Plague in the United States, 1982

Allan M. Barnes, Ph.D. Jack D. Poland, M.D.

Plague Branch Division of Vector-Borne Viral Diseases Center for Infectious Diseases Introduction Bubonic plague is a flea-transmitted disease of rodents caused by Yersinia pestis and is transmissible to humans by vector fleas or direct contact with infected animals. The disease in animals is characterized by explosive and often devastating sporadic epizootics among susceptible rodent and flea populations. During epizootic amplification, it tends to expand its distribution geographically, often for great distances, and to involve chance victims among ecologically associated animal species, including humans who enter or live in the affected areas. Epizootics among both wild and commensal rodents are self-limiting (1) and ultimately move on or recede to focal areas, at times seeding new pockets of infection that may persist for a period or occasionally remaining as new nidi of infection. A principal concern involves the transfer of plague to urban or rural commensal rat populations, with the result being epidemic plague transmission (2,3). Another is that humans and domestic animals that contract bubonic plague may develop secondary pneumonia and continue the chain of transmission via infectious airborne droplets to other persons, thus creating a pneumonic plague epidemic (4). Human plague is not common in the United States, but reported cases have averaged 16 a year since 1974. The case-fatality ratio has remained high (18%), despite the availability of effective antibiotic therapy. The humans most frequently affected are less than 20 years of age and are concentrated in two regions: the Southwest (Arizona, southern Colorado, New Mexico) and the Pacific States (California, southern Oregon) (5). Materials and Methods Plague surveillance in the United States has both passive and active elements. As required by the International Health Regulations of the World Health Organization (6), all human cases detected in the United States are reported internationally as well as locally and nationally. Criteria used to determine the status of a reported case are as follows:

1. Suspected plague

1. Compatible clinical and epidemiologic features

2. Suspicious-looking organisms seen in or isolated from clinical specimens 2. Presumptive plague

3. Positive fluorescent antibody test for Y. pestis in clinical specimens

4. Isolate from clinical specimen demonstrating biochemical reactions consistent with Y. pestis

5. A single (convalescent-phase) serum specimen positive for plague and not explainable on the basis of prior infection or vaccinationŐlf2ĺ 3. Confirmed plague

6. Isolate identified as Y. pestis

7. A significant (fourfold or greater) rise in antibody in paired (acute- and convalescent-phase) serum specimens

8. A significant (fourfold or greater) fall in antibody titer between a convalescent-phase and a "postconvalescent-phase" serum specimen In the United States, only presumptive and confirmed plague cases are included in official reporting since several other diseases can resemble bubonic plague. All reported cases are investigated epidemiologically by state and local health agencies and/or CDC 1) to confirm the infection as plague, 2) to determine the locality in which the infection was acquired, 3) to determine the possible animal (or human) source of infection, and 4) to locate, observe, and if necessary, treat case contacts or others thought to have been exposed to infection. Information thus obtained provides a basis for 1) informing the medical community about cases and diagnostic and therapeutic methods, 2) informing the public about the presence of plague and the means of avoiding infection and for getting their cooperation with health authorities in reporting events among susceptible animal populations, and 3) planning and implementing vector-control operations to reduce or eliminate the opportunity for human exposure. CDC maintains liaison not only with health agencies but also with an informal surveillance network of biologically trained persons in other fields--e.g., park managers, game managers, agricultural agents, foresters, and others who report unusual numbers of sick or dead rodents or rabbits, unusual disappearances of animal populations, or unusually large rodent populations. Information from such observers, followed by submission of specimens for laboratory studies, has been instrumental in the early detection of epizootic plague and implementation of control measures to prevent human exposure.

Serologic surveys of wild carnivore and domestic dog populations carried out by CDC in collaboration with state health agencies, the Indian Health Service, and the U.S. Fish and Wildlife Service Predator Damage Control Program form a major component of an active plague surveillance program. Both dogs and wild carnivores have been shown to produce detectable antibody to the specific fraction 1 antigen of Y. pestis following the ingestion of plague-infected material, but they usually do not become clinically ill. Serum specimens collected by the several agencies are tested in passive hemagglutination tests (7), the data are collated and analyzed, and the results are returned to state health agencies. Rodent surveys and/or control activities may be undertaken on the basis of data on carnivores indicating the presence of epizootic plague in areas of human risk.

Plague in animals and flea vectors examined as a result of surveillance activities is usually diagnosed by inoculation of laboratory mice followed by isolation and identification attempts on tissues of mice that die after being inoculated. For instance, flea specimens are pooled in groups of less than or equal to 25 by date, location, host source, and flea species. The fluorescent-antibody test is used on tissues of animals found dead in the field because it can provide early presumptive diagnosis for evaluating the potential risk to humans and the need for control. Results Nineteen cases of human plague were reported in the United States in 1982, the largest number since 1975 and the second largest since 1925 (Figure 1). One or more cases occurred in each of seven western states (Figure 2, Table 1). Texas reported its first case since 1920 and its first from a wild-animal source, although wild-rodent plague is identified frequently in West Texas. In the past 10 years, the case-fatality ratio has remained relatively constant; in 1982, three (15.7%) of the 19 reported cases were fatal. Patients ranged in age from 4 to 55 years. As in previous years, most patients were young: there were five cases each in the 0- to 9-year and the 10- to 19-year age groups. Eleven patients were male; eight were female. Four patients developed plague pneumonia and thus became potentially infective to others via the respiratory route. A 22-year-old veterinarian's assistant (Table 1, Patient 5) developed primary plague pneumonia (pneumonic plague) following face-to-face exposure to a sick cat. The human patient, a resident of Cheyenne, Wyoming, survived; the domestic cat died, and plague pneumonia was diagnosed at necropsy. Nine (47.4%) of the 19 human plague cases reported in 1982 occurred in American Indians--seven of them on the Navajo Reservation in northeastern Arizona and northwestern New Mexico. The attack rate for Navajos, based on a 1982 population total of 156,902 (Indian Health Service data) was 4.5 cases/100,000 population. In 1981 and 1982 combined, there were 13 cases in Navajos, for an average annual attack rate of 4.1/100,000. The seven 1982 cases on the Navajo Reservation were preceded by widespread evidence of plague activity among rodents, as indicated by serosurveys among dogs belonging to American Indians. Of a total of 853 serum specimens obtained from dogs by the Indian Health Service by June 1982, 135 (16%) had detectable antibody to Y. pestis, and 102 (76%) of the 135 positives had titers of more than or equal to 128, indicating recent infection. A case investigation in May (Table 1, Patient 4) revealed a widespread plague epizootic affecting Ammospermophilus leucurus, the antelope ground squirrel, and its flea, Thrassis bacchi, inhabitants of the saltbush ecological community (Atriplex-Sarcobatus) in much of the Southwest. In a larger survey, the A. leucurus epizootic was found to have swept through hundreds of square miles of saltbush landscape in western San Juan and McKinley counties of New Mexico. Other rodent species in adjacent habitats also were involved in epizootics. Discussion Natural foci of plague infection among rodents and their fleas are widespread in the western United States, and plague epizootics among susceptible rodent species occur frequently throughout the West. The geographic extent and intensity of these epizootics suggest that they will continue and indicate the continued need for plague surveillance and preventive control programs in the western states. Human cases, however, occur with greatest frequency in two regions--a southwestern region that includes northeastern Arizona, southern Colorado, southernmost Utah, and all of northern and part of southern New Mexico, and a Pacific region that includes much of California, southern Oregon, and far-western Nevada. Human cases outside these two regions have been few and scattered, and have usually been acquired through direct contact with plague-infected animals rather than by the usual flea-bite transmission. The factors and their interactions responsible for differences in human exposure from one region to another are poorly defined. The presence in abundance of susceptible rodent species living close to humans is obviously important. It also has been postulated that the willingness of various vector fleas to bite humans plays an extremely important role. Such fleas as Diamanus montanus on ground squirrels in both the Pacific and Southwest regions and Thrassis bacchi on antelope ground squirrels in the Southwest are known to be important and abundant rodent-to-human vectors.

Of equal importance are the lifestyles of persons who live in areas where plague is enzootic and periodically epizootic. In the Southwest, many people choose to live in "natural" settings, contributing to an increase in rodent populations and thus to the level of risk of exposure to plague. Others, because of culture and occupation (e.g., many Navajo Indians), live directly among rodent populations--prairie dogs, rock squirrels, and antelope ground squirrels--that are subject to periodic epizootics. That Navajos are victims of plague more frequently than other ethnic groups should not be surprising. Those with greater control over their environment could, given the appropriate information, reduce their risk by reducing rodent harborage, by avoiding fleas, and by judiciously using insecticides on pets that might harbor fleas.

Since certain high-risk ethnic/cultural groups live in geographic areas in which epizootic plague occurs, early therapy for persons with suspected cases should be considered. A decision to initiate therapy on clinical plus epidemiologic grounds should reduce the high case-fatality ratio. When a person with a moderate-to-high risk of exposure to plague hosts or vectors has fever and axillary or groin pain, it would be prudent to obtain blood cultures and serum specimens and then to initiate specific antibiotic therapy for Y. pestis. Patients who are not so acutely ill as to require hospitalization should have oral tetracycline or chloramphenicol administered on an outpatient basis. When outpatient treatment is given, the patient should be followed actively for 1-3 days to ensure a satisfactorily response to therapy and to mount an appropriate public health response if laboratory tests support the diagnosis of plague.

Patients who appear acutely ill and toxic at initial examination, usually after 3-4 days of illness, should have blood cultures obtained quickly (within a few minutes) and be given a plague-specific antibiotic (e.g., chloramphenicol, tetracycline, or gentamicin) intravenously. Clinical samples that can be obtained after antibiotic therapy has been started include lymph node aspirate, sputum or throat culture, culture of draining lesions, or, if indicated, biopsy of suspicious-looking lesions. White-blood-cell and differential counts should be done and a peripheral smear or lymph-node aspirate should be directly examined as early as possible to further direct the therapeutic regimen, i.e., to determine whether treatment for other agents in addition to Y. pestis should be considered.

This liberal regimen undoubtedly will result in treating febrile patients who are later shown not to have had plague, but should lead to a substantial reduction in the number of deaths caused by Y. pestis--if not completely limit fatal cases to those among patients with fulminating septicemia or others with atypical clinical presentations that do not appear to support a diagnosis of plague.

To define the impact and benefit of applying this aggressive therapeutic approach, the Plague Branch, Center for Infectious Diseases, is interested in receiving reports of cases, including patients with suspected but unconfirmed as well as confirmed and presumptive plague, and the treatment applied.

References

1. Meyer KF. The ecology of plague. Medicine 1942;21:143-74.

2. Miles VI, Kinney AR, Stark HE. Flea host relationships of associated Rattus and native wild rodents in the San Francisco Bay area of California, with special reference to plague. Am J Trop Med Hyg 1957;6:41-3.

3. Hudson BW, Quan TJ. Serologic observations during an outbreak of rat-borne plague in the San Francisco Bay area of California. J Wild Dis 1975;11:431-6.

4. Poland JD, Barnes AM. Plague. In Steele JF, ed. CRC handbook series in zoonoses, section A: bacterial, rickettsial, and mycotic diseases. Boca Raton, Fla.:CRC Press, 1979;1:515-56.

5. Barnes AM. Surveillance and control of plague in the United States. Symp Zool Soc Lond 1982;50:237-70.

6. World Health Organization. International health regulations (1969). Geneva: World Health Organization, 1971:1-99.

7. World Health Organization. Multipurpose serological surveys and WHO serum reference banks: report of a WHO scientific group. WHO Tech Rep 1970;454:1-95.

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