SlideShare verwendet Cookies, um die Funktionalität und Leistungsfähigkeit der Webseite zu verbessern und Ihnen relevante Werbung bereitzustellen. Wenn Sie diese Webseite weiter besuchen, erklären Sie sich mit der Verwendung von Cookies auf dieser Seite einverstanden. Lesen Sie bitte unsere Nutzervereinbarung und die Datenschutzrichtlinie.
SlideShare verwendet Cookies, um die Funktionalität und Leistungsfähigkeit der Webseite zu verbessern und Ihnen relevante Werbung bereitzustellen. Wenn Sie diese Webseite weiter besuchen, erklären Sie sich mit der Verwendung von Cookies auf dieser Seite einverstanden. Lesen Sie bitte unsere unsere Datenschutzrichtlinie und die Nutzervereinbarung.
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
(Hang’ombe 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,
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.,
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).
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)
Figure 1.World distribution of plague,1998
•1000- 3000 cases
reported annually across
•Africa , Asia
•Andes Mountain Regions
•US (19-40 cases a year
mostly in Western areas
such as New Mexico and
•About 15% of reported
humans with plague die
(Campbell and Dennis,
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).
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).
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 2–6 days, when the bacteria is
◦ General malaise
◦ 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
Septicemic plague (Campbell and Dennis, 1998).
◦ Seizures in children
◦ General malaise
Note: Patient may die before any symptoms appear
Pneumonic plague (Spread person to person)
(Campbell and Dennis, 1998)
◦ Chest pain
◦ 100% mortality if not treated
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 × 0.5μm) or in short chains in smears
(Guarner et al., 2002).
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
using a monoclonal anti-F1 Y.
pestis antibody on formalin-
fixed tissue samples
Plate 1 (Guarner et al., 2002).
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
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).
(B) 72 h,
(C) 96 h,
(D) 96 h
center , 2007.
POSITIVE WEAKLY POSITIVE NEGATIVE
NON MOTILE MOTILE
POSITIVE WEAKLY POSITIVE NEGATIVE
• Catalase positive
• Urease, indole and oxidase
• Non-motile at 35 -370C
(Wadsworth Centre, 2007)
There are no widely available rapid diagnostic tests for
plague (American Public Health Association, 1995).
Tests that would be used to confirm a suspected
diagnosis—antigen 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).
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
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).
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.,
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
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
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
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
Campbell, G.L. and Dennis, D.T. (1998). Plague and other Yersinia infections. In: Fauci AS,
Braunwald E, Isselbacher KJ, et al, eds.Harrison’s 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:
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
Hang’ombe, 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
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
http://www.idsociety.org/bt/biotemplate.cfm?template= 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 :93–112
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
Slack, P. (1989). The Black Death past and present. Trans R Soc Trop Med Hyg;
Wadsworth Centre (2007). Laboratory Features of Yersinia Pestis. New York State
Department of Health.