Lecture 17:

Bacteria Distribution Virulence Factors (VF) Diseases Notes Haemophilus present in almost *small, sometimes pleomorphic. all individuals, *requires blood for growth on agar media. (haemo: blood primarily *Growth stimulating factors needed in Philos: lover) colonizing the media: mucosal (pleomorphic) (1) hemin (X factor for “unknown factor”) & membranes of the (2) nicotinamide adenine dinucleotide (NAD; respiratory tract also called V factor for “vitamin”) 1 H. influenzae H. influenzae 1.The surface of many, but not all, *A common cause of disease in unvaccinated *After introduction of the vaccine, more (particularly strains of H. influenzae is covered children: than half of all invasive disease is now serotype b with a six antigenic serotypes (a through a. meningitis: fever, sever headache, & caused by nonencapsulated (nontypeable) [biotype I]) is f) & antiphagocytic polysaccharide systemic signs. strains which are opportunistic pathogens that can cause infections of the upper and uncommon in capsule (polyribitol phosphate [PRP], b. epiglottitis [obstructive laryngitis]: lower airways. the upper which contains ribose, ribitol, and initial pharyngitis, fever, and difficulty *Treatment: systemic H. influenzae respiratory tract phosphate >> antibodies against it breathing and progressing to cellulitis and (type b: the most infections require prompt antimicrobial develop because of natural infection, swelling of the supraglottic tissues, with significant pediatric therapy because the mortality rate in vaccination with purified PRP, or the obstruction of of the airways pathogen in many patients with untreated meningitis or passive transfer of maternal c. cellulitis countries of the epiglottitis approaches 100%. antibodies. (capsule is a major VF) *Pneomonea (in elderly with underlying chronic world & was *Identification & diagnosis: responsible for more 2. Adhesins mediate colonization of pulmonary disease): inflammation and -A presumptive identification of H. than 95% of all the oropharynx consolidation of the lungstypically caused by influenzae can be made by the Gram invasive 3. Cell wall components of the nontypeable strains. stain morphology and demonstration of Haemophilus bacteria damage the respiratory *In the absence of specific opsonic antibodies a requirement for both X and V factors. infections) epithelium. directed against the polysaccharide capsule, -The immunologic detection of H. Then translocation across both high-grade bacteremia can develop. influenzae antigen, specifically the PRP epithelial and endothelial cells occurs *H. influenzae and S. pneumoniae are the two most capsular antigen, is a rapid and sensitive the and the bacteria can enter the blood. common causes of acute and chronic otitis and species sinusitis way to diagnose H. influenzae type b most disease 2 H. aegyptius (the commonly acute purulent conjunctivitis Koch-Weeks bacillus) associated with 3 Chancroids (STD common in men): 5 to 7 days H. ducreyi disease after exposure (occupation period) , a tender papule with an erythematous base develops on the genitalia or perianal area. 4 H. parainfluenzae Bacteremia, endocarditis, opportunistic infections

 All bacteria in this file are Gram Negative bacteria

Aggregatibacter colonize the can spread from the mouth into the blood and (A. human mouth then stick to a previously damaged heart valve actinomycetemcomitan or artificial valve, leading to the development of s & A. aphrophilus) endocarditis. 1 A. *often found in association with localized *facultative anaerobe, non-motile actinomycetemcomi aggressive periodontitis bacterium tans *endocarditis *bite wound infections *frequency: It's commonly found Pasteurella found as P. multocida causes: Bite wound infections, * genus of facultatively anaerobic, commensals in chronic pulmonary disease, bacteremia, fermentative coccobacilli (coccobacilli) the oropharynx of (P.multocida>> common meningitis. healthy animals P. canis causes: Bite wound infections *Most human infections result from animal P. canis>> uncommon) contact (e.g., animal bites, scratches, Both are human pathogens shared food). Vibrio lipopolysaccharides consisting of lipid *facultatively anaerobic, fermentative, (Rods) A (endotoxin), core polysaccharide, oxidase positive, with polar flagella rods and an O polysaccharide side chain. *Growth media description: can grow on a variety of simple media within a broad temperature range (from 14° C to 40° C). The O polysaccharide is used to And tolerate a wide range of pH (e.g., pH subdivide Vibrio species into of 6.5 to 9.0) but are susceptible to serogroups ( cholerae O1 and O139 stomach acids. are vibrio serotypes) All species require sodium chloride (NaCl). *Most species are halophilic (“salt- loving”). *grow naturally in estuarine and marine environments worldwide & Pathogenic vibrios can also flourish in waters with chitinous shellfish . 1 V. cholerae *Cholera complex A-B toxin: The active The majority of individuals exposed to toxigenic *Strains other than O1 & O139 of V. (cholerae O1 and portion of the A subunit ↑ adenylate V. cholerae O1 have asymptomatic infections or cholerae generally do not produce O139 are the only to cyclase activity > ↑cAMP > self-limited diarrhea; however, some individuals cholera toxin and do not cause epidemic hypersecretion of water and electrolytes. produce cholera develop severe, rapidly fatal diarrhea with rice disease. *toxin co-regulated pilus (TCP): toxin and are water stools (colorless and odourless, free of *Transmission: Cholera is spread by surface receptor site for the associated with protein, and speckled with mucus) contaminated water and food rather bacteriophage CTXΦ permitting it to move with the abrupt onset of watery diarrhea and epidemics of into the bacterial cell, where it becomes than direct person-to-person spread, vomiting. Fever is rare. 8 cholera) integrated into the V. cholerae genome; because a high inoculum (e.g., >10

 All bacteria in this file are Gram Negative bacteria

mediates adherence to intestinal mucosal *The resulting severe fluid and electrolyte loss organisms is required to establish infection cells. (encoded on VPI-1) can lead to dehydration, painful muscle in a person with normal gastric acidity.). *Chemotaxis protein (adhesin factor) cramps, metabolic acidosis (bicarbonate loss), *usually seen in communities with poor *Accessory cholera enterotoxin: ↑ and hypokalemia and hypovolemic shock sanitation. fluid secretion. (potassium loss), with cardiac arrhythmia and *Identification & diagnosis: *Zonula occludens toxin: ↑ intestinal renal failure. -Immunoassays for the detection of permeability. cholera toxin or the O1 and O139 *Neuraminidase: ↑GM1 binding sites for **V. cholerae O1 does not produce a capsule, lipopolysaccharides are used for the cholera toxin. so infections with this organism do not spread diagnosis of cholera in endemic areas.

* occupation period: 2 to 3 days (can be beyond the confines of the intestine. **How cholera strains gain toxicity? <12 hours) Virulence of V. cholerae involved *Treatment: Patients with cholera acquisition of first a sequence of must be promptly treated with fluid and genes including the toxin co-regulated electrolyte replacement (↓ mortality pilus (TCP) on what is termed the rate from 70% to 1%) before the vibrio pathogenicity island (VPI-1), resultant massive fluid loss leads to followed by infection with the hypovolemic shock. bacteriophage CTXΦ that encodes the *Some statistics: It is estimated that 3 to genes for the two subunits of cholera 5 million cases of cholera and 120,000 toxin (ctxA and ctxB). deaths occur worldwide each year. Seven major pandemics of cholera have occurred since 1817, resulting in thousands of deaths and major socioeconomic changes. *Note: Chocolate agar contains heated blood and named chocolate just for the similar brown colour.

*More info. about H. influenzae:

-Most of the H. influenzae type b infections now occur in children who are not immune (because of Satellite phenomenon incomplete vaccination or a poor response to the vaccine) and in elderly adults with waning caused by H. influenzae immunity.

-Antibodies directed against the capsule greatly stimulate bacterial phagocytosis and complement- mediated bactericidal activity

-When vaccines containing purified PRP antigens conjugated to protein carriers (i.e., diphtheria toxoid, tetanus toxoid, meningococcal outer membrane protein) were introduced in December 1987, a protective antibody response in infants aged 2 months and older was produced, and systemic disease in children younger than age 5 was virtually eliminated in the United States.

 All bacteria in this file are Gram Negative bacteria

Lecture 18: All are opportunistic pathogens

Bacteria Description Virulence Factors (VF) Diseases Notes

Pseudomonas Motile, *Adhesins : *Pulmonary Infections: asymptomatic *has broad environmental distribution because it can use (rods) straight or (1) flagella, (2) pili, (3) colonization (in patients with Cystic many organic compounds as sources of carbon and nitrogen. *Members of the genus are found in soil, decaying organic slightly lipopolysaccharide (LPS), and Fibrosis and other chronic lung diseases) curved, (4) alginate (a mucoid or benign inflammation of the bronchials matter, vegetation, and water. Also found throughout the P. aeruginosa (most aerobic, exopolysaccharide that forms (tracheobronchitis) to severe necrotizing hospital environment. And is resistant to many antibiotics important pathogen oxidase + rods a prominent capsule ) bronchopneumonia. >> Previous therapy and disinfectants. of the group which typically *Toxins and Enzymes : with broad-spectrum antibiotics and use *infections are primarily opportunistic. has intrinsically arranged in 1. Exotoxin A (disrupts of mechanical ventilation equipment *The underlying conditions required for most infections: resistant to many pairs protein synthesis by blocking predispose to infection. (1) the presence of the organism in a moist reservoir and antibiotics) peptide chain elongation in *Skin and Soft-Tissue Infections: burn (2) compromised host defenses (e.g., cutaneous trauma, P. aeruginosa eukaryotic cells ). wounds (most recognized) & Folliculitis elimination of normal microbial flora as a result of smells fruity, 2. Two elastases, LasA (assosiated with immersion in antibiotic usage, neutropenia) "grape-like" (serine protease) and LasB contaminated water e.g. hot tubs) ,"fresh- (zinc metalloprotease), act *Urinary Tract Infections: assosiated with *Identification & diagnosis: The presence of tortilla" synergistically to degrade long-term indwelling urinary catheters. cytochrome oxidase (detected in a rapid 5-minute test) & Produces elastin, related to lung *Ear Infections: range from external otitis differentiate them from Enterobacteriaceae. blue-green parenchymal damage. (“swimmer’s ear” so swimming is an *Treatment: combination of antibiotics for serious pigment 3. Phospholipase C is a heat- important risk factor) to invasive infections. pyocyanin. labile hemolysin that breaks destruction of cranial bones. -antimicrobial therapy for Pseudomonas infections is down lipids and lecithin, *Eye Infections : Occur after initial frustrating because the bacteria are typically resistant to Pyocyanin catalyzes the production facilitating tissue destruction trauma to the cornea (e.g., abrasion from most antibiotics and the infected patient has compromised of superoxide and hydrogen 4. Exoenzymes S and T are contact lens). immune defences peroxide, toxic forms of oxygen. extracellular toxins *Bacteremia and Endocarditis: *Antibiotic resistance gained by (the low rate of movement This pigment also stimulates facilitating bacterial spread, characterized by ecthyma gangrenosum. of antibiotics through the outer membrane pores into the interleukin (IL)-8 release, leading to tissue invasion, and necrosis. -Mortality rate in affected patients is bacterial cell, combined with the rapid efflux of antibiotics with enhanced attraction of neutrophils higher with P. aeruginosa. efflux pumps . Also acquired and adaptive resistance)

Burkholderia 1. B. cepacia complex: * colonize a variety of moist environmental surfaces and B. cepacia complex, a- Pulmonary infections: Patients are opportunistic pathogens >> like P. aeruginosa B. gladioli, & B. particularly susceptible to pulmonary infections with B. cepacia complex and B. pseudomallei gladioli are those with Cystic fibrosis, in *pseudomallei is of public health importance in whom infections can progress to endemic areas, particularly in northeast Thailand, significant destruction of pulmonary Vietnam, and northern Australia, causing melioidosis. tissue. b- Opportunistic infections: UT infections ( in catheterized patients, bacteremia (in  All bacteria in this file are Gram Negative bacteria

immunocompromized patients with *Transmission of Melioidosis: contracted through contaminated IV catheters) direct contact with contaminated soil and surface 2. B. pseudomallei: asymptomatic waters. colonization to abcess formation & *Melioidosis Occupation period: range from one day to Melioidosis many years; generally symptoms appear two to four weeks after exposure. Acinetobacter *strictly respiratory tract & pulmonary *opportunistic pathogens (coccobacilli) aerobic, infections (in patients receiving oxidase- respiratory therapy), UT infections, & negative, wound infections (traumatic;military plump conflicts, &nosocomial wounds) ; they coccobacilli. also cause septicemia ** A. baumannii (frequent cause of hospital-acquired pneumonia, especially of late-onset, ventilator-associated pneumonia) Moraxella strictly * Over the last 20 to 30 years, the * The peak rate of colonisation by M. catarrhalis appears M. catarrhalis aerobic, bacterium has emerged as a genuine to occur around 2 years of age, with a striking difference in oxidase- pathogen and is now considered an colonization rates between children and adults (very high positive, important cause of upper respiratory to very low). diplococci. tract infections (in otherwise healthy children and elderly people) * M. catarrhalis is a nosocomial pathogen *important cause of lower respiratory tract infections (in adults with chronic obstructive pulmonary disease (COPD)) Legionella *Slender, Legionellae are facultative L. pneumophila affects the lungs and *Legionella acquired its name after an outbreak of a then- (Rods) pleomorphic intracellular bacteria ( infect present in one of two forms : unknown "mystery disease" sickened 221 persons, causing

L. pneumophila rods and replicate in (1) an influenza-like illness (referred to as 34 deaths, at a convention of the American Legion. *obligatively macrophages and amoeba ). Pontiac fever (self-limited, febrile illness) (cause of 90% of all *Transmission: Human infections are most commonly aerobic and Cytokines released by the (2) a severe form of pneumonia (i.e., Legionella infections) associated with exposure to contaminated aerosols (e.g., nutritionally infected macrophages legionnaires disease). air conditioning cooling towers, whirlpool spas, showerheads, fastidious stimulate a robust water misters). (They require inflammatory response that *The organisms can survive in moist environments for a

media is characteristic of infections long time. Legionnaires disease is characteristically supplemented with Legionella *The medium most commonly used for the isolation of more severe and, if untreated, promptly with cysteine). legionellae is buffered charcoal yeast extract (BCYE) agar causes considerable morbidity.

 All bacteria in this file are Gram Negative bacteria

Bordetella extremely *Pertussis toxin (A-B toxin) pertussis or whooping cough *Transmition: mainly by respiratory droplets. (Coccobacillus) small (0.2 to inactivates the protein that Pertussis: a toxin-mediated human *Even under ideal conditions, recovery of B. pertussis in B. pertussis 0.5 × 1 μm), controls adenylate cyclase disease (human is the only reservoir). culture is difficult. fastidious, activity, ↑ cAMP levels and a strictly subsequent ↑ in respiratory *vaccines contain inactivated pertussis toxin, filamentous aerobic, secretions and mucus hemagglutinin, and pertactin coccobacillus. production. -Since widespread use of the vaccine began, incidence has decreased more than 75% compared with the pre-vaccine *The bacteria attach to the cilia era. of the respiratory epithelial cells, produce toxins that *incubation period: 7-10 days. paralyze the cilia, and cause

inflammation of the respiratory tract, which interferes with the * In the summer of 1976, public attention was focused on clearing of pulmonary an outbreak of severe pneumonia that caused many secretions. deaths and the clearance of mucus is impaired. This stage is characterized by the classic whooping cough paroxysms

**The oxidase test is used to identify bacteria that produce cytochrome c oxidase, an enzyme of the bacterial electron transport chain. (note: All bacteria that are oxidase positive are aerobic, and can use oxygen as a terminal electron acceptor in respiration. This does NOT mean that they are strict aerobes. Bacteria that are oxidase-negative may be anaerobic, aerobic, or facultative; the oxidase negative result just means that these organisms do not have the cytochrome c oxidase that oxidizes the test reagent. They may respire using other oxidases in electron transport.)

 All bacteria in this file are Gram Negative bacteria

Lecture 19: Bacteria Description Virulence Factors Diseases Transmission Notes (VF) Campylobacter Small (0.2 to lipooligosaccharides the most common cause of bacterial *zoonotic *Microaerophilic: grow best in an atmosphere of (Rods) 0.5 μm wide (LOSs lack O-antigen gastroenteritis infections with a reduced O2 (5% to 7%) and increased CO2 (5% to and 0.5 to 5.0 in LPS) *most commonly > acute enteritis variety of animals 10%) (C. jejuni μm long), with diarrhea (stools may be bloody serving as C. jejuni grows better at 42°C than at 37°C. responsible for most motile, curved, on gross examination ), fever, and reservoirs. *The organisms are killed when exposed to infections) oxidase +, severe abdominal pain. *Contaminated gastric acids, (so conditions that decrease or catalase + rods *Uncommon> Guillain-Barré poultry are neutralize gastric acid secretion favor disease. syndrome & reactive arthritis are responsible for *Identification & diagnosis: well-recognized complications. more than half of A presumptive identification of isolates is based ((Probably through molecular the infections in on growth under selective conditions, typical mimicry)) developed microscopic morphology, and positive oxidase *C. jejuni GI disease characteristically countries. and catalase tests. produces histologic damage to the *Uncommon to *Some statistics: Microbiological findings among US mucosal surfaces of the jejunum and be transmitted by emergency department patients presenting with 549 other parts of the intestine. food handlers. episodes of bloody diarrhea at 11 Emergency ID NET sites. Helicobacter spiral rods *urease *Colonization with H. pylori invariably fecal-oral route. *Growth of H. pylori and other helicobacters (rods) resembling *urease byproducts leads to gastritis requires a complex medium in microaerophilic campylobacters that mediate localized - acute gastritis: a feeling of fullness, ((Humans are the conditions. H. pylori is tissue damage: nausea, vomiting, and primary reservoir *H. pylori adheres to gastric mucosa and is responsible for All gastric mucinase, hypochlorhydria. for H. pylori, and usually not recovered in stool or blood 85% of the gastric helicobacters, phospholipases, & - chronic gastritis: disease confined to colonization is specimens ulcers and 95% of vacuolating cytotoxin including H. the gastric antrum or involve the believed to *H. pylori adapt to the acidic conditions of the duodenal A (VacA> damages pylori, are entire stomach persist for life the stomach by using their motility, ulcers. epithelial cells by highly motile >>Chronic gastritis will progress to unless the host is chemotaxis, urease production, and other producing vacuoles) (corkscrew *cytotoxin-associated peptic ulcers. specifically mechanisms. It also colonizes a narrow- motility) and gene (cagA) interferes The ulcers develop at the sites of treated)) protected niche near the surface of epithelial produce an with the normal intense inflammation, (the junction cells abundance of cytoskeletal structure between the corpus and antrum *Identification & diagnosis: urease of the epithelial cells (gastric ulcer) or the proximal Since H. pylori adheres to gastric mucosa , H. duodenum (duodenal ulcer)) pylori can be detected by histologic examination *Chronic gastritis increases the risk of of gastric biopsy specimens, but identification is gastric cancer and MALT lymphoma usually done by non-invasive methods, A number (mucosa-associated lymphoid tissue of polyclonal and monoclonal immunoassays for B-cell lymphomas) H. pylori antigens excreted in stool have been developed and demonstrated to have sensitivities and specificities exceeding 95%.  All bacteria in this file are Gram Negative bacteria

Bartonella coccobacillary facultative B. henselae causes cat-scratch transmitted by Incubation period: prolonged (2 to 6 weeks). (coccobacillary or or bacillary rods intracellular disease, 1–3 weeks after inoculation vectors such as bacillary rods) with fastidious bacteria (acquired after exposure to cats (e.g., ticks, fleas, sand growth scratches, bites, contact with the flies, and B. henselae, B. requirements contaminated feces of cat fleas)) mosquitoes bacilliformis, & B. Symptoms>> typically include a non- Quintana painful bump or blister at the site of injury & painful & swollen lymph nodes B. bacilliformis causes Carrion's disease B. Quintana causes trench fever Rickettsiaceae aerobic rods Obligate transmitted by *grow only in the cytoplasm of eukaryotic cells. ectoparasites such (Rods) intracellular *Seen best with Giemsa stain. bacteria (The primary as fleas, lice, mites, *Rickettsia is subdivided into the spotted fever clinical manifestations and ticks. group and the typhus group appear to result from So,, the distribution *All age groups are at risk for rickettsial infections the replication of of rickettsial during travel to endemic areas. bacteria in endothelial diseases is cells, with subsequent determined by the damage to the cells and distribution of the leakage of the blood arthropod vessels) host/vector.

Mortality Rickettsiaceae without Disease Reservoir vector distribution Clinical presentation Rash treatment

type period

Eschar

Incubation % R. rickettsii Rocky Ticks, Hard ticks (dog Western Canada, continental US, 7 Abrupt onset; fever headache, >90%; macular; No 10-25 mountain wild tick, wood tick) Mexico, Panama, Argentina, Brazil, malaise, myalgias, nausea, centripetal spotted fever rodents Bolivia, Colombia, Costa Rica vomiting, abdominal pain spread R. prowazekii Epidemic Humans Human body Mountainous regions of Central & 8 Abrupt onset; fever headache, 20-80%; No 20 (louse-borne) louse Eastern Africa (Burundi, Rwanda, chills, myalgias, arthralgia macular; typhus Ethiopia), Central & South centrifugal America, Asia. spread Tickborne spotted fever rickettsioses are the most frequently reported travel-associated rickettsial infections, while Epidemic typhus caused by R. prowazekii infection is rarely reported among tourists but can occur in impoverished communities and refugee populations where body lice are prevalent.

 All bacteria in this file are Gram Negative bacteria

Lecture 20: All are related to sexual transmitted disease (STD)

Bacteria Description Diseases Transmission Notes

Treponema thin, helical (0.1 *Syphilis (common STD found world wide) *The most common *T. pallidum has not been cultured regularly in vitro T. pallidum to 0.5 × 5 to 20 - Patients infected with syphilis are at increased risk for route of spread is by because they are dependent on host cells for many (The most μm),bacterial transmitting and acquiring HIV when genital lesions are direct sexual contact. metabolites (e.g. purines, pyrimidines, amino acids). important Spirochetes present *Syphilis cannot be Moreover, they’re extremely sensitive to oxygen treponemal (too thin to be - Syphilis undergoes 3 phases: spread through (microaerophilic or anaerobic) seen with light species that 1. primary phase is characterized by skin lesions (chancres) contact with *Identification & diagnosis: microscopy so causes human at the site where the spirochete penetrated inanimate objects -darkfield microscopy or immuno-fluorescent stains traditional 2. secondary phase, the clinical signs of disseminated such as toilet seats must be used for visualization and diagnosis. disease; the diagnostic tests disease appear, (e.g. skin lesions over the entire body, (since the bacteria is -For diagnosis of syphilis, serology is the most causative agent such as gram very labile to drying for Syphilis) stain and fever, headache). Symptoms resolve within weeks. important tool, with tests like Treponema pallidum microscopy are of 3. Late syphilis severely damages organs involved (e.g., and disinfectants) . particle agglutination (TP-PA) test (Gelatin particles little value) neurosyphilis, cardiovascular syphilis) leading to various *Other routes include sensitized with T. pallidum antigens are mixed with symptoms (e.g. dementia or blindness) congenitally (from an dilutions of the patient’s serum. If antibodies - infected mother) or by against T. pallidum- are present, the particles **If the patient is not treated, syphilis cause systemic transfusion with agglutinate, indicating the patient has been infected devastating damage. contaminated blood. and developed antibodies). ***Between 2000 and 2012, the incidence of newly *Treatment: Syphilis be controlled only through the acquired disease has increased each year. practice of safe-sex techniques and adequate treatment with antibiotics. Borrelia Spirochetes Lyme disease and relapsing fever *Hard ticks are the *stain well with dyes such as Giemsa and stain In untreated patients > hematogenous dissemination will major vectors for lyme poorly with gram stain, but have an outer membrane occur within days to weeks of the primary infection. This disease. similar to gram-negative bacteria stage is characterized by systemic signs of disease (e.g., *The ticks *Identification & diagnosis: severe fatigue, headache, fever, malaise). contaminate the bite Because culture is generally unsuccessful, diagnosis *60% of patients with untreated Lyme disease will develop wound with borreliae of diseases caused by borreliae is by serology (Lyme arthritis present in saliva or disease) or microscopy (relapsing fever). *Tickborne diseases can have similar signs & symptoms: feces. fever/chills, aches & pains, rash Chlamydia 0.3 µm in *Trachoma (leading cause of preventable blindness): *Eye-to-eye *Unlike other bacteria, it has a unique most common diameter, with chronic inflammatory granulomatous process of eye transmission of developmental cycle, forming metabolically inactive bacterial STDs a unique life surface, leading to corneal ulceration, scarring, pannus trachoma is by infectious forms (elementary bodies [EBs]) and in humans & cycle formation and blindness. droplet, hands, metabolically active noninfectious forms (reticulate the leading __Infections occur predominantly in children, who are the contaminated bodies [RBs]). chief reservoir of C. trachomatis in endemic areas. clothing, and flies that  All bacteria in this file are Gram Negative bacteria cause of *Urogenital infections: transmit ocular Virulence factor: Obligate intracellular parasites infectious -Most genital tract infections in women are asymptomatic discharges from the (they use host cell ATP for their energy requirements & blindness (80%) eyes of infected damage is thought to be caused by intracellular worldwide. -Most C. trachomatis genital infections in men are children to the eyes of replication and destruction of infected cells upon symptomatic, 25% of the infections will be inapparent. uninfected children. release) -It can cause cervicitis in women and urethritis & proctitis *Infects epithelial cells, *Identification & diagnosis: in both men and women. which are found on the C. trachomatis infection can be diagnosed (1) on the mucous membranes of basis of cytologic, serologic, or culture findings, (2) the urethra, endocervix, through the direct detection of antigen in clinical endometrium, fallopian specimens, and (3) through the use of nucleic acid– tubes, anorectum, based tests. respiratory tract, and conjunctivae. Neisseria *aerobic, coccoid shaped (0.6 to 1.0 μm in diameter) bacteria arranged in pairs (diplococci) *Identification & diagnosis: (Coccoid) *All are oxidase + & most are catalase + *Both strains are strictly human pathogens. properties that combined with the Gram stain *Gonococci attach to mucosal cells, penetrate into the cells and multiply, and then pass through the morphology allow a rapid, presumptive cells into the subepithelial space where infection is established. identification of a clinical isolate . 1 N. fastidious (only *Gonorrhea N. gonorrhoeae in a clinical specimen is always gonorrhoeae grows on -Genital infection in men is primarily restricted to the considered significant. enriched urethra (purulent urethral discharge and dysuria) > all *incubation period: 2-5 days. (Gonorrhea chocolate agar infected men have acute symptoms (symptomatic) *Virulence factors: 2nd most and other -half of all infected women have mild or asymptomatic Pilin, Por protein, Opa protein, Rmp protein, commonly supplemented infections transferrin- lactoferrin- & haemoglobin- binding reported media) *Gonococcemia : Disseminated infections with proteins, LOS, IgA1 protease, β-lactamase STD in the septicaemia and infection of skin and joints (occur in US after 1% to 3% of infected women and in a much lower chlamydia) percentage of infected men) 2 N. *Meningitis: begins abruptly with headache, meningeal N. meningitidis can colonize the nasopharynx of meningitidis signs, and fever; however, very young children may have healthy people without producing disease (not only nonspecific signs such as fever and vomiting. significant in clinical specimen) *Meningococcemia (Septicaemia) with or without *ability to cause disease is determined by antigenic meningitis differences in the polysaccharide capsule *Meningococcal disease occurs in patients who lack *Meningitis mortality approaches 100% in untreated specific antibodies directed against the polysaccharide patients. capsule and other expressed bacterial antigens: (1) children younger than 2 years (antibodies from the mother are disappearing) (2) Patients with deficiencies in C5, C6, C7, or C8 of the complement system (6000-fold greater risk) (3) Post-splenectomy patients  All bacteria in this file are Gram Negative bacteria

Lecture 21: Mycoplasma

Mycoplasma *Don't have a *M. pneumoniae infects respiratory tract; typically results (Mycoplasma and Ureaplasma organisms are the M. pneumoniae cell wall & their in asymptomatic carriage but can cause: smallest free-living bacteria). They are unique is a strict cell membrane Respiratory disease occurs worldwide throughout the among bacteria because they do not have a cell wall human contains sterols year.: and their cell membrane contains sterols. pathogen. *pleomorphic -tracheobronchitis (most common) shapes varying -pneumonia: referred to as primary atypical pneumonia **Absence of the cell wall renders the mycoplasmas from 0.2 to 0.3 can also develop, with a patchy bronchopneumonia seen resistant to penicillins, cephalosporins, vancomycin, μm coccoid on chest radiographs and other antibiotics that interfere with synthesis of forms to rods *M. genitalium infects genitourinary tract & can cause the cell wall. 0.1 to 0.2 μm in nongonococcal urethritis (NGU) and pelvic inflammatory *Identification & diagnosis: width and 1 to 2 disease. -The most sensitive diagnostic tests are PCR μm long. amplification tests of species-specific gene targets. -(Microscopy is of no diagnostic value because mycoplasmas stain poorly with the Gram stain. Likewise, antigen tests have poor sensitivity and specificity and are not recommended.)

Saba Alfayoumi

 All bacteria in this file are Gram Negative bacteria