Lyme Disease

Total Page:16

File Type:pdf, Size:1020Kb

Lyme Disease Pondicherry Journal of Nursing Vol S, Issue1, December'11 -Marcl1'12 LYME DISEASE Ms. Snvithri K B INTRODUCTION Hard-bodied ticks of the genus lxodes arc the main vectors of Lyme Lyme disease, or Lyme disease. borreliosis is an emerging infectious disease caused by three species of Lyme spirochetes have been bacteria belonging to the genus found in insects as well as ticks. It has BoITelia The disease is named after the been found in semen and breast milk, town of Lyme, Connecticut, USA, but transmission has not been known to where a number of cases were take place through sexual contact. identified in 1975. Although Allen Transmission across the placenta Steere realized Lyme disease was a during pregnancy has not been tick-home disease in 1978, the cause of demonstrated. the disease remained a mystery until 1981, when B. burgdorferi was identified by Willy Burgdorfer. ETIOLOGY Borrelia bacteria, the causative agent of Lyme disease. It is caused by Gram-negative, spirochetal bacteria from the genus Borrelia. The Borrelia species that cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato. It made up of three closely related species namely B. burgdorferi sensu stricto B. afzelii, and B. garinii TRANSMISSION Lyme disease is classified as a zoonosis, as it is transmitted to humans from a natural reservoir among rodents by ticks that feed on both sets of hosts. Ms. Savithri KB, Lecturer, Vel RS Deer Tick medical college - College of Nursing, life cycle Avadi, Chennai. 17 Pond/cherry Journal of Nursing Vol S, lssue1, December'll -1\,f Q,.c,_,, .1.< targeted by antibodies, an0 variation of the VlsE surface tg~i~ . k . Prote· inacttvatmg ey immune compon 111, ii such as complement, and hiding . ellts extracellular matnx,. which ll} th e interfere with the function of imllllllay factors une PATHOPHYSIOLOGY In the brain, B. burgdorferi n.. ••iay induce astroc~es . to undergo Borrelia burgdorferi can spread astrogliosis (prohferatton followed b throughout the body during the course apoptosis), which may contribute t~ of the disease , and has been found in neurodysfunction. The spirochetes rnay the skin, heart, joint, peripheral nervous also induce host cells to secrete system, and CNS. B. burgdorferi is products toxic to nerve cells and cause injected into the skin by the bite of an cognitive impairment. infected Ixodes tick. IMMUNOLOGICAL STUDIES Tick saliva, which accompanies the spirochete into the skin during the Exposure to the Borrelia feeding process, contains substances bacterium during Lyme disease that disrupt the immune response at the possibly causes a long-lived and site of the bite. The spirochetes damaging inflammatory response, a multiply and migrate outward within form of pathogen-induced autoimmune the dermis. Days to weeks following disease. The production of this reaction the tick bite, the spirochetes spread via might be due to a form of molecular the bloodstream to joints, heart, mimicry, where Borrelia avoid being nervous system, and distant skin sites, killed by the immune system by where their presence gives rise to the resembling normal parts of the body's variety of symptoms of disseminated tissues. disease. SIGNS AND SYMPTOMS The spread of B. burgdorferi is aided by the attachment of the host Lyme disease can affect protease plasmin to the surface of the multiple body systems. Not all patients spirochete. If untreated, the bacteria with Lyme disease will have all may persist in the body for months or symptoms. The incubation period from even years, despite the production of B. infection to the onset of symptoms is burgdorferi antibodies by the immune usually one to two weeks, but system. The spirochetes may avoid the can be much shorter (days) immune response by decreasing or much longer (months to years). expression of surface proteins that are A circular, expanding rash called erytbe.DIS 18 Pondicherry Journal of Nursing Vol S, /ssue1, December'11 - March'12 chronicum migrans (EM), which swelling), cramps, stiffness, muscle occurs at the site of the tick bite 3 to 30 twitches, numbness and tingling, days after the tick bite. The rash is red, shooting pains, and lower back or wann, painless & the innermost portion neck pain. remains dark red and becomes indurated; the outer edge remains red; • Circulatory system: too fast or and the portion in between clears, too slow heart rate, irregular giving the appearance of a bullseye. heartbeat (palpitations), EM occurs in about 80% of infected inflammation of the heart patients. muscle or arteries, and chest pam. • Respiratory system: sinusitis, difficulty breathing, and pneumonias, sore throat, hoarseness, • Skin: rashes, itching, crawling sensations, benign cysts and nodules, and skin discoloration. • Eyes: pain, inflammation, blurred or double vision, retinal damage, floaters, flashing lights, light sensitivity, dry eye, and blindness. • Ears: itching, earache, buzzing, ringing, and sound sensitivity. • Digestive tract: nausea, vomiting, diarrhea, constipation, loss of appetite, mild liver Characteristic bullseye rash caused by Lyme abnonnalities, and disease Borre/ ial lymphocytoma on the cheek function spleen tenderness and • Central Nervous System: enlargement. migraines, dizziness, brain fog, poor • Genitourinary tract: memory, poor sleep, lack of verbal inflammation of the urethra and fluency, confusion or disorientation, bladder, pelvic pain, testicular decreased ability to concentrate, pain, and loss of sexual desire. facial nerve tics or paralysis, sore • General: tiredness, lack of jaw, mood & all the psychiatric stamina, fever, vague discomfort, disorders. irritability, nervousness or • Muscles, joints, and bones: pains anxiety, and weight loss or gain. that come and go (with or without 19 Vol 5, /ssue1, December'JJ ~ .1 .. ~P:o~n~d1~·ch~e~ny ~ J~o:u~m:a!!l~of~N:r~,r.~'S1~·nio __iiiiiiiii ________iiiiiiiiiiiii.&iiiiiiiiiiiiiiii~iiiiiiiiiiiiii;;~ ~ ..,q,,.c~. 1 Late persistent infection Laboratory testing < After several months, The most widely usect . test serologies, which measure 8 a. untreated or inadequately treated 1 1 'b d' . eveis i patients may go on to develop specific anti o ies m a patient's b! 01 severe and chronic symptoms that These tests may be negative in °oQ_ affect many parts of the body, infection, as the body may not earl) . 'fi h~ including the brain, nerves, eyes, produced a s1gn1 1cant quantit i joints and heart. Chronic neurologic antibodies. The serological labo y Of rato symptoms occur in up to 5% of tests most widely available ~ untreated patients. employed are the Western blot anq . a~~ ELISA. · Hi~h titers of either A polyneuropathy that immunoglobulm G (IgG) involves shooting pains, numbness, immunoglobulin M (IgM) antibodies ~r 0 and tingling in the hands or feet Borrelia antigens indicate disease b • Ut may develop. A neurologic lower titers can be misleading, because syndrome called Lyme the IgM antibodies may remain after encephalopathy is associated with the initial infection, and IgG antibodies subtle cognitive problems, Lyme may remain for years. arthritis usually affects the knees PREVENTION DIAGNOSIS Attached ticks should be Lyme disease is diagnosed removed promptly, as removal within clinically based on symptoms, 36 hours can reduce transmission rates. objective physical findings (such as Protective clothing includes a hat, long­ erythema migrans, facial palsy or sleeved shirts and long trousers tucked arthritis) or a history of possible into socks or boots. Light-colored exposure to infected ticks, as weII clothing makes the tick more easily as serological blood tests. Because visible before it attaches itself. People of the difficulty in culturing should use special care in handling and Borrelia bacteria in the laboratory, allowing outdoor pets inside homes diagnosis of Lyme disease is because they can bring ticks into the typically based on the clinical exam house. findings and a history of exposure to endemic Lyme areas. Lyme A more effective, community disease may be misdiagnosed as wide method of preventing Lyme multiple sclerosis, rheumatoid disease is to reduce the numbers of arthritis, fibromyalgia, chronic primary hosts on which the deer tick fatigue syndrome, lupus, Crohn's depends, such as rodents, other small disease or other autoimmune and mammals, and deer. Reduction of the neurodegenerati ve diseases. deer population may, over time, helP break the reproductive cycle of the deer 20 Pond/cherry Journal ofNursing Vol 5, Issue 1, December'11 - March'12 ticks and their ability to flourish in Alternative choices are cefuroxime and suburban and rural areas. cefotaxime. Treatment of pregnant women is similar, but tetracycline TICK REMOVAL should not be used. Folk remedies for tick removal MANAGEMENT tend to be ineffective, offer no NURSING advantages in preventing the transfer of Health Education regarding · the disease, and may increase the risks of prevention of Lyme disease transmission or infection. The best People should use special care in method is simply to pull the tick out handling and allowing outdoor pets with tweezers as close to the skin as inside homes because they can bring possible, without tw1stmg, and ticks into the house. Protective avoiding crushing the body of the tick clothing includes a hat, long-sleeved or removing the head from the body. shirts and long trousers tucked into socksor boots. Light-colored clothing VACCINATION makes the tick more easily visible A recombinant vaccme against before it attaches itself. To remove Lyme disease, based on the outer the tick pull the tick out with tweezers surface protein A (OspA) of B. as close to the skin as possible, without burgdorferi, was developed by twisting, and avoiding crushing the GlaxoSmithKline. In clinical trials body of the tick or removing the head involving more than 10,000 people, the from the body. vaccine, called LYMErix, was found to REFERENCES confer protective immunity to Borrelia in 76% of adults and 100% of children • Rapini, Ronald P.; Bolognia, Jean L.; with only mild or moderate and Jorizzo, Joseph L. (2007). Dennatology: 2- Volume Set.
Recommended publications
  • Antibodies of Patients with Lyme Disease to Components of the Ixodes Dammini Spirochete
    Antibodies of patients with Lyme disease to components of the Ixodes dammini spirochete. A G Barbour, … , E Grunwaldt, A C Steere J Clin Invest. 1983;72(2):504-515. https://doi.org/10.1172/JCI110998. Research Article Lyme disease is an inflammatory disorder of skin, joints, nervous system, and heart. The disease is associated with a preceding tick bite and is ameliorated by penicillin treatment. A spirochete (IDS) isolated from Ixodes dammini ticks has been implicated as the etiologic agent of Lyme disease. We examined the antibody responses of Lyme disease patients to IDS lysate components in order to further understand the pathogenesis of this disease. The components were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose, reacted with patients' sera, and the bound IgG was detected with 125I-labeled protein A (western blot). We found that (a) Lyme disease patients had antibodies to IDS components (b) most patients studied had antibodies to two components with apparent subunit molecular weights of 41,000 and 60,000, and (c) the patients' antibody responses during illness and remission were specific, for the most part, for the IDS. In contrast to the findings with Lyme disease sera, sera from controls showed little reactivity with IDS components in either the western blots or a derivative solid-phase radioimmunoassay. FIGURE 1FIGURE 2FIGURE 3FIGURE 4FIGURE 5 Find the latest version: https://jci.me/110998/pdf Antibodies of Patients with Lyme Disease to Components of the Ixodes dammini Spirochete ALAN G. BARBOUR, Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, Hamilton, Montana 59840 WILLY BURGDORFER, Epidemiology Branch, Rocky Mountain Laboratories, Hamilton, Montana 59840 EDGAR GRUNWALDT, 44 South Ferry Road, Shelter Island, New York 11964 ALLEN C.
    [Show full text]
  • Prevalence of Lyme Disease in the US Is 10-Times Higher Than
    Prevalence of Lyme Disease in the US Is 10-Times Higher Than Previously Reported By Dr. Mercola It‟s now been fairly well-established that chronic inflammation is an underlying factor in most chronic illnesses. Diseases, such as Parkinson's, multiple sclerosis, cardiomyopathy, gastritis, and chronic fatigue, are all turning out to be expressions of chronic infections. Lyme disease appears to be a major, yet oftentimes hidden, player. This may sound shocking to you, but diagnosing Lyme is very difficult, so the actual number of cases is high relative to reporting. According to preliminary statistics1, 2 just released by the Centers for Disease Control and Prevention (CDC), approximately 300,000 new cases of Lyme disease are diagnosed in the US each year. This is about 10 times higher than the officially reported number of cases, indicating that the disease is being vastly underreported. The data was presented by CDC officials at the 2013 International Conference on Lyme Borreliosis and Other Tick-Borne Diseases in Boston in the middle of August. As reported in the featured article by Medical News Today3: “This agrees with studies reported in the 1990s that showed the actual number of Lyme diseases cases in the US was likely to be three to twelve times higher than reported... Lyme disease is the most commonly reported tick-borne illness in the US.” What Is Lyme disease? Lyme disease was named after the East Coast town of Lyme, Connecticut, where the disease was first identified in 1975.4 The disease was first referred to as "Lyme arthritis" due to the presentation of atypical arthritic symptoms in children that lived in that city.
    [Show full text]
  • Clinical Spectrum of Lyme Disease
    European Journal of Clinical Microbiology & Infectious Diseases (2019) 38:201–208 https://doi.org/10.1007/s10096-018-3417-1 REVIEW Clinical spectrum of Lyme disease Jesus Alberto Cardenas-de la Garza1 & Estephania De la Cruz-Valadez1 & Jorge Ocampo-Candiani 1 & Oliverio Welsh1 Received: 4 September 2018 /Accepted: 30 October 2018 /Published online: 19 November 2018 # Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Lyme disease (borreliosis) is one of the most common vector-borne diseases worldwide. Its incidence and geographic expansion has been steadily increasing in the last decades. Lyme disease is caused by Borrelia burgdorferi sensu lato, a heterogeneous group of which three genospecies have been systematically associated to Lyme disease: B. burgdorferi sensu stricto Borrelia afzelii and Borrelia garinii. Geographical distribution and clinical manifestations vary according to the species involved. Lyme disease clinical manifestations may be divided into three stages. Early localized stage is characterized by erythema migrans in the tick bite site. Early disseminated stage may present multiple erythema migrans lesions, borrelial lymphocytoma, lyme neuroborreliosis, carditis, or arthritis. The late disseminated stage manifests with acordermatitis chronica atrophicans, lyme arthritis, and neurological symptoms. Diagnosis is challenging due to the varied clinical manifestations it may present and usually involves a two-step serological approach. In the current review, we present a thorough revision of the clinical manifestations Lyme disease may present. Additionally, history, microbiology, diagnosis, post-treatment Lyme disease syndrome, treatment, and prognosis are discussed. Keywords Lyme disease . Borrelia burgdorferi . Tick-borne diseases . Ixodes . Erythema migrans . Lyme neuroborreliosis History posteriorly meningitis, establishing a link between both mani- festations.
    [Show full text]
  • The Lyme Times V 25 No 2
    ABOUT LYMEDISEASE.ORG 25th Anniversary Issue We advocate nationally for quality accessible healthcare for patients with Lyme and other tick-borne diseases. We are committed to shaping health policy through advocacy, legal and ethical analysis, education, physician training and medical research. We communicate our message in print and online. We connect and educate the patient community through net- working and state online support groups. We take the pulse of the Lyme community through patient surveys. We analyze and archive information in our quarterly journal, The Lyme Times, and maintain an educational website at lymedisease.org. We publish regularly in peer- reviewed medical and health policy publications. Online Support Groups Participate in education and advocacy activities in your state. Learn about local resources and receive technical support for your efforts. Exchange information and patient support conveniently from your home. To find your own LymeDisease.org is grateful for the special online state-based group, go to: health.groups.yahoo.com/ support of the following sponsors: group/(yourstatename)lyme. Jill & Ira Auerbach Website Sandy Berenbaum, LCSW, BCD Dolly Curtis Visit our extensive educational website at lymedisease. Marcia Datson org. Discover the basics at Lyme 101, read news and Brian Fallon, MD analysis, and check the events calendar. Sign up for our free Ken & Kerry Fordyce email newsletter. Suzanne MacDonald Fratus Facebook In Memory of Paul E. Lavoie, MD Georgia Lyme Disease Association Keep on top of developing news and share your own ex- Thora Graves periences and opinions by joining the conversation on our Bob Lane, PhD Facebook page: facebook.com/lymedisease.org.
    [Show full text]
  • Discovery of the Lyme Disease Spirochete and Its Relation to Tick Vectors
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central THE YALE JOURNAL OF BIOLOGY AND MEDICINE 57 (1984), 515-520 Discovery of the Lyme Disease Spirochete and Its Relation to Tick Vectors WILLY BURGDORFER, Ph.D. Department of Health and Human Services, Public Health Service, National Institutes ofHealth, National Institute ofAllergy and Infectious Diseases, Epidemiology Branch, Rocky Mountain Laboratories, Hamilton, Montana Received November 16, 1983 The various hypotheses concerning the etiologic agent of erytheina chroniicum migranis of Europe and of Lyme disease in the United States are reviewed, and an account of evenlts tllat led to the discovery of the causative spirochetal agent in Ixodes dammini is presented. Spiro- chetes morphologically and antigenically similar, if not identical to, the organism detected in L. dammini were also found for the first time in Ixodes pacificus and Ixodes ricinus, the vectors hitherto incriminated, respectively, in western United States and Europe. In most infected ticks, spirochetal developmenit was found to be limnited to the midgut. Ticks with generalized infections were shown to transmit spirochetes via eggs, but inifectionis de- creased in intensity and became restricted to the central ganglion as filial ticks developed to adults. Although the mechanisms of transmission to a host are still under inlvestigation, the spiro- chetes may be transmitted by saliva of ticks with generalized infectionis and possibly also by regurgitation of infected gut contents, or even by means of infected fecal material. Ever since the first description of Erythema chronicum migrans (ECM) in Europe [1] and of Lyme disease in the United States [2], tick-transmitted toxins, viruses, rickettsiae, and spirochetes have been considered as possible causes of these ailments.
    [Show full text]
  • Willy Burgdorfer Oral History
    INTRODUCTORY NOTE Deirdre Boggs: I interviewed Dr. Willy Burgdorfer on tape in three different sessions, beginning on July 10, 2001, and ending in August. After reading the transcribed version of the interviews, Dr. Burgdorfer wished to make some changes and refinements to the answers that he gave to the interview questions. He finished making the desired changes at the beginning of October 2001. The following transcription reflects Dr. Burgdorfer's oral responses to the interview questions as later edited and supplemented by Dr. Burgdorfer. This is Deirdre Boggs of Historical Research Associates interviewing Dr. Willy Burgdorfer in Hamilton, Montana on July 10, 2001. The interview is being done at the request of the National Institutes of Health. DB: Dr. Burgdorfer, I'd like to begin by asking you where you grew up and what your first language was? WB: I was born and grew up in Basel, Switzerland. Basel is in the northwest corner of the country where German is spoken, so my mother tongue is German. DB: Where and how did you learn to speak English? WB: I became exposed to the English language for four years in gymnasium. DB: Can you still speak German? WB: Oh, yes. DB: And do you ever speak German anymore? WB: Yes, I do. Some of my correspondence is still written in German. DB: Although you've been speaking English for many years. Isn't that true? WB: Yes. DB: For over 50 years? WB: That's true. DB: Did your parents encourage you to attend university? 1 WB: Yes, both my mother and father did.
    [Show full text]
  • Lyme Disease
    Rochester Institute of Technology RIT Scholar Works Theses 5-1-1996 Lyme disease Carolyn Nichols Follow this and additional works at: https://scholarworks.rit.edu/theses Recommended Citation Nichols, Carolyn, "Lyme disease" (1996). Thesis. Rochester Institute of Technology. Accessed from This Thesis is brought to you for free and open access by RIT Scholar Works. It has been accepted for inclusion in Theses by an authorized administrator of RIT Scholar Works. For more information, please contact [email protected]. o6160678 RDDDblbDb?fl ROCHESTER INSTITUTE OF TECHNOLOGY A Thesis Submitted to the Faculty of The College of Imaging Arts and Sciences in Candidacy for the Degree of MASTER OF FINE ARTS LYME DISEASE By Carolyn H. Nichols May 1, 1996 APPROVALS Adviser: Glen Hintz ._----- Date: -4~<t3:::--- Associate Adviser: Robert Wabnitz Date: -3/-J.dtJ:J---- Associate Adviser: Bob Heischman 7 Date: -----~--..L----20,L;h /71 Special Assistant to the Dean for Graduate Affairs: Date: ~ _ Dean, College of Imaging Arts and Sciences: Margaret Lucas, PhD. Date: _ I, Carolyn H Nichols, hereby grant permIssIOn to the Wallace Memorial Library of RIT to reprocduce my thesis in whole or in part. Any reproduction will not be for commercial use or profit. CONTENTS SECTIONI - Lyme Disease ? History 1 ? Geographic Ranges 2 ? Incidence of Lyme Disease 2 ? Ticks 3 Tick Identification Tick Biology Tick-Borne Diseases ? Life Cycles 5 Ixodes Tick Life Cycle Spirochete Life Cycle ? Borrelia Spirochetes 7 Spirochete Identification Spirochete Biology ? Transmission of Lyme Disease 8 Tick Bite Other Additional Spirochete Carriers Transovarial Transmission Maternal Transmission Blood Transmission Pretender" ? Symptoms: "The Great 1 2 Rash (erythmia migrans) Stages 1-3 ? Testing 1 5 ? Treatment 1 6 ? Veterinary Concerns 1 7 ? Effects on Children and the Elderly 1 8 ? Decrease Strategies for the Existence of Lyme Disease...
    [Show full text]
  • MOTILITY and CHEMOTAXIS in the LYME DISEASE SPIROCHETE BORRELIA BURGDORFERI: ROLE in PATHOGENESIS by Ki Hwan Moon July, 2016
    MOTILITY AND CHEMOTAXIS IN THE LYME DISEASE SPIROCHETE BORRELIA BURGDORFERI: ROLE IN PATHOGENESIS By Ki Hwan Moon July, 2016 Director of Dissertation: MD A. MOTALEB, Ph.D. Major Department: Department of Microbiology and Immunology Abstract Lyme disease is the most prevalent vector-borne disease in United States and is caused by the spirochete Borrelia burgdorferi. The disease is transmitted from an infected Ixodes scapularis tick to a mammalian host. B. burgdorferi is a highly motile organism and motility is provided by flagella that are enclosed by the outer membrane and thus are called periplasmic flagella. Chemotaxis, the cellular movement in response to a chemical gradient in external environments, empowers bacteria to approach and remain in beneficial environments or escape from noxious ones by modulating their swimming behaviors. Both motility and chemotaxis are reported to be crucial for migration of B. burgdorferi from the tick to the mammalian host, and persistent infection of mice. However, the knowledge of how the spirochete achieves complex swimming is limited. Moreover, the roles of most of the B. burgdorferi putative chemotaxis proteins are still elusive. B. burgdorferi contains multiple copies of chemotaxis genes (two cheA, three cheW, three cheY, two cheB, two cheR, cheX, and cheD), which make its chemotaxis system more complex than other chemotactic bacteria. In the first project of this dissertation, we determined the role of a putative chemotaxis gene cheD. Our experimental evidence indicates that CheD enhances chemotaxis CheX phosphatase activity, and modulated its infectivity in the mammalian hosts. Although CheD is important for infection in mice, it is not required for acquisition or transmission of spirochetes during mouse-tick-mouse infection cycle experiments.
    [Show full text]
  • Rocky Mountain Labs: NIAID’S Montana Campus
    Rocky Mountain Labs: NIAID’s Montana campus Karen Honey J Clin Invest. 2009;119(2):240-240. https://doi.org/10.1172/JCI38528. News The Division of Intramural Research (DIR) is a branch of the National Institute of Allergy and Infectious Diseases (NIAID). A fact not widely known about the DIR is that more than 20% of its research is conducted in western Montana at the Rocky Mountain Laboratories (RML) (Figure 1). Furthermore, RML soon will house one of the very few biosafety level four (BSL4) facilities — laboratories with the strictest levels of biosafety, biocontainment, and security — in the US. The DIR conducts basic, translational, and clinical research related to immunology, allergy, and infectious diseases, with the aim of promoting the development of new vaccines, therapeutics, and diagnostics to improve human health. At RML, the specific research focus is infectious microorganisms that cause disease in humans and animals. This focus reflects the history of RML, whose most well-known alumni are probably Herald Rea Cox and Gordon Davis, who were involved in identifying Coxiella burnetii, the vector-borne bacterium that causes Q fever, and Willy Burgdorfer, who isolated Borrelia burgdorferi, the vector-borne spirochete that causes Lyme disease. Even before the first RML building was completed in 1928, researchers were working in the area (in makeshift cabins and tents) to determine the cause of Rocky Mountain spotted fever, a disease that in the early 1900s was lethal in nearly four out of every five cases […] Find the latest version: https://jci.me/38528/pdf News Rocky Mountain Labs: NIAID’s Montana campus The Division of Intramural Research traveled to work in the area each summer the future impact of the new microscope that (DIR) is a branch of the National Institute of was Howard Ricketts, from the University the Microscopy Unit will house, which is the Allergy and Infectious Diseases (NIAID).
    [Show full text]
  • Pathogenesis of Relapsing Fever
    Curr. Issues Mol. Biol. 42: 519-550. caister.com/cimb Pathogenesis of Relapsing Fever Job Lopez1, Joppe W. Hovius2 and Sven Bergström3 1Department of Pediatrics, Section of Tropical Medicine, Baylor College of Medicine and Texas Children's Hospital, Houston TX, USA 2Center for Experimental and Molecular Medicine, Amsterdam Medical centers, location Academic Medical Center, University of Amsterdam, 1105 AZ, Amsterdam, The Netherlands 3Department of Molecular Biology, Umeå Center for Microbial Research, Molecular Infection Medicine Sweden, Umeå University, Umeå, Sweden *Corresponding author: [email protected] DOI: https://doi.org/10.21775/cimb.042.519 Abstract outbreaks of RF. One of the best recorded Relapsing fever (RF) is caused by several species of descriptions of RF came from the physician John Borrelia; all, except two species, are transmitted to Rutty, who kept a detailed diary during his time in humans by soft (argasid) ticks. The species B. Dublin, where he described the weather and illnesses recurrentis is transmitted from one human to another in the area during the mid-1700’s (Rutty, 1770). by the body louse, while B. miyamotoi is vectored by Interestingly, the fatality rate was very low and most hard-bodied ixodid tick species. RF Borrelia have of the affected people did recover after two or three several pathogenic features that facilitate invasion relapses. and dissemination in the infected host. In this article we discuss the dynamics of vector acquisition and RF symptoms also were described in detail by field subsequent transmission of RF Borrelia to their medics during the 1788 Swedish-Russian war. The vertebrate hosts. We also review taxonomic Swedish navy conquered the Russian 74-cannon challenges for RF Borrelia as new species have been battleship Vladimir and its 783 men crew at a battle in isolated throughout the globe.
    [Show full text]
  • History, Rats, Fleas, and Opossums. II. the Decline and Resurgence of Flea-Borne Typhus in the United States, 1945–2019
    Tropical Medicine and Infectious Disease Review History, Rats, Fleas, and Opossums. II. The Decline and Resurgence of Flea-Borne Typhus in the United States, 1945–2019 Gregory M. Anstead Medical Service, South Texas Veterans Health Care System and Department of Medicine, University of Texas Health San Antonio, San Antonio, TX 78229, USA; [email protected] Abstract: Flea-borne typhus, due to Rickettsia typhi and R. felis, is an infection causing fever, headache, rash, and diverse organ manifestations that can result in critical illness or death. This is the second part of a two-part series describing the rise, decline, and resurgence of flea-borne typhus (FBT) in the United States over the last century. These studies illustrate the influence of historical events, social conditions, technology, and public health interventions on the prevalence of a vector-borne disease. Flea-borne typhus was an emerging disease, primarily in the Southern USA and California, from 1910 to 1945. The primary reservoirs in this period were the rats Rattus norvegicus and Ra. rattus and the main vector was the Oriental rat flea (Xenopsylla cheopis). The period 1930 to 1945 saw a dramatic rise in the number of reported cases. This was due to conditions favorable to the proliferation of rodents and their fleas during the Depression and World War II years, including: dilapidated, overcrowded housing; poor environmental sanitation; and the difficulty of importing insecticides and rodenticides during wartime. About 42,000 cases were reported between 1931–1946, and the actual number of cases may have been three-fold higher. The number of annual cases of FBT peaked in 1944 at 5401 cases.
    [Show full text]
  • Arnold Markowtiz, MD
    10/21/2020 WHY SHOULD YOU CARE? TICK ASSOCIATED DISEASE IN MICHIGAN WITH AN EMPHASIS ON Incidence –most common tick borne disease in US LYME DISEASE CDC est. 330,000 cases – more than Breast cancer and and HIV combined Great imitator – MS, Parkinson’s, Rheumatoid Arthritis, Attention Deficit Disorder, Chronic Fatigue Syndrome, Long term medical impact Economic and social impact – cost of testing, # tested, PTLD Our role as physicians: dx and treatment Satisfaction of giving someone their life back 1 2 THE HIGH COST OF LYME DISEASE DISTRIBUTION: MICHIGAN LYME DISEASE RISK 2000 VS. 2020 3 4 INCREASE DISTRIBUTION IN UNITED STATES 5 6 1 10/21/2020 EARLY HISTORY RECENT HISTORY Europe: 1883 – atrophic rash Dr. A. Buchwald Named ACA Acrodermatitis chronica atrophicans 1902 Arvid Afzelius 1909 ECM/Ixodes (Garrin- Bujadoux) Bannwarth syndrome 1941 USA – Polly Murray -1975 – 39 children, 12 adults Allen C. Steere Investigated, published 1977 Wilhelm "Willy" Burgdorfer - 1982 isolated organism Serology available 1983 7 8 MY EXPERIENCE ORIGINAL CDC GUIDELINES FOR LYME 1995 Clinical Description A systemic, tick-borne disease with protean manifestations, including dermatologic, rheumatologic, neurologic, and cardiac abnormalities. The best clinical marker for the disease is the initial skin lesion, erythema migrans (EM), that occurs among 60%-80% of patients. Clinical Criteria Erythema migrans, OR At least one late manifestation, as defined below, and laboratory confirmation of infection Laboratory Criteria for Diagnosis Isolation of Borrelia burgdorferi from clinical specimen, OR Demonstration of diagnostic levels of immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies to the spirochete in serum or cerebrospinal fluid (CSF), OR Significant change in IgM or IgG antibody response to B.
    [Show full text]