- Causative agent
- Natural distribution
- Types and clinical signs of plague in animals and humans
- Infection control
- Use of plague as a biological weapon
Plague is an infectious disease of animals and humans caused by the bacterium Yersinia pestis.
Plague is widely distributed throughout the world and occurs mainly as a flea-borne disease of small wild animals, including lagomorphs such as cottontails and jackrabbits, and rodents (woodrats, ground squirrels, mice, voles, tree squirrels and chipmunks). Carnivores such as dogs, cats, coyotes, foxes, bobcats, lynx and mountain lions may become infected and develop clinical signs. Canids tend to experience less severe illness and disease than felids, and may have inapparent infections. Domestic and wild cats are susceptible and about 50% of affected animals will die. Natural infection of some livestock species has been reported, though it is uncommon. People most often contract plague from the bite of infected fleas. They may also be exposed by handling tissues of infected animals, especially rodents and rabbits; by inhalation of infectious respiratory droplets from people or pets with plague pneumonia; or through manipulation of laboratory cultures without using biosafety precautions.
Enzootic plague is associated with semiarid environments. Foci exist on all continents except Australia and Antarctica. In North America, plague is found in animals and their fleas from the Pacific Coast to the Great Plains, and from southwestern Canada to Mexico. Most human cases in the United States, are contracted in New Mexico, Arizona, Colorado, Nevada, Oregon and California.
Plague is transmitted among small, wild mammals such as rodents by fleas. North American rodents tend to be very susceptible to plague infection, with essentially 100% susceptibility and 90 – 100% mortality. A few rodent species such as grasshopper mice and kangaroo rats display variable levels of resistance, but this phenomenon is rare.
Types and clinical signs of plague in animals and humans
Plague primarily affects wild and domestic rodents. Rabbits and hares are sometimes affected. Cats are also very susceptible. Rare cases have developed in goats, sheep, and camels. The source of infection for carnivores, goats, sheep, and camels is most likely contact with or ingestion of infected animals, rather than fleabites.
Rodents—In rodent populations, plague may be subacute, mild, or severe and acute with high fatality rates. In the acute form, rodents develop hemorrhagic buboes (swollen lymph nodes) and splenomegaly, without evidence of other internal lesions, and succumb within 3 to 5 days of infection. Rodents affected by subacute plague develop necrotic buboes and necrotic nodules in the liver, spleen, and lungs, with death 6 or more days after infection. Clinical signs in the acute and subacute forms include nasal bleeding, petechia, abscess formation, and pneumonitis. The resolving form of plague is characterized by lymphadenopathy with focal purulent necrosis.
Cats—Abscesses, lymphadenopathy (especially of the submandibular and cervical lymph nodes), lethargy, and high fever are typical signs in cats infected with Y. pestis. Secondary pneumonia may also be present. Pathologic lesions include necrotic nodules in the spleen and liver and evidence of suppurative pneumonia. Mortality is approximately 50% among experimentally infected cats.
Dogs—Dogs inoculated orally with Y. pestis react only with fever. All orally infected dogs have developed antibodies and recovered. ogs have been less commonly reported with clinical signs of plague than cats; however, over the last 5 years, reports of dogs with diagnosed Y. pestis infections have become more common, reinforcing that a diagnosis of plague must always be considered in plague-endemic areas in animals that present with signs of lethargy, fever, dyspnea, and/or hemoptysis and a history that could be compatible with exposure to rodents and/or their fleas.
Humans—Most naturally occurring cases of plague in humans result from the bite of an infected flea. Clinical signs usually develop within 2 to 6 days of the flea bite and include sudden onset fever, chills, headache, muscle aches, vomiting, nausea, abdominal and/or back pain, and weakness. A bubo (an acutely swollen and painful lymph node) may develop in any regional lymph node site, but most often appears in the axillary, cervical, or inguinal regions, about 24 hours after symptom onset. The skin overlying the bubo is frequently reddened, warm, and edematous (bubonic plague). Some individuals may develop septicemia without a bubo (primary septicemic plague) or septicemia may occur secondary to bubonic plague. Gangrene (hence the name ‘black death’), coagulopathies, and multiple organ failure may result from advanced plague septicemia.
Secondary pneumonic plague develops in about 10 to 15% of patients with bubonic or primary septicemic plague by hematogenous spread of Y. pestis to the lungs. Pneumonic plague patients may present with cough, chest pain, bronchopneumonia and hemoptysis. Primary pneumonic plague caused by inhalation of Y. pestis is rare, but has been acquired from handling cats with pneumonic plague. In addition to respiratory disease, patients with pneumonic plague often show gastrointestinal signs such as nausea, abdominal pain, vomiting and diarrhea. Other types of plague in humans include plague meningitis and plague pharyngitis. The case fatality rate for untreated bubonic plague in humans is about 50%. Untreated primary septicemic plague and pneumonic plague are invariably fatal. Antibiotic treatment has reduced fatalities from bubonic plague. Pneumonic and septicemic plague also respond if treated promptly with an appropriate antibiotic.
Yersinia pestis may be identified microscopically by examination of Gram, Wright, Giemsa or Wayson's stained smears of peripheral blood, sputum, and bubo or cerebrospinal fluids. Finding bipolar-staining, Gram-negative bacillus permits a rapid presumptive diagnosis of plague. Bacteria can also be identified through culture of clinical specimens in appropriate media. Phagocytolysis, immunofluorescence, agglutination, phage typing, or PCR tests are also useful for diagnosis. A four-fold rise in antibody titer in patient serum is also diagnostic.
Prevention of plague is based on control flea vectors and avoidance of rodents. In areas where natural foci exist, surveillance for plague cases and epizootic plague activity is important. Some species, such as dogs and coyotes, may serve as sentinels by checking antibody titers. Preventing contact between rodent fleas, infected small wild mammals and domestic pets is critical for plague case prevention. Cats and dogs should be kept indoors and food and shelter should be denied to rodents around residences and recreational areas. Owners should apply flea control products to their pets regularly.
Human and animal plague are reportable diseases in the United States. Local and state health departments, state wildlife department, state agriculture departments should immediately be notified of any suspect cases. State level departments will assume responsibility for federal reporting of cases. Veterinarians that suspect plague in their patients should inform laboratories when specimens are submitted, to ensure that proper biosafety protocols are followed.
Y. pestis is sensitive to sunlight and heat and does not survive for long periods outside a host. A household bleach solution, with a contact time of 30 minutes, may be used effectively for decontamination prior to normal cleaning. Organic material will quickly denature a bleach solution; therefore, if organic material is present, cleaning should precede decontamination.
Use of plague as a biological weapon
Use of Y. pestis as a biological weapon would most likely involve aerosolization of the bacterium. The presence of hemoptysis in previously healthy patients with fever, cough, shortness of breath, chest pain, and rapid death would suggest the possibility of plague.