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Fatal Human Plague -- Arizona and Colorado, 1996

In 1996, five cases of human plague, of which two were fatal, were reported in the United States; both decedents had septicemic plague that was not diagnosed until after they died. This report summarizes the investigation of the two fatal cases and underscores the need for health-care providers in areas with endemic plague to maintain a high level of awareness about the risk for plague in their patients. Patient 1

On August 2, 1996, an 18-year-old resident of Flagstaff, Arizona, was taken to a local outpatient clinic because of a 2-day history of fever, pain in his left groin, and diarrhea. On examination, he was afebrile, had a pulse rate of 126 beats per minute, respiration rate of 20 breaths per minute, and blood pressure of 130/81 mm Hg. Left groin swelling and tenderness were noted. A groin muscle strain was diagnosed and attributed to a fall 2 days earlier. He was treated with nonsteroidal anti-inflammatory agents, instructed about using a liquid diet, and released. On August 3, the patient reported feeling weak, had difficulty breathing, and collapsed while taking a shower. Emergency medical assistance was called, and the patient experienced cardiac arrest while emergency medical technicians were on site. He was transported to a hospital emergency department (ED) and pronounced dead shortly after arrival.

On August 8, cultures of blood samples obtained in the ED were presumptively positive for Yersinia pestis by fluorescent antibody staining and confirmed by specific bacteriophage lysis at the laboratory of the Arizona State Department of Health. Additional isolates from postmortem brain, liver, lung, and vitreous fluid cultures were confirmed as Y. pestis at CDC. An epidemiologic investigation by public health officials indicated that the patient most likely became infected on July 27 as the result of bites by Y. pestis-infected fleas while walking through a prairie dog (Cynomys gunnisoni) colony in Navajo County. High antibody titers to the fraction 1 (F1) antigen of Y. pestis were detected in two of four pet dogs living in houses near the prairie dog colony. Dog owners were advised about the risk for plague and instructed to restrain their pets and to periodically dust them with insecticide. Prairie dog burrows within one half mile of the residences were dusted with insecticide to control flea populations. Patient 2

On August 17, 1996, a 16-year-old resident of western Colorado had onset of pain followed by numbness in her left arm and left axillary pain. During August 18-19, she had chills, fever, and several episodes of vomiting. On August 19, she was evaluated at a local hospital ED. Findings included a temperature of 97.4 F (36.3 C), pulse rate of 100 beats per minute, respiration rate of 16 breaths per minute, and blood pressure of 103/59 mm Hg; a chest radiograph was interpreted as within normal limits. She was discharged with a diagnosis of possible brachial plexus injury related to a fall from a trampoline on August 14. She was prescribed analgesics, and an appointment with a neurologist was scheduled.

On August 21, she was found semiconscious at home and taken to the same hospital. She was confused and complained of neck pain and generalized soreness. Findings on examination included a temperature of 102.5 F (39.2 C), pulse rate of 170 beats per minute, respiration rate of 50 breaths per minute, and blood pressure of 130/70 mm Hg. Within an hour of arrival at the hospital, she experienced respiratory arrest and was intubated. Numerous gram-positive diplococci were detected in a blood smear, and a chest radiograph revealed bilateral pulmonary edema. She was administered 2 g ceftriaxone intravenously and transferred to a referral hospital with diagnoses of septicemia, disseminated intravascular coagulation, adult respiratory distress syndrome, and possible meningitis. A gram stain of sputum revealed rare white blood cells and no bacteria; she was treated for gram-positive sepsis. However, her condition rapidly deteriorated, and she died later that day.

On August 23, blood and spinal fluid cultures obtained on August 21 grew an unidentified gram-negative rod and Streptococcus pneumoniae. On August 26, Yersinia pseudotuberculosis was initially identified in cultures of blood and respiratory aspirate using a rapid microbiologic identification device. This blood culture isolate subsequently was presumptively identified as Y. pestis at the Utah Division of Laboratory Services and confirmed as Y. pestis at CDC.

An environmental investigation by health officials revealed evidence of an earlier extensive prairie dog die-off adjacent to the patient's residence. High antibody titers to the F1 antigen of Y. pestis were present in serum specimens from four of five family dogs and one of three family cats. The seropositive cat had a submandibular lesion consistent with a healing abscess. Family members reported that the cat had been recently ill and had been closely cared for by the decedent. Investigators concluded that the decedent was probably exposed to Y. pestis by direct contact with infectious material while handling the cat. None of 10 flea pools or 13 rodents (least chipmunk, Tamias minimus {four}; deer mouse, Peromyscus maniculatus {six}; and house mouse, Mus musculus {three}) collected on the property tested positive for Y. pestis or for antibody to Y. pestis, respectively. Because the diagnosis was established after the standard 7-day maximum plague incubation period had elapsed, antibiotic prophylaxis of family members and medical personnel was not instituted.

Reported by: M Tenborg, B Davis, MS, D Smith, Coconino County Health Dept, Flagstaff; C Levy, MS, B England, MD, State Epidemiologist, Arizona Dept of Health Svcs. B Koehler, Delta County Health Dept, Delta; D Tanda, J Pape, MS, R Hoffman, MD, State Epidemiologist, Colorado Dept of Public Health and Environment. R Fulgham, MS, B Joe, J Cheek, MD, Indian Health Svc. Bacterial Zoonoses Br, Div of Vector-Borne Infectious Diseases, National Center for Infectious Diseases; Div of Applied Public Health Training (proposed), Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: In the United States, most cases of human plague are reported from New Mexico, Arizona, Colorado, and California (1,2). The principal forms of plague are bubonic, septicemic (primary or secondary), and pneumonic (primary or secondary). From 1947 through 1996, a total of 390 cases of plague were reported, resulting in 60 (15.4%) deaths. Of these, bubonic plague accounted for 327 (83.9%) cases and 44 (13.5%) deaths; primary septicemic plague, for 49 (12.6%) cases and 11 (22.4%) deaths; and primary pneumonic plague, for seven (1.8%) cases and four (57.1%) deaths. Seven (1.8%) cases were unclassified, including one (14.3%) death (CDC, unpublished data, 1997). During 1965-1989, a total of 27 persons with plague were treated at the Gallup Indian Medical Center in New Mexico. Of these, classic signs of bubonic plague were present in only 10 (37%); provisional diagnoses in other patients included apparent upper respiratory tract infections, nonspecific febrile syndromes, gastrointestinal or urinary tract infections, or meningitis (3). The syndromes in both patients described in this report initially were attributed to injuries and treated with analgesics.

Bubonic plague may not be considered by a physician if swollen, tender lymph nodes are not detected or present on physical examination. Evidence of regional lymphadenitis should prompt a suspicion of plague in a patient who lives in or has recently visited an area with endemic plague. Septicemic plague without obvious lymphadenopathy is more difficult to diagnose because the manifestations are nonspecific (e.g., elevated temperature, chills, abdominal pain, nausea, vomiting, diarrhea, tachycardia, tachypnea, and hypotension) (4).

A patient with clinical signs of sepsis and a history of possible plague exposure, particularly during the spring, summer, and fall months, should be aggressively managed as having plague. Even before a specific laboratory diagnosis is obtained, anti-biotic therapy should be initiated with streptomycin; alternatives include gentamicin, chloramphenicol, and the tetracyclines. The penicillins and cephalosporins are not effective in treating plague, although these drugs frequently show activity in vitro (5).

In suspected cases of plague, several samples of blood should be collected for culture during a 45-minute period before initiation of antibiotic treatment, unless such a delay is contraindicated by the patient's condition. The direct immunofluorescence test for the rapid presumptive identification of Y. pestis F1 antigen should be applied to appropriate clinical materials (e.g., lymph node aspirates, culture isolates, or blood films), and if pneumonic plague is suspected, tracheal washes or sputum smears. Rapid microbiologic identification devices may not include adequate Y. pestis profiles in their database and, therefore, may misidentify Y. pestis as Y. pseudotuberculosis (6 ). Acute- and convalescent-phase serum specimens should be obtained to detect antibodies to the Y. pestis F1 antigen by using passive hemagglutination assay or enzyme-linked immunosorbent assay methods. Patients with suspected Y. pestis infections should be reported immediately to local or state health departments to enable prompt initiation of appropriate public health control and prevention activities. In the United States, testing of clinical specimens and isolates from suspected plague patients should be coordinated through state health departments and sent to CDC's Diagnostic and Reference Laboratory Section, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases (telephone {970} 221-6400), for confirmation of Y. pestis (7).

Control measures to prevent human plague include surveillance for plague in rodents and rodent predators as well as public education (8,9). When epizootic plague is detected, local health-care providers and the public should be alerted about possible risks. Warnings can be posted at identified epizootic foci (e.g., campgrounds and trailheads), and rodent flea-control measures should be considered. Public education efforts should focus on promoting personal protection measures, including 1) avoiding areas with known epizootic plague; 2) avoiding sick or dead animals; 3) using repellents, insecticides, and protective clothing during potential exposures to rodent fleas; and 4) using gloves when handling animals killed by trapping or hunting. Persons residing in areas with wild rodent plague should keep their dogs and cats free of fleas and restrict pets from wandering. Because plague in cats is especially contagious, persons caring for sick cats should take precautions to avoid exposure to potentially infectious exudates or secretions. Sources of rodent food (e.g., garbage and animal food) and harborage (e.g., brush piles and junk heaps) should be eliminated in the peridomestic environment.

References

  1. CDC. Human plague -- United States, 1993-1994. MMWR 1994;43:242-6.

  2. CDC. Prevention of plague: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996;45(no. RR-14):5.

  3. Crook LD, Tempest B. Plague: a clinical review of 27 cases. Arch Intern Med 1992;152:1253-6.

  4. Hull HF, Montes JM, Mann JM. Septicemic plague in New Mexico. J Infect Dis 1987;155:113-8.

  5. Craven RB. Plague. In: Hoeprich PD, Jordan MC, Ronald AR, eds. Infectious diseases: a treatise of infectious processes. 5th ed. Philadelphia, Pennsylvania: J.B. Lippincott Company, 1994: 1302-12.

  6. Wilmoth BA, Chu MC, Quan TJ. Identification of Yersinia pestis by BBL Crystal Enteric/ Nonfermenter Identification System. J Clin Microbiol 1996;34:2829-30.

  7. Gray LD. Escherichia, Salmonella, Shigella, and Yersinia. In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology. 6th ed. Washington, DC: ASM Press, 1995:454.

  8. Poland JD, Quan TJ, Barnes AM. Plague. In: Beran GW, ed. CRC handbook of zoonoses. Boca Raton, Florida: CRC Press, 1994:93-112.

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




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