yersinia pestis

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1. BY ADELOYE ADERINSOLA DORA 2. Yersinia pestis , the cause of bubonic and pneumonic plague in humans, persists in populations of wild rodents in many parts of the world and is transmitted primarily by the bites of infected fleas (Poland et al., 1994). Plague caused by Yersinia pestis is categorized as a rare disease. The disease rarely occurs but when it strikes, the consequences can be devastating (Hangombe et al, 2012). The infectious source of the disease was not understood until Alexandre Yersin investigated the Hong Kong epidemic in the mid-1890s (Gross, 1995). 3. Although Y. pestis is usually transmitted by the bite of an infected flea or inhalation of aerosolized droplets from a person with pneumonic plague, the enteropathogenic Yersiniae are ubiquitous in the environment and are transmitted by ingestion of contaminated food or water (Eppinger et al., 2007). Infection by the bacterium Yersinia pestis is most often associated with the infamous Black Death of the middle Ages, a pandemic that cost Europe a third of its population in the 14th and 15th centuries. (Slack, 1989). 4. Three major league pandemics have been recorded in human history: in the 6th century, in the 14th century known as the black death which killed up to an estimated 17 to 28 million people (Drancourt and Raoult, 2008), and at the end of 19th century following the spread of infection from china (Prentice and Rahalison, 2007). Plague is a seasonal disease, with most reported human cases occurring between March and October (Orloski and Lathrop, 2003) 5. Figure 1.World distribution of plague,1998 1000- 3000 cases reported annually across the world Africa , Asia Northeastern Brazil Andes Mountain Regions US (19-40 cases a year mostly in Western areas such as New Mexico and Arizona) About 15% of reported humans with plague die (Campbell and Dennis, 2001). 6. After being ingested by a flea from a rodent host, Y. pestis multiplies in the flea gut and expresses a coagulase that clots ingested blood, occluding the proventriculus (an organ between the stomach and esophagus of the flea), rendering the flea blocked, that is, unable to move food (blood) from its esophagus to its midgut (Hinnebusch, 1997). Thus, the flea repeatedly attempts to feed, and because it is unable to ingest the blood, it regurgitates the newly infected blood back into the bloodstream of the mammal on which it is feeding, therefore transferring the microorganism from the flea to the mammal. (Hinnebusch, 1997). 7. Approximately 25,000 to 100,000 Y. pestis organisms are inoculated into the skin of the mammal host during this process. (Reed et al., 1970). The bacteria migrate through cutaneous lymphatics to regional lymph nodes where they are phagocytosed but resist destruction (Butler, 1995). They rapidly multiply, causing destruction and necrosis of lymph node architecture with subsequent bacteremia, septicemia, and endotoxemia that can lead quickly to shock, disseminated intravascular coagulation, and coma(Butler, 1995). 8. Patients typically develop symptoms of bubonic plague 2 to 8 days after being bitten by an infected flea (Campbell and Dennis, 1998). Bubonic plague (Campbell and Dennis, 1998). Incubation period of 26 days, when the bacteria is actively replicating. General malaise Fever Headache and chills occur suddenly at the end of the incubation period Swelling of lymph nodes resulting in buboes, the classic sign of bubonic plague Death can occur in less than 2 weeks 9. Septicemic plague (Campbell and Dennis, 1998). Hypotension Hepatosplenomegaly Delirium Seizures in children Shock General malaise Fever Note: Patient may die before any symptoms appear 10. Pneumonic plague (Spread person to person) (Campbell and Dennis, 1998) Fever Chills Coughing Chest pain Dyspnea Hemoptysis Lethargy Hypotension Shock 100% mortality if not treated 11. Yersinia pestis can be identified in the laboratory by both bacteriologic and serologic methods (Guarner et al., 2002). Diagnosis can be made from a variety of samples, including blood, aspirates from involved lymph nodes, skin scrapings, cerebrospinal fluid, urine, and sputum (Guarner et al., 2002). Yersinia pestis appears as a pleomorphic gram negative rod and may appear as a single cell (1.0-2.0 0.5m) or in short chains in smears (Guarner et al., 2002). 12. The organism gives a bipolar closed-safety pin appearance on Giemsa, Wright, or Wayson stains (but not on Gram stain) (Guarner et al., 2002). The organism also may be identified via immunohistochemical staining using a monoclonal anti-F1 Y. pestis antibody on formalin- fixed tissue samples Plate 1 (Guarner et al., 2002). 13. Yersinia pestis colonies grown on CIN agar Colonies are smooth, opaque, and round but may have irregular edges. Under magnification, colonies can be smooth or finely granular and might have a raised center with a flat periphery (fried egg appearance) or a hammered copper appearance (Brubaker, 1991). Colonies are visible on plates after 48 hours, and it is recommended that plates be incubated for a total of 7 days before being discarded(Smego et al., 1999). 14. A B C D Yersinia pestis growth on BA at (A)48 h, (B) 72 h, (C) 96 h, (D) 96 h Fried egg Plate 2. wadsworth center , 2007. 15. POSITIVE WEAKLY POSITIVE NEGATIVE CATALASE TEST NON MOTILE MOTILE MOTILITY TEST POSITIVE WEAKLY POSITIVE NEGATIVE OXIDASE TEST POSITIVENEGATIVE UREASE TEST Catalase positive Urease, indole and oxidase negative Non-motile at 35 -370C (Wadsworth Centre, 2007) 16. There are no widely available rapid diagnostic tests for plague (American Public Health Association, 1995). Tests that would be used to confirm a suspected diagnosisantigen detection, IgM enzyme immunoassay, immunostaining, and polymerase chain reaction are available only at some state health departments, the CDC, and military laboratories (American Public Health Association, 1995). The routinely used passive hemagglutination antibody detection assay is typically only of retrospective value since several days to weeks usually pass after disease onset before antibodies develop (American Public Health Association, 1995). 17. Prompt initiation of appropriate antimicrobial treatment is essential. Human deaths from plague usually occur because of delays in treatment with appropriate antimicrobials either because of a delay in seeking medical care or misdiagnosis by health care providers (Infectious Diseases Society of America, 2003). The treatment of choice for humans with plague is streptomycin (Inglesby et al., 2000). Gentamicin has been used successfully to treat humans with plague and for animal control in veterinary medicine (Inglesby et al., 2000). 18. Doxycycline is an appropriate choice for less complicated cases. Other treatment options include tetracycline and chloramphenicol. Sulfonamides can be used but only if other antimicrobials are not available (Inglesby et al., 2000). Antibiotics preferably should be administered intravenously, unless a mass casualty or outbreak situation results in the overwhelming of health care facilities, in which case orally administered tetracycline, doxycycline, or ciprofloxacin is considered an acceptable alternative (Infectious Diseases Society of America,2003). 19. 1. Far from being a historic medical curiosity, this zoonotic disease continues to be a threat to the health of humans and animals throughout the world, including Eurasia, Africa, and North and South America. 2. Prompt diagnosis and immediate onset of treatment is key to reducing the mortality rates that usually follow this disease condition. 20. American Public Health Association (1995). Plague. In: Benenson AS, ed. Control of Communicable Diseases Manual. 353-358. Brubaker, R.R. (1991). Factors promoting acute and chronic diseases caused by Yersinia. Clin Microbiol Rev.;4:309-324. Butler, T. (1995). Yersinia species (including plague). In:Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases.NewYork, NY: Churchill Livingstone :2070-2078 Campbell, G.L. and Dennis, D.T. (1998). Plague and other Yersinia infections. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds.Harrisons Principles of Internal Medicine. New York, NY: McGraw-Hill: 975-983 Eppinger, M.,. Rosovitz, M. J., Fricke, W. F., Rasko, D. A., Kokorina, G., Fayolle, C., Lindler, L. E., Carniel, E. and Ravel, J. (2007).The complete genome sequence of Yersinia pseudotuberculosis IP31758, the causative agent of Far East scarlet-like fever. Genet. 3: e142 Gross, L. (1995). How the plague bacillus and its transmission through fleas were discovered: reminiscences from my years at the Pasteur Institute in Paris. Proc Natl Acad Sci U S A.;92:7609-7611 Hangombe, B. M., Samui, K. L., Nakamura, I., Kaile, D., Mweene, A. S., Kilonzo, B. S., Sawa, H., Sugimoto, C. and Wren, B. W. (2012). Evidence of Yersinia pestis DNA from fleas in an endemic plague area of Zambia. BMC Res. Notes 5:72 21. Hinnebusch, B.J. (1997). Bubonic plague: a molecular genetic case history of the emergence of an infectious disease. J Mol Med. 75:645-652 Infectious Diseases Society of America (2003). Plague Available at pl_summary.htm. Accessed December 27, 2003. Inglesby, T.V., Dennis, D.T., Henderson, D.A., et al. (2000). Plague as a biological weapon: medical and public health management.JAMA.;283:2281-2290 Poland, J.D., Quan, T.J. and Barnes, A.M. (1994). Plague. In: Beran GW, ed. Handbook of zoonoses. Boca Raton, FL: CRC Press :93112 Reed, W.P., Palmer, D.L., Williams, R.C. Jr., et al. (1970). Bubonic plague in the Southwestern United States: a review of recent experience. Medicine (Baltimore).;49:465-486 Slack, P. (1989). The Black Death past and present. Trans R Soc Trop Med Hyg; 83:461463 Wadsworth Centre (2007). Laboratory Features of Yersinia Pestis. New York St


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