Exposure Protocols

Contents Introduction ...... 4 Flowchart – First Aid and Medical Response Protocol for Human Blood and/or Tissues and MDRO Incidents ...... 6 Medical Surveillance for Primary Blood Products ...... 8 Human Immunodeficiency Virus (HIV);...... 8 Hepatitis B Virus (HBV); ...... 8 Hepatitis C Virus (BVC); ...... 8 Treponema pallidum ...... 8 Human T-Lymphotropic Virus (HTLV); ...... 12 Leptospira interrogans; ...... 12 Creutzfedlt-Jacob agent, Kuru agent ...... 12 Medical Surveillance Breast Milk ...... 15 Human Immunodeficiency Virus (HIV);...... 15 Human T-Lymphotropic Virus (HTLV); ...... 15 Cytomegalovirus (CMV); ...... 15 Creutzfedlt-Jacob agent, Kuru agent ...... 15 Medical Surveillance Inventory ...... 21 Group A (S. pyogenes); ...... 21 Staphylococcus intermedius; ...... 21 Staphylococcus hyicus; ...... 21 Streptococcus Group B (S. agalactiae) ...... 21 Streptococcus Group C (S. zooepidemicus, S. equi, and S. dysgalactiae); ...... 24 Streptococcus Group D;...... 24 Streptococcus pneumoniae; ...... 24 Candida albicans ...... 24 Listeria monocytogenes; ...... 29 Nocardia spp.; ...... 29 Streptococcus salivarius (S. viridans); ...... 29

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 1 of 92 Revised: January 26, 2017

Pseudomonas aeruginosa ...... 29 Proteus spp.; ...... 34 Bacillus cereus; ...... 34 Citrobacter diversus; ...... 34 Enterobacter spp. (E. cloacae, E. aerogenes) ...... 34 influenzae; ...... 39 Pasteurella sp.; ...... 39 spp.; ...... 39 Staphylococcus aureus (MRSA, MSSA, VISA, hVISA, VRSA) ...... 39 Bordatella bronchiseptica; ...... 46 Serratia sp.; ...... 46 Klebsiella spp.; ...... 46 Vancomycin-resistant Enterococci (VRE) ...... 46 Medical Surveillance Sewage Bacteria ...... 54 pneumophila; ...... 54 Mycobacterium spp.; ...... 54 Shigella spp.; ...... 54 ...... 54 (enterotoxigenic); ...... 59 Escherichia coli (uropathogenic); ...... 59 Escherichia coli (entero-hemorrhagic), ...... 59 Escherichia coli (septicemia causing) ...... 59 Staphylococcus aureus (MRSA, MSSA, VISA, hVISA, VRSA); ...... 62 Salmonella enterica spp.; ...... 62 Aeormonas hydrophilia; ...... 62 Campylobacter coli...... 62 difficile; ...... 69 Clostridium botulinum; ...... 69 Yersinia enteracolitica; ...... 69 ...... 69 Clostridium perfringens; ...... 76 Klebsiella spp.; ...... 76

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 2 of 92 Revised: January 26, 2017

Actineobacter spp...... 76 Medical Surveillance Sewage Viruses ...... 80 Norovirus; ...... 80 Adenovirus serotypes 1-5, and 7; ...... 80 Adenovirus serotypes 40 and 41; ...... 80 Hepatitis A Virus ...... 80 Hepatitis E Virus; ...... 84 Coxsackievirus; ...... 84 Human Rotavirus ...... 84 Medical Surveillance Sewage – Other ...... 88 Giardia lamblia; ...... 88 Cryptosporidum parvum; ...... 88 Schistosoma spp.; ...... 88 Naegleria fowleri ...... 88

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 3 of 92 Revised: January 26, 2017

Introduction

Within this binder are a list of some of the hazards you, or other researchers in this lab, could conceivably be exposed to during the course of your research. Please note that they are not listed alphabetically. This was done in order to facilitate simple adding and removal of organisms as required.

The lists and information within are not meant to be alarmist or to frighten. Rather, their purpose is to inform and help direct emergency responses to exposure events. Not every exposure will result in infection or illness. Some exposures will carry a higher risk of infection than others and this will be dependent on:

- the virulence of the organism(s) and/or nature of the material(s) in question; - how much is known about the organism(s) and or material(s) with which work is being carried out; - mode(s) of transmission; - route of exposure; - the required infectious dose of the pathogen(s) or suspected pathogen(s) in question, and if possible, an estimation as to whether or not that threshold was reached.

Deciding whether or not you are at risk for infection after an exposure is not up to you – a professional medical assessment is required to determine this. For this reason, regardless of perceived risk, in the event of any exposure with any of the materials that are contained in this binder, remain calm and follow the post-exposure protocols listed below:

1) Remove any contaminated PPE and personal effects immediately;

2) Evacuate yourself from the area in which the exposure took place;

3) Wash any potentially exposed skin/mucous membrane/hair areas thoroughly with soap and running water for 10 to 15 minutes;

4) Encourage bleeding if exposure involves a sharps injury or puncture and keep washing for a minimum of 15 minutes;

5) Yourself or someone else must inform your supervisor, senior laboratory staff, or the biosafety officer of the exposure;

6) Get immediate medical attention.

The flow chart on the following pages is to assist you and your supervisor (and your medical team – emergency room physician, family physician or public health office if required) in managing exposure risks and treatment methods following an exposure.

Please note that you MUST REPORT ANY AND ALL EXPOSURES.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 4 of 92 Revised: January 26, 2017

Reporting exposures and completing an incident report, allows us - collectively you, your supervisor, your colleagues, and the university community – to learn from the incident and possibly make policy or behavioral change requirements in order to prevent similar future incidents.

Another important reason for reporting exposures is to prevent exposure of other individuals following the incident. In other words, if an exposed person is infectious and does not know, or does know and is not instructed in the proper way to prevent infecting others, additional infectious events will not be prevented.

A third reason that illustrates why reporting an exposure is important, is that after an infectious exposure to many of the risks listed in this binder, serious signs or symptoms of infection may take weeks, months, or years to present themselves. If an exposure is not reported, not only may exposed individuals not get needed acute medical treatment, but they may also have more difficulty in the future, securing critical medical support if/when infection manifests itself symptomatically.

Any questions or concerns about the information within this binder can be directed to the TRU Biosafety Officer, Dr. Peter Fairman ([email protected]) and (250-320-5158).

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 5 of 92 Revised: January 26, 2017

Flowchart – First Aid and Medical Response Protocol for Human Blood and/or Tissues and MDRO Incidents

Immediately wash Contact Public Were materials tested to YES thoroughly with soap and Health Office be free of HIV, Hepatitis water for 5 minutes with NO and arrange for B, and Hepatitis C? repeated application of soap tetanus

NO while washing. booster, baseline Report incident to Minimal tissue amount Tetanus bloodwork, and and short contact time on supervisor and biosafety Booster in other follow- intact, healthy skin? office. last 10 years? YES ups. NO Complete incident form. Contact Public YES Mucous membrane Immediately flush affected Health Office to determine exposure? (eyes, nose, area(s) at an eyewash YES mouth) station for 10-15 minutes. when baseline blood work NO Immediately wash should be scheduled. Exposure in/on wound thoroughly with soap and water for 5 minutes with or chapped skin Seek emergency medical help YES gentle massage and immediately at Royal Inland OR repeated application of soap Hospital and tell them you have while washing. A larger splash and been exposed to human material contact time on intact If available, apply an at work. It is crucial to get skin? antiseptic. antiretroviral treatment within 2 NO hours of exposure. Get baseline bloodwork done. Assist supervisor in Cut or needlestick injury completion of Incident Report the incident to your with contaminated YES report and WorkSafe forms. supervisor. object? Contact your physician or Request attending medical staff TRU Health Services and to send information to TRU arrange for health Health Services or your family monitoring. physician.

Consult with TRU OSEM about prevention and outcome follow-up.

IMPORTANT:

NO MATTER YOUR COURSE OF ACTION Take the information sheets within this binder that corresponds with the organism(s) and/or material(s) to which you may have been exposed to the administering medical authorities.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 6 of 92 Revised: January 26, 2017

Pathogen identification, Mode of Transmission, Incubation Period, Period of Communicability, Infectious Dose, Typical Presenting Symptoms, Mode(s) of Decontamination, and Emergency Response:

Primary Blood Products

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 7 of 92 Revised: January 26, 2017

Medical Surveillance for Primary Blood Products Human Immunodeficiency Virus (HIV); Hepatitis B Virus (HBV); Hepatitis C Virus (BVC); Treponema pallidum

Pathogen Human Immunodeficiency virus Hepatitis B Virus (HBV) Hepatitis C Virus (HCV) Treponema pallidum Identification (HIV)

Mode(s) of HIV is transmitted either by exposure HBV is transmitted by percutaneous M ainly parenterally by T. pallidum is transmitted by Transmission to mucosa or parenterally via or mucosal exposure to infected contaminated needles and other percutaneous or mucosal exposure contaminated needles. blood or other body fluid. sharps. to infected blood or other body fluid.

Incubation Variable. Commonly the time from Usually 24-180 days (average 60-90 Ranges from 2 to 12 weeks. acquired via mucosal Period infection to the development of days). The variation depends on the exposure has an incubation of 10- detectable antibodies is generally 1 to amount of virus in the inoculum, 90 days, although it is usually 21 3 months; however, the time from HIV mode of transmission, and other host days. Secondary venereal syphilis infection to diagnosis of AIDS had an factors. usually arises 6 weeks to 6 months observed range of less than 1 year to post infection. Tertiary venereal 15 years or longer. syphilis has its onset months to years after initial infection. The primary stage of endemic syphilis arises approximately 2 to 4 weeks after inoculation. Secondary stage occurs 3 to 6 months post- inoculation and tertiary stage occurs as early as 6 months or as late as several years after initial symptoms. Period of Early after HIV infection and is All persons who are Hepatitis B All infected persons are If present in a blood sample, it may Communicability thought to last throughout the life of antibody positive are potentially potentially infectious. survive for as long as 120 hours at the infected individual. Infectiousness infectious, and blood can be 4°C. Otherwise it may not be is related to viral load. infectious for several weeks before viable, but caution must still be the onset of clinical symptoms. exercised. Infectious Dose(s) Unknown. Unknown. Unknown. 57 organisms by injection.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 8 of 92 Revised: January 26, 2017

Typical Acute infection is accompanied by Acute hepatitis B infection: Persons Acute HCV infection : If mucosal, acute infection can Presenting non-specific “flu-like” and with acute hepatitis B infection may Asymptomatic in most patients manifest as a painless and Symptoms “mononucleosis-like” symptoms such be asymptomatic or present with a (60-75%). The syndrome of regional . Acute as myalgia, arthralgia, diarrhoea, clinical picture varying from mild to acute hepatitis is often parenteral infection may be nausea, vomiting, headache, severe hepatitis. Persons with preceded or accompanied by asymptomatic Clinical

hepatosplenomegaly, weight loss, and symptomatic acute HBV infections symptoms of fatigue, myalgia, manifestations of the secondary neurological symptoms. can show signs and symptoms that low-grade fever, right upper stage include a symmetric Typically, when the patient’s CD4+ include nausea, abdominal pain, quadrant pain, nausea, maculopapular rash involving the T-cell count falls below 500 cells/µL, vomiting, fever, jaundice, dark urine, vomiting, jaundice, mild palms and soles, generalized syndromes indicative of depressed changes in stool colour, and hepatosplenomegaly, lymphadenopathy, fever, malaise, cell mediated immunity can appear. hepatomegaly or splenomegaly as maculopapular rash, and raised lesions (condylomata lata), Examples include orophayngeal and well as signs of liver dysfunction. arthralgia. These symptoms and alopecia. Tertiary syphilis may recurrent vulvovaginal candidiasis, Chronic hepatitis B infection: may last for 2 to 12 weeks. include gummatous syphillis where , recurrent or Defined as the persistence of Chronic HCV gummatous lesions may form on multidermatomal herpes zoster, Hepatitis B antibodies for more than infection: malaise, nausea, any organ or tissue, cardiovascular , infections due 6 months. Persons with chronic HBV abdominal pain and pruritis. syphilis, which usually manifests as to Rhodococcus equi, pelvic infection may be asymptomatic or Fluctuating alanine transferase aortic disease and neurosyphillis. inflammatory disease, oral hairy may suffer from symptoms such as levels are characteristic. The Neurosyphilis can manifest as acute leukoplakia associated with Epstein- fatigue, anorexia, nausea, abdominal late sequelae of chronic HCV syphilitic meningitis, Barr virus, cervical dysplasia, long discomfort and liver dysfunction. infection include serious health meningovascular syphilis or as lasting diarrhoea, idiopathic They are at substantially increased consequences such as chronic paresis or tabes doraslis. thrombocytopenic purpura, and risk for developing chronic liver hepatitis, cirrhosis, and peripheral neuropathy. Late-stage diseases, including cirrhosis of the hepatocellular carcinoma. If disease refers to the period when the liver and primary hepatocellular cirrhosis develops, patients patient’s CD4+ T-cell count falls carcinoma. may experience jaundice, below 200 cells/µL. The loss of the splenomegaly, ascites, integrity of cell-mediated immune oesophageal varices, and responses allows ubiquitous hepatic encephalopathy. environmental organisms with limited Extrahepatic manifestations are virulence to become life threatening uncommon but may include pathogens. Examples of conditions (as mixed essential cryo- set out by the US Centers for Disease globulinaemia, membranous or Control and Prevention) include membrano-proliferative candidiasis of bronchi, , lungs glomerulo-nephritis, non- or oesophagus, invasive cervical Hodgkin’s lymphoma, cancer, coccidioidomycosis, Sjorgren’s syndrome, lichen cryptococcosis, cryptosporidiosis, planus, and porphyria cutanea cytomegalovirus disease (other than tarda. liver, spleen, or nodes), cytomegalovirus retinitis (with loss of vision), HIV-related encephalopathy, herpes simplex, histoplasmosis, isosporiasis, Kaposi’s sarcoma,

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 9 of 92 Revised: January 26, 2017

Burkitt’s lymphoma, immunoblastic lymphoma, primary lymphoma of the brain, Myco-bacterium avium complex, Myco-bacterium tuberculosis, Pneumocystis jirovecii , recurrent pneumonia, progressive multifocal leukoencephalopathy, recurrent salmonella septicaemia, toxoplasmosis of the brain, and wasting syndrome due to HIV. Mode(s) of HIV is susceptible to fresh 2% Treatment of HBV diluted in HCV RNA is readily degraded Susceptible to 70% ethanol, 2% Decontamination glutaraldehyde, 2% Jodopax (detergent phosphate buffered saline with 1% by 2% glutaraldehyde when glutaraldehyde, 1% sodium and iodine), hypochlorite, iodine, non-ionic detergent (Triton X-100) added to biological samples at hypochlorite. phenolics, and to a lesser extent 70% plus 0.3% tri-n-butyl-phosphate leads 37°C, and soaking laboratory ethanol, NaOH, isopropanol, and to HBV inactivation. HBV is also equipment in 3%

Ultraviolet (UV) light. inactivated by formaldehyde, glutaraldehyde is effective at glutaraldehyde, sodium hypochlorite limiting HCV transmission. (5,000 ppm available chlorine), Phenolic compounds (0.4 to quaternary ammonium compounds, 3%) are effective at inhibiting and alcohols (70-80%). Moist heat at HCV binding and infectivity in 98°C for 1 minute will partially VERO cell cultures. inactivate HBV in a 1:10 serum Furthermore, treatment of HCV dilution. Incubation at 60°C for 10 diluted in phosphate buffered hours (pasteurisation) will also saline with 1% non-ionic inactivate HVB. detergent (Triton X-100) plus 0.3% tri-n-butyl-phosphate leads to inactivation. Also pasteurization is effective. Emergency If exposure is suspected wash area Following exposure to HBV the If exposure is suspected, If exposure is suspected, suspected Response thoroughly and encourage bleeding if, affected area should be washed suspected wash area thoroughly wash area thoroughly and sharps or puncture injury. Emergency immediately with soap and water. and encourage bleeding if, encourage bleeding if, sharps or post-exposure prophylaxis (PEP) must Seek emergency medial attention. sharps or puncture injury. Seek puncture injury. Seek emergency be sought immediately and initiated Mucous membranes and conjunctivae emergency medical attention. medical attention. Medical

within 72 hours of the suspected should be irrigated thoroughly with Medical surveillance is surveillance is recommended. exposure event. HIV postexposure water. If the material involved is recommended before initiating Penicillin provides the most prophylaxis regimens are based on the known to contain HBV or be positive any HCV treatment. There is effective treatment for all stages of nature of the exposure. The majority of for Hepatitis B antibodies then no demonstrated benefit disease cause by Treponema HIV exposures will warrant a two drug hepatitis B immunoglobulin (HBIG) associated with rapid PEP and pallidum. Those who are allergic to regimen, using 2 NRTIs or 1 NRTI and should be given, ideally within 48 HCV. If HCV exposure is penicillin can take tetracycline, 1 NtRTI. Combinations include: hours of exposure. Seven drugs are suspected, an HCV RNA doxycycline, or erythromycin. zidovudine (ZDV) and lamivudine licensed in the United States for antibody test will be carried out Ceftriaxone may be considered as (3CT) or emtricitabine (FTC); treatment of HBV infection: shortly after exposure and then an alternative for treatment of early stavudine (d4T) and 3TC or FTC; and interferon-α, pegylated interferon α- again after 12 weeks. If syphilis in pregnancy.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 10 of 92 Revised: January 26, 2017

tenofovir (TDF) and 3TC or FTC. The 2a, lamivudine, adefovir, entecavir, observed to be positive, Chloramphenicol may also be used addition of a third or fourth drug telbivudine, and tenofovir. Previously treatment may be utilized and to treat neurosyphilis. should be considered for exposures unimmunised adults exposed to may consist of mono-therapy that pose an increased risk of HBsAg positive blood should receive with pegylated interferon transmission. The preferred drugs in HBIG as soon as possible as well as (addition of polyethylene this case are proteinase inhibitors such immunization with HB vaccine unless glycol to interferon-α) and as lopinavir/ritonavir (LPV/RTV). natural immunity can be confirmed. combined therapy of pegylated Two types of HB vaccine have been interferon with ribavirin, or licensed and shown to be highly standard interferon with effective against all subtypes of HBV. ribavirin, are common methods The first, prepared from plasma from of treating HCV infection. HBsAg-positive persons, is still widely used. The second is synthesised using recombinant DNA.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 11 of 92 Revised: January 26, 2017

Primary Blood Products - continued

Human T-Lymphotropic Virus (HTLV); Leptospira interrogans; Creutzfedlt-Jacob agent, Kuru agent

Pathogen Human T-Lymphotropic Virus (HTLV) Leptospira interrogans Creutzfedlt-Jacob agent, Kuru agent Identification

Mode(s) of Infections can occur from blood and mucosal Direct contact with infected urine or tissues; The mode of transmission of most cases is Transmission exposure. occasionally through ingestion of contaminated food unknown. or by inhalation of droplet aerosols of contaminated fluids.

Incubation Unknown. Usually 10 days with a range of 4-19 days. 15 months to 2 years. Period

Period of Unknown. Human-to-human transmission is possible. Direct transmission from person to person is rare; CNS and other tissues are infectious throughout Communicability leptospires may be excreted in urine for usually 1 symptomatic illness; lymphoid and other organs month but has been observed as long as 11 months probably infectious before signs of illness appear. after the acute illness. Infectious Dose(s) Unknown. Unknown. Unknown.

Typical Acute HTLV Fever, headache, chills, severe malaise, vomiting, Insidious onset of confusion, progressive dementia, Presenting infection is rarely suspected or diagnosed. Adult T- myalgia and conjunctival suffusion; occasionally myoclonic jerks with spasticity, wasting and coma; Symptoms cell leukemia or lymphoma (ATLL) occurs in 1-2% meningitis, rash and uveitis; sometimes jaundice, slight elevation of CSF proteins; death usually of those infected. Symptoms present 20-30 years after renal insufficiency, anemia and hemorrhage of the occurs in less than 1 year. CNS disease with infection. Of those who develop ATLL, more than skin; clinical illness lasts 3 days to few weeks, often cerebellar ataxia, incoordination, tremors, rigidity,

two thirds develop leukemia while the remainder biphasic; may have asymptomatic infection; low case progressive wasting and death within 3-9 months. develop lymphoma. Prognosis is approximately 1 fatality rate but increases with age. year after development of ATLL. ATLL has five types: asymptomatic, pre-leukemic, chronic/smouldering, lymphoma, and acute. The smouldering type presents with skin lesions and involvement of the bone marrow. The chronic stage is associated with elevated circulating leukemic cells and usually progresses to the acute type within two

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 12 of 92 Revised: January 26, 2017

years. The acute phase is an aggressive form of leukemia and is accompanied by hypocalcaemia, elevated lactate dehydrogenase (LDH), skin lesions, lymphadenopathy, lymphomatous meningitis, lytic bone lesions, spleen or liver involvement and immune-deficiency. HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) has a shorter latency period than ATLL. HAM/TSP is a progressive and chronic myelopathy, with preferential damage to the thoracic spinal cord. Symptoms include muscle weakness of lower limbs, hyperreflexia, sphincter disorders, impotence, sensory disturbances and lower back pain. Mode(s) of Susceptible to 1% sodium hypochlorite, 2% Susceptible to 1% sodium hypochlorite, 70% ethanol, Resistance to commonly used disinfectants is well Decontamination glutaraldehyde, 4% chlorhexidine, 70% ethanol, 0.3% glutaraldehyde, formaldehyde. Sensitive to moist heat recognized: formaldehyde, glutaraldehyde, ethanol, hydrogen peroxide, iodophores, phenolics, and (121° C for at least 15 min). and iodine. Immersion in undiluted bleach (60,000 quaternary ammonium compounds. Can be ppm available chlorine) for 1 hour is only partially inactivated by steam sterilization at 121ºC for a effective. Disinfection should be carried out using

minimum of 15 minutes and UV light. 1N sodium hydroxide at room temperature for 1 hour (shorter treatments have occasionally not inactivated the pathogen). Resistant to ultraviolet and ionizing radiation, ultrasonication, nucleases, boiling, heat; autoclaving - 15 to 30 min at 121°C or 132°C will not effectively inactivate pathogen, 1 hour at 132°C is recommended). Contaminated electrodes stored in ethanol-formalin for several years were found to cause CJD in chimpanzee. Emergency If exposure is suspected, wash area thoroughly and If exposure is suspected, wash area thoroughly and If exposure is suspected, wash area thoroughly with Response encourage bleeding if, sharps or puncture injury. Seek encourage bleeding if, sharps or puncture injury. Seek NaOH and encourage bleeding if, sharps or emergency medical attention. No established therapy. emergency medical attention. Monitor for symptoms puncture injury. Seek emergency medical attention. Combination therapy of Zidovudine (AZT) and of illness; confirm serologically; isolation of Monitor for symptoms of illness - clinical signs - interferon alpha (INF-α) is used with some success to leptospires from blood, CSF or urine. Doxycycline diagnosis based on EEG, histopathological

improve prognosis. treatment within 4 days of onset, combination of findings, transmission to animals from tissue amoxycillin and erythromycin can be effective; samples from suspected specimens. resistant to penicillin prophylaxis.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 13 of 92 Revised: January 26, 2017

Pathogen identification, Mode of Transmission, Incubation Period, Period of Communicability, Infectious Dose, Typical Presenting Symptoms, Mode(s) of Decontamination, and Emergency Response:

Primary Breast Milk

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 14 of 92 Revised: January 26, 2017

Medical Surveillance Breast Milk Human Immunodeficiency Virus (HIV); Human T-Lymphotropic Virus (HTLV); Cytomegalovirus (CMV); Creutzfedlt-Jacob agent, Kuru agent

Pathogen Human Immunodeficiency Virus Human T-Lymphotropic Virus Cytomegalovirus (CMV) Creutzfedlt-Jacob agent, Kuru Identification (HIV) (HTLV) agent

Mode(s) of HIV is transmitted either by exposure Lab acquired infections have been Inhalation of concentrated The mode of transmission of most Transmission to mucosa or parenterally via reported and Infections can occur aerosolized materials, droplet cases is unknown. Accidental contaminated needles. Blood, semen, from mucosal exposure as well as exposure of mucous parenteral inoculation; risk of vaginal secretions, cerebrospinal fluid, accidental parenteral inoculation. membranes of the eyes, nose, infection from aerosols, droplets, synovial fluid, peritoneal fluid, pleural Blood samples and bodily fluids or mouth, ingestion, and exposure of intact skin, gastric

fluid, pericardial fluid, amniotic fluid, (i.e. CSF, breast milk, blood etc.) are accidental parenteral and mucous membranes is not other specimens containing visible potential sources of HTLV. inoculation are the primary known. No documented laboratory- blood, breast milk, unscreened or hazards associated with associated infections with inadequately treated blood products, herpes viruses including spongiform encephalopathies and infected human tissues are all Cytomegalovirus. No lab however, consequences of infection potential sources of HIV. acquired infections have been are grave. Infections have been reported. Urine, blood, breast observed via blood, CSF, and breast milk, tears, stool, semen, milk in animal studies. respiratory secretions (nasopharyngeal secretions, saliva, throat washings, and bronchoalveolar lavage fluid) and cervical secretions are all potential sources of CMV infection. Incubation Variable. Commonly the time from Unknown. Worldwide - Cytomegalovirus 15 months to 2 years. Period infection to the development of (CMV) is a universally detectable antibodies is generally 1 to distributed pathogen with 3 months; however, the time from HIV approximately 40-100% of the infection to diagnosis of AIDS had an world's population having observed range of less than 1 year to CMV antibody present in 15 years or longer. blood as evidence of infection. Incubation period is generally 1-4 months post- CMV infection.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 15 of 92 Revised: January 26, 2017

Period of Early after HIV infection and is Unknown period of communicability, CMV virus can persist in CNS and other tissues are infectious Communicability thought to last throughout the life of but, human-to-human transmission is body fluids such as urine, throughout symptomatic illness; the infected individual. Infectiousness possible. saliva, and seminal fluids for lymphoid and other organs probably is related to viral load. many years, or can remain infectious before signs of illness dormant until reactivation of appear. latent infection. Transmission occurs through direct contact with body fluids from symptomatic or asymptomatic persons excreting the virus, thus infection may be transmitted between humans and from adults to children through childbirth and breastfeeding. Infectious Dose(s) Unknown Unknown. Unknown Unknown.

Typical Acute infection is accompanied by HTLV-1 primarily causes adult T-cell CMV infection is common Insidious onset of confusion, Presenting non-specific “flu-like” and leukemia/ and usually asymptomatic in progressive dementia, myoclonic Symptoms “mononucleosis-like” symptoms such lymphoma and topical spastic healthy children and adults, jerks with spasticity, wasting and as myalgia, arthralgia, diarrhoea, parapareis/HTLV-1 associated but can cause severe disease coma; slight elevation of CSF nausea, vomiting, headache, hepato- myelopathy. It also causes uveitis, in newborns and immuno- proteins; death usually occurs in less

splenomegaly, weight loss, and infective dermatitis and compromised children or than 1 year. CNS disease with neurological symptoms. lymphadenitis. adults. CMV is the most cerebellar ataxia, incoordination, Typically, when the patient’s CD4+ T- HTLV-2 is a less pathogenic strain common cause of congenital tremors, rigidity, progressive cell count falls below 500 cells/µL, and has been associated with milder infection, affecting 0.2-2.4% wasting and death within 3-9 syndromes indicative of depressed cell neurological disorders and chronic of all infants, and also of months. mediated immunity can appear. pulmonary infections. HTLV-3 viral-based mental retardation Examples include oropharyngeal and and HTLV-4 have not been and hearing deficit in children recurrent vulvovaginal candidiasis, associated with specific illnesses. of developing countries. bacillary angiomatosis, recurrent or Acute HTLV Infections are often recurrent, multidermatomal herpes zoster, infection is rarely suspected or caused by reactivation of listeriosis, infections due diagnosed. Adult T-cell leukemia or latent virus (especially in to Rhodococcus equi, pelvic lymphoma (ATLL) occurs in 1-2% of immunocompromised patients inflammatory disease, oral hairy those infected. Symptoms present 20- such as bone marrow or other leukoplakia associated with Epstein- 30 years after infection. Of those who transplant recipients), Barr virus, cervical dysplasia, long develop ATLL, more than two thirds reinfection may also occur lasting diarrhoea, idiopathic develop leukemia while the due to the antigenic diversity thrombocytopenic purpura, and remainder develop lymphoma. of the virus. Infection may peripheral neuropathy. Late-stage Prognosis is approximately 1 year cause a mononucleosis-like- disease refers to the period when the after development of ATLL. syndrome with prolonged patient’s CD4+ T-cell count falls ATLL has five types: asymptomatic, fever (lasting 2-3 weeks),

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 16 of 92 Revised: January 26, 2017

below 200 cells/µL. The loss of the pre-leukemic, chronic/smouldering, malaise, atypical integrity of cell-mediated immune lymphoma, and acute. The lymphocytosis, cervical responses allows ubiquitous smouldering type presents with skin lymphadenitis, mild hepatitis, environmental organisms with limited lesions and involvement of the bone and encephalitis. Both virulence to become life threatening marrow. The chronic stage is primary CMV infection, or pathogens. Examples of conditions (as associated with elevated circulating reactivation can cause serious set out by the US Centers for Disease leukemic cells and usually progresses illness in immuno-suppressed Control and Prevention) include to the acute type within two years. patients (for example patients candidiasis of bronchi, trachea, lungs The acute phase is an aggressive form with AIDS, patients with or oesophagus, invasive cervical of leukemia and is accompanied by leukemia or lymphoma who cancer, coccidioidomycosis, hypocalcaemia, elevated lactate are receiving chemotherapy, cryptococcosis, cryptosporidiosis, dehydrogenase (LDH), skin lesions, and recipients of organ cytomegalovirus disease (other than lymphadeno-pathy, lymphomatous transplants on immuno- liver, spleen, or nodes), meningitis, lytic bone lesions, spleen suppressive therapy). The cytomegalovirus retinitis (with loss of or liver involvement and immune- major symptoms of the vision), HIV-related encephalopathy, deficiency. HTLV-1-associated disease in organ transplant herpes simplex, histoplasmosis, myelopathy/tropical spastic recipients include fever, isosporiasis, Kaposi’s sarcoma, paraparesis (HAM/TSP) has a shorter myalgia, malaise, arthralgia, Burkitt’s lymphoma, immunoblastic latency period leucopenia, thrombo- lymphoma, primary lymphoma of the than ATLL. HAM/TSP is a cytopenia, and hepatitis. brain, Myco-bacterium progressive and chronic myelopathy, , caused by CMV avium complex, with preferential damage to the infection in bone marrow Myco-bacterium tuberculosis, thoracic spinal cord. Symptoms transplant recipients is Pneumocystis jirovecii pneumonia, include muscle weakness of lower associated with significant recurrent pneumonia, progressive limbs, hyperreflexia, sphincter morbidity and mortality (50- multifocal leuko-encephalopathy, disorders, impotence, sensory 90%). CMV infection recurrent salmonella septicaemia, disturbances and lower back pain. in HIV patients may spread to toxoplasmosis of the brain, and visceral organs, resulting in wasting syndrome due to HIV. chorioretinitis, gastrointestinal infections (esophagitis, gastritis, and ulcerative colitis), polyradiculo- myelopathy, and neurological disorders. Mode(s) of HIV is susceptible to fresh 2% Susceptible to 1% sodium Cytomegalovirus has been Resistance to commonly used Decontamination glutaraldehyde, 2% Jodopax (detergent hypochlorite, 2% glutaraldehyde, 4% shown to be susceptible to disinfectants is well recognized: and iodine), hypochlorite, iodine, chlorhexidine, 70% ethanol, 0.3% 7.5% povidone-iodine. formaldehyde, glutaraldehyde, phenolics, and to a lesser extent 70% hydrogen peroxide, iodophores, Although not much ethanol, and iodine. Immersion in ethanol, NaOH, isopropanol, and phenolics, and quaternary ammonium information is available on undiluted bleach (60,000 ppm

Ultraviolet (UV) light. HIV can remain compounds. Can be inactivated by disinfectants specific for available chlorine) for 1 hour is only viable in blood in syringes at room steam sterilization at 121°C for a CMV, most herpes viruses are partially effective. Disinfection temperature for 42 days, and in blood minimum of 15 minutes and UV susceptible to 30% ethanol should be carried out using 1N and cerebrospinal fluid from autopsies and isopropanol, 1% sodium sodium hydroxide at room

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 17 of 92 Revised: January 26, 2017

for up to 11 days. Although drying in light. HTLV-1 and HTLV-2 can hypochlorite, formaldehyde, temperature for 1 hour (shorter the environment is known to cause a survive in stored blood for 8-9 days. 0.12% ortho- phenylphenol, treatments have occasionally not rapid reduction in HIV concentration, and 0.04% glutaraldehyde. inactivated the pathogen). Resistant under experimental conditions, Cell- Inactivated by heat (56 °C for to ultraviolet and ionizing radiation, free HIV dried onto a glass coverslip 30 min), low pH, UV light, ultrasonication, nucleases, boiling, in 10% serum can survive for longer cycles of freezing/thawing. heat; autoclaving - 15 to 30 min at than 7 days, depending on the initial Cytomegalovirus can survive 121°C or 132°C will not effectively titre. on dry inanimate surfaces inactivate pathogen, 1 hour at 132°C (persistence varies from only is recommended). Contaminated a few hours up to 7 days); electrodes stored in ethanol-formalin blanket for 2 hours; plexiglass for several years were found to for 4-8 hours. cause CJD in chimpanzee. Emergency If exposure is suspected wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash area Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding if, area thoroughly and thoroughly with NaOH and sharps or puncture injury. Emergency sharps or puncture injury. Seek encourage bleeding if, sharps encourage bleeding if, sharps or post-exposure prophylaxis (PEP) must emergency medical attention. No or puncture injury. Since puncture injury. Seek emergency be sought immediately and initiated established therapy available. CMV infection resolves medical attention. Monitor for

within 72 hours of the suspected Monitor for symptoms. HTLV is spontaneously in normal symptoms of illness - clinical signs - exposure event. HIV postexposure detected in blood serum by healthy patients, antiviral diagnosis based on EEG, prophylaxis regimens are based on the identifying antibodies using ELISA. treatment is not usually histopathological findings, nature of the exposure. The majority of Other methods of detection include recommended. If exposed transmission to animals from tissue HIV exposures will warrant a two drug particle agglutination assays and individual is chronically samples from suspected specimens. regimen, using 2 NRTIs or 1 NRTI and Western Blotting. For the immuno-compromised, 1 NtRTI. Combinations include: identification of specific viral Intravenous ganciclovir or zidovudine (ZDV) and lamivudine sequences, PCR is used. Limited oral valganciclovir are the (3CT) or emtricitabine (FTC); therapy is available for HTLV first line drugs for therapy for stavudine (d4T) and 3TC or FTC; and infections. ATL treated with CMV infection. Intravenous tenofovir (TDF) and 3TC or FTC. The chemotherapy. Zidovudine (AZT) cidofovir and foscarnet are addition of a third or fourth drug and alpha interferon have shown used as alternatives. Once should be considered for exposures some response and improved the symptomatic improvement that pose an increased risk of ATL prognosis. Other treatments are has been achieved, these transmission. The preferred drugs in currently under investigation drugs can also be used for this case are proteinase inhibitors such including arsenic, trioxide, chronic maintenance therapy as lopinavir/ritonavir (LPV/RTV). proteasome inhibitors, retenoids, in patients with CMV retinitis There is no available vaccine for HIV angiogenesis inhibitors and cellular or neurological disease. No infection. immunotherapy. Antiretroviral vaccine is licensed for treatments using lamivudine and high prevention of cytomegalovirus dose interferon alpha and interferon infection. beta is used for HTLV-1-associated myelopathy/tropical spastic parparesis. Uveitis is treated with topical and systemic corticoids to improve sight. Infective dermatitis is

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 18 of 92 Revised: January 26, 2017

treated with antibiotics. There is no available vaccine for HTLV 1 or 2.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 19 of 92 Revised: January 26, 2017

Pathogen identification, Mode of Transmission, Incubation Period, Period of Communicability, Infectious Dose, Typical Presenting Symptoms, Mode(s) of Decontamination, and Emergency Response:

Laboratory Bacterial Inventory – Bacteria

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 20 of 92 Revised: January 26, 2017

Medical Surveillance Inventory Bacteria Streptococcus Group A (S. pyogenes); Staphylococcus intermedius; Staphylococcus hyicus; Streptococcus Group B (S. agalactiae)

Pathogen Streptococcus Group A (S. pyogenes) Staphylococcus intermedius Staphylococcus hyicus Streptococcus Group B Identification (S.agalactiae)

Mode(s) of Transmission via respiratory droplets, Inhalation of infectious aerosols, C ontamination of Transmission is possible through Transmission hand contact with nasal discharge and contamination of mucocutaneous mucocutaneous lesions, and contact with contaminated objects skin contact with lesions are lesions, and accidental inoculation are accidental inoculation are the and/or surfaces. Accidental the most important modes of the primary hazards associated with primary hazards associated parenteral inoculation, ingestion, transmission. The pathogen can be working with this pathogen. Direct with working with this inhalation of infectious aerosols and

found in its carrier state in the anus, contact with infectious material and pathogen. Contact between direct contact are the primary vagina, skin and and contact objects may also be a source of exposed intact and inflamed hazards when working with this with these surfaces can spread the transmission. skin and infectious material pathogen. Streptococcus infection. and contaminated objects can agalactiae has been isolated from Inhalation of infectious aerosols and also be a source of blood, cerebrospinal fluid, joint contamination of mucocutaneous transmission. fluid, peritoneal fluid, pleural fluid, lesions are the primary laboratory bone, vaginal, throat and rectal hazards associated with working with cultures, aerosols and feces. This this pathogen. The bacterium can bacterium has been found to survive survive on a dry surface for 3 days to months in dry dust in buildings. 6.5 months. is usually because of contamination of skin lesions or wounds with the infectious agent. Incubation Usually 1 to 3 days. Variable and indefinite, however Unknown due to lack of Unknown. Period most commonly incubation is 4-10 available data. days. Period of If untreated, patients with streptococcal As long as a purulent lesion is present Unknown due to lack of Variable and indefinite in some Communicability are infective during the or as long as the carrier state exists. available data. cases as symptom-free humans carry acute phase of the illness, usually 7-10 the pathogen in their throat, days, and for one week afterwards; genitourinary tract and their rectum. however, if antibiotics are used, the infective period is reduced to 24 hours. The bacterium can remain in the body in its carrier state without causing

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 21 of 92 Revised: January 26, 2017

illness in the host for weeks or months and is transmissible in this state. Infectious Dose(s) Unknown Unknown. Unknown in humans. Unknown.

Typical This bacterium is responsible for a This bacterium is responsible for a This bacterium is responsible Infection symptoms depend on the Presenting wide array of infections. It can cause wide array of infections. It may cause for a wide array of infections. part of the body that is infected. Symptoms streptococcal sore throat which is fever, tissue inflammation, tissue It has been implicated as a Bacteremia and sepsis can manifest characterized by fever, enlarged swelling (edema), purulent skin causative agent in toxic shock as fever, chills, and low alertness. tonsils, tonsillar exudate, sensitive infections, skin , , syndrome, cellulitis, Pulmonary infections can present as

cervical lymph nodes and malaise. If wound infections, nail bed infections, bacteremia, septicemia, and pneumonia, the symptoms of which untreated, strep throat can last 7-10 gastroenteritis, bacteremia, otitis, spondylodiscitis. Based on can include: fever and chills, cough, days. (pink-red rash and septic arthritis, endocarditis, , animal models, it may also rapid breathing or difficulty fever) as well as impetigo (infection of mastoiditis, pneumonia, meningitis, cause vomiting, purulent skin breathing, and chest pain. Skin and the superficial layers of skin) and and brain abscesses. S. intermedius infection, and wound soft tissue can manifest as swelling, pneumonia are also caused by this also produces exotoxins, which if infection. Symptoms may redness, pain, and elevated bacterium. Septicaemia, otitis media, ingested, can cause symptoms similar vary and S. hyicus infection temperature. Infected areas may also mastitis, cellulitis, , myositis, to that of food-poisoning including has been mistaken as acute S. be full of pus or other drainage. If osteomyelitis, septic arthritis, abdominal cramping, diarrhea, aureus infection. the infection involves bones or meningitis, endocarditis, pericarditis, vomiting, loss of appetite, fever, joints, it may present as fever, chills, and neonatal infections are all less weakness, nausea, and headaches. swelling and stiffness that prevents common infections due to S. pyogenes. normal joint range of motion. Streptococcal , acute rheumatic fever (joint inflammation, carditis and CNS complications), post-streptococcal glomerulonephritis (inflammation, hematuriia, fever, edema, hypertension, urinary sediment abnormalties and severe kidney pain) and necrotizing fasciitis (rapid and progressive infection of subcutaneous tissue, massive systematic inflammation, hemorrhagic bullae, crepitus and tissue destruction) are some of the more serious complications involving S.pyogenes infections. Mode(s) of Susceptible to 1% sodium Susceptible to 4% chlorhexidine in 10% sodium hypochlorite Susceptible to 2-5% phenol, 1% Decontamination hypochlorite, 4% formaldehyde, 2% 70% ethanol, 6.5% sodium solution. Bacteria are sodium hypochlorite, 4% glutaraldehyde, 70% ethanol, 70% hypochlorite, 0.3% stabilized susceptible to moist heat formaldehyde, 2% glutaraldehyde, propanol, 2% peracetic acid, 3-6% glutaraldehyde in 70% ethanol, 0.3% (121°C for at least 15 70% ethanol, 70% propanol, 2% hydrogen peroxide and 0.16% iodine. stabilized glutaraldehyde in distilled peracetic acid, 3-6% hydrogen

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 22 of 92 Revised: January 26, 2017

Bacteria are susceptible to moist heat water, and 1% formaldehyde minutes) and dry heat (170°C peroxide, and iodine. Sensitive to (121°C for at least 15 minutes) and dry solutions. Bacteria are susceptible to for at least 1 hour). moist heat at 55°C for 30 minutes. heat (170°C for at least 1 hour). The moist heat (121°C for at least 15 Bacteria are also susceptible to bacterium can survive on a dry surface minutes) and dry heat (170°C for at moist heat (121°C for at least 15 for 3 days to 6.5 months. least 1 hour). minutes) and dry heat (160-170°C for at least 1 hour). Fecal streptococci can be inactivated by ozone. This bacterium has been found to survive months in dry dust in buildings. Emergency If exposure is suspected wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash area Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding if, area thoroughly and thoroughly and encourage bleeding sharps or puncture injury. Seek sharps or puncture injury. Seek encourage bleeding if, sharps if, sharps or puncture injury. Seek emergency medical attention. Monitor emergency medical attention. or puncture injury. Seek emergency medical attention. for symptoms. Confirm infection by Infections with this bacterium are emergency medical attention. Monitor for symptoms and confirm

bacteriological and serological testing, often mistaken as S. aureus Infections with this bacterium by culture of blood or CSF. latex bead agglutination, fluorescent infections. It can be differentiated via can be mistaken as S. aureus Serology can be used to determine antibody staining or ELISA. a negative or weak maltose test, a infections. It can often be the Lancefield group. Susceptible to Appropriate antibiotic treatment is positive arylamidase test, delayed reliably differentiated and penicillin or a combination of necessary for a S. pyogenes infection. mannitol fermentation, via identified via 16S rRNA or ampicillin and an Penicillin is used for Polymerase Chain Reaction nuc gene analysis. Penicillin aminoglycoside. Streptococcus infections (pharyngitis) and macrolides identification, Ribotyping, Pulse-field has been observed to be an agalactiae is also sensitive to or lincosamides are used if there are gel electrophoresis, Pyrolysis-mass effective antibiotic in S. vancomycin, , allergies. Clindamycin may be used in spectrometry, Multilocus enzyme hyicus infection treatment. clindamycin, erythromycin, cases of necrotizing fasciitis and electrophoresis. Some antibiotic cotrimoxazole, and ceftriaxone. It is surgical debridement of the affected resistance has been also observed in generally resistant to macrolides and area is necessary. S. some clinical settings. Many clindamycin resistance has also pyogenes infections are susceptible to a Staphylococcus species are β-lactam occurred. No vaccine is currently variety of drugs: β-lactams such as resistant and therefore the use of available for S. agalactiae. penicillin, as well as erythromycin, penicillins, ampicillin, and clindamycin, imipenem, rifampin, amoxicillin, which are all β-lactam vanomycin, macrolides and antibiotics in a clinical setting may lincomycin; however, certain strains of not be effective. Resistance to the bacterium have been found to tetracycline, streptomycin, and resistant to macrolides, lincomycin, methicillin has also been observed. chloramphenicol, tetracyclines and cotrimoxazole.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 23 of 92 Revised: January 26, 2017

Medical Surveillance Inventory – Bacteria (cont)

Streptococcus Group C (S. zooepidemicus, S. equi, and S. dysgalactiae); Streptococcus Group D; Streptococcus pneumoniae; Candida albicans

Pathogen Streptococcus Group C (S. Streptococcus Group D Streptococcus Candida albicans Identification zooepidemicus, S. equi, and S. pneumoniae dysgalactiae) Mode(s) of Inhalation of infectious aerosols, Inhalation of infectious aerosols, I nfectious cells can be Most infections result from the Transmission accidental parenteral inoculation, and contamination of mucocutaneous disseminated via microaerosol patient’s own flora, rather than from contamination of mucocutaneous lesions, and accidental inoculation are droplets created by coughing cross infection. Although rare, lesions are the primary hazards the primary hazards associated with or sneezing, or person-person nosocomial transmission has also associated with working with this working with this pathogen. Direct oral contact can also facilitate been reported to occur from

pathogen. Direct contact with contact with infectious persons, infection. Person to person inanimate surface, from hands of infectious persons, materials, and materials, and objects can also transmission is common, but health care workers or between objects can also facilitate transmission facilitate transmission. Blood, urine, infection is infrequent as patients. In laboratories, the primary wound samples, and feces are all healthy individuals carry S. hazards are skin contact with potential carriers of this bacterium. In pneumoniae contaminated personnel, surfaces, and addition, Enterococci can grow and in the nasopharyngeal region cultures. Also through accidental survive in harsh environments, and without any presence of parenteral inoculation and trauma of can persist almost anywhere infection. Sputum, nasal or cutaneous barrier. Epithelial including soil, plants, water, and throat swabs, blood, scrapings, lesion exudates, sputum, food. Can survive 5 days to 4 months cerebrospinal fluids, and brochoalveolar lavage, and blood can on dry inanimate surfaces. respiratory secretions can all all be infectious. C. albicans can be infectious. Primary survive on inanimate surfaces for 24 laboratory hazards include: hours to 120 days, and on palms for accidental inhalation of about 45 minutes. C. albicans has aerosols containing bacterial been isolated from bed-sheets, cots, cells, accidental inoculation, and wash-basins of nurseries, and it direct mucous-to-person has also been found to be able to contact. Streptococcus spp. survive and grow in distilled water at can survive in dental plaque room temperature. The fungus can for up to 7 days, in dust for up survive on drying in darkness for 5 to 20 days, on glass for 1 – 11 hours, and 1 hour if also exposed to days, and up to 180 days in light. frozen fish. Incubation Unknown. Unknown. Unknown, but speculated to Unknown. Period be 1 to 3 days.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 24 of 92 Revised: January 26, 2017

Period of If untreated, patients with streptococcal Unknown, but likely for as long as In humans, these bacteria are Although rare, person to person Communicability pharyngitis are infective during the persistence of infection or symptoms, often located in the upper transmission can occur. acute phase of the illness, usually 7-10 but symptoms not required. respiratory tracts of healthy days, and for one week afterwards; individuals where they however, if antibiotics are used, the colonize and multiply. infective period is reduced to 24 hours. Communicable period is The bacterium can remain in the body therefore variable. May be in its carrier state without causing communicable via coughing illness in the host for weeks or months or sneezing, likely for as long and is transmissible in this state. as persistence of infection or symptoms, but symptoms not required. Infectious Dose(s) Unknown Unknown. Unknown for humans. Mice Unknown. developed sepsis or pneumonia when infected with 107 or 108 cfu, and after infection with 104 bacteria, S. pneumoniae are able to cross the blood-brain barrier. Typical This bacterium is responsible for a Enterococci infection will vary S. pneumonia C. albicans is a commensal pathogen Presenting Symptoms wide array of infections. It can cause according to the site of infection. colonizes in the mucosal as it is a member of the acute illness which is characterized by If bloodstream infection (bacteremia surfaces of the nasopharynx gastrointestinal, oropharyngeal and pharyngitis leading to sore throat, or septicemia), fever, elevated heart and upper respiratory airway, female genital flora. However, it is fever, enlarged tonsils, tonsillar rate, and malaise are common. In and symptoms of also an opportunistic pathogen in

exudate, sensitive cervical lymph severe cases shock can result which is inflammation appear as the humans, as it can cause disease in nodes and malaise. Skin and soft-tissue indicated by dizziness, confusion, bacteria migrate into the immunodeficient and immuno- infections including pyroderma, hypotension, weakness and fainting sterile parts of the airway. It is competent individuals that can be cellulitis, wound infections, abcesses, that can lead to life threatening the most common etiological life-threatening. The most frequent erysipelas, and necrotizing fasciitis can conditions. Urinary tract infections agent of community-acquired clinical form is thrush/oral also result from dermal exposure and present as pain or burning during pneumonia and otitis media, candidiasis, where infection can be infection. Septicaemia, septic arthritis, urination, back pain, difficulty and the second most prevalent observed on the tongue, palate or endophthalmitis, myositis, urinating, frequent urination, or fever. cause of bacterial meningitis other mucosal surfaces and is osteomyelitis, pneumonitis, meningitis, Wound, and soft tissue infections in Israel characterized by single or multiple, endocarditis, nephritis, may be red with warm skin and (Neisseria meningitides ragged white patches. Esophageal glomerulonephritis, and sinusitis can swelling, pain, and may or may not being the first). Early candidiasis is manifested by also result from infection with Group have pus or pus drainage. They are symptoms include shaking inflammatory patches that develop on C streptococcal species. Streptococcal also associated with endocarditis and chills and high fever, and the esophagus, causing painful toxic shock-like syndrome consisting in some cases pneumonia which is coughs producing pink to swallowing and substernal chest pain. initially of dizziness, confusion, and characterized by fever, coughing, rusty coloured sputum. If left In immuno-compromised patients the development of large patches of shaking chills, and shortness of untreated, sustained fever and (such as those with HIV infection), reddened skin which can lead to pleuritic pain will develop, as similar lesions can also occur on the

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 25 of 92 Revised: January 26, 2017

hypotension, necrotizing fasciitis, and breath, especially when climbing well as sinusitis, endocarditis, small intestine and stomach. Chronic eventual multi organ system failure stairs. arthritis, and peritonitis. When mucocutaneous candidiasis is a rare (respiratory, renal, and liver). pneumococci migrate to the genetic disease, which occurs in lungs, they can cause individuals with defects in immune pneumonia, or can enter the response against Candida. It involves blood stream and cause chronic infections of the skin, hair, bacteremia or septicemia. face, scalp and hands, and can further Uncontrolled colonization disseminate to deeper tissues and of S. pneumonia in the lung, major body organs such as kidneys, meninges, or middle ear will heart and brain, which may lead to cause pneumococcal lysis, septicimea (candidemia – Candida in which can trigger blood) and death. Infections of the inflammation. Mortality rate nail (paronychial and onychomycotic of pneumococcal pneumonia candidosis), superficial invasion of is 5 – 10% despite mucous membranes, cutaneous antimicrobial treatment, a infections of the macerated skin (in higher mortality rate as been crural folds, diaper area in infants), observed in patients with eye infections such as pneumococcal bacteremia, as endophthalmitis are also examples of it has been approximately 25 infections caused by C. albicans. – 29% in the past four decades. S pneumoniae infection is an important cause of bacterial co-infection in patients with and can increase the morbidity and mortality in these patients. Mode(s) of Susceptible to 1% sodium Susceptible to 70% isopropyl alcohol, Exposure to 0.5% Candida albicans strains can be Decontamination hypochlorite, 4% formaldehyde, 2% 70% ethanol, 0.041% sodium glutaraldehyde, 1% sodium killed effectively with sodium glutaraldehyde, 70% ethanol, 70% hypochlorite, phenolic and quaternary hypochlorite, iodines, 70% hyphochlorite (5% and 0.5%), iodine propanol, 2% peracetic acid, 3-6% ammonia compounds, and ethanol, and formaldehyde (2%) and potassium iodide (4%) hydrogen peroxide and 0.16% iodine. glutaraldehyde. Resistant to 3% (effective at higher within 30 seconds. Chlorhexidine

Bacteria are susceptible to moist heat hydrogen peroxide. Enterococci are temperatures than 20˚C) have acetate (0.5%) is able to completely (121°C for at least 15 minutes) and dry killed by temperatures in excess of been shown to disinfect S. kill C. albicans strains within 5 heat (170°C for at least 1 hour). 80°C. pneumonia. Cells can be minutes. C. albicans strains are inactivated by heat suspension resistant to calcium hydroxide. C. in a water bath at 56˚C for 30 albicans isolates are also susceptible minutes. to 70% ethanol, 0.5% ecodiol and a combination of 1.2% sodium hyphochlorite and 0.5% ecodiol. UV light has been shown to reduce fungal load, but is ineffective in killing the

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 26 of 92 Revised: January 26, 2017

yeast completely. Most microorganisms are also inactivated by moist heat (121°C for 15 min- 30 min). Emergency Response If exposure is suspected wash area If exposure is suspected wash area If exposure is suspected, wash If exposure is suspected, wash area thoroughly and encourage bleeding if, thoroughly and encourage bleeding if, area thoroughly and thoroughly and encourage bleeding if sharps or puncture injury. Seek sharps or puncture injury. Seek encourage bleeding if, sharps sharps or puncture injury. Seek emergency medical attention. Monitor emergency medical attention. or puncture injury. Seek immediate emergency medical for symptoms. Confirm infection by Monitor for symptoms. Diagnosis is emergency medical attention. attention. Appropriate biotherapy and bacteriological and serological testing, via isolation of enterococci from Monitor for symptoms. Gram- ongoing surveillance are latex bead agglutination, fluorescent clinical specimens. Confirm infection negative stains or bacteriology recommended. Direct examination of antibody staining or ELISA. by bacteriological and serological studies of direct smears from the fungus or the fungus in culture in Appropriate antibiotic treatment is testing, latex bead agglutination, nasal fluid, fluid from lesions, the clinical specimen can confirm the necessary for a Group C Streptococcus fluorescent antibody staining or or areas of inflammation can presence of infection if key infection. Antibiotic effectiveness may ELISA. Treatment with penicillin or be used to detect symptomatic characteristics (size and shape of vary from case to case and condition to ampicillin for infections such as or asymptomatic infections. yeast, presence of pseudophypahe, condition. Group C Streptococcal , peritonitis, and ELISA, PCR fingerprinting blastoconidia, chlamydospores, and species have demonstrated wound infections. Combination analysis, and radiography absence of arthroconidia and capsule) susceptibility to a variety of drugs: β- therapy of a cell wall- active agent techniques are also useful for are observed. Other methods include lactams such as penicillin, as well as (penicillin, ampicillin or vancomycin) diagnosis. Administer biochemical tests, serological erythromycin, clindamycin, imipenem, and an aminoglycoside is required for appropriate drug treatment. methods such as RIA and ELISA, and rifampin, vanomycin, macrolides and the treatment of endocarditis and Inflammation caused by molecular biology methods such as lincomycin; however, certain strains of possibly meningitis. Most strains pneumococcal lysis makes the REA (restriction enzyme analysis) the bacterium have been found to remain susceptible to penicillin, treatment of pneumococcal PCR, and PGFE (pulse-field gel resistant to macrolides, lincomycin, ampicillin, and vancomycin. Strains diseases less effective with electrophoresis). Eliminating chloramphenicol, tetracyclines and resistant to β-lactams, antibiotics alone, and even predisposing factors such as cotrimoxazole. aminoglycosides and, increasingly, highly effective bactericidals administration of antibiotics, steroids, vancomycin have been described. such as β-lactam may actually and immuno-suppressants; humidity, Strains have also been identified enhance the harmful effects of local maceration, vaginal pH, which carry genetic elements the disease in some cases. removal of infected catheter can help conferring resistance to Susceptible to penicillin, in resolving infections. Susceptibility chloramphenicol, tetracyclines, tetracycline, cefotaxime, has been shown for amphotericin B, macrolides, lincosamides, quinolones, levofloxacin, erythromycin, nystatin, flucytosine, the azoles, and streptogramins. and fluoroquinolones, echinocandins, and combination drug especially moxifloxacin and therapies. Topical and oral azoles gatifloxacin. The bacteria may such as butoconazole, clotrimazole, display full susceptibility to triazole, and econazole lipogel can be telithromycin, vancomycin, used against vaginal candidiasis. and linezolid. Multi-drug Systemic antifungals such as resistant S. pneumoniae is fluconazole or itraconazole can be emerging. It displays high used to treat mucocutaneous candida resistance to penicillin, as infections. Voriconazole, and well as to erythromycin,

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 27 of 92 Revised: January 26, 2017

cefotaxime, levofloxacin, echinocandins can be effective tetracycline, TMP/SMX, β- against cutaneous candidiasis lactam agents, macrolides, although an azole is preferred, and chloramphenicol, and invasive candidiasis can be treated ceftriaxone, with with caspofungin, or lipid fluoroquinolone-resistant formulations of amphotericin B. strains being resistant to Posaconazole is used to treat oral, but ciprofloxacin and levofloxacin not systemic candidiasis. treatments. Recent widespread Resistance of C. albicans to use of a pneumococcal fluconazole has been associated with capsular polysaccharide (CPS) repeated use of this drug, particularly conjugate vaccine reduces the in immuno-suppressed patients who incidences of carriage of the are taking this drug chronically for bacteria in children, and, as a prophylaxisis. Resistance to result, herd immunity has also echinocandins has also been reported. been observed. Protection, however, is serotype-specific, but development of promising vaccines are focusing on viral pneumococcal proteins that are common to all serotypes. Pneumococcal vaccination is recommended in Canada for infants less than 2 years of age, adults over 65 years and others at high risk of invasive pneumococcal disease. Currently available vaccines are the pneumococcal conjugate vaccine (PCV7) which is effective against 7 serotypes, and it has been shown to be effective for children less than 2 years of age. The pneumococcal polysaccharide vaccine (PPV23) is effective against 23 serotypes.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 28 of 92 Revised: January 26, 2017

Medical Surveillance Inventory – Bacteria (cont)

Listeria monocytogenes; Nocardia spp.; Streptococcus salivarius (S. viridans);

Pathogen Listeria monocytogenes Nocardia spp. Streptococcus salivarius (S. Pseudomonas aeruginosa. Identification viridans)

Mode(s) of The predominant mode of L. Inhalation of infectious aerosols, dust, Inhalation of infectious P.aeruginosa Transmission monocytogenes transmission is by contamination of mucocutaneous aerosols, contamination of have been found to survive within ingestion of contaminated food. L. lesions, and accidental parental mucocutaneous lesions, and droplet nuclei and can remain in monocytogenes can also be transmitted inoculation are the primary hazards accidental inoculation are the aerosols for long periods of time, thus transplacentally from mother to child associated with working with this primary hazards associated there is evidence of potential airborne

during pregnancy and via the birth pathogen. Nocardia have been with working with this transmission. Contact with canal during birth. Direct contact with isolated from sputum, sinus tissues, pathogen. Direct contact with contaminated water is also a major diseased animals may lead to bronchial aspirates, pus, and rarely infectious persons, materials, route, but since the oral infectious transmission to farmers and from urine and blood. and objects can also facilitate dose is thought to be very high, routes veterinarians during the birthing of transmission. Blood, that pose the greatest health risk are domestic farm animals. Nosocomial peritoneal fluid, cerebrospinal skin exposure (for example, in infections and person-to-person fluid, and oropharyngeal contaminated hot tub water) and lung transmission (excluding vertical) are secretions are all potential exposure from inhaling aerosols recognised but rare. carriers of this bacterium. discharged from infected respiratory L. monocytogenes is commonly found Studies in the 1930s and tracts. The bacterial can often enter in nature, particularly in association 1940s suggest that S. the body through injuries and with soil. Blood, cerebrospinal fluid, salivarius can survive on wounds. The use of contaminated faeces, placenta, skin lesions, pus, drinking glass rims and mechanical respiratory ventilators in amniotic fluid, menstrual blood, utensils for at least a couple of hospital settings is also a common lochia, respiratory secretions, days; however, genetic source of nosocomial infections. meconium, gastric aspirate, animal identification was not Inhalation of infectious aerosols, tissues/specimens, and infected organs available at this time, and it is contamination of mucocutaneous such as brain and liver are all potential unknown whether species- lesions, and accidental inoculation are sources of infection. Accidental specific identification was the primary hazards associated with autoinoculation, exposure to the tissues possible. working with this pathogen. of experimentally infected animals, Pseudomonas can survive for months and on dry surfaces and inanimate L. monocytogenes objects, and are one of the bacteria most frequently isolated from patients with nosocomial infections; humidity

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 29 of 92 Revised: January 26, 2017

cultures, are the primary hazards can improve persistence. Growth associated with working with this observed in distilled water can pathogen. survive up to months with minimal nutrients. Incubation Can vary depending on the mode of Unknown. Unknown. Varies according to infection, eye Period transmission and dose received, but infection can appear 24 – 72 hours typically ranges from 1 to 4 weeks, and after infection. can be as high as several months. Febrile gastroenteritis as a result of L. monocytogenes has a short incubation period, typically 18 to 20 hours. Period of Unknown, however person to person The bacterium is not transmitted Unknown, but human to Spread of infection from person-to- Communicability transmission, while recognized as from human to human but rather human transmission has been person is speculated to be highly possible, is rare. through external contact with it in the recorded. possible during infection, especially environment. amongst patients. Infectious Dose(s) The approximate infective dose of L. Unknown. Unknown. Unknown. monocytogenes is estimated to be 10 to 100 million colony forming units (CFU) in healthy hosts, and only 0.1 to 10 million CFU in individuals at high risk of infection. Typical Although relatively rare, human Nocardial infections are S. salivarius has been As opportunistic pathogens, Presenting Symptoms listeriosis is often severe and mortality predominantly opportunistic associated with a variety of Pseudomonas sp. often invades the rates can approach 50%. Certain infections. As such, patients who are infections. The most common host tissue and cause infection and factors predispose individuals to immunosuppressed (transplant reports refer to meningitis, bacteremia in immuno-compromised infection with L. monocytogenes, such patients and patients with HIV, and bacteraemia. Other cases hosts (e.g., HIV/AIDS, cystic

as neonates, pregnancy, leukemia, systematic lupus erythematosis, include pericarditis, fibrosis, , and severe Hodgkin’s disease, diabetes mellitus, chronic granulomatous disease, spontaneous bacterial chronic obstructive pulmonary alcoholism or cirrhosis and malignancies, trauma, or intravenous peritonitis, acute jejunitis, disease, burns, malignancy, or immunosuppressive or cytostatic catheters) are at higher risk of pancreatic , diabetes mellitus). The common site therapy. Most commonly, listeria contracting . Nocardial multimicrobial endocarditis, of infection is the lower respiratory causes a mild febrile illness however, infections occur in three main forms: early neonatal sepsis, tract, and severity ranges from several types of listeriosis disease pulmonary, systemic, and cutaneous. sinusitis, endophthalmitits, colonization without immunological manifestations are recognised; for Pulmonary infections usually cause and femoral response to severe necrotizing instance, listeriosis in pregnancy, acute, chronic, or relapsing broncho- osteitis. It must be noted, broncho-pneumonia; such severe listeriosis of the central nervous pneumonia that sometimes spreads to however, that although S. infection in patients with cystic system (CNS), febrile gastroenteritis, cavities and pleura. Symptoms salivarius frequently enter the fibrosis is almost impossible to glandular listeriosis, local listeriosis, include coughing, dyspnea, and fever. bloodstream, infections eradicate once established in the typhoid listeriosis, and atypical Pulmonary infection can lead to with S. salivarius are rare due airways. Pseudomonal pneumonia listeriosis. systemic or neurologic complications to their low virulence. Many often develops from oro-pharyngeal Listeriosis in pregnancy: Occurs such as meningitis and brain patients with S. contamination or secondary mostly during the third trimester, and abscesses. salivariusbacteraemia have bacteremia, and is also a common

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 30 of 92 Revised: January 26, 2017

is characterised by a “flu like” illness Nocardia brain abscesses are predisposing local factors cause of nosocomial ventilator-related with symptoms such as fever, chills, commonly found in the brain stem, such as mucosal disruption pneumonia in intensive care settings. malaise, arthralgia, back pain, and basal ganglia, and cerebral cortex, and/or serious underlying Infections also include endocarditis, diarrhoea. In many cases the infection and the mortality rate for patients diseases, such as malignancy osteomyelitis, urinary tract infections, is subclinical or unapparent; however, who develop brain abscesses is about or liver cirrhosis. gastrointestinal infections, meningitis, intrauterine infection of the foetus can 50%. Systemic infections and, commonly, septicaemia. P. lead to foetal death, spontaneous of Norcardia are rare and commonly aeruginosa is the most common agent abortion, premature delivery, or the occur in immuno-compromised associated with infection and birth of a foetus that dies shortly after individuals. Cutaneous infection, inflammation during contact lens birth. Surviving newborns with called mycetoma, is characterized by wear. The bacteria colonize on lenses listeriosis are often classified as “early pustules, fever, tender lymphadenitis and produce proteases to kill or onset” or “late onset”. Early onset in local lymph nodes, abscess, and invade corneal cells, an infection that neonatal listeriosis due to yellow-white grainy discharge. can lead to scarring and vision loss. transplacental infection often presents Mycetoma can affect the underlying The species is also the most virulent as pneumonia and/or sepsis. Severe bone and is most common in adult with a mortality rate of 30%, which disease can result in widespread males who walk bare foot or who can be higher depending on granulomas (granulomatosis have burn injuries. With appropriate predisposing conditions. P. infantisepticum). Late onset neonatal antibiotic treatment, it is usually aeruginosa can also readily colonize listeriosis is said to occur from healed within a few weeks, though it on open wounds, causing infections, infection during birth, with neonates may take up to 3 months for full abscesses, and sepsis, with edema showing symptoms of meningitis one clearance. and/or discoloration of unburned skin to several weeks after birth. In both at wound margins and green pigment early and late onset neonatal listeriosis, in subcutaneous fat. P. aeruginosa is the mortality rate ranges from 20 to also associated with swimmer’s ear 30%. (otitis externa). Other Pseudo- Listeriosis of the CNS: Meningitis is monas species are also opportunistic; the most frequently recognised listerial however, cases of infection are rare. infection. Common symptoms of listeriosis of the CNS include high fever, nuchal rigidity, tremor and/or ataxia, and seizures. The most common form of non-meningitic form of CNS listeriosis is encephalitis involving the brainstem (rhombencephalitis)Febrile gastroenteritis: A non-invasive form of listeriosis that manifests as symptoms typical of gastroenteritis, for example, fever, diarrhoea, and vomiting. Glandular listeriosis: Resembles infectious mononucleosis with swelling of the salivary glands and nuchal lymph nodes.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 31 of 92 Revised: January 26, 2017

Local listeriosis: Can manifest as papules and pustules on the hands and arms following direct contact with infectious material, and can be accompanied by constitutional symptoms (fever, myalgia, and/or headache). Typhoid listeriosis: Characterised by high fever and is particularly frequent in immunocompromised individuals. Atypical listeriosis: Rare cases of have been described with symptoms such as endocarditis, purulent (mononuclear) pleural exudates, pneumonia, , and abscesses. Mode(s) of At room temperature, L. Susceptible to 2-5% phenol, 1% Susceptible to 5.25% sodium Susceptibility has been shown for 1% Decontamination monocytogenes is susceptible to sodium hypochlorite, 4% hypochlorite, and cresophene sodium hypochlorite, 70% ethanol, sodium hypochlorite, iodophor formaldehyde, 2% glutaraldehyde, (30% paramonochlorophenol, 2% glutaraldehyde, and compounds, and quaternary 70% ethanol, 70% propanol, 2% 5% thymol, 0.1% formaldehyde; however, it has been ammonium compounds. Five to 10- peracetic acid, 3-6% hydrogen dexamethasone), 21% alcohol, found to be resistant to disinfectants

fold higher concentrations of the above peroxide, and iodine. Bacteria are and 2.0% chlorohexidine. that are used to treat drinking water compounds are required at 4°C. L. susceptible to moist heat (121°C for Streptococcal species are such as chlorine, chloramines, ozone, monocytogenes can be inactivated by at least 15 minutes) and dry heat inactivated at low pH. and iodine. Certain adapted stains ozone, high pressure (500MPa), and (160-170°C for at least 1 hour). It is Bacteria are susceptible to have been found to be able to grow in high temperatures (at least 70°C for 2 able to remain viable for 8 hours at moist heat (121°C for at least disinfectants; however, isopropyl minutes). L. monocytogenes can 50°C. 15 minutes) and dry heat alcohol 4% v/v or ethyl alcohol 6% tolerate cold temperature environments (170°C for at least 1 hour). v/v are effective disinfectants. well, and can survive at low pH. Inactivation and sterilization using moist heat should be at 121°C for 15 minutes or longer, dry heat at 170- 250 °C or higher for 30 minutes or more. Emergency Response If exposure is suspected wash area If exposure is suspected wash area If exposure is suspected, wash If exposure is suspected, wash area thoroughly and encourage bleeding if, thoroughly and encourage bleeding if, area thoroughly and thoroughly and encourage bleeding if sharps or puncture injury. Seek sharps or puncture injury. Seek encourage bleeding if, sharps sharps or puncture injury. Seek emergency medical attention. Monitor emergency medical attention. or puncture injury. Seek immediate emergency medical for symptoms. Listeriosis can be Monitor for symptoms. ELISA for emergency medical attention. attention. Appropriate biotherapy and diagnosed in the laboratory by detection of Nocardia -specific Monitor for symptoms. ongoing surveillance are cultivation of the organism, and mAbs,PCR, sequence-based Confirm infection using gram- recommended. Aminoglycoside with demonstration of the infectious agent identification methods, and stain, followed by isolation of β-lactam penicillin is usually the first or its products in tissues or body fluids. microscopic observation can be used the organism from blood or line of treatment. Aggressive Several commercially available kits to identify the presence of species in cerebrospinal fluid culture. treatment can avoid development of exist for the detection of L. the host Appropriate antibiotic chronic infection. Wounds should be

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 32 of 92 Revised: January 26, 2017

monocytogenes. These rapid therapy is used to treat clinical PCR has also been used to cleaned with surgical detergent procedures are based on ELISA and disease caused by this bacterium. In identify disinfectants and/or topical PCR technology; however, none have some cases of mycetoma, surgical S. salivarius in clinical antibacterial ointments, such as been validated for use as a diagnostic drainage may be needed. Most samples. Antibiotic therapy, mupirocin. Pseudomonas tool. Treatment for human listeriosis species are susceptible to typically with ceftriaxone, spp. are resistant to many antibiotics. with ampicillin or amoxicillin together trimethoprim-sulfamethoxazole, amoxicillin, and/or Susceptibility to extended-spectrum with gentamicin is the primary choice amikacin, ampicillin, carbenicillin, vancomycin. Treatment is penicillins (such as ticarcillin, of therapy. The recommended course broad-spectrum cephalosporins, delivered depending on the azlocillin, and piperacillin), of treatment is ampicillin for 2 to 4 minocycline, erythromycin, manifestation of the infection, aminoglycosides, cephalosporins, weeks. The addition of gentamicin for ciprofloxacin, clindamycin, for example patients suffering fluoroquinolones, polymixins, and the 2 weeks should be considered for imipenem, and cotrimoxazol, but from meningitis due monobactams. Multi-drug resistant immunocompromised patients. An resistant to penicillin and to S.salivarius strains are emerging, such as against alternative therapy for individuals antituberculous, and antifungal may require mechanical carbenicillin, cephalosporins, allergic to β-lactams is intravenous co- agents. ventilation. Sensitive to ceftazidime, and ciprofloxacin. trimoxazole. Susceptible to most broad various antibiotics, including spectrum and gram-positive spectrum ciprofloxacin, levofloxacin, antibiotics, except the cephalosporins metronidazole, penicillin, are active against L. monocytogenes in amoxicillin, ceftriaxone, vitro. In vivo, the most active are clindamycin, rifampicin, ampicillin and amoxicillin. gentamycin, cefuroxime, moxifloxacin, ceftoxime, and vancomycin. Certain strains of S. salivarius have shown partial resistance to penicillin, ceftriaxone, erythromycin, and meropenem.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 33 of 92 Revised: January 26, 2017

Medical Surveillance Inventory – Bacteria (cont)

Proteus spp.; Bacillus cereus; Citrobacter diversus; Enterobacter spp. (E. cloacae, E. aerogenes)

Pathogen Proteus spp Bacillus cereus Citrobacter diversus. Enterobacter spp. (E. cloacae, E. Identification aerogenes)

Mode(s) of Proteus spp. are part of the human The primary mode of transmission is Transmission is possible Transmission is through direct or Transmission intestinal flora and can cause infection via the accidental ingestion of B. through accidental ingestion indirect contact of infected specimens upon leaving this location. They may cereus contaminated materials. It or parenteral inoculation with with mucous membranes, parenteral also be transmitted through ingestion forms spores and spreads easily. In contaminated materials. inoculation, trauma of the cutaneous or by accidental parenteral inoculation. hospitals, B. cereus can also be Person-to-person transmission or mucocutaneous barriers, aerosols,

The specific, natural mode of transmitted via contact with is also possible. Human feces, and ingestion. Direct or indirect transmission, however, has not been contaminated fabrics. In the brain abscesses, cerebral contact of mucosal surfaces with identified. In the laboratory, accidental laboratory, accidental parenteral fluids, laboratory mice, eye, infectious agent (e.g. bacteria can contact with aerosols, parenteral inoculation, trauma of the cutaneous urine, intestines, umbilicus, transfer from contaminated hands or inoculation, trauma of the cutaneous or or mucocutaneous barriers, and/or skins pustules, hands, contaminated urinals) or, in the case mucocutaneous barriers, and/or ingestion of contaminated material environmental sources (soil, of endogenous flora, through transfer ingestion of contaminated material are are all infectious risk factors. Lab water) are possible sources of to adjacent, susceptible, sterile body all infectious risk factors. Urine tract, samples at risk for infectious material infectious contamination. sites. Entero-bacteriaceae can also be wound, blood, and in some cases, CSF, contamination may include stool spread through the fecal-oral route. stool, tears, and respiratory fluid may samples, food specimens, and soil Infected urine, feces, respiratory all be infectious sources of this group samples. B. cereus survives in soil secretions, wound exudates, blood, of pathogens. Proteus spp. survive and on vegetation, and is generally water, soil, and plants are all potential only for a few days on inanimate heat-resistant and thus may survive sources of infectious contamination. surfaces; and only 1 to 2 days in the thermal food processing with or case of P. vulgaris. They also survive without injury to cells. well within the environment in soil, water, and sewage. Incubation Unknown. The diarrheal form of B cereus has an Unknown in adults. In Unknown. Period onset period of 8-16 h while the neonates time ranges from emetic form has an onset period of 1- hours to days. 6 h. Recovery is usually complete in 24 h. Period of Proteus spp. are not known to be Not known to be transmitted from Unknown. Variable. In some cases, the bacteria Communicability transmitted from person-to-person. person-to-person. can be present as resident flora in the absence of symptoms and can be

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 34 of 92 Revised: January 26, 2017

transmitted for as long as the carrier state persists. Infectious Dose(s) Unknown. In diarrheal illness, the toxin Via ingestion: Approximately Unknown, however, approximately responsible is produced by organisms 10 7 CFU/mL. Parenteral 1000 cells have been considered in the small intestine and infective inoculation dose unknown. infectious, similar to the infectious dose is 104-109 cells per gram of dose of the pathogenic food. The emetic toxin is preformed bacteria , and indigested in food (about 105- Escherichia coli O157, and Listeria 108 cells per gram in order to produce monocytogenes 4b. sufficient toxin). Typical Generally, affect the upper urinary B. cereus causes self-limiting (24-48 Citrobacter Enterobacter Presenting Symptoms tract (common site of infection), hours) food-poisoning syndromes (a normally cause urinary tract spp., particularly causing infections such as urolithiasis diarrheal type and an emetic type), infections, blood stream E. aerogenes (stone formation in kidney or bladder), opportunistic infections and is infections, intra abdominal and E. cloacae, cystitis, and acute . Rare associated with clinical infections sepsis, brain abscesses, and have been associated with nosocomial

cases of bacteraemia, associated such as endophthalmitis and other pneumonia and other neonatal outbreaks, and are considered with UTIs, with Proteus spp. have also ocular infections. The diarrheal form infection, such as meningitis, opportunistic pathogens. been reported. Other infections include of B. cereus food poisoning is neonatal sepsis, joint infection Enterobacter spp. can cause septicaemia and wound infections. characterized by abdominal cramps, or general bacteremia. CNS numerous infections, including After attachment and colonization profuse watery diarrhea, and rectal infections are more common cerebral abscess (mental process within the urinary tract, Proteus spp. tenesmus, and, occasionally, fever for infants under 2 months old inhibition, decreases speech, release urease, which catalyzes the and vomiting. The emetic form of than for older children or sensation and motor skills, changes in conversion of urea into ammonia and B. cereus food poisoning is immunocompromised adult vision and personality and vomiting), CO2. This causes a decrease in the characterized by nausea, vomiting, patients, but rare cases have pneumonia (cough, fever, shaking urine pH and may eventually lead to and malaise, occasionally with been reported. May cause chills, shortness of breath, especially the formation of kidney or bladder diarrhea. B. cereus can cause wound neonatal meningitis that can when climbing stairs), meningitis stones. P. mirabilis causes the most infections, bacteremia, septicaemia, lead to brain abscesses. (fever, cold hands and feet, infections among all Proteus spp. meningitis, pneumonia, central Citrobacter drowsiness, confusion, irritability, nervous system infections, infections can be fatal, with severe muscle pain, blotchy skin, endocarditis, pericarditis, respiratory 33-48 % overall death rates, sever headache, and stiff ), infections, and peripheral infections. and 30% for neonates. Infant septicemia (fecer and shaking chills, Infection in immunocompromised survivors may experience or a very low body temperature, individuals can be life-threatening. B. significant damage to CNS, decreased urination, rapid pulse, rapid cereusstrains which harbour a including profound breathing, nausea and vomiting, and plasmid bearing B. anthracis-like retardation, hemiparesis, diarrhea), wound infection (increased virulence factors can cause severe seizures, etc. pain, redness, swelling, and warmth pneumonia in immuno-competent around the area, red streaking people. extending from the area, pus drainage, and fever), urinary tract infection (upper back and side (flank) pain high fever shaking and chills nausea, vomiting, pelvic pressure lower abdomen discomfort frequent,

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 35 of 92 Revised: January 26, 2017

painful urination blood in urine), and abdominal cavity/intestinal infections (tenderness, pain, bloating, nausea and vomiting, diarrhea, constipation, loss of appetite). In addition, Enterobacter spp. have been noted in intravascular device-related infections, and surgical site infections (primarily postoperative or related to devices such as biliary stents). Many species can cause extra-intestinal infections, for example, Enterobacter sakazakii, has been associated with brain abscesses in infants and with meningitis. Mortality rates for bacterial meningitis range from 40-80%. Mode(s) of Generally susceptible to a number of Gluteraldehyde is a chemical agent Phenolic disinfectants, 1% While information specific Decontamination disinfectants including phenolic used to sterilize bacillus- sodium hypochlorite, 70% to Enterobacter compounds, hypochlorites (1% sodium contaminated material. Spores can be ethanol, formaldehyde, spp. is not available, most species in hypochlorite), alcohols (70% ethanol), killed by 1% sodium hypochlorite, glutaraldehyde, iodophore and the family Entero-bacteriaceae are formaldehyde (18.5 g/L; 5% formalin paracetic acid, activated hydrogen paracetic acid are effective susceptible to 70-80 % ethanol and

in water), glutaraldehyde, and iodines peroxide, chlorine dioxide, against most vegetative bacteria are also (0.075 g/L). Bacteria are generally formaldehyde, iodine, acids, alkali. Citrobacter. Ethanol (0.41M), susceptible to 1% sodium sensitive to moist heat (121 °C for at These chemical agents should be chlorhexidine detergent scrub, hypochlorite, glutaraldehyde, least 15 minutes) and dry heat (160 to highly concentrated and required hexachlorophene or iodophor formaldehyde, iodines, hydrogen 170 °C for at least 1 hour). greater time of contact to kill spores. preparations and bleach may peroxide, peracetic acid, and Oazolidinones are also effective also be effective. 90% of quaternary ammonium compounds. antibacterial agents for B. cereus. B. the Citrobacter Enterobacter sakazakii have been cereus can be inactivated by pulse organisms may be killed after shown to be inactivated by pulsed electric field in 0.15 % NaCl 15 minutes at 230 electric fields and high hydrostatic solution. MPa. Citrobacter are also pressure. While additional B. cereus spores can be resistant to inactivated by UV, information specific heat and radiation, but heating at microwave, gamma radiation, to Enterobacter spp. is unavailable, 100°C for 5 minutes results in cellular moist heat (121°C for at least most vegetative bacteria can be damage to the membranes and 20 min) and dry heat (165- inactivated by moist heat (121 °C for ribosomes. Gamma irradiation at 2-5 170°C for 2 h). 15 min- 30 min) and dry heat (160- kGy is required to inactivate B. 170 °C for 1-2 hours). cereus cells.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 36 of 92 Revised: January 26, 2017

Emergency Response If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash area thoroughly and encourage bleeding if thoroughly and encourage bleeding if area thoroughly and thoroughly and encourage bleeding if sharps or puncture injury. Seek sharps or puncture injury. Seek encourage bleeding if sharps sharps or puncture injury. Seek immediate emergency medical immediate emergency medical or puncture injury. Seek immediate emergency medical attention. Proteus spp. can be attention. Monitor for symptoms. B. immediate emergency medical attention. Monitor for symptoms. diagnosed by isolation and cereus strains can be isolated and attention. Monitor for Stool specimen should be observed differentiation with chromogenic grown in laboratory media at 37°C. symptoms. Citrobacter can be for presence of blood or mucous. media (i.e. by means of cultured Specimen isolated from contaminated detected by serological Enterobacter species can be isolated organisms from urine and bloods human stool can be grown with methods, molecular methods, by plating into MacConkey agar, samples). Administer appropriate tryptic soy broth with polymyxin. The or polymerase chain reaction eosin methylene blue agar or blood antibiotic therapy where necessary. organism can be isolated in B. (PCR) generated DNA finger agar. PCR assays for the detection Other than that, treatment is mainly for cereusmedium, i.e. in mannitol, egg prints from mother to child. and identification of Enterobacter symptoms. Proteus spp. are generally yolk, polymyxin B agar (MEYP) or Infection can also be spp. have also been developed. susceptible to broad-spectrum polymyxin B, egg yolk, mannitol, confirmed by other Administer appropriate antibiotics cephalosporins, aminoglycosides, and bromthymol blue agar (PEMBA). bacteriological and serological accounting for local antimicrobial imipenem. Immunological assays, polymerase means. Administer susceptibility patterns. Most Entero- P. mirabilis is also susceptible to chain reaction and biological tests, appropriate drug therapy. bacter spp. are susceptible to trimethoprim-sulfamethoxazole, have been used to detect the Citrobacter spp. are cefepime, aminoglycosides, ampicillin, amoxicillin, and enterotoxin activity of B. cereus. susceptible to fluoroquinolones, and trimethoprim- piperacillin. P. vulgaris and P. Isolation of greater than aminoglycosides, sulfamethoxazoleTigecycline has penneri are also susceptible to 105 organisms/g from contaminated chloramphenicol, been shown effective in vitro. cefoxitin, cefepime, and aztreonam. food can confirm B. cereus imipenim/cilastatin, Enterobacter spp. are resistant to P. mirabilis is resistant to contamination. Administer trimetoprim, and ampicillin; first- and second- nitrofurantoin. Resistance to appropriate drug therapy with trimetoprim/sulfamethazole. generation cephalosporins; and ciprofloxacin may develop with supportive treatment. Oral Resistance has been shown cephalothin. unrestricted use.P. vulgaris and P. rehydration therapy is the treatment against cephalosporins, penneri are resistant to piperacillin, for acute food poisoning syndromes, ceftazidime , pipera- amoxicillin, ampicillin, cefoperazone, and antibiotics are seldom required. cillintazobactam, cefuroxime, and cefazolin. P. Patients are given corticosteroids and antipseudomona penicillins, penneri is more resistant to penicillin antibiotics as a first line treatment for ampicillin, cephalothin, and than P. vulgaris. Resistance to β- eye infections from B. cereus. carbenicillin. Prophylaxis lactamases among Proteus spp. is Whenever gram-positive rods are consists of antibiotics such as emerging. Carbapenem resistance, discovered in the blood or the amoxicillin and a beta- including pan-resistant isolates, have cerebrospinal fluid of an lactamase inhibitor. been described in India. immunocompromised patient with clinical signs of infection, the empiric antibiotic treatment should cover B. cereus (B. cereus is usually sensitive to clindamycin, aminoglycosides, vancomycin, chloramphenicol, and erythromycin). In cases of an acute non-inflammatory infectious diarrhea, a pharmacologic prophylaxis with

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 37 of 92 Revised: January 26, 2017

bismuth subsalicylate in a dose of two tablets four times daily with meals and at bedtime may be useful. Duration of use should not exceed 3 weeks. B. cereus is susceptible to imipenem and vancomycin, and most strains are sensitive to chloramphenicol, aminoglycosides, ciprofloxacin, erythromycin, and gentamicin. Some strains were moderately sensitive to clindamycin and tetracycline. Clindamycin with gentamicin, given early, is the best treatment for ophthalmic infections from B. cereus. B. cereus produce large amounts of β lactamase and are resistant to penicillin, ampicillin, cephalosporins, trimethoprim.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 38 of 92 Revised: January 26, 2017

Medical Surveillance Inventory – Bacteria (cont)

Haemophilus influenzae; Pasteurella sp.; Salmonella enterica spp.; Staphylococcus aureus (MRSA, MSSA, VISA, hVISA, VRSA)

Pathogen Pasteurella sp. Salmonella enterica spp. Staphylococcus aureus (MRSA, Identification MSSA, VISA, hVISA, VRSA)

Mode(s) of Respiratory droplet transmission as Transmission occurs primarily by bites Primary hazards when working Ingestion of food containing Transmission well as via contact with discharge and scratches of infected animals, with Salmonella enterica are enterotoxins. Vertical transmission from nose and throat during animal licks on injury site, respiratory accidental parenteral inoculation, during vaginal delivery is uncommon. infectious periods. The portal of entry droplets, and infected meat. exposure of non-intact Person-to-person transmission occurs is most commonly the nasopharynx. Cockroaches may spread mucocutaneous and cutaneous through contact with a purulent lesion or

Bacteria may be in the cerebrospinal if they come in contact with food. barriers, and ingestion. The risk with a carrier. Unsanitary conditions fluid, serum, urine, blood, pleural Laboratory hazards include laboratory associated with aerosol exposure and crowded community settings fluid, joint fluid and middle ear animal bites, exposure to infectious is not yet known. increase exposure to S. aureus. Infection aspirates. Lab acquired infections are aerosols, contact with broken Human infection usually occurs may be spread from person-to-person caused by inhalation, autoinoculation, cutaneous or mucocutaneous barriers, when consuming contaminated through health care workers or patients. or ingestion. does not survive long and parenteral inoculation. Infected foods and water, contact with Nasal colonization can lead to auto- term in the environment, but can bite wounds and abscesses, pus, infected feces, as well as contact infection. Trauma of cutaneous barrier, survive more than 18 hrs in mucous bronchial secretion, CSF, and blood with infective animals, animal parenteral inoculation, ingestion of and 12 hrs on plastic. may contain feed, or humans. Foods that pose infected material, and contact with Pasteurella spp. P. multocida may a higher risk include meat, aerosols are the primary lab associated survive in air (5% after 45 min), in poultry, milk products, and egg hazards. Direct contact with open cuts distilled water and ocean water (14 products. In hospitals, the and lesions of skin is also a risk. May days at 4°C, less than 24 hours at bacteria have been spread by become carrier by touching 37°C), and in pig slurry (3 days at 4°C personnel in pediatric wards, contaminated surfaces and objects with and 6 days at 37°C). It may also either on their hands or on intact epidermis. Infective stages may survive in blood. inadequately disinfected scopes. be present in CSF, joint aspirates, blood, Flies can infect foods which can abscesses, aerosols, faeces, and urine. also be a risk for transmission to Survives on carcasses and organs (up to humans. Serotype Choleraesuis 42 days), floors (less than 7 days), glass can survive in wet swine feces (46 hours), sunlight (17 hours), UV (7 for at least 3 months and in dry hours), meat products (60 days), coins swine feces for at least 13 (up to 7 days), skin (30 minutes to 38 months. Serotype Dublin can days). Depending on colony size, S. survive in feces spread on aureus can survive on fabrics from days concrete, rubber, and polyester to months.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 39 of 92 Revised: January 26, 2017

for almost six years. Serotype Typhimurium can survive in cattle slurry for 19-60 days, cattle manure for 48 days, soil for 231 days, and water for up to 152 days. Flies have been shown to excrete certain serotypes for 8 days and bed bugs can excrete bacilli for up to 21 days. Certain serotypes have been shown to survive on fingertips for up to 80 minutes, depending on the inoculum size. Salmonella serotypes have been found to live up to 63 days on lettuce, 231 days on parsley, 32 weeks in pecans, 10 months on refrigerated cheddar cheese, 9 months in butter, up to 63 days in frozen yogurt, and up to 20 weeks on frozen minced beef and chicken. Incubation 2-4 days. Depends on site of infection, but For non-typhoidal , If ingested, 30 minutes to 8 hours is Period generally less than 24 hours. the incubation period is variable, expected, otherwise symptoms may depends on the inoculum size, appear 1 to 10 days post infection. and usually ranges between 5 However, people may be colonized and 72 hours. For , intermittently or for months-years the incubation period can be before a symptomatic infection occurs, between 3 and 60 days, although if at all. most infections occur 7-14 days after contamination. The incubation period for typhoid fever is highly variable and depends on inoculum size, host susceptibility, and the bacterial strain. Period of Not highly contagious. Secondary Pasteurella spp. may be transmitted Humans can spread the disease Communicable period is as long as a Communicability infection may occur in the case of during colonization. Human-to-human for as long as they shed the purulent lesion is present or carrier state particularly close contact with communicability is suspected, but not bacterium in their feces. Certain persists. infected individuals. Not confirmed. carriers shed the bacteria for communicable 48 h after initiation of years and 5 % of patients efficient antibiotic treatment. recovering from non-typhoidal salmonellosis can shed the

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 40 of 92 Revised: January 26, 2017

bacteria for 20 weeks. Animals can have a latent or carrier state where they excrete the organism briefly, intermittently or persistently. Infectious Dose(s) Unknown. Unknown. Unknown for parental At least 100,000 organisms in humans. inoculation. For ingestion, the infectious dose varies with the serotype. For non-typhoidal salmonellosis, the infectious dose is approximately 103 bacilli. For enteric fever, the infectious dose is about 105 bacilli by ingestion. Patients with achlorhydria, depressed cell-mediated immunity, or who are elderly may become infected with at a lower infectious dose. The infectious dose may also be dependent on the level of acidity in the patient’s stomach. Typical Infection with Haemophilus 50% of pasteurellosis cases in Europe Salmonella enterica can cause Staphylococcus aureus is an Presenting Symptoms influenzae (type b) can cause and America are infected bites or four different clinical opportunistic pathogen that can cause a meningitis (50% of all cases - adults scratches from animals, usually cats manifestations: gastroenteritis, variety of self-limiting to life- and children), (17%), and dogs 20-80% of cat bites and 3- bacteremia, enteric fever, and an threatening diseases in humans. The pneumonia (15%), septic arthritis 18% dog bites will be infected. 3-48h asymptomatic carrier state. It is bacteria are a leading cause of food

(8%), cellulitis (6%), osteomyelitis after infection, substantial local more common in children under poisoning, resulting from the (2%), or generalized bacteremia cellulitis, sometimes accompanied with the age of 5, adults 20-30 year consumption of food contaminated with (2%). A small proportion of children low fever, appear. If this infection olds, and patients 70 years or enterotoxins. Staphylococcal food (0.5-3%) children will have progresses, subcutaneous abscess, older. intoxication involves rapid onset of asymptomatic infections. Meningitis osteomyelitis, pneumonia, Gastroenteritis: Gastroenteritis nausea, vomiting, abdominal pain, may begin as minor upper respiratory endocarditis, septic arthritis, or “food poisoning” is usually cramps, and diarrhea. Symptoms usually infection. Symptoms include pericarditis, brain abscess, liver characterized by sudden nausea, resolve after 24 hours. Animal bites can behavioural or mental status change, abscess, renal abscess, vomiting, abdominal cramps, result in local infections, cellulitis, fever, vomiting, headaches, and signs bacteremia/septicaemia, conjunctivitis, diarrhea, headache chills and erythema, tenderness, mild fever, of meningeal irritation such as and may develop. 25% of fever up to 39 ºC. The symptoms adenopathy, and lymphangitis (rarely). bulging fontanelle in infants, or stiff the cases present as respiratory tract can be mild to severe and may Scalded skin syndrome is caused by neck in older children or adults. In diseases, which may include last between 5-7 days. The exfoliative toxins secreted on the adults, complete recovery is common epiglottitis, sinusitis, tracheobronchitis, Typhimurium serotype is the epidermis and mostly affects neonates with treatment, but for children there pneumonia, empyema, and pulmonary most common cause of and young children. Other skin is a 2-5% mortality rate, even with abscesses. Rarely, it may also present gastroenteritis and there are an conditions caused by Staphylococcal treatment. Sequelae such as hearing as malakoplakia and as a estimated 1.3 billion cases and 3 exfoliative toxins include blisters, skin loss, mental retardation, seizures, granulomatous pulmonary lesion. The million deaths annually (1.4 loss, , furuncles, impetigo,

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 41 of 92 Revised: January 26, 2017

vision loss, and motor and speech remainder of cases appear as urinary million cases and 600 deaths in , abscesses, poor temperature delay may develop in 15-30% of tract infections, sepsis, or meningitis. the US alone) due to non- control, fluid loss, and secondary cases. Epiglotitis is an acute infection Pasteurellosis may lead to death with typhoidal Salmonella. In well infection. S. aureus can also cause of the upper airway that causes an overall mortality rate of 30% among resourced countries with low necrotizing fasciitis in immuno- oedema and inflammation of the reported cases. levels of invasive complications, compromised individuals, although this and adjacent tissues and the mortality rate due to non- is very rare. Necrotizing fasciitis is life- may lead to complete airway typhoidal Salmonella is lower threatening and causes severe morbidity. obstruction in hours. Symptoms then 1%; however, in developing Certain strains of S. aureus produce the include severe sore throat and fever. countries, the mortality rate can superantigen TSST-1, which is Speaking, swallowing or breathing be as high as 24%. Bacteremia: responsible for 75% of toxic shock may be impaired and respiration may Bacteremia occurs in 3-10% of syndrome (TSS) cases. The clinical be noisy. To assist with breathing, individuals infected presentation of TSS is severe and acute patients may adopt a tripod or with Salmonella entericaand symptoms include high fever, vascular sniffing posture. Airways obstruction certain serotypes (particularly collapse, vomiting, diarrhea, myalgia, results in a 5-10% mortality rate. serotype Choleraesuis) have hypotension, erythematous rash, Cellulitis often affects the face, head higher mortality rates. desquamation, and involvement of at or neck. Cellulitis causes localized Immunosuppressed individuals least 3 organs. Mortality is very high tissue inflammation and may lead to and patients with comorbid and death can occur within 2 hours. proptosis, loss of visual acuity, medical conditions (e.g. HIV- Deep infections include endocarditis, limitation of extraoccular movement AIDS, diabetes, mellitus, peritonitis, necrotizing pneumonia, and death. 12-25% of affected malignancy, corrhosis, chronic bacteremia, meningitis, osteomyelitis, children may have concomitant granulomatous disease, sickle septic arthritis, and infections of bones, meningitis. Other illnesses associated cell disease, lymphoproliferative joints and organs. with infection include pneumonia disease, or collagen vascular (pulmonary infection with purulent disease) have a higher risk of excretion), osteomyelitis (bone developing bacteremia due to infection), septic arthritis (joint a Salmonella infection. infection) and pericaditis (infection of Bacteremia can cause septic the pericardial membrane surrounding shock; endocarditis, especially in the heart). patients older then 50 or with heart conditions; infection of the aorta, especially in patients with pre-existing atherosclerotic disease; liver, spleen, and biliary tract infections in patients with underlying structural abnormalities; mesenteric lymphadenitis; osteomyelitis in long bones and vertebrae; urinary tract infection; pneumonia; pulmonary abscess; brain abscess; subdural and epidural empyema; meningitis;

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 42 of 92 Revised: January 26, 2017

CNS infections (rarely); and death. Enteric fever: Also known as typhoid fever, this infection is caused by serotypes Typhi and Paratyphi. Enteric fever is characterized by fever (rising within 72 hours after the onset of illness) and headache, brachycardia, faint rose-colored rash on the abdomen and chest, anorexia, abdominal pain, myalgias, malaise, diarrhea (more common in children) or constipation (more common in adults), hepatosplenomegaly, segmental ileus, meningismus, and neuropsychiatric manifestations. Less common symptoms are sore throat, cough, and bloody diarrhoea. Complications include myocarditis, encephalopathy, intravascular coagulation, infections of the biliary tree and intestinal tract, urinary tract infection, and metastatic lesions in bone, joints, liver, and meninges. The most severe complication (occurs in about 3% of patients) is haemorrhage due to perforations of the terminal ileum of proximal colon walls. If untreated, the fever can last for weeks; however, with proper antimicrobial therapy, patients usually recover within 10-14 days. The disease is milder in children and, if treated, has a mortality rate of less then 1%; untreated cases can have a mortality rate greater then 10 %. Mode(s) of Phenolic disinfectants, 1% sodium Phenolic disinfectants, 1% sodium Gram negative bacteria are Susceptible to 70% ethanol, Decontamination hypochlorite, 70% ethanol, hypochlorite, 70% ethanol, susceptible to 2-5% phenol, 1% clorhexidine, 1% hypochlorite, 70%

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 43 of 92 Revised: January 26, 2017

formaldehyde, glutaraldehyde, formaldehyde, glutaraldehyde, sodium hypochlorite, 4% ethanol, formaldehyde, glutaraldehyde, iodophore and peracedic acid are iodophore, and peracetic acid are formaldehyde, 2% iodophore, and peracetic acid are effective disinfectants. Inactivated effective against Pasterella spp. glutaraldehyde, 70% ethanol, effective against Serratia sp.; also by UV, microwave, and Pasteurella spp. are inactivated by UV, 70% propanol, 2% peracetic inactivated by UV, microwave, gamma gamma radiation, moist heat (121°C microwave, gamma radiation, moist acid, 3-6% hydrogen peroxide, radiation, moist heat (121°C for at least for at least 20 min), and dry heat heat (121°C for at least 20 min), and quaternary ammonium 20 min), and dry heat (165-170°C for 2 (165-170°C for 2 h. dry heat (165-170°C for 2 h). compounds and iodophors; h). however, Salmonella spp. is resistant to nitrites. Susceptible to moist heat (121°C for at least 15 minutes) and dry heat (170°C for at least 1 hour). Salmonella spp. can also be disinfected with ozone. Emergency Response If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash area thoroughly and encourage bleeding if thoroughly and encourage bleeding if area thoroughly and encourage thoroughly and encourage bleeding if sharps or puncture injury. Seek sharps or puncture injury. Seek bleeding if sharps or puncture sharps or puncture injury. Seek immediate emergency medical immediate emergency medical injury. Seek immediate immediate emergency medical attention. attention. The primary treatment attention. Monitor for symptoms and emergency medical attention. Appropriate biotherapy and ongoing for Haemophilus influenzae is confirm bacteriologically and by PCR. Confirm diagnosis by isolation surveillance are recommended. appropriate antibiotics. Intravenous Give appropriate antibiotic therapy. from stool or blood and by antibiotics are often required but Sensitive to penicillins and serotyping to identify the depending on illness, oral doxycycline. Antibiotics such as serotype. Treatment depends on administration may follow for 7-10 penicillin or derivative are given with the clinical symptoms presented days. If airways are blocked, more clinical observation of infected bites. by the patient. Gastrotenteritis: invasive procedures may be indicated. Fluid and electrolyte Susceptible to chloramphenicol and replacement as well as control of third generation cephalosporins (e.g. the nausea and vomiting are the cefotaxime, ceftriaxone, and usual treatments for these cefuroxime). Resistance has been symptoms. Antibiotic treatment shown for ampicillin, co-trimoxazole, is not usually used; however, it clarithromycin, tetracycline, may be necessary for neonates, chloramphenicol, and rifampicin. children, the elderly, and the Currently, vaccination targets immunosuppressed, in which the PRP antigen and is effective case ciproflaxin, co-trimoxazole, for Hibbut not other Haemophilus ampicillin, and cephalosporins influenzae serotpyes. Vaccine is may be used. Bacteremia: usually given between 2 months and Antibiotic treatment is used to five years of age. Rifampin treat bacteremia (e.g. prophylaxis is indicated for direct ciproflaxin, co-trimoxazole, contacts, as directed by a doctor. ampicillin, or cephalosporins), Pregnant women should not receive especially for neonates, children, prophylactic treatment. the elderly, and the

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 44 of 92 Revised: January 26, 2017

immunosuppressed. Asymptomatic carrier state: Carriers can be treated with ciproflaxin in order to reduce the spread of the infectious agent. Susceptible to chloramphenicol, ciproflaxin, amoxicillin, co- trimoxazole, trimethprim- sulfonamid, cephalosporins and norfloxacin. Some resistance to chloramphenicol has been reported and, in 1989, 32% of strains were multi-drug resistant.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 45 of 92 Revised: January 26, 2017

Medical Surveillance Inventory – Bacteria (cont)

Bordatella bronchiseptica; Serratia sp.; Klebsiella spp.; Vancomycin-resistant Enterococci (VRE)

Pathogen Bordetella bronchiseptica Serratia sp. Klebsiella spp. Vancomycin-resistant Enterococci Identification (VRE)

Mode(s) of Transmission can occur through direct Ingestion of contaminated foods and Klebsiella spp. can be Inhalation of infectious aerosols, Transmission contact with respiratory secretions, direct contact. Nosocomial transmitted through skin contamination of mucocutaneous fomites, or inhalation of infected transmission may occur by hand contact with environmentally lesions, and accidental inoculation are aerosol. Primary lab hazards include contact from hospital personnel and contaminated surfaces and/or the primary hazards associated with parenteral inoculation, contact with other patients. Accidental parenteral objects; examples include working with this pathogen. Direct

non-intact cutaneous and inoculation, droplets exposure of Loofah sponges, medical contact with infectious persons, mucocutaneous barriers, and exposure mucous membrane, infectious equipment, sewage, and blood materials, and objects can also of mucous membranes to infectious aerosols, and ingestion and contact products. Fecal transmission facilitate transmission. Blood, urine, aerosols. Bordetella species survive with non-intact mucocutaneous and has also been suggested for wound samples, and feces are all only for a few hours in respiratory cutaneous barriers. Fomites may some cases of bacteremia potential carriers of this bacterium. In secretions. B. bronchiseptica has been also spread Serratia. S. caused by Klebsiella spp. K. addition, Enterococci can grow and shown to survive for 24 weeks in marcescens may survive from 3 rhinoscleromatis can be survive in harsh environments, and phosphate-buffered saline and lake days to 2 month on dry, inanimate transmitted from person-to- can persist almost anywhere water at 10°C and at 37°C, without any surfaces, and 5 weeks on dry floor. person via airborne secretions; including soil, plants, water, and nutritional supplement. The organism may survive less than however, prolonged contact food. Can survive 5 days to 4 months B. bronchiseptica 4 days in a blood bag under aerobic with infected individuals is on dry inanimate surfaces. can also survive in soil for 45 days. conditions and 20 days in semi- required for infection. K. anaerobic/ granulomatis are sexually anaerobic conditions. It has been transmitted. They may also be also reported to survive in contact vertically transmitted (from lens disinfectant (with mother to child) or by chlorheximide), double-distilled accidental inoculation. water, non-medicated hand soap, but Transmission rates between no duration has been reported for partners are low (<50%) those cases. Serratia spp. are found compared to other sexually in feces, wound exudates, transmitted diseases. Sources respiratory specimen, blood, eye for clinical samples culture, and urine. of Klebsiella spp. primarily include samples from respiratory tract (RT;

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 46 of 92 Revised: January 26, 2017

nasopharyngeal samples) and urinary tract (UT), and blood. Laboratory hazards include direct contact of mucosal membranes with contaminated surfaces and/or object, and inhalation of infectious airborne secretions, accidental parenteral inoculation and/or ingestion. Incubation Unknown; however, one report Unknown. Not clearly understood. Unknown. Period described a 5-year-old girl who According to some sources, became sick 10-12 days after being the incubation period for K. exposed to an infected rabbit. Other granulomatis is usually 1 to 6 human infections with this pathogen weeks. have been reported but none of the cases was incubation period described. Period of Unknown, but spread of infection from Serratia sp. may be transmissible Members of Klebsiella spp. Unknown, but likely for as long as Communicability person-to-person via respiratory between people but rates are can be transmitted from persistence of infection or symptoms, droplets is possible during infection. unknown. person-to-person; however, but symptoms not required. the communicability period is unknown. Approximately one-third of people carry Klebsiellae in their stools; detection rates according to different studies vary from 5% to 36%. Detection rates in nasopharynx vary from 1% to 6%. Hospital personnel have been shown to frequently carry Klebsiellae on their hands. Infectious Dose(s) Unknown. Unknown. Unknown. According to one Unknown. source, 108 Klebsiella organisms per gram of feces are required to produce damage. Typical B. bronchiseptica Serratia sp. are opportunistic Klebsiella spp. have been Enterococci infection will vary Presenting Symptoms is primarily a respiratory tract pathogens and are one of the ten identified as important according to the site of infection. pathogen found in a variety of animals. most common causes of bacteremia common pathogens for If bloodstream infection (bacteremia It causes atrophic in swine, in North America. They are nosocomial pneumonia (7 to or septicemia), fever, elevated heart

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 47 of 92 Revised: January 26, 2017

kennel cough in dogs, with nasal responsible for a variety of 14% of all cases), septicaemia rate, and malaise are common. In turbinate inflammation and turbinate infections, including bacteremia, (4 to 15%), urinary tract severe cases shock can result which is atrophy. It has been implicated as an pneumonia, intravenous infections, infection (UTIs; 6 to 17%), indicated by dizziness, confusion, infrequent cause of infection in osteomyelitis, endocarditis, and wound infections (2 to 4%), hypotension, weakness and fainting humans, primarily in immuno- rarely, endogenous and exogenous intensive care unit (ICU) that can lead to life threatening compromised patients exposed to endophthalmitis. Symptoms of infections (4 to 17%), and conditions. Urinary tract infections infected animals, although infections infection may include heachache, neonatal septicaemias (3 to present as pain or burning during have also been reported in fever, chills, hypotension, vomiting, 20%). Klebsiella urination, back pain, difficulty immunocompetent individuals as well. respiratory distress, erythema, spp. can also cause urinating, frequent urination, or fever. Woolfrey et al., 1991 described 25 ocular pain, periorbital swelling, bacteremias and hepatic Wound, and soft tissue infections patients with B. cellulitis, ear aches, ear discharge, infections, and have been may be red with warm skin and bronchiseptica infections, 56% of and hypopyon (pus in the eyes). The isolated from a number of swelling, pain, and may or may not whom had an immuno-compromising mortality rate from bacteremia due unusual infection, including have pus or pus drainage. They are factor and all except 3 had an exposure to endocarditis, primary gas- also associated with endocarditis and to an infected animal. These Serratia sp. 6 months after infection containing mediastinal in some cases pneumonia which is individuals presented with varied is 37%. Serratia infections in abscess, peritonitis, acute characterized by fever, coughing, clinical manifestations such as neonates are frequent (11-15% in cholecystitis, crepitant shaking chills, and shortness of nosocomial tracheobronchitis, acute neonatal intensive care unit) and myonecrosis, , breath, especially when climbing maxillary sinusitis, peritonitis, may include bloodstream infection necrotizing fasciitis, psoas stairs. septicemia and bacteremia in immuno- (42%), conjunctivitis (26%), muscle abscess, fascial space compromised individuals and pneumonia (13%), urinary tract infections of the head and /pertussis-like disease infection (8%), meningitis (7%), and neck, and septic in healthy individuals. Many B. surgical site infections. Other arthritis. They are also bronchiseptica infections have been infections in infants are documented important opportunistic reported in human immunodeficiency (otitis externa, enterocolitis and pathogens, particularly among virus-infected patients, as Dworkin et omphalitis, gastroenteritis, septic the immuno-compromised. al., 1999 described 9 patients with B. arthritis, and intraperitoneal : Infection bronchiseptica infection/abcess), but are rare. Risk of the upper lobe is more infections, all of whom had at least one factors include birth weight, use of common. Symptoms include: AIDS defining condition. These mechanical ventilation, and fevers, chills, and patients presented with pneumonia, gestational age (under 37 weeks are leukocytosis with red currant sinusitis or . Two cases of at greater risk). The mortality rate in jelly-like sputum. Rare meningitis with B. bronchiseptica have neonates is 44%. complications include lung also been reported. Severe cases of infection involving necrosis illness due to B. bronchiseptica are and sloughing of the entire often found to be co-infections with lobe. Chronic nose toxigenic inflammation has also been . observed as ozena, or . Central nervous system (CNS) infections including meningitis and cerebral abscesses. Clinical symptoms

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 48 of 92 Revised: January 26, 2017

include: headaches, fever, altered consciousness, seizures, and septic shock. Can also cause urinary tract infections, pyogenic liver abscesses (symptoms including fever, right-upper- quadrant pain, nausea, vomiting, diarrhoea or abdominal pain, and leukocytosis. Abscesses occur predominantly in the right lobe and are solitary.) and donovanosis or granuloma, a chronic ulcerative disease that primarily affects the genitalia. Symptoms include development of small papule or at the site of inoculation that later develop into large red ulcers (lesions) that extend along the moist folds of the genitalia. Mode(s) of Information specific to B. Phenolic disinfectants, 1% sodium Gram-negative bacteria are Susceptible to 70% isopropyl alcohol, Decontamination bronciseptica is not available, but most hypochlorite, 70% ethanol, generally susceptible to a 70% ethanol, 0.041% sodium vegetative bacteria have been shown to formaldehyde, glutaraldehyde, number of disinfectants, hypochlorite, phenolic and quaternary be susceptible to low concentrations of iodophore, and peracetic acid are including phenolic ammonia compounds, and chlorine (<1ppm), 70% ethanol, effective against Serratia compounds, hypochlorites glutaraldehyde. Resistant to 3%

phenolics such as orthophenylphenol spp. Serratia spp. are inactivated by (1% sodium hypochlorite), hydrogen peroxide. Enterococci are and ortho-benzyl-para-chlorophenol, UV, microwave, gamma radiation, alcohols (70% ethanol), killed by temperatures in excess of 2% aqueous glutaraldehyde, peracetic moist heat (121°C for at least 20 formaldehyde (18.5 g/L; 5% 80°C. acid (0.001% to 0.2%). Information min), and dry heat (165-170°C for 2 formalin in water), specific to B. bronchiseptica in not h). glutaraldehyde, and iodines available, but most vegetative bacteria (0.075 g/L). Reduction in the can be inactivated by moist heat growth and metabolic activity (121°C for 15 min- 30 min) and dry of K. pneumoniae at heat (160-170°C for 1-2 hours). temperatures >35 °C has been reported. Significant growth reduction has been demonstrated at 60 °C; however, the bacteria still show some metabolic activity (i.e. not completely

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 49 of 92 Revised: January 26, 2017

inactivated). Bacteria can be inactivated by moist heat (121°C for 15 min- 30 min) and dry heat (160-170°C for 1-2 hours). Emergency Response If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected wash area thoroughly and encourage bleeding if thoroughly and encourage bleeding area thoroughly and thoroughly and encourage bleeding if, sharps or puncture injury. Seek if sharps or puncture injury. Seek encourage bleeding if, sharps sharps or puncture injury. Seek immediate emergency medical immediate emergency medical or puncture injury. Seek emergency medical attention. attention. Monitor for symptoms. attention. Appropriate biotherapy immediate medical attention. Monitor for symptoms. Diagnosis is Diagnosis can be made by culturing and ongoing surveillance are Monitor for symptoms. Other via isolation of enterococci from the bacteria from clinical specimens, or recommended. Serratia spp. are tests include isolating strains clinical specimens. Confirm infection via molecular methods such as PCR. usually susceptible to of the bacteria or typing by bacteriological and serological MacConkey agar or Regan-Lowe agar aminoglycosides, fluoroquinolones, different isolates. This is often testing, latex bead agglutination, (RL agar) media can be used for and co-trimazole. necessary for investigation of fluorescent antibody staining or culturing B. bronchiseptica from Many Serratia spp. isolates (39- endemic and epidemic ELISA. Treatment with penicillin or clinical specimens. Since B. 73%) are resistant to gentamicin. nosocomial infections and ampicillin for infections such as bronchiseptica is sensitive to They are all resistant to penicillins also for epidemiological urinary tract infection, peritonitis, and cephalexin, cephalexin is replaced by and cephalosporin. investigations from the wound infections. Combination methicillin or oxacillin in the RL agar environment. therapy of a cell wall- active agent media to allow its growth. Administer Klebsiellae can be isolated by (penicillin, ampicillin or vancomycin) appropriate drug therapy. No specific growth in media. Although and an aminoglycoside is required for guidelines have been described for the there are specific chromogenic the treatment of endocarditis and treatment of B. bronchiseptica. media available for isolating possibly meningitis. Although this Patients are generally treated with these bacteria from specific most strains remain susceptible to aminoglycosides, extended-spectrum samples, Klebsiellae grow some antibiotics, this strain is third-generation penicillin, well on blood and non- resistant to vancomycin. Some tetracycline, and susceptibility to differential media. Biotyping strains have also been identified quinolone and trimethoprim- and serotyping are two which carry genetic elements sulfamethoxazole is variable but it can common forms of typing conferring resistance to generally be administered to children methods used for chloramphenicol, tetracyclines, as oral treatment. Antibiotics course of typing Klebsiella spp. macrolides, lincosamides, quinolones, 2 to 4 weeks is recommended to treat Serotyping is the most widely and streptogramins. the disease. Longer courses, of up to 6 used technique for typing months, have been required for these bacteria which involves treatment in some patients. No detection of capsular antigens vaccines or prophylaxis are available by means of antisera. for humans. Susceptible in vitro to Serotyping tests include: aminoglycosides (amikacin, quelling reaction, gentamicin, and tobramycin), immunofluorescence, double- penicillins such as azlocillin, diffusion gel precipitation, mezlocillin, piperacillin, and counter-current immuno- ticarcillin, broad septrum electrophoreses, Staphylococc

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 50 of 92 Revised: January 26, 2017

cephalosporins, tetracyclines, us coagulation, and latex erythromycin, choramphenicol, and coagulation methods. trimethoprim-sulfamethoxazole. B. Biotyping is not preferred due bronchiseptica strains are usually to the large number of resistant to streptomycin, primary reactions and the amount of penicillins such as penicillin G and time required to complete ampicillin, miocycline, erythromycin, these tests. Molecular typing and ceftriaxone. methods are also being developed, although they are not commonly used. These include: plasmid analysis, ribotyping, PFGE, and random amplified polymorphic DNA analysis, all of which have been successfully used to track strains epidemiologically. Administer appropriate antibiotic therapy where necessary. Klebsiella spp. are known to show resistance to penicillins, especially ampicillin and carbenicillin. Since more and more strains of Klebsiella spp. appear to be developing and harbouring extended-spectrum beta- lactamases (ESBLs), cephalosporinases, and carbapenemases, resistance of Klebsiella spp. to current antibiotics appears to be increasing. According to results from some studies in Europe and USA, ranges of susceptibility were as follows: ceftazidime (92-95%), ceftriaxone (96-98%), cefotaxime (96%), piperacillin-tazobactam (90- 97%), imipeneum (98-100%), gentamicin (95-96%), amikacin (98-99%),

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 51 of 92 Revised: January 26, 2017

triethoprimsulfamethoxazole (SXT) (88-90%). Resistance values tend to be higher for strains isolated from ICU patients compared to non-ICU patients. Pan-resistant isolates have been identified in the Indian subcontinent.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 52 of 92 Revised: January 26, 2017

Pathogen identification, Mode of Transmission, Incubation Period, Period of Communicability, Infectious Dose, Typical Presenting Symptoms, Mode(s) of Decontamination, and Emergency Response:

Untreated Sewage

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 53 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Bacteria ; Mycobacterium spp.; Shigella spp.; Helicobacter pylori

Pathogen Legionella pneumophila Mycobacterium spp. Shigella spp. Helicobacter pylori Identification

Mode(s) of Can be transmitted by aerosols and Nosocomial, direct contact with a Organisms are spread through The exact route of transmission is Transmission aspiration of contaminated water and contaminated environment. the fecal-oral route, and unknown, but acquisition is likely sewage. Lab infection hazards include Mycobacteria are able to survive for transmission is typically to occur during childhood accidental ingestion of the pathogen, weeks to months on inanimate through one of three through faecal–oral or oral–oral direct contact of open wounds/site of objects if protected from mechanisms: ingestion of contact or during gastrointestinal

injury with the pathogen, exposure to sunlight. NTM contaminated foods (washed tract transit disorders. aerosols, and accidental parenteral species are widely distributed in with fecally contaminated Transmission may also occur inoculation. Sources of L. nature and have been found in water, or handled with poor through food-borne, airborne, or pneumophila in the laboratory include sewage, natural water, tap water, hygiene, commonly in tossed waterborne pathways, as the expectorated sputum, lower respiratory soil, water used in showers and salads, chicken, and shellfish); sewage system has been found to specimens, pleural fluid, blood, surgical solutions. NTM can be drinking contaminated water be an agent of dissemination. In pericardial fluid, kidney, liver, spleen, isolated from sputa, exudates from (or in swimming pools); or by its coccoid form, it can survive up myocardium and soft tissues. Other lesions, tissues, environmental person-to-person contact by to one year in a river-water sources include water samples from samples (soil, water), and from anal sexual contact. Spread of microcosm, and remains water systems and fresh water sources. wounds. MAC has also been infection linked to flies has also culturable for more than 10 days isolated from blood, and stool been recorded. Organisms can in 4˚C water. specimens of infected individuals. also be found in stool samples, Lab infection hazards include Primary lab infection hazards but rarely in blood lab samples. accidental ingestion of the include ingestion of the pathogen, The primary lab infection pathogen, direct contact of open direct contact of open wounds/ hazard is accidental ingestion, wounds/site of injury with the site of injury with the pathogen, however, direct contact of open pathogen, exposure to aerosols, exposure to aerosols, and accidental wounds/site of injury with the and accidental parenteral parenteral inoculation. pathogen, exposure to aerosols, inoculation. H. pylori may be and accidental parenteral located in the oral cavity, inoculation are also potential gastrointestinal and hepatobiliary hazards. regions of infected mammals and Shigella species have been birds. They can also be found in recently identified to be the tissues of the small intestine, most frequently identified saliva, gastric juice, and faeces. agent of laboratory-acquired infections because of their high

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 54 of 92 Revised: January 26, 2017

virulence and low infectious dose. Incubation Incubation period for Legionnaires' Infection with M. marinum has an Ranges from 1 – 7 days. Acute Unclear as symptoms usually do Period disease is 2-14 days. Pontiac fever has incubation period of about 2-3 diarrhea can develop within 1 – not appear until adulthood and an incubation period of 30 to 90 hours weeks. 2 days. Symptoms and observable symptoms may never (with 24-48 hours being most may occur within 12 develop (known as silent common). – 50 hours. infections). Major symptoms such as abdominal pain, heartburn, and nausea have been observed 3 – 4 days after ingestion of the bacteria. Period of No person -to-person transfer has been Not generally transferred from Agents begin to be shed in Variable and indefinite. Communicability documented. No documentation of human to human. Transmission is feces 4 weeks after infection, Transmission between people zoonotic (animal-to-human) or animal- dependent on accidental ingestion or and it is communicable as long usually occurs through oral-oral to-animal transmission cases have been contact with contaminated material as the organisms are present in routes. Carriers can be infectious described. source(s). excrement. Although rare, and symptom free. asymptomatic carriers can also spread the infection for up to some months. Infectious Dose(s) Unknown. Unknown. Infection can result from Unknown for humans. Infection ingestion of 10 – 200 in the Rhesus monkey occurred organisms. with a minimum of 104 H. pylori bacteria intake by orogastrical inoculation. Typical L. pneumophila Non-tuberculous mycobacteria Ingested pathogens can survive H. pylori are not invasive, but Presenting infection can cause Legionnaires' (NTM) infections occur mainly in gastric acidity and cause illness colonize in the human stomach’s Symptoms disease, a severe form of pneumonia. immunosuppressed individuals, by infecting the colonic mucosa antral region and gastric mucosal The symptoms of Legionnaire's disease although immunocompetent patients and multiplying in the colonic surfaces where they release include confusion, headache, can also be affected. Non epithelial cells, and spreading pathogenic proteins that induce

diarrhoea, abdominal pain, fever, tuberculous mycobacteria cause laterally to adjacent cells. cell injury and inflammation. This chills, and myalgia as well as a non- many different diseases in humans: Infection may be mild and can result in clinical symptoms of productive cough. Mortality rate is Pulmonary disease: Pulmonary asymptomatic, but it is most infection, such as duodenal ulcer reported to be 15-25%. diseases are caused mainly by M. commonly characterized by and gastric adenocarcinoma. Pontiac fever is a non-pneumonic form kansasii, MAC, and rarely by M. acute intestinal infections upon Other common illnesses as a of L. pneumophila infection. malmoense, M. xenopi, M. ingestion, resulting in mild result of infection include Symptoms are flu-like, including fever, asiaticum, M. simiae and M. szulga. watery diarrhea to severe gastroenteritis, diffuse antral tiredness, myalgia, headache, sore Pulmonary disease may show inflammatory bacillary gastritis, and gastric throat, nausea, and cough may or may different clinical patterns: dysentery or shigellosis, carcinoma. H. pylori is a Class I not be present. Pontiac fever is self tuberculosis like infiltrates, nodular manifested by severe human carcinogen according to limited and requires no hospitalization bronchiectasis, solitary nodules, and abdominal cramps, nausea and the World Health Organization. or antibiotic therapies. There are no diffuse infiltrates. vomiting, fever, tenesmus, Infection can last a lifetime in the anorexia, and stool containing host if not properly treated,

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 55 of 92 Revised: January 26, 2017

reported deaths associated with Pontiac Lymphadenitis: caused mainly blood and mucus. Further causing chronic gastritis which fever. by MAC, M. scrofulaceum, M. complications include Reiter’s can lead to peptic gastroduodenal Although up to 85-90% of cases can be haemophilum, M. syndrome which has been ulcer disease. The rate of attributed to L. pneumophila, fortuitum, M. kansasii. associated with S. flexneri, mortality varies with country and approximately half of the remaining 49 Cutaneous and soft tissue infections severe dehydration, intestinal age, but is generally low, being species in the genus have caused (skin ulcers): Cutaneous or skin perforation, toxic mega colon, around 2 – 4%. disease in humans. It is conjectured infections may be associated bacteremia, toxaemia, that up to 40% of cases involving these with M. marinum, M. ulcerans, M. septicaemia, seizures, toxic rare pathogens, attributed to species fortuitum, and M. chelonei . M. encephalopathy with headache and groups other than L. marinumcan cause cutaneous and alterations of pneumophila sero-group 1, are missed infection on exposure of broken skin consciousness, septic shock and clinically if commercially available to contaminated freshwater fish convulsions (very rare), and urine antigen detection kits, which tanks. The disease is characterized haemolytic uremic syndrome, target only L. pneumophila sero-group by a formation of a single which have been linked to 1, are used exclusively for diagnosis. papulonodular lesion confined to Shiga toxin (a potent cytotoxin Sources of L. pneumophila in the one extremity, which with time may produced by S. dysenteriae that laboratory include expectorated become ulcerative. M. can also cause other neurotoxic sputum, lower respiratory specimens, ulcerans causes cutaneous skin effects). Virulence pleural fluid, blood, pericardial fluid, ulcers which may vary from a of Shigella is temperature- kidney, liver, spleen, myocardium and localized nodule to widespread regulated, as organisms are soft tissues. Other sources include ulcerative or non-ulcerative disease able to invade HeLa cells at water samples from water systems and including osteomyelitis. 37°C, and cannot do so in fresh water sources. Other infections associated vitro at 30°C. Infections are with NTM include enteritis, usually self-limiting, but can musculoskeletal disease, bursitis, become life-threatening in CNS disease, corneal infections, and immunocompromised patients otitis media. Disseminated infection or if not properly treated. and bacteremia may also occur. Severity of infection depends Disseminated infection occurs on the host, dose, and mainly in immuno-suppresed serotype. S. dysenteriae is the individuals, and may involve liver, most pathogenic species, with a spleen, bone marrow. Patients with fatality rate up to 20%, disseminated infection present with whereas S. sonnei usually cause nonspecific symptoms such as fever, mild forms of shigellosis. malaise, weight loss, anorexia, abdominal pain and night sweats. Mode(s) of L. pneumophila The vegetative state is susceptible to Susceptible to 1% sodium Readily inactivated by free Decontamination is susceptible to 1% solutions of disinfectants such as 70% ethanol, hypochlorite, 70% ethanol, 2% chlorine, iodine treatments can sodium hypochlorite, 2% phenol, 2% 0.1% sodium hypochlorite, and glutaraldehyde, iodines, inhibit its vacuolation toxin gluteraldehyde, isopropyl alcohol, and 0.1N NaOH. Spores may be phenolics, and formaldehyde . activity, thus practices used for formaldehyde. L. pneumophila resistant to disinfectants. Toxins are Organisms can be heat-killed treating drinking water, apart

can be inactivated in water inactivated (more than 99.7%) by 20 by steaming using an autoclave from ozonolysis, should be by UV light, and temperatures of 80 °C minutes exposure to 3 mg/L free for 1 hour at 100˚C under sufficient for disinfecting H.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 56 of 92 Revised: January 26, 2017

for 0.4 minutes when in its aqueous available chlorine (FAC; similar to normal atmospheric pressure. pylori as well. Exposing H. environment. Autoclave conditions of the military disinfection procedure), Can survive up to months on pylori to 1.1mg/L residual 121 °C for 15 minutes. L. and 84% inactivated by a treatment dry surfaces, up to 10 days in chlorine for 45 minutes is enough pneumophila is found naturally in most of 20 minutes at 0.4 mg/L FAC citric juices and carbonated soft to eradicate the pathogen fresh water sources, including lakes, (similar to municipal water drinks, several days on (biocidal properties of chlorine ponds, and rivers. It is also found in treatment procedures). Toxin is contaminated vegetables, over are optimized at lower pH levels, cooling towers, plumbing systems, destroyed after heating for 5 minutes 3 hours on fingers, 2 – 28 days such as around 98 days. recommended to sterilize with dry MacConkey agar. Flies can culturing H. pylori in the Clinical specimens will usually support heat (2 hours at 160°C) by carry Shigellafor up to 20 – 24 laboratory is difficult as it needs the survival of L. pneumophila for up autoclaving (20 minutes at 121°C, 1 days. adequate conditions of to 1 week. atm pressure) and/or by irradiation. desiccation, air supply, and Survives well in soil, water and temperature, it is likely that it agricultural products. does not survive well outside of its host; however, in its coccoid form, it can survive up to one year in a river-water microcosm, and remains culturable for more than 10 days in 4˚C water. Emergency If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding area thoroughly and encourage area thoroughly and encourage sharps or puncture injury. Seek if, sharps or puncture injury. Seek bleeding if, sharps or puncture bleeding if, sharps or puncture immediate medical attention. Monitor immediate medical attention. injury. Seek immediate medical injury. Seek immediate medical for symptoms. Diagnosis can be Monitor for symptoms. Diagnosis attention. Monitor for attention. Monitor for symptoms.

confirmed via identification of L. of NTM infection can be done via symptoms. Serological testing Presence of H. pylori can be pneumophila, often isolated from culture of clinical specimens and of stool isolates can distinguish confirmed by culture, blood respiratory secretions, by culturing, identification using phenotypic and confirm serogroups. antigen detection, urease immunofluorescent staining, urine characteristics (growth rate, colony Administer appropriate drug detection, or bacterial metabolite antigen tests, PCR or serologic tests. pigmentation and biochemical tests); therapy. Oral rehydration or detection in the infected Respiratory fluoroquinolones and the histopathological examination to electrolyte replacement in individual’s breath. Administer newer macrolides are used to treat L. demonstrate the presence of dehydrated patients can lead to appropriate drug therapy. H. pneumophila pneumonia. Treatment granuloma in aspirates or biopsies; recovery within days. pylori is rapidly developing typically lasts 7-10 days or in the case serotyping methods; isoenzyme and Antibiotics usually are not antibiotic resistance, so antibiotics of immunosuppressed patients, 21 protein electro-pherogram based needed in mild cases, but can be applied with a proton days. Pontiac fever usually does not methods; should be administered for pump inhibitor or a bismuth require antimicrobial therapy. L. and PCR, DNA fingerprinting and infections involving S. compound. Such dual, triple or pneumophila is susceptible to identification using gene probes. A dysenteriae. Antimicrobials quadruple treatments have been erythromyin, clarithromycin, combination of several antibiotics may reduce duration of found to be more effective than

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 57 of 92 Revised: January 26, 2017

azithromycin, tetracycline, moxifloxin, over long periods of time is infection, carriage state of the administering one antibiotic and levofloxacin. Aminoglycosides recommended for treatment patient, and mortality. Other alone. Sensitivity has been such as gentamicin, kanamycin and of NTM infections. The most treatments aids for severe cases established for clarithromycin, streptomycin are active against L. important antibiotics used in include mechanical ventilation, amoxicillin, tetracycline, pneumophila; however, there are antimyco-bacterial therapy include: anticonvelsants, and inotropics. imipenem, cefaclor, minocycline, mutant strains that show resistance to rifampin, isoniazid, ethambutol, simethicone, gabexate mesilate, streptomycin. Beta-lactam antibiotics macrolides (clarithromycin, and ketoconazole. Strains have (i.e. penicillin, cephalosporins) are azithromycin), quinolones been found to show resistance to ineffective against L. pneumophila. (ciprofloxacin, moxifloxacin, antibodies such as clarithromycin, gatifloxacin), aminoglycosides erythromycin, ofloxacin, and (streptomycin, amikacin) and metronidazole, and show low linezolid. Surgery may be useful in levels of resistance to tetracycline, removing debridement in soft tissue amoxicillin, fluoroquinolones, diseases caused by NTM species, and rifabutin. Omeprazole, and in managing cervical clarithromycin, and lymphadenitis. Surgery can also be metronidazole can be used along with antibiotic therapy to administered if early symptoms of reduce the bacterial load and to cure infection such as heartburn, life threatening symptoms such as nausea, or severe epigastic cramps hemoptysis. Combinational drug are experienced. Recombinant therapy is used as different species urease (rUrease) and parenteral are susceptible and resistant to vaccine containing H. different drugs. Drug susceptibility pylori antigens (CagA, VacA, and tests are performed on isolated NAP) in combination with organisms to guide proper aluminum hydroxide as an therapy. M. kansasii is susceptible to adjuvant have been found to be first line tuberculosis drugs effective vaccines against H. (rifampin, isoniazid, pyrazinamide pylori, although they cannot and ethambutol). M. marinum is prevent re-infection. resistant to pyrazinamide, and MAC organisms, unlike M. kansasii, are resistant to first line tuberculosis drugs.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 58 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Bacteria – (cont)

Escherichia coli (enterotoxigenic); Escherichia coli (uropathogenic); Escherichia coli (entero-hemorrhagic), Escherichia coli (septicemia causing)

Pathogen Escherichia coli (enterotoxigenic) Escherichia coli (uropathogenic) Escherichia coli, (entero- Escherichia coli (septicemia Identification hemorrhagic) causing)

Mode(s) of Ingestion of contaminated food or Ingestion of contaminated food or Ingestion of contaminated food Ingestion of contaminated food or Transmission other materials; fecal-oral other materials; fecal-oral or other materials; fecal-oral other materials; fecal-oral transmission. The primary lab transmission. The primary lab transmission; person-to-person transmission. The primary lab infection hazard is accidental infection hazard is accidental transmission (extremely high). infection hazard is accidental ingestion, however, direct contact of ingestion, however, direct contact of The primary lab infection ingestion, however, direct contact

open wounds/site of injury with the open wounds/site of injury with the hazard is accidental ingestion, of open wounds/site of injury pathogen, exposure to aerosols, and pathogen, exposure to aerosols, and however, direct contact of open with the pathogen, exposure to accidental parenteral inoculation are accidental parenteral inoculation are wounds/site of injury with the aerosols, and accidental parenteral also potential hazards. Sources also potential hazards. Sources pathogen, exposure to aerosols, inoculation are also potential of entero-toxigenic E. coli, in the of entero-toxigenic E. coli, in the and accidental parenteral hazards. Sources of entero- laboratory include contaminated food laboratory include contaminated inoculation are also potential toxigenic E. coli, in the laboratory products, faeces, and sewage. food products, faeces, and sewage. hazards. Sources of entero- include contaminated food hemorrhagic E. coli, in the products, faeces, and sewage. laboratory include contaminated food products, faeces, and sewage. Incubation Between 14 and 30 hours. 3-8 days. 2-8 days. Unknown. Period

Period of Can last from days to months. Can be transferred from human to Can last from days to months. Not transferred from human to Communicability human via heterosexual intercourse human. Transmission is as well as via accidental ingestion or dependent on contact with contact with contaminated material contaminated material source(s). source(s). Infectious Dose(s) The infectious dose of ETEC in adult Unknown. Appears to have low infectious Unknown. is estimated to be at least dose, may be similar to that of 108organisms, but the young, the Shigella spp.,10 organisms by elderly and the infirm may be ingestion. susceptible to lower numbers.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 59 of 92 Revised: January 26, 2017

Typical Patients with ETEC enteritis usually Burning during urination, frequent Hemorrhagic colitis, intestinal Bacteraemia which can lead to Presenting have an abrupt onset of watery urges to urinate with very little disease accompanied by septicemia (symptoms: fever, a Symptoms diarrhea that does not contain blood, passage of urine, foul smelling, cramps and abdominal pain; rapid heart rate, shaking chills, pus, or mucus (nondysenteric). The cloudy, or bloody urine, fever, initially watery, followed by low blood pressure, diarrhea is usually mild to moderate in chills, pelvic pain in women, rectal bloody diarrhea; low grade gastrointestinal symptoms

severity, but some patients may have pain in men, and pain in the lower fever; last about 8 days; 5-10% (abdominal severe fluid loss. Low-grade fever, back, abdomen, hips, or flank. of hemorrhagic colitis victims pain, nausea, vomiting, nausea, and abdominal pain may also may develop hemolytic uremic and diarrhea), rapid breathing, be present. Dehydration may become syndrome (HUS); affects all and/or confusion). severe or life threatening in neonates ages, higher death rates occur and children, necessitating aggressive in elderly and young; can cause fluid and electrolyte replacement. A thrombo-cytopenic purpura self-limited course, with resolution in (TTP) in elderly. 2-5 days, is most common in adult travelers who acquire the disease, though some strains of the organism may produce a disease lasting much longer, with a median duration of illness of 7 days. There are an estimated 800,000 deaths each year due to ETEC. Mode(s) of Susceptible to a combination of 2,2- Susceptible to a combination of 2,2- Susceptible to many Susceptible to a combination of Decontamination dibromo-2-cyanoacetamide (DBA) dibromo-2-cyanoacetamide (DBA) disinfectants - 1% sodium 2,2-dibromo-2-cyanoacetamide with sodium iodide (20:80 parts), with sodium iodide (20:80 parts), hypochlorite, 70% ethanol, (DBA) with sodium iodide (20:80 iodine, 2 % glutaraldehyde, quaternary iodine, 2 % glutaraldehyde, phenolics, glutaraldehyde, parts), iodine, 2 % ammonium (20°C, 0.5 min), quaternary ammonium (20°C, 0.5 iodines, formaldehyde. Heat glutaraldehyde, quaternary

hypochlorite (0.525%, 20°C, 0.5 min), min), hypochlorite (0.525%, 20°C, sensitive, inactivated by moist ammonium (20°C, 0.5 min), phenolic (20°C, 0.5 min), and ethyl 0.5 min), phenolics (20°C, 0.5 min), heat (121° C for at least 15 hypochlorite (0.525%, 20°C, 0.5 alcohol (70%, 20°C, 0.5 min). Ozone and ethyl alcohol (70%, 20°C, 0.5 min) and dry heat (160-170° C min), phenolics (20°C, 0.5 min), can inactivate E. coli. E. coli are also min). E. coli are also sensitive to for at least 1 hour). Survives and ethyl alcohol (70%, 20°C, 0.5 sensitive to heat treatment, especially heat treatment, especially at well in contaminated feces and min). E. coli are also sensitive to at temperatures of 70°C or higher. Can temperatures of 70°C or higher. Can soil, only small reduction in heat treatment, especially at survive for 1.5 hours to 16 months on survive for 1.5 hours to 16 months organism number over 2 temperatures of 70°C or higher. dry inanimate surfaces. on dry inanimate surfaces. months Can survive for 1.5 hours to 16 months on dry inanimate surfaces. Emergency If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding area thoroughly and encourage area thoroughly and encourage sharps or puncture injury. Seek if, sharps or puncture injury. Seek bleeding if, sharps or puncture bleeding if, sharps or puncture immediate medical attention. Monitor immediate medical attention. injury. Seek immediate medical injury. Sepsis is a genuine for symptoms. Stool culture is a Monitor for symptoms. Strain attention. Monitor for medical emergency. Seek

common method used to identify E. identification by molecular and symptoms; confirm immediate medical attention. coli. ETEC can be detected using non- biochemical means is necessary to bacteriologically, DNA probe Monitor for symptoms. Adequate radioactively labeled oligonucleotides determine proper antibiotic to detect Verotoxins VT1 and organ perfusion should be ensured

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 60 of 92 Revised: January 26, 2017

DNA probes and PCR targeted against treatment. Antibiotic treatment, VT2. Electrolyte fluid therapy; and hypotension should be the LT and ST genes. ELISA can also typically with trimethoprim antibiotics may be administered managed with with intravenous be used to detect LT and ST. /sulfamethoxazole, ciprofloxacin, in very severe cases. Sensitive administration of supplementary Treatment with Fosfomycin, Nirtofurantoin, to a wide spectrum of fluids. Ventilatory support should trimethoprim/sulfamethoxazole (TMP- Levofloxacinm Cephalexin, antibiotics. be provided for patients with SMX) or quinolones reduces the Ceftrialone, Azithromycin, and progressive hypoxia, hypercapnia, duration of diarrhea. Treatment of fluid Doxycycline may be effective for altered sensorium, or respiratory and electrolyte loss is usually achieved eradication of the infecting strain. muscle fatigue. Blood glucose through oral rehydration. The use of However, there is documentation of must be maintained and if present, the World Health Organization Oral increases in antibiotic resistance, disseminated intravascular Rehydration Salts (ORS) solution has allergic reaction to certain coagulation must be managed via been recommended. Intravenous pharmaceuticals, alteration of transfusion. Strain identification rehydration may be necessary for normal gut flora, and failure to by molecular and biochemical infants, individuals with excessive prevent recurrent infections. means is necessary to determine vomiting, or those with severe proper antibiotic treatment. dehydration. Bismuth subsalicylate Antibiotics should initially be may decrease the amount of diarrhea given intravenously. Ideally, and the duration of disease. antibiotic treatment should start Antimicrobial therapy is generally not within an hour of diagnosis to indicated, because of the self-limited reduce the risk of serious nature of this disease. Susceptible to complications or death. carbapenem, fosfomycin-trometanol, Intravenous nitrofurantoin, and bovine apo- antibiotics are usually replaced by lactoferrin. E. coli can be resistant to tablets after two to four days. chloramphenicol, β lactams, nalidixic acid, ampicillin, and ciprofloxacin. Fluoroquinolones such as ciprofloxacin enhance toxin production.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 61 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Bacteria – (cont)

Staphylococcus aureus (MRSA, MSSA, VISA, hVISA, VRSA); Salmonella enterica spp.; Aeormonas hydrophilia; Campylobacter coli.

Pathogen Staphylococcus aureus, (MRSA, Salmonella enterica spp. Campylobacter coli Identification MSSA, VISA, hVISA, VRSA)

Mode(s) of Ingestion of food containing Human infection usually occurs Infection is spread via fecal- Oral ingestion of bacteria from Transmission enterotoxins. Vertical transmission when consuming contaminated oral transmission during direct contaminated food, contaminated during vaginal delivery is uncommon. foods and water, contact with ingestion or drinking of drinking water, and sewage. Person-to-person transmission occurs infected feces, as well as contact contaminated water or foods. Contact with animals and their through contact with a purulent lesion with infective animals, animal feed, Infection can also be feces is also a source of infection.

or with a carrier. Unsanitary conditions or humans. Foods that pose a higher transmitted by eating Primary lab infection hazards and crowded community settings risk include meat, poultry, milk contaminated meat, dairy, include: accidental ingestion, increase exposure to S. aureus. products, and egg products. In shrimp, or fish. Primary lab direct contact of open wounds/site Infection may be spread from person- hospitals, the bacteria have been infection hazards include of injury with the pathogen, to-person through health care workers spread by personnel in pediatric ingestion of the pathogen, exposure to aerosols, and or patients. Nasal colonization can lead wards, either on their hands or on direct contact of open wounds/ accidental parenteral inoculation. to auto-infection. Lab infection hazards inadequately disinfected scopes. site of injury with the pathogen, Campylobacter include accidental ingestion of the Flies can infect foods which can also exposure to aerosols, and can survive for many weeks in pathogen, direct contact of open be a risk for transmission to humans. accidental parenteral water at 4°C, but only a few days wounds/site of injury with the Primary lab infection hazards inoculation. The bacteria have above 15°C, and for 2-10 hours pathogen, exposure to aerosols, and include ingestion of the pathogen, been isolated from feces, when exposed to drying. Nearly accidental parenteral inoculation. direct contact of open wounds/ sputum, urine, bile, pus, all water sources are Laboratory sources of infection site of injury with the pathogen, surgical wounds, medicinal contaminated with C. coli. include, but are not limited to: CSF, exposure to aerosols, and accidental leeches, normal flora, spleen, joint aspirates, blood, abscesses, parenteral inoculation. pleural fluid, placenta, skin aerosols, faeces, urine, and All Salmonella enterica subspecies lesion, throat, gall bladder, contaminated water sources. (with the exception of serotype hospital water supplies, dialysis Typhi) are found in blood, urine, fluids, and blood plasma feces, food and feed and products. environmental materials. Serotype Typhi is found in blood, urine, feces and bile. Incubation Onset of symptoms after consuming For non-typhoidal salmonellosis, the The reported incubation period 1 to 10 days. Period contaminated food is usually 30 incubation period is variable, for Aeromonas-associated minutes to 8 hours. Colonies of S. depends on the inoculum size, and diarrhea is 1 to 2 days.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 62 of 92 Revised: January 26, 2017

aureus can be carried for an usually ranges between 5 and 72 Aeromonas’ infections undetermined amount of time; some hours. For typhoid fever, the contracted via recreational individuals may carry it chronically, incubation period can be between 3 sporting activities, such as and some may carry it intermittently. and 60 days, although most swimming occur as early as infections occur 7-14 days after 24h post exposure. Cellulitis is contamination. The incubation the most frequent soft tissue period for typhoid fever is highly infection and is usually variable and depends on inoculum accompanied by systemic signs size, host susceptibility, and the developing within 8 to 48 h. bacterial strain . The length of time from initial A. hydrophila infection to bacteremia ranges from 1 to 38 days. Period of Communicable period is as long as a Humans can spread the disease for It can be transferred from Not generally transferred from Communicability purulent lesion is present or carrier as long as they shed the bacterium in human-to-human by contact human to human. Transmission is state persists. their feces. Certain carriers shed the with infected wounds, feces or dependent on accidental ingestion bacteria for years and 5 % of blood. The pathogen can also or contact with contaminated patients recovering from non- be transferred during sports; material source(s). typhoidal salmonellosis can shed the especially when played in bacteria for 20 weeks. Animals can muddy environments involving have a latent or carrier state where transfer of infected soil. they excrete the organism briefly, intermittently or persistently. Infectious Dose(s) At least 100,000 organisms in humans. The infectious dose varies with the The infectious dose for humans As low as 500 organisms by serotype. For non-typhoidal and animals is greater than 1010 ingestion. One volunteer study salmonellosis, the infectious dose is organisms. found that 9000 bacteria were approximately 103 bacilli. For required to infect 50 percent of enteric fever, the infectious dose is subjects. about 105 bacilli by ingestion. Patients with achlorhydria, depressed cell-mediated immunity, or who are elderly may become infected with at a lower infectious dose. The infectious dose may also be dependent on the level of acidity in the patient’s stomach. Typical Staphylococcus aureus is an Salmonella enterica can cause four Infection with Aeromonas A major agent of gastroenteritis Presenting opportunistic pathogen that can cause a different clinical manifestations: hydrophila can result in and acute enterocolitis in humans, Symptoms variety of self-limiting to life- gastroenteritis, bacteremia, enteric gastrointestinal or non- and also of acute diarrheal threatening diseases in humans. The fever, and an asymptomatic carrier gastrointestinal complications. illnesses in developed countries. bacteria are a leading cause of food state. It is more common in children Symptoms of gastrointestinal Typical symptoms include watery

poisoning, resulting from the infection range from watery diarrhea that may contain red or

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 63 of 92 Revised: January 26, 2017

consumption of food contaminated under the age of 5, adults 20-30 year diarrhea to dysenteric or bloody white blood cells, inflammatory with enterotoxins. Staphylococcal food olds, and patients 70 years or older. diarrhea. Chronic infection is enterocolitis, abdominal pain, intoxication involves rapid onset of Gastroenteritis: Gastroenteritis or also possible. Non- fever, malaise, nausea and nausea, vomiting, abdominal pain, “food poisoning” is usually gastrointestinal complications vomiting. Symptoms usually last cramps, and diarrhea. Symptoms characterized by sudden nausea, that may arise subsequent to A. for about a week, with relapses usually resolve after 24 hours. Animal vomiting, abdominal cramps, hydrophila infection include occurring in 5-10% of cases if bites can result in local infections, diarrhea, headache chills and fever hemolytic syndrome and untreated, and persistent cellulitis, erythema, tenderness, mild up to 39 ºC. The symptoms can be kidney disease, cellulitis, symptoms may be observed in fever, adenopathy, and lymphangitis mild to severe and may last between wound and soft-tissue immuno-compromised patients. A (rarely). Scalded skin syndrome is 5-7 days. The Typhimurium infection, meningitis, large number of campylobacter caused by exfoliative toxins secreted serotype is the most common cause bacteremia and septicemia, infections are asymptomatic; on the epidermis and mostly affects of gastroenteritis and there are an ocular infections, pneumonia however, although the illness is neonates and young children. Other estimated 1.3 billion cases and 3 and respiratory tract infections, generally mild, many skin conditions caused by million deaths annually (1.4 million urinary tract infection in complications can be preceded by Staphylococcal exfoliative toxins cases and 600 deaths in the US neonates, osteomyelitis, enteritis, including bacteremia, include blisters, skin loss, pimples, alone) due to non- peritonitis and acute hepatitis, cholecystitis, furuncles, impetigo, folliculitis, typhoidal Salmonella. In well cholecystitis. Severe infection pancreatitis, urinary tract abscesses, poor temperature control, resourced countries with low levels can result from non resolved infection, abortion, myocarditis fluid loss, and secondary infection. S. of invasive complications, the intermittent diarrhea, which can and meningitis. In developing aureus can also cause necrotizing mortality rate due to non- occur months after the initial countries where infections are fasciitis in immunocompromised typhoidalSalmonella is lower then infection. A. hydrophila can endemic, the majority of individuals, although this is very rare. 1%; however, in developing cause disease in aquatic symptomatic cases occur in young Necrotizing fasciitis is life-threatening countries, the mortality rate can be animals, such as red leg disease children. and causes severe morbidity. as high as 24%. in frogs which is caused by Certain strains of S. aureus produce Bacteremia: Bacteremia occurs in 3- endotoxin and haemolysin the superantigen TSST-1, which is 10% of individuals infected produced by the bacteria and responsible for 75% of toxic shock with Salmonella entericaand certain can be fatal. syndrome (TSS) cases. The clinical serotypes (particularly serotype presentation of TSS is severe and acute Choleraesuis) have higher mortality symptoms include high fever, vascular rates. Immunosuppressed collapse, vomiting, diarrhea, myalgia, individuals and patients with hypotension, erythematous rash, comorbid medical conditions (e.g. desquamation, and involvement of at HIV-AIDS, diabetes, mellitus, least 3 organs. Mortality is very high malignancy, corrhosis, chronic and death can occur within 2 hours. granulomatous disease, sickle cell Toxic shock syndrome is associated disease, lymphoproliferative disease, with vaginal colonization with toxin- or collagen vascular disease) have a producing S. aureus during higher risk of developing bacteremia menstruation, complications with due to a Salmonella infection. at other sites, Bacteremia can cause septic shock; or complications of surgical endocarditis, especially in patients procedures. Deep infections include older then 50 or with heart endocarditis, peritonitis, necrotizing conditions; infection of the aorta,

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 64 of 92 Revised: January 26, 2017

pneumonia, bacteremia, meningitis, especially in patients with pre- osteomyelitis, septic arthritis, and existing atherosclerotic disease; infections of bones, joints and organs. liver, spleen, and biliary tract infections in patients with underlying structural abnormalities; mesenteric lymphadenitis; osteomyelitis in long bones and vertebrae; urinary tract infection; pneumonia; pulmonary abscess; brain abscess; subdural and epidural empyema; meningitis; CNS infections (rarely); and death. Enteric fever: Also known as typhoid fever, this infection is caused by serotypes Typhi and Paratyphi. Enteric fever is characterized by fever (rising within 72 hours after the onset of illness) and headache, brachycardia, faint rose-colored rash on the abdomen and chest, anorexia, abdominal pain, myalgias, malaise, diarrhea (more common in children) or constipation (more common in adults), hepatosplenomegaly, segmental ileus, meningismus, and neuropsychiatric manifestations. Less common symptoms are sore throat, cough, and bloody diarrhoea. Complications include myocarditis, encephalopathy, intravascular coagulation, infections of the biliary tree and intestinal tract, urinary tract infection, and metastatic lesions in bone, joints, liver, and meninges. The most severe complication (occurs in about 3% of patients) is haemorrhage due to perforations of the terminal ileum of proximal colon walls. If untreated, the fever can last for weeks; however, with proper antimicrobial therapy, patients usually recover within 10-14 days.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 65 of 92 Revised: January 26, 2017

The disease is milder in children and, if treated, has a mortality rate of less then 1%; untreated cases can have a mortality rate greater then 10%. Mode(s) of Susceptible to 70% ethanol, Gram negative bacteria are Susceptibility has been shown Inactivation can be achieved by Decontamination clorhexidine, 1% sodium hypochlorite, susceptible to 2-5% phenol, 1% for 1% sodium hypochlorite, using >1.5% concentration of 2% glutaraldehyde, 0.25% sodium hypochlorite, 4% 2% glutaraldehyde, 70% NaCl. A related pathogen C. benzalkonium chloride, and formaldehyde, 2% glutaraldehyde, ethanol, iodines, phenolics, and jejuni is susceptible to 10 mg/L formaldehyde. Staphylococcus 70% ethanol, 70% propanol, 2% formaldehyde. It is also iodophor, 1:50 000 quaternary

aureus can grow in a pH of 4.2 to 9.3 peracetic acid, 3-6% hydrogen sensitive to silver in water and ammonium compound, 0.15% and in salt concentrations of up to peroxide, quaternary ammonium free chlorine. Exposure to phenolic compound, 70% ethyl 15%. Enterotoxins are resistant to compounds and iodophors; temperatures of 62oC or greater alcohol or 0.125% glutaraldehyde temperatures that would destroy the however, Salmonella spp. is for more that a few minutes is all with a contact time of 1 minute bacilli. Sensitive to dry heat treatment resistant to nitrites. Susceptible to lethal to A. hydrophila. The or 5mg/L of hypochlorite with a of 160-170oC for at least an hour, but moist heat (121°C for at least 15 bacteria can be inactivated by contact time of 5 minutes. not to moist heat treatment. Survives minutes) and dry heat (170°C for at moist heat (121°C for 15 min - Inactivated by heat (70°C for 1 on carcasses and organs (up to 42 least 1 hour). 30 min) and dry heat (160- min), hydrostatic pressure (450 days), floors (less than 7 days), glass Salmonella spp. can also be 170°C for 1-2 hours). The MPa at 15°C for 30 s), and pH (46 hours), sunlight (17 hours), UV (7 disinfected with ozone. Serotype bacteria can also be inactivated levels below 5.0 and above 9.0. hours), meat products (60 days), coins Choleraesuis can survive in wet by ultrasonic waves delivered Campylobacter cells can enter a (up to 7 days), skin (30 minutes to 38 swine feces for at least 3 months and under high pressure (200 KPa) viable but nonculturable state days) (citation needed). Depending on in dry swine feces for at least 13 and elevated temperatures (40 (VBNC) when subject to stress. colony size, S. aureus can survive on months. Serotype Dublin can °C). Simultaneous sonication at This is thought to improve their fabrics from days to months. survive in feces spread on concrete, temperature higher than 70°C survival in the environment, as it rubber, and polyester for almost six and 0.5 MPa is also effective. has been observed to survive years. Serotype Typhimurium can Aeromonas hydrophila can freezing for several months in survive in cattle slurry for 19-60 survive in large volumes of frozen poultry, minced meat, and days, cattle manure for 48 days, soil open water, ground water, soil, other cold food products. for 231 days, and water for up to as well as polluted lakes and Campylobacter can survive for 152 days. Flies have been shown to rivers and sewage. many weeks in water at 4°C, but excrete certain serotypes for 8 days only a few days above 15°C, and and bed bugs can excrete bacilli for for 2-10 hours when exposed to up to 21 days. Certain serotypes drying. have been shown to survive on fingertips for up to 80 minutes, depending on the inoculum size. Salmonella serotypes have been found to live up to 63 days on lettuce, 231 days on parsley, 32 weeks in pecans, 10 months on refrigerated cheddar cheese, 9 months in butter, up to 63 days in

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 66 of 92 Revised: January 26, 2017

frozen yogurt, and up to 20 weeks on frozen minced beef and chicken. Emergency If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding area thoroughly and encourage area thoroughly and encourage sharps or puncture injury. Seek if, sharps or puncture injury. Seek bleeding if, sharps or puncture bleeding if, sharps or puncture immediate medical attention. Monitor immediate medical attention. injury. Seek immediate medical injury. Seek immediate medical for symptoms. In outbreak settings, Monitor for symptoms. Confirm attention. Monitor for attention. Monitor for symptoms.

food poisoning can be diagnosed on diagnosis by isolation from stool or symptoms. The bacteria can be Campylobacter infection can be clinical grounds with food cultured blood and by serotyping to identify detected by PCR. confirmed by culturing and for S. aureus. Toxic shock syndrome the serotype. Treatment depends on Aeromonas spp. samples can be identification of bacteria in stool. can be indicated with a clinical the clinical symptoms presented by isolated and confirmed on Recent Campylobacter infections diagnosis and isolation of S. the patient. ampicillin dextrin agar forming can be identified using serologic aureus strain, TSST-1, or enterotoxins Gastrotenteritis: Fluid and yellow colour colonies. tests. Administer proper B or C. This can be achieved using electrolyte replacement as well as Confirmation by laboratory antimicrobial therapy. Treatment ELISA, reverse passive latex control of the nausea and vomiting tests can be performed by is primarily supportive as most agglutination, or PCR. Scalded skin are the usual treatments for these (positive), triple infections are self-limiting. syndrome can be diagnosed clinically, symptoms. Antibiotic treatment is sugar iron agar (glucose Antibiotic therapy may be with presence of Nikolsky’s sign and not usually used; however, it may be fermenting), or Biolog required in more serious cases identification of S. aureus retrieved necessary for neonates, children, the detection methods. particularly in young, elderly or from the infection site. Bacteremia and elderly, and the immunosuppressed, Administration of antibiotics immunocompromised patients. deep site infections are confirmed with in which case ciproflaxin, co- such as ciprofloxacin, co- Erythromycin is the drug of direct microscopic examination of trimoxazole, ampicillin, and trimoxazole, Gentamicin, or choice for treating Campylobacter clinical specimen. Treatment of cephalosporins may be used. Amikacin. Intravenous fluid gastroenteritis. Susceptible to abscesses usually does not need Bacteremia: Antibiotic treatment is replacement in combination macrolides, fluoroquinolones, antibiotic therapy; appropriate drainage used to treat bacteremia (e.g. with oral antibiotics is effective aminoglycosides, is usually sufficient. Proper antibiotic ciproflaxin, co-trimoxazole, in lessening infection chloramphenicol, nitrofurantoin therapy is required for more serious ampicillin, or cephalosporins), symptoms. Sensitivity has been and tetracycline. Antibiotic infections. Many strains of especially for neonates, children, the confirmed for fluoroquinolones resistant strains are emerging Staphylococcus aureus have increasing elderly, and the immunosuppressed. (ciproflaxin), aminoglycosides particularly to fluoroquinolones resistance to multiple antibiotic Enteric fever: Chloramphenicol is (except streptomycin), and erythromycin. Antibiotic classes. Methicillin resistant strains are the most common antibiotic used for tetracycline, chloramphenicol, resistance strains are emerging common causes of nosocomial enteric fever although ampicillin, carbapenems, polymyxin, particularly to fluoroquinolones, infection. Increasing resistance to trimethoprim-sulfonamid, streptomycin, gentamicin, and macrolides, trimethoprim, beta vancomycin is being documented in cephalosporins, ciproflaxin, and trimethoprim-sulfametho- lactam antibiotics, including many hospitals. norfloxacin are also being used to xazole. Almost penicillin and most treat the disease. all Aeromonas spp. are resistant cephalosporins, as well as to Asymptomatic carrier state: Carriers to penicillin, ampicillin, tetracycline, quinolone and can be treated with ciproflaxin in amoxicillin, ticarcillin, kanamycin. order to reduce the spread of the carbenicillin, and cephalothin. infectious agent. Susceptible to chloramphenicol, ciproflaxin, amoxicillin, co- trimoxazole, trimethprim-

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 67 of 92 Revised: January 26, 2017

sulfonamid, cephalosporins and norfloxacin. Some resistance to chloramphenicol has been reported and, in 1989, 32% of strains were multi-drug resistant.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 68 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Bacteria – (cont)

Clostridium difficile; Clostridium botulinum; Yersinia enteracolitica; Campylobacter jejuni

Pathogen Clostridium difficile Clostridium botulinum Campylobacter jejuni Identification

Mode(s) of Transmission mainly occurs through Food borne botulism: Ingestion of Human -to-human transmission Oral ingestion of bacteria from Transmission the fecal-oral route, via contaminated contaminated food containing toxin. has been reported rarely in contaminated food, contaminated foods, fomites, or hands. C. Infection is commonly associated schools, daycares and hospitals. drinking water. Contact with difficile overgrowth and toxin with commercially processed foods Nosocomial infections and animals and their feces is also a production can occur in immuno- that had undergone poor processing, blood transfusion related source of infection. Primary lab

compromised patients from their storage, and improper preservation. infections by this bacterium infection hazards include: natural flora. Nosocomial transmission Wound botulism: Contamination of have been reported. Fecal-oral accidental ingestion, direct has also been reported, where wounds with spores of neurotoxin transmission from animal-to- contact of open wounds/site of infections were transmitted via hospital producing Clostridium species and human or consumption of injury with the pathogen, staff and contaminated equipment. The is seen almost exclusively in contaminated foods (raw pork exposure to aerosols, and primary lab infection hazard is injection drug users, particularly products, undercooked pork, accidental parenteral inoculation. accidental ingestion of the pathogen or those who partake in injection of tofu and unpasteurized milk Campylobacter associated toxins, however, direct black-tar heroin into skin tissue. have been shown to be a source can survive for many weeks in contact of open wounds/site of injury Intestinal (infant) botulism: of outbreaks) and untreated water at 4°C, but only a few days with the pathogen, exposure to Ingestion of spores. Sources include water are also common modes above 15°C. aerosols, and accidental parenteral honey and infant milk powder. of transmission. Also found in inoculation are also potential hazards. Adult infectious botulism: Ingestion untreated sewage. Laboratory samples at risk of infection of clostridial spores, rather than The primary lab infection include, but are not limited to: Human toxin, which then colonize the gut to hazards are accidental ingestion fecal and excretion samples, produce their neurotoxin directly in of the pathogen, direct contact contaminated food products, sewage, the gut. of open wounds/ soil, and bowel luminal contents or Iatrogenic botulism: Side effect of site of injury with the pathogen, tissue. injection of purified toxin. exposure to aerosols, and Inhalational botulism: Occurs due to accidental parenteral absorption of botulinum toxin by the inoculation. mucous membrane of the nose. The primary lab infection hazards are accidental ingestion of the pathogen or associated toxins, direct contact of open wounds/

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 69 of 92 Revised: January 26, 2017

site of injury with the pathogen, exposure to aerosols, and accidental parenteral inoculation. Incubation 5-10 days with a range of 1 day to The shorter the incubation period, The incubation period for this 1 to 10 days. Period weeks following antibiotic treatment the more severe the disease and the bacterium is between 3-10 for AAD (antibiotic associated higher the case fatality rate. days. diarrhea). Food-borne botulism: Usually 12 to 72 hrs after ingestion of toxin, depending on the dose. Wound botulism: The median period is 7 days. Adult infectious botulism: Unknown. Intestinal botulism: Unknown. Inhalational botulism: Not well defined, but it is longer than for food borne botulism, and is estimated at 12-80 hours. Period of Indefinite. Low risk of transmission Not generally transferred from Variable. Although rare, the Not generally transferred from Communicability from person-to-person, although human to human. Transmission is disease can be spread from human to human. Transmission is nosocomial transmission from dependent on accidental ingestion or human-to-human and bacteria dependent on accidental ingestion contaminated hands, instruments such contact with contaminated material can still be present in stool or contact with contaminated as endoscopes, and the environment source(s). weeks after the clinical material source(s). have been reported. Asymptomatic symptoms have ceased. patients can also act as a reservoir for the transmission of this pathogen within the hospital. Infectious Dose(s) Unknown. Cells/spores are not normally toxic The infectious dose is of As low as 500 organisms by for healthy adults. Botulinum toxin 108 bacteria or more orally. ingestion. One volunteer study is the most potent toxin known, with found that 9000 bacteria were an estimated oral or injected toxic required to infect 50 percent of dose (serotype A) of 0.001 μg/kg subjects. body weight, and an estimated lethal dose by inhalation exposure in humans of approximately 0.07 μg/kg body weight. Type A toxin is more potent than types B and E and causes the longest lasting disease. Typical C. difficile is the main cause of Rare but serious paralytic disease, Yersinia enterocolitica Campylobacter jejuni cause Presenting nosocomial antibiotic- associated caused by a neurotoxin formed infection is characterized by gastroenteritis, with the most Symptoms diarrhea. Antibiotics or any other during the growth of the spore- enteritis, enterocolitis common symptom being diarrhea procedures that disrupt the normal forming bacterium C. botulinum (or (particularly in children), fever (sometimes bloody) that lasts 2- intestinal microbiota can lead to the rarely, C. argentinense, C. (39°C), watery stools, 10 days, as well as mild to severe

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 70 of 92 Revised: January 26, 2017

overgrowth and production of toxin butyricum, or C. baratii ). This abdominal pain and acute abdominal pain, fever, malaise, by C. difficile, which leads to clinical neurotoxin binds to the mesenteric lymphadenitis nausea and vomiting. Symptoms manifestations of infection. The neuromuscular junction and blocks (which may mimic last for about a week but relapses diarrhea may range from a few days of excitatory synaptic transmission by appendicitis). In some cases, occur in 5-10% of untreated intestinal fluid loss to life-threatening inhibiting acetylcholine release, acute terminal ileitis and cases. Although a large number pseudo-membranous colitis. In causing (flaccid) paralysis, and enteric fever can occur (violent of campylobacter infections are diarrhea without pseudo-membranous sometimes fatal . and relatively acute asymptomatic and mild, many colitis (PMC), feces have a foul odor The fatality rate of botulism is 5 to epigastric or abdominal pain complications have been reported and are not bloody. Abdominal pain 10%. caused by penetration of larvae in young children and immuno- with or without pyrexia may also be Food-borne botulism: The classic through the stomach or lower compromised patients, including present along with diarrhea. PMC is form of botulism is caused by the small intestine mucosa, bacteremia, hepatitis, associated with intense inflammation ingestion of preformed toxin in especially the ileum. Nausea, cholecystitis, pancreatitis, of the colon and formation of pseudo- contaminated food. Symptoms vomiting, and fever may abortion, myocarditis and membranes on the intestinal mucosal include double vision, drooping occur). 1-3 weeks after the meningitis. C. jejuni has been surface. Patients with PMC also have eyelids (ptosis), slurred speech, initial clinical symptoms, associated with post-infection more systemic side effects. Rare difficulty swallowing and muscle reactive arthritis (joint pain and sequelae, most commonly extracolonic manifestations of C. weakness that is symmetric and swelling) and erythema Guillain-Barré syndrome and difficile infection include bacteremia, descends through the body (first nodosum (reddish, painful, reactive arthritis. All strains of C. intra-abdominal abscess, osteomyelitis, shoulders are affected, then upper tender lumps jejuni possess a gene coding for visceral abscess, empyema, toxic arms, lower arms, thighs, calves, most commonly located in the cytolethal distending toxin, megacolon, colonic perforation, and etc.). Death is usually due to front of the legs. The tender however not all strains produce it. reactive arthritis. The production of respiratory failure and may occur as lumps, or nodules, of erythema The role of these toxins in disease exotoxins A and B facilitates tissue soon as 24 hours after onset of nodosum range in size from is not known. Motility is required damage, which results in cell necrosis symptoms. one to five centimeters. The for full virulence, and some and ulceration, diarrhea and fluid Wound botulism: Occurs by nodular swelling is caused effectors associated with secretion, and colitis. The strain with contamination of a wound with by inflammation in the fatty virulence are secreted through the ribotype 027, also known as North spores from neurotoxin- layer of skin) may occur which flagellum. America Pulsotype (NAP) 1, is one of producing Clostridium species in the can last about 6 months after the most pathogenic types of C. environment and subsequent infection. In rare instances, difficile, and the severity of this strain germination of these spores and complications can include is based on its unusually high levels of production of toxin in the anaerobic meningitis (symptoms: can toxin A and B production, its milieu of an abscess. The toxin is include fever, cold hands and production of a third toxin known as released into the bloodstream and feet, vomiting, severe the binary toxin, and its resistance to symptoms may take up to 2 weeks headache, stiff neck, severe fluoroquinolone antibiotics. Another to appear. muscle pain, pale blotchy skin, new hypervirulent Intestinal (infant) botulism: Results rash confusion, C. difficile strain 078 (NAP7/8), has almost exclusively from spore sleepiness, and seizures), been associated with severe diarrhea ingestion and subsequent growth endophthalmitis (progressive and high mortality rates have been and toxin production in the intestine, deterioration of vision, light reported from The Netherlands and affecting infants under 1-year-old. sensitivity, pain and swelling other countries, including Canada. The first clinical sign is usually around the eye), conjunctivitis constipation, but this disease has a (symptoms can include: wide spectrum of clinical severity, redness in white of eye or

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 71 of 92 Revised: January 26, 2017

ranging from mild illness with eyelid, increased amount of gradual onset, to sudden infant death tears, thick yellow discharge on due to respiratory failure. With eyelashes after sleep, green or appropriate intensive care, almost white discharge from eye, itchy 100% of infants with botulism make eyes, burning eyes, blurred a full recovery. Infants with vision, increased sensitivity to botulism are lethargic, feed poorly, light), myocarditis (chest pain, have a weakened cry, exhibit ptosis, arrhythmias, shortness of and floppy neck, and may progress breath, fluid retention, joint to generalised flaccidity and swelling, fatigue), pneumonia respiratory compromise. (symptoms: cough with or Adult infectious botulism: Rare. without mucus, fever, shaking, Caused by the intestinal colonization chills, and shortness of breath, of C. botulinum / other neurotoxin especially during physical producing species, followed by in exertion), pulmonary abscess vivo toxin production in a manner (fever and chills, rapid heart similar to infant botulism. Patients rate, profuse sweating, often have a history of immuno- prolonged period of poor compromise, abdominal surgery, health, loss of appetite, weight bowel disease, or recent antibiotic loss, chest pain, deep cough therapy. Inhalational botulism: Is that may produce foul smelling not a naturally occurring disease, but of bloody sputum), hepatitis has occurred in laboratory workers (abdominal pain, dark urine, due to inhalation of aerosolized fever, joint pain, lossof toxin. Inhalational botulism leads to appetite, nausea and vomiting, neurological symptoms similar to weakness and fatigue, those of food-borne botulism, but yellowing of skin and whites of with a longer incubation period. eyes - jaundice), cholangitis Iatrogenic botulism: Side effects (chills, fever, abdominal pain, resulting from the therapeutic clay coloured stools, dark intramuscular injection of Botox urine, nausea and vomiting, (purified, diluted A neurotoxin). jaundice), peritonitis Characterized by clinical weakness (abdominal pain, bloating, and electro-physiological fever, nausea and vomiting, abnormalities. loss of appetite, diarrhea, low urine output, thirst), glomerulo- nephritis (blood or excess protein in urine, high blood pressure, frequent night time urination, bubbly or foamy urine, abdominal pain, frequent nosebleeds), urethritis (burning on urination, frequent urination

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 72 of 92 Revised: January 26, 2017

with only small amounts of urine passed on each occasion, anal or oral infections, urgent need to urinate, bloody or yellowish discharge from the penis, blood in urine, urethral itching), cellulitis (pain, inflammation, fast growing sore or rash, tight, glossy, swollen skin appearance, pus filled center, fever), haemolytic anaemia (low RBC, dark urine, jaundice, heart murmur, increased heart rate, enlarged spleen, enlarged liver), thyroiditis (fatigue, depression, cold intolerance, weight gain, dry skin and hair, muscle cramps, constipation, decreased concentration and sleepiness, leg swelling, puffy eyes; severe symptoms include a slow heart rate, low body temperature, heart failure and coma), pharyngitis (sore throat, sneezing, cough, headache, fatigue, body aches, chills, fever), and septicaemia (symptoms: fever, a rapid heart rate, shaking chills, low blood pressure, gastrointestinal symptoms (abdominal pain, nausea, vomiting, and diarrhea), rapid breathing, and/or confusion). The infection is a greater health risk for immuno-suppressed individuals and if untreated, the mortality rate due to septicaemia can be up to 50%. Mode(s) of Spores are generally resistant to The vegetative state is susceptible to Susceptible to 2-5% phenol, C. jejuni is susceptible to 10 Decontamination disinfection. Clostridium spores are disinfectants such as 70% ethanol, 1% sodium hypochlorite, 70% mg/L iodophor, 1:50 000

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 73 of 92 Revised: January 26, 2017

resistant to ethyl and propyl alcohols. 0.1% sodium hypochlorite, and ethanol, 4% formaldehyde, 2% quaternary ammonium High level disinfectants such as 2% 0.1N NaOH. Spores may be glutaraldehyde, 2% peracetic compound, 0.15% phenolic glutaraldehyde can kill spores within resistant to disinfectants. Toxins are acid, 3-6% hydrogen peroxide compound, 70% ethyl alcohol or 20 minutes. 8% formaldehyde and 20 inactivated (more than 99.7%) by 20 and 0.16% iodine. Bacteria are 0.125% glutaraldehyde all with a ppm sodium hypochlorite are also minutes exposure to 3 mg/L free sensitive to moist heat (121°C contact time of 1 minute or effective against bacterial spores. available chlorine (FAC; similar to for at least 12 minutes) and dry 5mg/L of hypochlorite with a Spores of the genus Clostridium the military disinfection procedure), heat (170°C for 1 hour). The contact time of 5 minutes. are generally heat resistant and can and 84% inactivated by a treatment bacterium can survive 448 days Inactivated by heat (70°C for 1 withstand temperature of 116°C for 3 of 20 minutes at 0.4 mg/L FAC in water between -4 and 8°C, min), hydrostatic pressure (450 hours, whereas their vegetative cells (similar to municipal water and 10 days in water between MPa at 15°C for 30 s) and gamma can be rapidly killed by temperatures treatment procedures). Toxin is 20 and 30°C. It can live up to irradiation. Campylobacter of only 55-65°C. Most spores can be destroyed after heating for 5 minutes 10 days in soil and cattle cells can enter a viable but inactivated by moist heat at 121°C for at greater than 85°C. Toxins are manure between -4 and 30°C. nonculturable state (VBNC) when 15-30 minutes. C. difficile is able to detoxified in air within 12 hours and subject to stress. This is thought survive in soil, sewage, meat, and following exposure to sunlight to improve their survival in the vegetables. within 1 to 3 hours. Spores are environment, as it has been highly resistant to heat and observed to survive freezing for desiccation; therefore, it is several months in frozen poultry, recommended to sterilize with dry minced meat, and other cold food heat (2 hours at 160°C) by products. Campylobacter can autoclaving (20 minutes at 121°C, 1 survive for many weeks in water atm pressure) and/or by irradiation. at 4°C, but only a few days in Survives well in soil, water and water above 15°C. agricultural products. Emergency If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding area thoroughly and encourage area thoroughly and encourage sharps or puncture injury. Seek if, sharps or puncture injury. Seek bleeding if, sharps or puncture bleeding if, sharps or puncture immediate medical attention. Monitor immediate medical attention. injury. Seek immediate medical injury. Seek immediate medical for symptoms. Detection of toxins in Monitor for symptoms. Since attention. Monitor for attention. Monitor for symptoms.

stool specimens is the Gold Standard botulism is a life threatening symptoms. The bacterium can Campylobacter infection can be test for diagnosis of C. condition, a rapid diagnosis is be isolated in stool, tissue confirmed by culturing and difficile infection. Detection of toxins essential and may require testing to samples, blood and pus. PCR identification of bacteria in stool. is done using cell culture assays, or differentiate botulism from other and ELISA can also be used to Recent Campylobacter infections Enzyme Immunoassay (EIA). neurological diseases. diagnose the disease. Although can be identified using serologic Diagnosis can also be done by Food borne botulism: Can be infections by Yersinia tests. Administer proper culturing the bacteria on appropriate diagnosed by demonstration of toxin enterocolitica are usually self antimicrobial therapy. Treatment media such as egg yolk agar-based in serum, stool, gastric aspirate or limiting, antibiotic treatment is is primarily supportive as most media or blood agar media. Two implicated food, or by culture of C. necessary for severe or infections are self-limiting. different approaches are commonly botulinum from a patient's gastric complicated cases. The Antibiotic therapy may be used for typing of C. difficilestrains aspirate or stool in a clinical case. antibiotics commonly used are required in more serious cases and include PCR-ribotyping and pulse The mouse bioassay is the most gentamicin, cotrimoxazole, and particularly in young, elderly or field gel electrophoresis (PFGE). reliable method for detection of ciprofloxacin. Surgery may be immunocompromised patients. Treatment should be supportive with botulinum. Wound botulism: Can be required to treat acute terminal Erythromycin is the drug of

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 74 of 92 Revised: January 26, 2017

rebalancing of fluid levels and diagnosed by demonstration of toxin ileitis. Yersinia enterocolitica is choice for treating Campylobacter electrolytes. Antibiotic treatment in serum, or by positive wound susceptible to chloramphenicol, gastroenteritis. Generally should be discontinued for antibiotic culture. Adult infectious botulism: fluoroquinolones, gentamicin, susceptible to macrolides, associated diarrhoea (AAD) infection. Can be diagnosed by demonstration tetracycline, and trimethoprim- fluoroquinolones, For patients who do not respond to of C. botulinum sulfa-methoxazole. It is aminoglycosides, drug withdrawal or are present with (or other neurotoxin producing generally resistant to penicillin chloramphenicol, nitrofurantoin, systemic illness, oral metronidazole is species) and/or toxins in a patient's and its derivatives and to gentamicin, and tetracycline. used for treatment. Oral vancomycin faeces or in autopsy specimens. narrow spectrum Antibiotic resistance strains are has been shown to be more effective Intestinal (infant) botulism: Since cephalosporins. emerging particularly to than metronidazole in treating the toxin is rarely found in the sera fluoroquinolones, macrolides, recurrent infections. Susceptible to of infants, faeces should be trimethoprim, beta lactam metronidazole and oral vancomycin. C. examined. An ELISA has been antibiotics, including penicillin difficile also demonstrates sensitivity developed for the detection of A and and most cephalosporins, as well to penicillins and cephalosporins in B toxins in children's faecal as to tetracycline, quinolone and vitro, but these drugs are not used for samples. Inhalational botulism: kanamycin. treatment because they can be Aerosolized toxin can not usually be destroyed by β- identified in serum or faeces, but lactamases/cephalosporinases may be detected by ELISA from produced by other intestinal bacteria nasal swabs. Iatrogenic botulism: and are, thus, ineffective for treatment Should be suspected if patient has in vivo. recently received Botox. An immuno-PCR assay capable of detecting neurotoxin type A in the femtogram range has been developed. Susceptible to penicillin, metronidazole, clindamycin, cephalothin, cefoxitin, cefotaxime, chloramphenicol, tetracycline, erythromycin, rifampin, and vancomycin (with some strain variation). Usually resistant to the aminoglycosides, and may be resistant to tetracyclines and cephalosporins (with some strain variation). Also resistant to nalidixic acid and sulpha-methoxazole- trimethoprim (SMX-TMP).

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 75 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Bacteria – (cont)

Clostridium perfringens; Klebsiella spp.; Actineobacter spp.

Pathogen Clostridium perfringens Klebsiella spp. Acineobacter spp. Identification

Mode(s) of Food Poisoning: Food -borne illness acquired by Klebsiella spp. can be transmitted through skin Acineob acter spp. can be transmitted through skin Transmission ingestion of large number of C. perfringens contact with environmentally contaminated surfaces contact with environmentally contaminated vegetative cells present in the food. Food sources are and/or objects; examples include Loofah sponges, surfaces and/or objects. Acinetobacter spp. are usually cooked meat, vegetables, fish or poultry medical equipment, sewage, and blood products. ubiquitous inhabitants of soil, water, and sewage dishes which have been stored at ambient Fecal transmission has also been suggested for some environments.

temperatures for a long time after cooking. Enteritis cases of bacteremia caused by Klebsiella spp. K. Infection is most commonly Necroticans: Ingestion of contaminated pork meat. rhinoscleromatis can be transmitted from person-to- associated with contact with wounds and burns or Gas / Anaerobic Cellulitis: Infection can person via airborne secretions; however, prolonged inhalation by susceptible individuals. Primary lab occur through contamination of wounds (fractures, contact with infected individuals is required for infection hazards include: accidental ingestion, bullet wounds) with dirt or any foreign material infection. K. granulomatis are sexually transmitted. direct contact of open wounds/site of injury with contaminated with C. perfringens. Primary They may also be vertically transmitted (from mother the pathogen, exposure to aerosols, and accidental laboratory hazards include: accidental ingestion of to child) or by accidental inoculation. Transmission parenteral inoculation. Acinetobacter has been the enterotoxin, direct contact of open wounds/site rates between partners are low (<50%) compared to isolated from 97% of natural surface water samples of injury with the pathogen, accidental parenteral other sexually transmitted diseases. Laboratory in numbers inoculation of the toxin. Sources can include: human hazards include direct contact of mucosal membranes of up to 100/ml. The organisms have been found to feces, suspect food in a food borne illness, blood, with contaminated surfaces and/or object, and represent 1.0–5.5% of the HPC bowel luminal contents or tissue from the involved inhalation of infectious airborne secretions, accidental flora in drinking-water samples and have been bowel in case of enteritis necroticans, wound parenteral inoculation and/or ingestion. isolated from 5–92% of distribution exudates, and sewage. water samples. Nosocomial infections with this bacteria are not uncommon. Incubation Food Poisoning : 8-24 hours . : 1-4 Not clearly understood. According to some sources, Unknown . Period days after the injury, but may also start within 10 the incubation period for K. granulomatis is usually 1 hours. to 6 weeks. Period of Not transferred from human to human. Transmission Members of Klebsiella spp. can be transmitted from Not transferred from human to human. Communicability is dependent on contact with contaminated material person-to-person; however, the communicability Transmission is dependent on contact with source(s) . period is unknown. Approximately one-third of contaminated material source(s). people carry Klebsiellae in their stools; detection rates according to different studies vary from 5% to 36%. Detection rates in nasopharynx vary from 1% to 6%. Hospital personnel

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 76 of 92 Revised: January 26, 2017

have been shown to frequently carry Klebsiellae on their hands. Infectious Dose(s) Unknown. Unknown. According to one source, Unknown. 108 Klebsiella organisms per gram of feces are required to produce damage. Typical Clostridial Food Poisoning: Food poisoning can be Klebsiella spp. have been identified as important Opportunistic pathogens that may cause urinary Presenting caused by C. perfringens entero-toxin (CPE) common pathogens for nosocomial pneumonia (7 to tract infections (symptoms: upper back and side Symptoms produced by C. perfringens spores in the small 14% of all cases), septicaemia (4 to 15%), urinary (flank) pain, fever, shaking and chills, nausea, intestine, which can germinate in foods such as meat tract infection (UTIs; 6 to 17%), wound infections (2 vomiting, pelvic pressure, lower abdomen and poultry. In the United States consumption of to 4%), intensive care unit (ICU) infections (4 to discomfort, frequent, painful urination, and blood

large amounts of C. perfringens is considered an 17%), and neonatal septicaemias (3 to in urine), pneumonia (symptoms: cough with or important cause of watery diarrhea. Main symptoms 20%). Klebsiella spp. can also cause bacteremias and without mucus, fever, shaking chills, and shortness of the disease are nausea, abdominal pain, and hepatic infections, and have been isolated from a of breath, especially during physical exertion), diarrhea. The disease is usually mild and self- number of unusual infection, including endocarditis, bacteraemia which can lead to septicemia limiting in healthy individuals, with symptoms primary gas-containing mediastinal abscess, (symptoms: fever, a rapid heart rate, shaking chills, resolving within 24 hours. Clostridial Myonecrosis peritonitis, acute cholecystitis, crepitant myonecrosis, low blood pressure, gastrointestinal symptoms (Gas Gangrene): C. perfringens is the most common pyomyositis, necrotizing fasciitis, psoas muscle (abdominal pain, nausea, vomiting, and diarrhea), cause of clostridial myonecrosis. The disease abscess, fascial space infections of the head and neck, rapid breathing, and/or confusion), secondary involves breakdown of muscle tissue due to the and septic arthritis. meningitis (symptoms: headache, stiff neck, action of potent exotoxins, alpha and theta, produced Respiratory disease: Infection of the upper lobe is and fever. In infants, these symptoms may be by the bacteria. It is manifested by severe pain, more common. Symptoms include: fevers, chills, and difficult to detect. Other symptoms edema, tenderness and pallor, followed by leukocytosis with red currant jelly-like sputum. Rare include vomiting, nausea, photophobia (sensitivity discoloration and hemorrhagic bullae, and complications include lung infection involving to light), confusion, sleepiness, and seizures) and production of gas at the site of wound. Systemic necrosis and sloughing of the entire lobe. Chronic wound infections (symptoms: increased pain, manifestations of the disease include shock, renal nose inflammation has also been observed. swelling, redness, and drainage). failure, hypotension, bacteremia with intravascular Central nervous system (CNS) infections: meningitis hemolysis leading to coma and death. Clostridial and brain abscesses. Clinical symptoms include: Cellulitis: C. perfringens is the most common cause headaches, fever, altered conciousness, seizures, and of clostridial cellulitis, which is often associated septic shock. Can also cause donovanosis or with local trauma or recent surgery. Infection is less granuloma, a chronic ulcerative disease that primarily systemic than in clostridial myonecrosis, with affects the genitalia. Symptoms include development localized infection and associated skin and soft of small papule or ulcer at the site of inoculation that tissue necrosis, but sparing of the fascia and deep later develop into large red ulcers (lesions) that extend muscles. Enteritis Necrotican (pigbel): Enteritis along the moist folds of the genitalia. necroticans is a life threatening infection involving ischemic necrosis of the jejunum. The often fatal disease is caused by C. perfringens type C, and is marked by hemorrhagic, inflammatory, or ischemic necrosis of the jejunum. Most cases occur sporadically, during outbreatks, or in underdeveloped countries. CNS manifestations of C. perfringens infection: CNS diseases due to C. perfringensinfection are rare. The main

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 77 of 92 Revised: January 26, 2017

manifestations of C. perfringens infection in CNS are meningitis and encephalitis. Clinical symptoms of the two diseases are similar and include tiredness, fever, headache, vomiting, hypersensitivity to light or noise, neck stiffness, or impaired consciousness and coma.

Mode(s) of Spores are resistant to most disinfectants and, when Gram-negative bacteria are generally susceptible to a 10% bleach, 70% ethanol, and 2% glutaraldehyde Decontamination susceptible, they require longer contact number of disinfectants, including phenolic solutions are all effective surface decontaminants. time. Clostridium spores are resistant to ethyl and compounds, hypochlorites (1% sodium hypochlorite), Acineobacter spp. can also be inactivated by moist propyl alcohols, chlorine dioxide. Spores of alcohols (70% ethanol), formaldehyde (18.5 g/L; 5% heat (15 minutes at 121°C) and dry heat (1 hour at clostridium species can be killed by high level formalin in water), glutaraldehyde, and iodines (0.075 160-170°C). Outside of the host, Acineobacter spp.

disinfectants such as 2% aqueous glutaraldehyde g/L). Reduction in the growth and metabolic activity can survive for long periods of time outside of within 3 hours, and 8% formaldehyde. Spores are of K. pneumoniae at temperatures >35 °C has been susceptible hosts on dry surfaceas, in water, soil, highly resistant to both heat, and gamma-irradiation. reported. Significant growth reduction has been and in sewage. Enterotoxin is heat labile and can be inactivated by demonstrated at 60 °C; however, the bacteria still heat treatment at 60oC for 5 minutes. show some metabolic activity (i.e. not completely Vegetative cells can be rapidly killed by dry heat at inactivated). Bacteria are also sensitive to moist heat 160-170°C for 1-2 hours or moist heat at 121°C for and dry heat. Klebsiella spp. grow rapidly on surfaces 15 min- 30 min. Spores can survive in soil, crevices, of potatoes and lettuce with counts exceeding food, decaying vegetation, marine sediments, 103 organisms per g of surface. They have been found sewage, internal cavities and in the anaerobic in Loofah sponges made from vegetable gourds. They conditions inside the meat rolls, animal carcasses, also survive well within wood and sawdust. They do feces, dehydrated and cooked food. not grow well on human skin and generally exists in infected individuals and/or surfaces, and the environment; surface water, sewage, soil, and on plants, where they can survive for extended periods of time. Emergency If exposure is suspected, wash area thoroughly and If exposure is suspected, wash area thoroughly and If exposure is suspected, wash area thoroughly and Response encourage bleeding if, sharps or puncture injury. encourage bleeding if, sharps or puncture injury. Seek encourage bleeding if, sharps or puncture injury. Seek immediate medical attention. Monitor for immediate medical attention. Monitor for symptoms. Seek immediate medical attention. Monitor for symptoms. Diagnosis is based mainly on clinical Other tests include isolating strains of the bacteria or symptoms. Strain identification by molecular and symptoms. Food borne illness: Diagnosis consists typing different isolates. This is often necessary for biochemical means is necessary to determine

of: 1) culture and characterization of the bacteria investigation of endemic and epidemic nosocomial proper antibiotic treatment. Acineobacter spp. including Gram-stain; 2) PCR amplification of the infections and also for epidemiological investigations commonly presents resistance to multiple enterotoxin (cpe) gene, as toxin production is from the environment. antimicrobial agents, occasionally including associated with its presence; and 4) detection of CPE Klebsiellae can be isolated by growth in media. carbapenems and polymyxins, and hence, it is in feces through toxin assay, cell culture assay, Although there are specific chromogenic media considered the paradigm of multidrug-resistant ELISA or RPLA (reverse-phase latex agglutination). available for isolating these bacteria from specific (MDR) or pandrug-resistant (PDR) bacterium. Enteritis Necroticans: Diagnosis consists of direct samples,Klebsiellae grow well on blood and non- MDR A. baumannii is a rapidly emerging of specimens from symptomatic patients, differential media. Biotyping and serotyping are two pathogen, especially in the intensive care setting, and culture and characterization of the bacteria. common forms of typing methods used for causing infections including bacteremia, Typing can be done using PCR assay for the cpa and typing Klebsiella spp. Serotyping is the most widely pneumonia/ventilator-associated pneumonia

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 78 of 92 Revised: January 26, 2017

cpb genes, which code for a- and b-toxins, used technique for typing these bacteria which (VAP), meningitis, urinary tract infection, central respectively. Gas gangrene/Anaerobic cellulitis: involves detection of capsular antigens by means of venous catheter-related infection, and wound Diagnosis consists of direct Gram stain smear of the antisera. Serotyping tests include: quelling reaction, infection. wound for the presence of short chains of large, fat immunofluorescence, double-diffusion gel gram positive rods with blunt ends from precipitation, counter-current symptomatic patients. Food poisoning: Self-limiting immunoelectrophoreses, Staphylococcus coagulation, disease. Therapy in mainly supportive; bowel and latex coagulation methods. Biotyping is not resection may be required for very severe cases. Gas preferred due to the large number of reactions and the Gangrene: Treatment mainly involves excision of all amount of time required to complete these tests. devitalized tissue in conjunction with antibiotic Molecular typing methods are also being developed, therapy with a combination of penicillin and although they are not commonly used. These include: clindamycin or tetracycline, which appear most plasmid analysis, ribotyping, PFGE, and random effective based on animal models. In vitro, amplified polymorphic DNA analysis, all of which chloramphenicol, metronidazole, and several have been successfully used to track strains epidemio- cephalosporins are active against C. perfringens. logically. Administer appropriate antibiotic therapy There have been a few reports of successful results where necessary. using hyperbaric oxygenation in adjunctive therapy. Anaerobic Cellulitis: Surgical debridement of the tissue and antibiotic therapy with penicillin or clindamycin. In case of drug resistance to clindamycin, second line antibacterial agents such as vancomycin can be used. Vaccination against CPB toxin of C. perfringens type C which causes Enteritis Necroticans was reported to decrease the incidence of the disease in New Guinea.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 79 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Viruses Norovirus; Adenovirus serotypes 1-5, and 7; Adenovirus serotypes 40 and 41; Hepatitis A Virus

Pathogen Norovirus (Norwalk virus) Adenovirus serotypes 1, 2, 3, 4, 5, Adenovirus (serotypes 40 and Hepatitis A Virus (HAV) Identification and 7 (excluding serotypes 40 and 41) 41) Mode(s) of Norovirus transmission is usually Respiratory and fecal-oral routes. The virus is transmitted via the HAV transmission usually occurs Transmission person to person through the fecal-oral Infection can also spread through fecal-oral route. Laboratory via the faecal-oral route. The most route. It can also be transmitted contaminated fomites, fingers, hazards include Ingestion, common reported source of HAV through the environment, contaminated ophthalmic solutions, and airborne exposure of mucous infection is household or other surfaces, food, water, fomites, and particulates. Laboratory hazards membranes to infective close contact with an infected

aerosols. Laboratory hazards include include Ingestion, exposure of aerosols, accidental ingestion, person. Other potential sources of Ingestion, exposure of mucous mucous membranes to infective and accidental parenteral infection include men having sex membranes to infective aerosols, aerosols, accidental ingestion, and inoculation. Most serotypes are with men, travel to countries accidentally ingestion, and accidental accidental parenteral inoculation. stable at 36 °C for a week, for where HAV is endemic, and from parenteral inoculation. Noroviruses Adenoviruses are very stable in the several weeks at room contaminated drugs and needles have a protein capsid protecting it from environment and persist for 7 days temperature, and for several following illicit drug use. the environment. They can survive in to 3 months on dry inanimate months at 4 °C. Adenoviruses Consumption of contaminated seawater, groundwater, fresh water, surfaces. They can also survive for are very stable in the food and water are infrequent soil, and inanimate surfaces for an weeks in tap water, sewage effluent environment and persist for 7 modes of transmission, and unknown period of time. Norwalk and sea water. Adenovirus type 2 days to 3 months on dry transmission by transfusion of virus cannot be cultivated under can survive on common inanimate surfaces. They can blood or blood products is even laboratory conditions as of yet. Feline environmental surfaces for up to 8 also survive for many days in rarer. Laboratory hazards include calicivirus, another member of this weeks at room temperature. tap water, sewage effluent, and Ingestion, exposure of mucous family, with similar structure, can sea water. membranes to infective aerosols, survive on glass surfaces for 21-28 accidental ingestion, and days at room temperature and for accidental parenteral inoculation. longer periods at 4°C. At 37°C, feline HAV is exceptionally stable at calicivirus survives over 24 hours. ambient temperature and at low pH, thus allowing it to survive in the environment and to be transmitted via contaminated foods and drinking water. Incubation Onset of symptoms usually takes 15- Approximately 2 to 14 days. 3 to 10 days. Average of 28 to 30 days (range Period 48 hours from the time of infection. of 15 to 50 days).

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 80 of 92 Revised: January 26, 2017

Period of Individuals can spread virus particles Children shed non enteric Low communicability between Maximum infectivity occurs in Communicability without showing symptoms of disease. adenovirus in throat and stool close contacts in the same the latter half of incubation and Those who have recovered from samples for 3 to 6 weeks following household. Virus shedding continues a few days after the symptoms and those who are lower respiratory infection or takes place during the acute onset of jaundice. Chronic asymptomatic can shed infectious virus generalized illness. Chance of stage of the disease, since shedding of HAV in faeces does particles up to three weeks after transmission is high in crowded and enteric adenoviruses are rarely not occur. exposure. closed settings such as day cares, recovered from stool samples boarding schools and long-term care more than a few weeks after facilities. Transmission between recovery from gastroenteritis. family members is common. In rare Asymptomatic individuals cases, virus shedding may last for 18 (mainly children) shed months or longer. adenoviruses in their stool. Infectious Dose(s) Less than 10 virions. Inhalation of as few as 5 adenovirus Unknown. Unknown. particles can cause disease in susceptible individuals. The National Institutes of Health lists the infectious dose for adenovirus serotype 7 as >150 viral units, administered as nasal drops. Typical Norovirus infection causes acute Adenovirus cause generally mild Adenovirus serotypes 40 and HAV only causes acute hepatitis Presenting gastroenteritis, characterized by rapid respiratory tract infections which are 41 cause acute gastroenteritis and is not associated with chronic Symptoms onset of nausea, vomiting, diarrhea, self-limiting and generally primarily in children. liver disease. Most individuals abdominal cramps, abdominal pain, asymptomatic despite virologic and Symptoms may include fever, infected with HAV develop non- mucus in stool, malaise, headache, and serologic proof of infection, and diarrhea, vomiting, and specific constitutional signs and

fever. The infection is usually resolved only around 45% of infections are abdominal pain, and last for symptoms followed by within 12 to 60 hours, although it can manifested by disease. It is a major approximately 10 days. gastrointestinal symptoms. last up to 120 days in elderly, young agent of acute respiratory disease, Respiratory symptoms can Symptoms include fever, malaise, children or immunocompromised mainly caused by serotypes 4 and 7, occur in some individuals. The anorexia, nausea, abdominal individuals, and these groups are at and is characterized by fever, disease is usually self-limiting discomfort, dark urine, and greatest risk for mortality and rhinitis, pharyngitis, cough, and in immunocompetent jaundice. The disease course increased morbidity. Up to 30% of conjunctivitis. Other common individuals; however rare typically lasts less than 2 months. Norovirus infections are illnesses can be observed in the fatalities can occur in immuno- In rare cases, HAV can cause asymptomatic, however, these respiratory tract, gastrointestinal compromised individuals. severe cases of fulminant hepatitis individuals are able to transmit the tract, and eyes (acute follicular Asymptomatic infections are with fatal outcomes in otherwise virus. conjunctivitis). Common diseases common, particularly in healthy adults. caused by various adenovirus children. serotypes are: Childhood febrile illness and pharyngo-conjunctival fever (1-3, 5, 7), pneumonia (1-3, 5, 7, 14), pertussis-like illness (1-3, 5, 19, 21), kerato-conjunctivitis (3, 8, 9, 19, 37), acute (11), upper respiratory

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 81 of 92 Revised: January 26, 2017

illness and hepatitis (1-3, 5, 7), and lower respiratory illness (3, 4, 7, 21). Mode(s) of Formulation R-82 for 10 minutes, 5- Adenoviruses are resistant to lipid Adenoviruses are resistant to HAV is inactivated by 1 % Decontamination 10% sodium hypochlorite for 10-20 disinfectants, but are inactivated by lipid disinfectants, but are sodium hypochlorite, minutes, peracetic acid or formaldehyde and chlorine. They inactivated by formaldehyde formulations of quaternary glutaraldehyde for 5 minutes. can be inactivated by contact with and chlorine. Adenoviruses can ammonium compounds and HCl, Noroviruses are inactivated by 1:5 dilution of bleach for 1 minute be inactivated by contact with and 2 % glutaraldehyde.

temperatures of 71.3°C for 1 minute. It or 2 minutes contact with alcohol- 1:5 dilution of bleach for 1-2 Inactivation of HAV can be can survive at pH 2.7 for at least 3 based hand gels. Adenovirus can be minutes, and by contact with achieved by heating to greater hours. UV radiation may have inactivated by heat: heating to 56 °C alcohol-based hand gels. than 85°C for 1 minute. intermediate effect. for 30 min, 60 °C for 2 min, and Adenovirus can be inactivated autoclaving will destroy infectivity. by heat: heating to 56 °C for 30 min, 60 °C for 2 min, and autoclaving will destroy infectivity. Adenovirus serotype 40 is also sensitive to UV radiation. Emergency If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding area thoroughly and encourage area thoroughly and encourage sharps or puncture injury. Seek if, sharps or puncture injury. Seek bleeding if, sharps or puncture bleeding if, sharps or puncture emergency medical attention. Monitor emergency medical attention. injury. Seek emergency injury. Seek emergency medical for symptoms and confirm clinically. Monitor for symptoms and confirm medical attention. Monitor for attention. Monitor for symptoms

Viral RNA can be detected in stool clinically. Infected cells can be symptoms of gastrointestinal of disease. Viral infection can be samples using reverse transcription observed by microscopy, and and/or respiratory illness. detected via RT- PCR, radio- PCR. ELISA is also available for adenoviruses can be detected using Enteric adenovirus infection immunoassay, ELISA, identifying noroviruses. No specific immuno-fluorescence, enzyme- can be detected by electron immunoblotting, and dot-blot therapy other than rest, oral linked immunoassay, or PCR for microscopy, agglutination tests, gold filtration. No specific rehydration and intravenous electrolyte antigen detection. No formally enzyme-linked immuno- treatment for HAV infection has replacement. No immunization approved effective antiviral agents sorbent assay, or by PCR. been shown to be effective. Bed currently available. exist for treatment of adenoviral Illness is generally self- rest and balanced nutrition are infections. Illness is generally self- limiting. Treatment is primarily recommended, as is the avoidance limiting and treatment is supportive. oral rehydration or, in serious of alcohol or other hepatotoxins. It has been suggested that immuno- cases, intravenous rehydration. Several inactivated HAV vaccines compromised patients may require Reports indicate that cidofovir have been shown to be effective drug treatment with cidofovir or may be effective against (highly immunogenic and safe). other antiviral drugs. A vaccine for adenoviruses; however, no Individuals who are known to adenovirus strains 4 and 7 was controlled trials have been have been exposed to HAV developed but is no longer in performed so far, and the drug should be administered HAV production (economic reasons). is not currently licensed for immune globulin (0.02ml/kg body use. weight) within two weeks of the initial exposure. Inactivated HAV vaccines are highly effective in

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 82 of 92 Revised: January 26, 2017

pre-exposure prophylaxis for laboratory workers and travellers to HAV endemic areas. There is also some evidence for effective post-exposure prophylaxis with HAV vaccine.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 83 of 92 Revised: January 26, 2017

Medical Surveillance Sewage Viruses – (cont)

Hepatitis E Virus; Coxsackievirus; Human Rotavirus

Pathogen Hepatitis E Virus (HEV) Coxsackievirus Human Rotavirus Identification

Mode(s) of Four modes of transmission of HEV infection Infection occurs through contact with infective secretions The most common mode of transmission for HRV Transmission have been reported: faecal-oral transmission, or excretions, and subsequent autoinoculation of mouth, is through faecal-oral spread, either from person-to- food-borne transmission, blood-borne nose, or eyes. It is possible that ingestion of contaminated person or contact with contaminated environmental transmission, and vertical transmission. The most water may contribute to infection. Intranasal and aerosol surfaces. The possibility of spread through faecally common mode of transmission of HEV, also transmission are possible for some variants through contaminated food and water also exists.

responsible for the majority of the HEV infection contaminated respiratory secretions. Laboratory hazards Transmission through respiratory droplets has also outbreaks, is through the faecal-oral route, usually include exposure of mucous membranes to infective been suggested; however, more investigation is by ingestion of contaminated water. Potential aerosols, accidental ingestion, and accidental parenteral required. Laboratory hazards include exposure of exists for food-borne transmission and some cases inoculation. mucous membranes to infective aerosols, have been observed where consumption of raw or accidental ingestion, and accidental parenteral uncooked meat from wild boar and deer has led to inoculation. HEV infection. Blood-borne transmission is rare but has been documented in some cases involving blood transfusions. Some cases of vertical (perinatal) transmission from mother-to- child have been documented, particularly in India, but this is considered to be of minor importance as a mode of transmission for HEV and more investigation is required. Person-to- person transmission and secondary household cases are uncommon, particularly in epidemic (poor hygienic) conditions. In non-endemic regions, where autochthonous cases have been observed, zoonotic transmission has been considered as the likely mode of transmission, but more investigation is required. Laboratory hazards include exposure of mucous membranes to infective aerosols, accidental ingestion, and accidental parenteral inoculation. Since HEV survives the conditions within the intestinal tract, it is considered relatively stable in acidic and mild alkaline conditions. Since HEV mainly spreads

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 84 of 92 Revised: January 26, 2017

through the faecal-oral route, it must be relatively stable under environmental conditions, possibly similar to HAV (i.e. in water and sewage for long periods). Incubation Incubation period for HEV infection in humans The incubation period for HRV infection is about 1-3 days. 1 -3 days Period ranges from 15-60 days with a mean 40 days.

Period of Unknown. Person-to-person transmission has Human-to-human transfer can occur readily through oral, Person -to-person transmission appears to be fairly Communicability been documented but appears to be uncommon. ocular, respiratory, or faecal-oral routes. Incubation period common through the faecal-oral route. Rotavirus HEV has been detected in the stools of infected varies with clinical course. shedding rate is the highest during the diarrhoeal patients after the onset of illness (jaundice) for up stage of the disease, which occurs during the first to 14 days. Maximal HEV shedding occurs during 2-5 days of illness. the incubation period and during early acute stage of the disease. Infectious Dose(s) Unknown. Unknown; however, 15-50 TCID has been shown to be Theoretically, a single infectious virus particle is infective in adult volunteers. capable of causing infection, although more than one infectious virus particle is generally required. The median infectious dose for rotavirus is 5.597. Typical The disease caused by HEV is generally self - Majority of infections are asymptomatic and self-limiting; HRV predominantly attacks enterocytes, which are Presenting Symptoms limiting with symptoms typical of acute viral however, infections may lead to a variety of rare mature villous epithelial cells in the small intestine. hepatitis including, jaundice, malaise, anorexia, conditions, some of which are life threatening. Clinical The disease caused by HRV is self-limiting in abdominal pain, nausea, fever, diarrhea, course can vary within and between strains of general, lasting for about 4-7 days, with symptoms discoloured stool and/or urine, and hepatomegaly. Coxsackievirus. similar to those caused by other gastrointestinal

Anicteric hepatitis and cholestasis are also Coxsackievirus group A associated conditions: hand-foot- agents, although the symptoms of HRV infections observed in some cases. Mortality rate due to and-mouth disease, herpangina, acute lymphatic or nodular are usually more severe. These include fever, infection by hepatitis E have been reported to be pharyngitis, aseptic meningitis, paralysis, exanthema, hand- vomiting, and non-bloody diarrhoea (often watery as high as 1 %; however, the mortality rate may foot-and-mouth disease (A10, A16), pneumonitis of and explosive). This usually leads to mild to severe reach up to 20 % in pregnant women with each infants, “”, hepatitis, infantile diarrhoea, acute dehydration (usually isotonic in nature); electrolyte passing trimester, making HEV infection the most hemorrhagic conjunctivitis (A24). imbalance; and in prolonged cases, to secondary severe hepatitis in pregnancy of all recognized Coxsackievirus group B associated conditions: diabetes, disaccharidase deficiency. Subsequent hepatitis viruses. Analysis of serum specimens pleurodynia, aseptic meningitis, paralysis, severe systemic gastroenteritis infections tend to be less severe collected from volunteer blood donors shows that infection in infants, meningoencephalitis, myocarditis, compared to previous infections. A temporal the prevalence of HEV varies from region-to- pericarditis, upper respiratory illness and pneumonia, rash, association of rotavirus infection with a variety of region but is higher in endemic countries/regions hepatitis, and pancreatitis,. Undifferentiated febrile illness disease conditions has been described, including as compared to developed countries. Hepatitis and viral parkinsonism may also be associated with upper and lower respiratory infection, caused by HEV is clinically indistinguishable Coxsackievirus group B infection; however, these are more intussusception, and others. An etiologic from hepatitis A disease. controversial. Most common conditions requiring association of rotavirus infection with necrotizing hospitalization are: enterocolitis, hemorrhagic gastroenteritis, and Hand-foot-and-mouth disease: characterized by fever and pneumatosis intestinalis in infancy has been vesicles on the mouth and extremities, sore throat, fever, suggested. Detection of rotavirus RNA in and anorexia. Usually self limiting and requires only cerebrospinal fluid of patients with gastroenteritis symptomatic treatment. suggests that neurological disorders such as

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 85 of 92 Revised: January 26, 2017

Aseptic meningitis/meningoencephalitis: Most common convulsions may be associated with HRV infection, clinical syndrome associated with enteroviruses, resulting but this has not been confirmed. in medical attention. The virus causes nonbacterial inflammation of the meninges associated with fever, headache, photophobia, and with no apparent parenchymal involvement. The infection can progress to meningoencephalitis with infection of the parenchyma, characterized by disturbed state of consciousness, focal neurologic signs, and seizures. While severe meningeal disease is usually self limiting, deaths have been reported. Myocarditis and dilated cardiomyopathy: Myocarditis is an inflammation of the myocardium associated with damage that is unrelated to ischemic injury, if infection /inflammation persist the syndrome may progress to dilated cardiomyopathy (in which the heart is enlarged), potentially leading to heart failure [very rare]. Mode(s) of HEV is susceptible to iodinated disinfectants Sensitive to formaldehyde, gluteraldehyde, strong acids, HRV, either in suspension or on inanimate Decontamination (0.075g/L or 1 % iodine). It may also be sensitive sodium hypochlorite (bleach), and free residual chlorine. surfaces, is susceptible to glutaraldehyde (2%); to hypochlorites (1 % sodium hypochlorite), Sensitivity is dependent on sufficient concentration, pH, chlorinated disinfectants (>20,000 p.p.m. chlorine); formaldehyde (18.5 g/L; 5 % formalin in water), and contact time and is reduced in presence of extraneous iodinated disinfectants (>10,000 p.p.m. iodine); and glutaraldehyde. HEV is more heat labile organic materials. Infectious viruses are usually resistant to combinations of quaternary ammonium compounds

than Hepatitis A virus (HAV) and most strains can many common laboratory disinfectants, including 70% with alcohols (>40%), some acids (HCl), some be inactivated at temperature ≥60°C for 15 ethanol, isopropanol, dilute Lysol, and quaternary bases (sodium metasilicate); and combinations of minutes or more(12). The heat sensitivity of HEV, ammonium compounds. Insensitive to lipid solvents, phenolic compounds with strong anionic however, depends on the heating conditions. including ether and chloroform. Stable in many detergents surfactants. Longer exposure times are required for Hepatitis E in PBS is inactivated quickly at 60°C, at ambient temperatures. Sensitive to UV mediated disinfecting contaminated surfaces as compared to but in an albumin solution is inactivated more inactivation. Drying conditions reduce viral titres, the contaminated suspensions/solutions. HRV has also slowly. When HEV is added to freeze-dried degree of which is dependent on the porosity of the surface been shown to be very susceptible to Lysol brand fibrinogen containing stabilizers and subjected to and presence of extraneous organic matter. Most are readily disinfectants (79% ethyl alcohol, 0.1% o- dry heat, it is inactivated to below detection limit inactivated at 42 °C, but stability and heat resistance is phenylphenol). Other disinfectants include formalin within 24 hours at 80°C, but is inactivated more increased in the presence of sulphydral reducing agents and (2%) and sodium hypochlorite (2%). HRV is slowly at 60°C. It is also susceptible to low magnesium cations. No antiviral medications are currently susceptible to strong acidic pH (<3.0). It is also storage temperatures (between -70°C and +8°C). approved. Although Pleconaril® has been used in clinical susceptible to heating above 50 °C (for 30 trials to treat severe Coxsackievirus infections, these have minutes), but is stabilized in 2M magnesium shown no important effects on morbidity or mortality. sulphate. Emergency Response If exposure is suspected, wash area thoroughly If exposure is suspected, wash area thoroughly and If exposure is suspected, wash area thoroughly and and encourage bleeding if, sharps or puncture encourage bleeding if, sharps or puncture injury. Seek encourage bleeding if, sharps or puncture injury. injury. Seek emergency medical attention. emergency medical attention. Monitor for symptoms; Seek emergency medical attention. Monitor for Monitor for symptoms of disease. Confirm using confirm by serology, virus isolation, or PCR from lesions symptoms. Electron microscopy is still the gold serological or nucleic acid tests, and by exclusion or nasopharyngeal and fecal specimens. The use of viral standard diagnostic technique for HRV; however, it of hepatitis A and B viruses. Serological tests culture is declining as not all serotypes will grow well in is slightly less sensitive and more expensive than involve enzyme-linked immunosorbent assays culture. Molecular typing has largely replaced serotyping. some new diagnostic techniques. These include (i.e. ELISA) for the detection of antibodies to No specific treatment is available. No general vaccine enzyme-linked immunosorbent assays (ELISAs)

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 86 of 92 Revised: January 26, 2017

HEV (IgM, IgA, and IgG), and nucleic acid tests available; however, one is under development for and latex agglutination assays used for the involve reverse transcription-polymerase chain Coxsackievirus induced heart disease. detection of HRV (group A) antigen in stool reaction (RT-PCR) assays for the detection of samples. Supportive therapy is needed to prevent HEV RNA in serum, bile, and/or faecal samples. dehydration by replacement of fluid and electrolyte Rest is recommended for infected individuals, losses. This can be done using the World Health since no specific treatment currently available. Organization (WHO) formulation or other commercial formulations, or through intravenous fluids in cases of severe diarrhoea, intractable vomiting, acidosis, and/or shock accompany the illness. Resumption of normal diet should be promoted after rehydration. In the past, the rhesus- human rotavirus reassortment-tetravalent vaccine (Rotashield) had been recommended for use by the US Advisory Committee on Immunization Practices (ACIP), but its use was suspended in 1999. Health Canada has approved RotaTeq and Rotarix vaccines in Canada; however, they are not part of the routine immunization programs that are currently available. RotaTeq is a live, oral, human- bovine, reassortment rotavirus vaccine developed from a strain of bovine rotavirus, approved by the US Food and Drug Administration (FDA). Rotarix is a live, oral human rotavirus vaccine developed from the most common strain of human rotavirus, also approved by FDA.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 87 of 92 Revised: January 26, 2017

Medical Surveillance Sewage – Other Giardia lamblia; Cryptosporidum parvum; Schistosoma spp.; Naegleria fowleri

Pathogen Giardia lamblia Cryptosporidium parvum Schistosoma spp. Naegleria fowleri Identification

Mode(s) of The infectious cysts of G. lamblia are Transmitted through the fecal-oral Transmission occurs in water N. fowleri enters the nasal Transmission excreted in large numbers in feces of route, direct contact with infected contaminated with feces or passage, carried in contaminated infected persons, and they contaminate humans or animals, contaminated urine. Free swimming cercariae water, then penetrates through the hands, drinking water, swimming pool, food or water and aerosols. directly penetrate through the mucosal layer and travels along and food. They can be transmitted by Laboratory hazards include skin to infect humans. the olfactory nerve to the brain.

the fecal-oral route, or contaminated ingestion and possible aerosol and Laboratory hazards include Ingestion of contaminated water food and water. Sexual behaviours that inoculation infection. Outside of a direct contact with does not lead to PAM. N. aid in transmission of G. lamblia host, C. parvum survive for 6 contaminated fluids, ingestion fowleri can survive in water at include oral-anal, genital-anal, and months at 20°C in the environment. and possible aerosol and temperature up to 45°C and at pH digital anal contact. Contaminated soil inoculation infection. Cercariae 4.6 - 9.5. and fomites can also contain infective may survive in water for about Primary laboratory hazards cysts. Cysts can survive in cold water 2 days. include aerosol inhalation and for several weeks to months. At mucocutaneous and parenteral 4°C Giardia lamblia cysts can survive inoculation. 11 weeks in water, seven weeks in soil, and one week in cattle feces. They remain infective for a significantly shorter period at warmer temperatures - i.e. 25°C. Trophozoites do not survive in the environment. Laboratory hazards include ingestion and possible aerosol and inoculation infection with contaminated water, faeces, and other materials. Incubation 7 to 14 days; however, the time from 7 to 10 days. Cercariae reach the portal The first symptoms appear 1-7 Period ingestion of the cysts to detection of venous system several days days after infection, and death the cysts may be longer than the post-infection. 4-6 weeks by PAM may occur 7-10 days incubation period, which can result in usually pass before egg after infection. the stool sample being negative at the production begins. Toxemic time of the onset of symptoms. schistosomiasis may develop 6- 8 weeks post infection. Urinary

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 88 of 92 Revised: January 26, 2017

schistosomiasis may develop 10-12 weeks post infection. Adult schistosomes may live 20 to 30 years. Period of Can be transmitted from person -to- Highly contagious. Human-to- Not directly transmitted from Not transmitted from person-to- Communicability person, especially persons with poor human transmission is common. person to person. person. fecal-oral hygiene, causing epidemics. Oocysts can be excreted up to 50 days after cessation of diarrhea. Infectious Dose(s) Human volunteers have been The median infectious dose in Unknown. Unknown. experimentally infected with as few as healthy adult volunteers is 132 10 cysts. oocysts. However, the infectious dose for humans is as low as 1-5 oocysts. Infectious dose is dependent on the immune status of the host, with immunodeficient persons being much more susceptible. Typical The majority of infections are C. parvum occurs worldwide and is Symptoms are related to the N. fowleri is the causative agent Presenting asymptomatic. In symptomatic ubiquitous in the environment. amount and location of eggs in of primary amoebic Symptoms individuals, patients may experience Cryptosporidiosis is in the top five the human host. Any species meningoencephilitis nausea, chills, low grade fever, most common causes of infectious of Schistosoma (PAM). PAM is an acute, epigastric pain and sudden onset of diarrhea around the globe. can cause acute fulminating, rapidly fatal disease

watery diarrhea. Diarrhea is often Prevalence varies based on climate schistosomiasis. Acute that is often observed after explosive and presents a foul smell and level of development, schistosomiasis is characterized exposure to fresh water, with without the presence of blood, gas, accounting for 0.1-2% of diarrheal by cercarial dermatitis and symptoms such as sore throat, bloating, mucus, or cellular exudate. illness in cooler and developed areas Katayama syndrome. Cercarial blocked nasal passages, fever, Most infections resolve spontaneously and 0.5-10% in warmer and dermatitis is unusual among vomiting, stiff neck, confusion, within six weeks. Chronic infections developing countries. Settings individuals exposed for the first and abnormal behaviour. Three to can occur and diarrhea leads to involving close contact with infected time such as visitors and four days after the onset of the dehydration, malabsorption, weight persons, including day-care centres, migrants, and is rare among initial symptoms, mental lost and impaired pancreatic function. which increase transmission. endemic populations, travellers confusion and coma occur. Death Chronic infections can last from Outbreaks have been associated with or migrants. The clinical usually occurs 3-4 days after months to years. G. lamblia are usually contaminated food, drinking, and presentation of acute coma. Time from infection to found in the upper small intestine, but recreational water. One outbreak schistosomiasis includes fever, death is 7-10 days. Mortality rate can be found in the gall bladder and in linked to contaminated drinking headache, generalized myalgia, is estimated at greater than 95%. biliary drainage. water affected over 400,000 abdominal pain, vertigo, individuals in Milwaukee, vomiting, bloody diarrhea, and Wisconsin. fatigue. When eggs become trapped in tissue, and they fail to clear, they can produce chronic schistosomiasis. The chronic disease, which is more

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 89 of 92 Revised: January 26, 2017

prevalent in endemic areas, is due to a granulomatous response to parasitic eggs. Clinical presentation includes inflammation, hyperplasia, ulceration, and occult blood in feces. It is possible that there is an association between chronic schistosomiasis and colorectal cancer. When eggs are deposited in the liver, symptoms can include portal hypertension, hepato- splenomegaly, liver fibrosis, hepatic coma, ascites, and esophogeal varices. The latter are late stages of pipestem fibrosis with liver cell function relatively preserved early in the disease course. S. japonicum and S. mansoni are primarily associated with hepatic and intestinal pathology, including diarrhoea, abdominal pain, and hepato- splenomegaly. Urinary schistosomiasis is caused by S. haematobium, and chronic S. hematobium infection is the major risk factor for urinary tract carcinoma in Africa. The clinical presentation includes dysuria, hematuria, proteinuria, calcification in the bladder, obstruction of the , , hydronephrosis, and renal failure. Secondary infection may occur with urinary schistosomiasis. It is associated with genital disease in 1 out of 3 infected women. S. haematobium is a

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 90 of 92 Revised: January 26, 2017

leading cause of bladder cancer. Lung and CNS involvement can occur, producing lesions in the brain (S. japonicum and S. mekongi) and spinal cord (S. mansoni and S. haematobium). Clinical manifestations of cerebral schistosomiasis include seizure, headache, acute encephalopathy, hemiparesis, and hemianopsia. Worms may survive for 30 years in the host. Mode(s) of Cysts are relatively resistant to C. parvum is susceptible to high 2% glutaraldehyde, sodium N. fowleri is susceptible to NaCl Decontamination chlorination but Giardia cysts in water concentration (> 6%) of hydrogen hypochlorite, 70% ethanol. at concentrations greater then 1%, can be inactivated with 4 mg/L of peroxide and ethylene oxide, ozone. Sensitive to low w/v. N. fowleri is susceptible to chlorine after 60 min at 5°C, at pH It is resistant to low concentration of temperatures; S. chlorine at concentrations of 0.5 levels 6, 7 and 8. A chlorine hydrogen peroxide, peracetic acid, japonicum does not develop at and 1.0 mg/L, ozone, and

concentration of 8 mg/L will sodium hypochlorite, phenolic, temperatures lower than Deciquam 222. Heating water to inactivate Giardia cysts at pH 6 and 7 quaternary ammonium compound, 15.4°C. 50°C for 5 minutes will kill all after contact for 10 min, and at pH 8 2% glutaraldehyde, ortho- forms of the amoebae. Both after 30 min. Also, at 25°C, phtalaldehyde, and 70% ethanol. amoeba and cysts can tolerate Giardiacysts will be killed when Inactivated by moist heat (e.g. temperature of 65°C for 1-3 exposed to 1.5 mg/L of chlorine for 10 121°C for 18 minutes), freezing (- minutes and temperatures below min at pH 6. 6% H2O2can be used as a 70°C for seconds or -20°C for 24 20°C inhibit reproduction. surface disinfectant or in disinfection hours), desiccation, and UV light. Degradation occurs when of spills. Giardia is inactivated by Use of “absolute” 1 μm filters. temperatures reach below 10°C. exposure to UV light (10 JM-2). Cysts Dehydration is lethal to N. are relatively resistant to ozonolysis. fowleri. Cysts are susceptible to boiling and freezing. Emergency If exposure is suspected, wash area If exposure is suspected, wash area If exposure is suspected, wash If exposure is suspected, wash Response thoroughly and encourage bleeding if, thoroughly and encourage bleeding area thoroughly and encourage area thoroughly and encourage sharps or puncture injury. Seek if, sharps or puncture injury. Seek bleeding if, sharps or puncture bleeding if, sharps or puncture emergency medical attention. Monitor emergency medical attention. injury. Seek emergency injury. Seek emergency medical for symptoms. Since the incubation Monitor for symptoms. Detection medical attention. Confirm attention. Monitor for symptoms.

time may be shorter than the period usually by direct microscopic through direct observation of Identification is done by required for detection of the cysts in observation of oocysts in stool eggs in stool or urine (S. microscopic examination of CSF the stool, giardiasis should not be specimens. Nucleic acid and antigen haematobium for presence of amoebic eliminated as a diagnostic possibility if detection methods have also been and rarely S. mansoni). If a organism. Molecular biology a single stool specimen is negative at developed. Illness is generally self- patient exhibits the clinical techniques such as PCR and real- the onset of symptoms. symptoms but lacks eggs in time PCR have been recently

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 91 of 92 Revised: January 26, 2017

Since Giardia is excreted limiting in immuno-competent faeces or urine, a biopsy of the developed for detecting N. intermittently, in 50% to 70% of patients. bladder or rectal mucosa can be fowleri. Treatment of PAM is cases, Giardia will be detected from a Rehydration and electrolyte therapy performed. ELISA and PCR rarely successful and depends on single stool specimen and in 90% of may be used in cases with severe can be used, as well as a Kato- prompt diagnosis and cases after three specimens. In general, diarrhea. Nitazoxanide is approved Katz thick smear. If too few administration of medication. The the initial diagnosis is made by for treatment of cryptosporidiosis in eggs are excreted, the usual course of treatment involves identification of trophozoites or cysts children aged 1 to 10 years in the miracidium-hatching method amphotericin B administered in in stool specimens, duodenal fluid, or USA. It has also showed promise in can be employed. Praziquantel combination with rifampin and small bowel tissue by direct immuno-compromised individuals. is the primary drug used other antifungals. N. fowleri is microscopic examination. Other Immuno-compromised patients are against schistosomiasis. susceptible to amphotericin B, techniques such as detecting soluble often treated with paromomycin, Artemether is not used where which is often used in stool antigens using enzyme letrazuril and azithromycin. Highly malaria is present to prevent combination with rifampin, immunoassay (EIA) or polymerase active antiretroviral therapy Plasmodium from developing orindazol, miconazol, chain reaction technique are also used. (HAART) is currently considered resistance. Many strains are sulisoxazole, or chloramphenicol. Dehydration and electrolyte the best treatment option for life- resistant to oxamniquine. Miltefosine and voriconazole has abnormalities should be treated threatening cryptosporidiosis in Resistance to praziquantel has also been found to be effective symptomatically. In immunocompetent AIDS patients. Susceptible to been documented in laboratory against infection. Resistance hosts, infection is self-limited; drug nitazoxanide. strains and in the field. of Naegleria spp. has been shown therapy can shorten the duration of against fluconazole and symptoms and prevent transmission. itraconazole. This area remains a Metronidazole, tinidazole, and growing concern when repeated nitazoxanide are indicated for first line doses are administered, especially treatment. Susceptible to in endemic regions. metronidazole, tinidazole, nitazoxanide, quinacrine, furazolidone, paramomycin, and albendazole.

Suggested Reference: http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/index-eng.php.

SEM 20.25.1 Exposure Protocols – Medical Surveillance Page 92 of 92 Revised: January 26, 2017