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Plague is a
highly virulent disease believed to have killed millions during three
historic human pandemics. Worldwide, it remains a threat to humans and
is a potential agent of bioterrorism.
Plague is caused by Yersinia pestis, a
plump, bipolar, staining coccobacillus.
The America, Africa, and Asia are
endemic areas.
Wild rodents such as squirrels,
chipmunks, mice, wood rats, and rabbits are reservoirs.
Transmission from animal to animal is
by fleas. Infected domestic animals bring the disease to humans by
direct contact or flea bites.
Plague may
present in a variety of clinical forms.
Bubonic disease,
pneumonic plague, and septicemic plague are seen in addition to a
number of other less common manifestations.
Two to eight
days after the flea bite, bubonic plague begins with chills, fever,
nausea, vomiting, and rapid respiration and pulse.
A painful lymphnode
(bubo) enlarged in the area drained by the bite.
The architecture of
the lymph node, including the capsule and perinodal fat, is
obliterated by necrosis, hemorrhage and finely granular material.
This material comprises solid masses of gram-negative coccobacilli, the
plague bacillus.
Blood cultures are positive in 50% of patients.
Petechiae and ecchymoses lead to the “black
death”, 60 to 90% of those affected dying within 24 hours if
untreated.
Toxemia may kill even when antibiotics have arrested the
growth of bacteria.
The virulence of the plague bacillus partly
reflects its resistance to phagocytosis and destruction.
Further more,
the bacillus elaborates an antigenic coat that, on the release of the
organisms from phagocytic cells, enhances their resistance to further
phagocytosis.
In primary systemic plague, the
bacteria are inoculated directly into the blood and do not produce a bubo.
Patients die from the overwhelming growth of the bacteria in the
blood stream.
Fever, prostration, and meningitis occur suddenly, and
death comes within 28 hours of onset.
All vessels contain bacilli, and
fibrin casts surround them in renal glomeruli and in dermal vessels.
In primary pneumonic plague, the
bacilli are inhaled in airborne particles from carcasses of animals or
from a patient’s cough.
48 to 60 hours after infection, there
is a sudden onset of high fever, cough, and dyspnea.
Radiographs demonstrate patchy
bronchopneumonia or confluent consolidation. The sputum teems with
bacilli.
Respiratory insufficiency and shock from endotoxin and
disseminated intravascular coagulation kill the patient in 1 to 2
days.
Lobular pneumonia is characterized by necrotic alveolar walls,
nodules of necrotic tissue and debris, intense hyperemia and
hemorrhage, and myriad bacilli in the alveoli. Neutrophils are scant.
The diagnosis is made by blood
culture and smears of aspirate from buboes, cerebrospinal fluid,
sputum and intratracheal aspirates.
Tetracycline or streptomycin are
effective if started early, and chloramphenicol is used in patients
with meningitis.
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