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At least 145 records · Page 8Linked to original sources
PubMed1987

[Detection of an inhibitor of the causative agent of plague active against strains of the plague microbe from an homologous focus. The effect of lithium chloride on detecting the inhibitor].

A nutrient medium containing 0.7 per cent of lithium chloride was tested and Yersinia pestis inhibitor was detected in 83.3 per cent of the strains on the growth tufts of 8 indicator strains isolated from a homologous focus. Lowering the lithium chloride concentration in the medium up to 0.6 per cent promoted detection of the inhibitor in a larger number of the tested strains (93.3 per cent). But even on this medium none of the indicator strains formed overall growth tufts. The subcultures of the indicator strains resistant to lithium chloride formed overall growth tufts on agar plates with lithium chloride and were sensitive to the inhibitor of the tested strains from the central Caucasus. However, during storage they lost their sensitivity to the inhibitor which did not permit their use as the test cultures.

Antibiosis↗
PubMed1999

Incidence of plague associated with increased winter-spring precipitation in New Mexico.

Plague occurs episodically in many parts of the world, and some outbreaks appear to be related to increased abundance of rodents and other mammals that serve as hosts for vector fleas. Climate dynamics may influence the abundance of both fleas and mammals, thereby having an indirect effect on human plague incidence. An understanding of the relationship between climate and plague could be useful in predicting periods of increased risk of plague transmission. In this study, we used correlation analyses of 215 human cases of plague in relation to precipitation records from 1948 to 1996 in areas of New Mexico with history of human plague cases (38 cities, towns, and villages). We conducted analyses using 3 spatial scales: global (El Niño-Southern Oscillation Indices [SOI]); regional (pooled state-wide precipitation averages); and local (precipitation data from weather stations near plague case sites). We found that human plague cases in New Mexico occurred more frequently following winter-spring periods (October to May) with above-average precipitation (mean plague years = 113% of normal rain/ snowfall), resulting in 60% more cases of plague in humans following wet versus dry winter-spring periods. However, we obtained significant results at local level only; regional state-wide precipitation averages and SOI values exhibited no significant correlations to incidence of human plague cases. These results are consistent with our hypothesis of a trophic cascade in which increased winter-spring precipitation enhances small mammal food resource productivity (plants and insects), leading to an increase in the abundance of plague hosts. In addition, moister climate conditions may act to promote flea survival and reproduction, also enhancing plague transmission. Finally, the result that the number of human plague cases in New Mexico was positively associated with higher than normal winter-spring precipitation at a local scale can be used by physicians and public health personnel to identify and predict periods of increased risk of plague transmission to humans.

Animals↗
PubMed1986

Experimental plague infection in South African wild rodents.

Susceptibility studies were undertaken to determine the response of some South African wild rodent species to experimental plague (Yersinia pestis) infection. A degree of plague resistance was found in three gerbil species captured in the plague enzootic region of the northern Cape Province, these being the Namaqua gerbil, Desmodillus auricularis, (LD50 1 X 10(6) organisms), the bushveld gerbil, Tatera leucogaster, (LD50 9.1 X 10(5)) and the highveld gerbil, T. brantsii (LD50 4 X 10(2)). Animals from a population of the four-striped mouse, Rhabdomys pumilio, captured in the plague area of Port Elizabeth, proved moderately resistant to experimental plague infection (LD50 1.3 X 10(4)) while those from another population of the same species captured in a plague-free area of the Orange Free State were extremely susceptible (LD50, 5 organisms). The response of both populations however was a heterogeneous one. Marked differences in susceptibility were also found between two populations of multimammate mice, Mastomys natalensis (2n = 32) although both originated from areas outwith the known distribution of plague in southern Africa. The 50% infectious dose was relatively high in T. leucogaster (3.2 X 10(2)) and D. auricularis (1.7 X 10(3)), but was low (2-16 organisms) in the other rodent species tested. The plague antibody response, determined by enzyme-linked immunosorbent assay (ELISA), was extremely short-lived in T. leucogaster, only 10% of inoculated animals remaining seropositive at low titres after 11 weeks. Antibodies persisted for only slightly longer in the sera of T. brantsii which were reinoculated with 2 X 10(3) plague organisms 6 weeks after initial challenge. The demonstration of the existence of both susceptible and resistant populations of R. pumilio and M. natalensis indicates that these species must be considered as potential plague reservoir hosts in parts of South Africa. The results suggest that resistance to plague infection in previously epizootic hosts in the northern Cape Province such as Tatera sp. and D. auricularis has arisen through continual selective pressure of the organism. If the findings are applicable to gerbil populations in other plague enzootic regions of South Africa it is probable that acquired plague resistance has been responsible for the absence of gerbil epizootics and consequently for the dramatic decline in human plague outbreaks in South Africa since 1950.

Animals↗
PubMed1997

Plague pneumonia disease caused by Yersinia pestis.

Plague is a zoonotic infection caused by Yersina pesits, a pleomorphic, gram-negative non-spore-forming coccobacillus that is more accurately classified as a subspecies of Y pseudotuberculosis. Animal reservoirs include rodents, rabbits, and occasionally larger animals. Cats become ill and have spread pneumonic disease to man. Dogs may be a significant sentinel animal as well as a reservoir, although do not usually become ill. Flea bites commonly spread disease to man. Person to person spread has not been a recent feature until the purported outbreak of plague and plague pneumonia in India in 1994. Other factors that increase risk of infection in endemic areas are occupation-veterinarians and assistants, pet ownership, direct animal-reservoir contact especially during the hunting season, living in households with an index case, and, mild winters, cool moist springs, and early summers. Clinical presentations include subclinical plague (positive serology without disease); plague pharyngitis; pestis minor (abortive bubonic plague); bubonic plague; septicemic plague; pneumonic plague; and plague meningitis. Most prominent of plague's differential diagnosis are Reye's syndrome, other causes of lymphadenitis, bacterial pneumonias, tularemia, and acute surgical abdomen. Treatment has reduced mortality from 40-90% to 5-18%. The drug of choice (except for plague meningitis) is streptomycin, with tetracyclines being alternatives. Parenteral cholamphenicol is the treatment of choice for plague meningitis. A tetracycline should be administered as chemoprophylaxis to all contacts over the age of 8 years. Plague vaccine is available, but is only partially protective.

Animals↗
PubMed1982

Pediatric plague.

The large reservoir of animal plague in the American West led to 121 cases of human plague from 1970 to 1980. The majority (55%) of recent cases have occurred in children 16 years of age and younger. In New Mexico 38 pediatric plague cases were reviewed to determine the epidemiologic, clinical, and laboratory feature of this disease. Thirty-one patients (82%) had bubonic plague and seven (18%) had primary septicemic disease. Primary septicemic plague had a significantly higher case-fatality ratio (71% vs 3%; P = .0002) and an increased risk of plague pneumonia (57% vs 6%; P = .01) compared with bubonic disease. Symptoms at onset, physical examination, and laboratory data at hospitalization (mean of three days after onset) were consistent with an acute, systemic febrile illness. Recovery from plague was slow, requiring an average of 5.9 days from initiation of effective antibiotics until fever lysis. Only a minority of plague patients were initially suspected to have plague, even by the time of hospitalization. Whereas clinical evidence, particularly in bubonic disease, should suggest plague, residing in or visiting a rural are of the West (especially from June through September) during the week prior to illness may be the only useful epidemiologic clue for the majority of patients who lack a history suggestive of exposure to animals or fleas. The importance of pediatric plague stems from the recent increase in cases, the significant increase in the proportion of all cases occurring in children, the public health implications of plague pneumonia (16% of cases), and the demonstrated potential for plague patients to travel to areas of the country unfamiliar with the disease and its sylvatic home in the American West.

Adolescent↗
PubMed1997

An overview of plague in the United States and a report of investigations of two human cases in Kern county, California, 1995.

Plague was confirmed in the United States from nine western states during 1995. Evidence of Yersinia pestis infection was identified in 28 species of wild or domestic mammals. Thirteen of the plague positive species were wild rodents; 15 were predators/carnivores. Yersinia pestis was isolated from eight species of fleas. Seven confirmed cases of human plague were reported in 1995 (New Mexico 3; California 2; Arizona and Oregon 1 each). Five of the seven cases were bubonic; one was septicemic and one a fatal pneumonic case. Months of onset ranged from March through August. In California, during 1995, plague was recorded from 15 of the 58 counties. Over 1,500 animals were tested, of which 208 were plague positive. These included 144 rodents and 64 predators/carnivores. Two confirmed human cases (one bubonic and one fatal pneumonic) occurred, both in Kern County. Case No. 1 was reported from the town of Tehachapi. The patient, a 23 year-old male resident, died following a diagnosis of plague pneumonia. The patient's source of plague infection could not be determined precisely. Field investigations revealed an extensive plague epizootic surrounding Tehachapi, an area of approximately 500-600 square miles (800-970 square kilometers). Case No. 2 was a 57 year-old female diagnosed with bubonic plague; she was placed on an antibiotic regimen and subsequently recovered. The patient lives approximately 20 miles (32 km) north of Tehachapi. Field investigations revealed evidence of a plague epizootic in the vicinity of the victim's residence and adjacent areas. Overall results of the joint field investigations throughout the entire Kern county area revealed a high rate of plague positive animals. Of the numerous samples submitted, 48 non-human samples were plague positive.

Adult↗
PubMed1998

[Pulmonic plague].

One hundred years after Yersin discovered Yersinia pestis during the plague epidemic in Hong Kong in 1894, human plague still has not been eliminated. The epidemic in 1994 in India, a country where no cases had been observed since 1996, raised great concern. Plague is an epizootic bacterial infection caused by a Gram negative coccobacillus, Y. pestis, transmitted by the bite of infected fleas. Bubonic plague is the most common form. Other clinical presentations include asymptomatic plague, abortive plague, pharyngeal plague, septicemic plague, meningeal plague, and primary or secondary pneumonic plague which is observed in 5 to 20% of cases. Plague is a highly communicable disease between humans despite antibiotic therapy which has reduced mortality by 80%. The prognosis depends on early diagnosis. Streptomycin and cyclines are the gold standard treatment.

Anti-Bacterial Agents↗
PubMed2000

Cases of cat-associated human plague in the Western US, 1977-1998.

Exposure to cats infected with Yersinia pestis is a recently recognized risk for human plague in the US. Twenty-three cases of cat-associated human plague (5 of which were fatal) occurred in 8 western states from 1977 through 1998, which represent 7.7% of the total 297 cases reported in that period. Bites, scratches, or other contact with infectious materials while handling infected cats resulted in 17 cases of bubonic plague, 1 case of primary septicemic plague, and 5 cases of primary pneumonic plague. The 5 fatal cases were associated with misdiagnosis or delays in seeking treatment, which resulted in overwhelming infection and various manifestations of the systemic inflammatory response syndrome. Unlike infections acquired by flea bites, the occurrence of cat-associated human plague did not increase significantly during summer months. Plague epizootics in rodents also were observed less frequently at exposure sites for cases of cat-associated human plague than at exposure sites for other cases. The risk of cat-associated human plague is likely to increase as residential development continues in areas where plague foci exist in the western US. Enhanced awareness is needed for prompt diagnosis and treatment.

Adolescent↗