1. IDENTIFICATION (Click for APHA Plague manual, 2000).

A specific zoonosis involving rodents and their fleas, which transfer the bacterial infection to various animals and to people. Initial signs and symptoms may be nonspecific with fever, chills, malaise, myalgia (muscular pain or tenderness), nausea, prostration, sore throat and headache. Commonly a lymphadenitis develops in those lymph nodes that drain the site of the flea bite, where there may be an initial lesion. This is bubonic plague, and it occurs more often in lymph nodes in the inguinal area (90%) (see figure) and less commonly in those in the axillary and cervical areas. The involved nodes become swollen, inflamed and tender and may suppurate. Fever is usually present. All forms, including instances in which lymphadenopathy is not apparent, may progress to septicemic plague with bloodstream dissemination to diverse parts of the body, that include the meninges. Endotoxic shock and disseminated intravascular coagulation (DIC) may occur without localizing signs of infection. Secondary involvement of the lungs results in pneumonia; mediastinitis or pleural effusion may develop. Secondary pneumonic plague is of special significance, since respiratory droplets may serve as the source of person to person transfer with resultant primary pneumonic or pharyngeal plague; this can lead to localized outbreaks or devastating epidemics. Though naturally acquired plague usually presents as bubonic plague, purposeful aerosol dissemination as a result of biowarfare or a terrorist event would be manifest primarily as pneumonic plague.

Untreated bubonic plague has a case-fatality rate of about 50%-60%. Plague organisms have been recovered from throat cultures of asymptomatic contacts of pneumonic plague patients. Untreated primary septicemic plague and pneumonic plague are invariably fatal. Modem therapy markedly reduces fatality from bubonic plague; pneumonic and septicemic plague also respond if recognized and treated early. However, patients who do not receive adequate therapy for primary pneumonic plague within 18 hours after onset of respiratory symptoms are not likely to survive.

Visualization of characteristic bipolar staining, "safety pin" ovoid, gram-negative organisms in direct microscopic examination of material aspirated from a bubo, sputum or CSF (cerebral-spinal fluid) is suggestive, but not conclusive, evidence of plague infection (see figure). Examination by FA test or antigen capture ELISA is more specific and is particularly useful in sporadic cases. Diagnosis is confirmed by culture and identification of the causal organism from exudate aspirated from buboes (inflamed and swollen lymph node), from blood, CSF or sputum, or by a fourfold or greater rise or fall in antibody titer. Slow growth of the organism at normal incubation temperatures may lead to misidentification by automated systems. The passive hemagglutination test (PHA) using Yersinia pestis Fraction-1 antigen is most frequently used for serodiagnosis. Medical personnel should be aware of areas where the disease is endemic and entertain the diagnosis of plague early; unfortunately, plague is often misdiagnosed, especially in travelers who develop illness after returning from an endemic area.