Plague is caused by Yersiniapestis, a gram-negative, nonmotile,nonsporulating bacillus.It is a zoonotic disease, and rodentsare the primary reservoir.Plague can present as bubonic,pneumonic, or primary septicemic disease.Y pestis is usually transmitted tohumans via the bites of infected fleas,causing the bubonic form of the disease.Primary septicemic and secondarypneumonic disease are muchless common. Primary pneumonicdisease results from aerosol exposureto an infected animal or human withplague pneumonia; however, it too hasbecome uncommon as a natural event.Nonetheless, primary pneumonicplague, or a similar illness, is the mostlikely manifestation following a bioterroristattack.1,2 Despite the substantialinvestment by the former Soviet Unionin this agent as a potential weapon,there is little experience from whichto predict the clinical consequencesof intentional aerosolization of thisorganism.
Plague is caused by Yersiniapestis, a gram-negative, nonmotile,nonsporulating bacillus.It is a zoonotic disease, and rodentsare the primary reservoir.Plague can present as bubonic,pneumonic, or primary septicemic disease.Y pestis is usually transmitted tohumans via the bites of infected fleas,causing the bubonic form of the disease.Primary septicemic and secondarypneumonic disease are muchless common. Primary pneumonicdisease results from aerosol exposureto an infected animal or human withplague pneumonia; however, it too hasbecome uncommon as a natural event.Nonetheless, primary pneumonicplague, or a similar illness, is the mostlikely manifestation following a bioterroristattack.1,2 Despite the substantialinvestment by the former Soviet Unionin this agent as a potential weapon,there is little experience from whichto predict the clinical consequencesof intentional aerosolization of thisorganism.
EPIDEMIOLOGY
Most natural cases of plagueoccur in Africa and Asia. Only a handfulof cases are reported each year inthe United States (Table). Plague isconsidered endemic in the southwesternUnited States; the attack rateamong Native Americans from thisregion is up to 10 times higher thanthat in other populations.
CLINICAL COURSE
Pneumonic plague in humansfollows an incubation period of 1 to 6(usually 2 to 3) days and is characterizedby acute onset of malaise, highfever, chills, and cough, with initiallywatery and then bloody sputum.Cervical buboes have been observedin experimental animal models. Chestfilms reveal patchy or consolidatedinfiltrates.
The disease progresses rapidly,producing dyspnea, stridor, cyanosis,and septic shock, resembling otherfulminant pneumonias.3 The timefrom clinical onset to death is usually4 to 5 days. Unlike inhalational anthrax,there is no brief recovery periodand no widening of the mediastinumon chest films.
DIAGNOSIS
Gram-stained lymph node aspirate,sputum, or cerebrospinal fluidwill reveal gram-negative coccobacilliwith polar bodies. Most organismsproduce capsular F1 antigen, whichcan be detected in serum samples byimmunoassay. Growth of the organismin vitro can be observed within 24hours of inoculation, but subsequentidentification takes longer and is mostefficiently undertaken when there isprior notification of the laboratory.
THERAPY
Streptomycin, gentamicin, tetracycline,fluoroquinolones, and chloramphenicolmay be effective if begunearly in the course of illness (less than24 hours after onset of symptoms).3Untreated pneumonic plague is invariablyfatal. Even with appropriate management,however, the case fatalityrate is approximately 50%.
Patients in whom the disease issuspected should be kept in a privateroom, and strict respiratory precautionsobserved. At a minimum, allpersons entering the patient's roomneed to wear a surgical-style mask, asshould the patient whenever he or sheleaves the room. These precautionsmust be observed until antibiotic treatmenthas been given for at least 72hours with symptomatic improvement.
There is no vaccine that hasproved to be effective in preventingor ameliorating pneumonic plague.