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Pneumonic Plague -- Arizona, 1992

On August 26, 1992, a 31-year-old male resident of Tucson, Arizona, died of an illness subsequently diagnosed as primary pneumonic plague. This is the 10th case of plague reported in the United States in 1992, the first pneumonic plague case this year, and the first plague fatality reported since 1987 (CDC, unpublished data). This report summarizes the investigation of this case by county, state, and federal public health officials in Arizona and Colorado.

On August 22, the man had onset of abdominal cramps, 2 days after returning home by private automobile from a friend's residence in Chaffee County, Colorado. On August 23, he had onset of fever (103 F [39.6 C]), nausea, vomiting, severe diarrhea, and cough. The next day, he consulted a primary-care physician because of diarrhea and vomiting. On examination, he was febrile (104 F [40 C]) and dehydrated; no abnormal chest sounds were heard, and there was no lymphadenopathy. He was treated for gastroenteritis with intramuscular prochlorperazine and lincomycin and given oral ciprofloxacin to be taken the following day. On August 25, he was hospitalized with cyanosis and septic shock. Chest radiograph revealed a right upper lobar pneumonia. A Gram stain of a sputum sample obtained at hospital admission showed numerous gram-negative rods. Antibiotic therapy with ceftazidime, erythromycin, and one dose each of penicillin and tobramycin was initiated for treatment of overwhelming sepsis and pneumonia. He died 24 hours after admission.

One week postmortem, biochemical tests at the hospital identified as Yersinia pestis an organism that had been isolated from sputum. The organism was also identified as Y. pestis by fluorescent antibody and bacteriophage tests at the state laboratory; this identification was confirmed by CDC. Antemortem blood and urine samples were culture negative. Postmortem cultures of blood, cerebrospinal fluid, and lung tissue were also negative.

After the patient died, a rapid microbiological testing device used at the hospital identified the organism isolated from sputum as Y. pseudotuberculosis. The testing device subsequently was determined not to have been programmed to recognize Y. pestis, thus delaying the initial identification of the organism.

All persons who had contact with the man after he became ill were considered to be at risk for plague, including two friends, the physician and his staff, one patient in the physician's waiting room, and hospital staff contacts. All contacts were traced and were asymptomatic 8 or more days after exposure. Although no contacts required prophylactic treatment (1), two nurses requested and received tetracycline for plague prophylaxis (2).

Investigation by Chaffee County public health officials indicated the patient had become infected on August 19 through respiratory exposure to an infected domesticated cat that he had removed from the crawlspace of a house in rural Chaffee County. The cat, reported to have submandibular abscesses and oral lesions consistent with feline plague, died on August 19 before being evaluated by a veterinarian and was cremated without diagnostic studies. A dead chipmunk found in the area where the cat lived was culture-positive for Y. pestis. Rodent die-off in a nearby arroyo was also evident.

On September 10-11, the house and rodent burrows within a 100-yard radius of the house were dusted with the insecticide carbaryl to control flea populations. Cats and dogs living at the house were dusted, and the owners were advised to continue periodic dusting of their pets.

Reported by: A Opulski, MD, E MacNeill, MD, C Rosales, MD, Pima County Health Dept. A Hartsough, MD, Pima County Forensic Science Center, Tucson; J Doll, PhD, C Levy, MS, M Fink, Vector and Zoonotic Disease Control Section, B Erickson, PhD, W Slanta, G Cage, MS, Div of State Laboratory Svcs, L Sands, DO, Acting State Epidemiologist, Arizona Dept of Health Svcs. J Lofgren, G Gentry, Chaffee County Health Dept; T Davis, MS, J Pape, RE Hoffman, MD, State Epidemiologist, Colorado Dept of Health. Bacterial Zoonoses Br, Div of Vector-Borne Infectious Diseases, National Center for Infectious Diseases; Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: Although plague has enzootic foci among wild rodent populations in North America from the Pacific coast eastward to Texas, Oklahoma, Kansas, and the Dakotas, human cases have been concentrated in two principal regions: 1) a southwestern area that includes New Mexico, northeastern Arizona, southern Colorado, and southern Utah and 2) a Pacific Coast region located in California, Oregon, and western Nevada (3). Pneumonic plague, which is rare in the United States, can spread among humans and can be rapidly fatal unless detected and treated early (1,4). Onset of symptoms for primary plague pneumonia usually occurs within 2-3 days after exposure (1).

Cases of pneumonic plague in the United States have occurred secondary to septicemic plague or as a result of direct exposure (i.e., primary) to respiratory droplets from infected cats (5,6). Health-care providers, especially in areas with enzootic plague, should suspect plague in persons with unexplained fever, suspected sepsis, or pneumonia with or without lymphadenopathy or a classic plague bubo (i.e., an enlarged, inflamed lymph node). Buboes may not be present in persons with septicemic or pneumonic plague (1,4); however, nausea, vomiting, diarrhea, and abdominal pain may be prominent features (1). Persons suspected to have pneumonic plague should be placed in respiratory isolation and reported immediately to public health authorities so that rapid diagnosis, environmental assessments, and control measures (including flea control, rodent control, health education, and investigation of contacts) can be initiated. Streptomycin is the treatment of choice for persons suspected to have plague; alternates include tetracycline, chloramphenicol, and sulfonamides (1,4).

Veterinarians and veterinary assistants in areas enzootic for plague are at risk for plague infection from infected cats or wild rodents. Cats with unexplained lymphadenopathy and/or oral or submandibular abscesses should be suspected of having plague, and procedures for appropriate laboratory testing should be followed. Reporting of suspected cases by veterinarians to public health officials is essential to identify and monitor animal sources of infection and to minimize the potential for transmission to humans.

This case underscores the need for manufacturers marketing rapid microbiological testing devices to ensure that identification of Y. pestis is possible or to advise users that isolates of Y. pestis will not be identified and alternative tests need to be performed. In addition, this report is a reminder that persons with pneumonic plague may travel during the incubation period or while ill to areas where plague does not occur. In such cases, plague may not be considered in the diagnosis, increasing the potential for death and transmission to other persons.


  1. Barnes AM, Quan TJ. Plague. In: Gorbach SL, Bartlett JG, Balacklow NR, eds. Infectious diseases. Philadelphia: WB Saunders, 1992:1285-91.

  2. CDC. Plague pneumonia -- California. MMWR 1984;33:481-3.

  3. Barnes AM. Surveillance and control of plague in the United States. In: Edwards MA, McDonnel U, eds. Animal disease in relation to conservation. New York: Academy Press, 1982:237-70.

  4. Craven RB, Poland JD. Plague. In: Last JM, Wallace RB, eds. Maxcy-Rosenau-Last public health and preventive medicine. 13th ed. Norwalk, Connecticut: Appleton and Lange, 1992:237-40.

  5. Werner SB, Weidmer CE, Nelson BC, et al. Primary plague pneumonia contracted from a domestic cat at South Lake Tahoe, Calif. JAMA 1984;251:929-31.

  6. Eidson M, Tierney LA, Rollag OJ, et al. Feline plague in New Mexico: risk factors and transmission to humans. Am J Public Health 1988;78:1333-5.

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