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PubMed1976

Bubonic plague from direct exposure to a naturally infected wild coyote.

An 11-year-old boy developed axillary bubonic plague and plague meningitis 3 days after skinning a dead coyote near Albuquerque, New Mexico. The coyoto carcass was recovered 10 days later, and Yersinia pestis was isolated from spleen and marrow of the animal. This is the first report of human plague from exposure to a coyote. A review of experimental and epidemiologic studies suggests that severe plague infection in members of the family Canidae is unusual, and that the risk of acquiring plague from direct contact with coyote tissues is minimal. Nevertheless, certain precautions are outlined for persons working with wild coyotes.

Ampicillin↗
PubMed1997

Bubonic plague: a molecular genetic case history of the emergence of an infectious disease.

Yersinia pestis, the bacterial agent of bubonic plague, is transmitted primarily by fleas and has been responsible for devastating epidemics throughout history. Y. pseudotuberculosis is a food- and water-borne pathogen that causes a much more benign enteric disease in humans. Despite these profoundly different pathogenesis strategies, the two bacteria are very closely related phylogenetically. Thus, identifying the specific genetic differences between them should provide an instructive case study in the evolution of microbial pathogenicity. Some key pathogenesis-related genes of Y. pestis and Y. pseudotuberculosis that have been described to date are compared in this review. Factors that potentiate plague transmission as well as disease are discussed, since dependence on the blood-sucking flea for transmission likely fueled the selection of virulent Y. pestis strains able to produce a high-density bacteremia. Retracing the evolutionary steps between these two Yersinia species may ultimately furnish a historical model for the sudden emergence of new human disease agents.

Animals↗
PubMedDate not supplied

[Rumors, fear or epidemy? The bubonic plague of 1913-1914 in the Atlantic coast of Columbia].

By the end of the 1800s, international trade and steam navigation made way for the third bubonic plague pandemy, which started in China in 1891 and reached America in 1898. This calamity apparently arrived in Columbia's coast between 1913 and 1915, during the apex of Pasteur medicine. The deficiencies of Columbian public scientific and sanitary apparat, concerning the emerging bacteriology and epidemiology, prevented the government and the medical body from reacting against the fear and rumor of epidemy, which negatively affected the trade. The authorities were also unable to fight this problem with adequate diagnosis, enferms treatment, urban sanitation, and isolation of infected places. These difficulties led to a confrontation between the government and the medical body, inciting an argument about the existence of the plague. This discussion was settled by the North American official medicine that, in its verdict, gave preference to the commercial interests of the United States, ignoring the sanitary urgencies of the Columbian Atlantic coast.

Colombia↗
PubMed1990

Bubonic plague in a child presenting with fever and altered mental status.

An 8-year-old Navajo boy presented to the emergency department with fever and altered mental status. Because the child lived in a plague-endemic area of the southwestern United States, antibiotics effective against Yersinia pestis were administered rapidly. Buboes were appreciated on physical examination, and the diagnosis of bubonic plague was confirmed by positive blood cultures. Characteristics and treatment of Yersinia pestis infection are discussed. The need for a high index of suspicion for the presence of plague in patients who present to the ED and who reside or have recently traveled in a plague-endemic area is emphasized.

Child↗
PubMed2001

Small rodents fleas from the bubonic plague focus located in the Serra dos Orgãos Mountain Range, State of Rio de Janeiro, Brazil.

Eleven species of fleas were collected from 601 small rodents, from November 1995 to October 1997, in areas of natural focus of bubonic plague, including the municipalities of Nova Friburgo, Sumidouro and Teresópolis, State of Rio de Janeiro, Brazil. Among 924 fleas collected, Polygenis (Polygenis) rimatus (Rhopalopsyllidae) was the predominant species regarding the frequency, representing 41.3% (N:382), followed by P. (Neopolygenis) pradoi, representing 20% (N:185) and Craneopsylla minerva minerva (Stephanocircidae), representing 18.9% (N:175). The host Akodon cursor harbored 47.9% of these fleas. Other six host species were infested by 52.1% of the remaining fleas. Fleas were found on hosts and in places within the focus not previously reported by the literature.

Animals↗
PubMed2006

Immunogenicity and protective immunity against bubonic plague and pneumonic plague by immunization of mice with the recombinant V10 antigen, a variant of LcrV.

In contrast to Yersinia pestis LcrV, the recombinant V10 (rV10) variant (lacking residues 271 to 300) does not suppress the release of proinflammatory cytokines by immune cells. Immunization with rV10 generates robust antibody responses that protect mice against bubonic plague and pneumonic plague, suggesting that rV10 may serve as an improved plague vaccine.

Animals↗
PubMedDate not supplied

[Outbreak of bubonic plague in Jacocha, Huancabamba, Perú ].

Climatic alterations arising in the north of Perú as a result of the El Niño phenomenon (ENSO) have caused variations in the crop volume, changes in the direction of rivers and probably an increase in the rodent population. In February 1999, in a native community in Jacocha, Huancabamba, Piura's mountains, Perú, an outbreak of bubonic plague appeared with five human cases, one of which lead to death. The diagnosis was confirmed by serology (passive hemaglutination). The presence of antibodies in dogs of localities close to Jacocha has confirmed the circulation of Yersinia pestis in the region. The outbreak was controlled by the local sanitary authorities' prompt action. This episode, after an epidemiological silence for more than four years, showed the necessity of intensifying the plague epidemiological surveillance system in this area.

Adolescent↗
PubMedDate not supplied

Effect of the bubonic plague epidemic on inbreeding in 14th century Britain.

The purpose of the study reported here was to further investigate a new method of estimating inbreeding in large, relatively isolated populations over historic times, as reported by Pattison (1999, 2001). The method is based on modeling the genealogical "paradox" and produces values of Pearl's coefficients of inbreeding as a function of time for any given population curve. In particular, this study demonstrates that the new method of estimating inbreeding may be used to examine the effect of unusual features in population curves on levels of inbreeding in that population. As an example, the medieval population "bump" that spans the 13th and 14th centuries in the population of Britain, which terminated abruptly with the outbreak of bubonic plague in 1348 AD, is examined. It is first assumed that the whole population was the adult (breeding) population, corresponding to minimum inbreeding. For this case it is found that, for distant generations, about 90% of the whole population occurs in any present-day British pedigree. This value compares favorably with the values of 85% and 80% reported by Wachter (1980) and Derrida et al. (1999, 2000), respectively. The population bump causes the curves for Pearl's coefficient, for minimum inbreeding, to have a plateau of about 96% over the period from about 1220 AD to 1380 AD. The effect of introducing a single known estimate of inbreeding into the model is to produce a more realistic situation where the adult (breeding) population is considerably less than the whole population. It is found that the maximum number of different ancestors in any generation, in the average British pedigree, is about 22900 individuals and occurs about 1220 AD. More importantly, and possibly contrary to expectation, it is now found that the population bump had virtually no effect on the level of inbreeding.

Consanguinity↗
PubMed2004

Flea-borne transmission model to evaluate vaccine efficacy against naturally acquired bubonic plague.

A flea-to-mouse transmission model was developed for use in testing new candidate vaccines for the ability to protect against flea-borne plague. The model was used to evaluate a recombinant fusion protein vaccine consisting of the Yersinia pestis F1 and V antigens. After one to three challenges with Y. pestis-infected fleas, 14 of 15 unvaccinated control mice developed plague, with an average septicemia level of 9.2 x 10(8) Y. pestis CFU/ml. None of 15 vaccinated mice developed the disease after similar challenges, and serological testing indicated that transmitted bacteria were eliminated by the immune system before extensive replication and systemic infection could occur. The transmission and development of disease in control mice correlated with the number of bites by blocked fleas but not with the total number of fleabites. The model provides a means to directly assess the efficacy of new vaccines to prevent naturally acquired bubonic plague and to study events at the vector-host interface that lead to dissemination and disease.

Animals↗
PubMed2006

RovA, a global regulator of Yersinia pestis, specifically required for bubonic plague.

The pathogenic species of Yersinia contain the transcriptional regulator RovA. In Yersinia pseudotuberculosis and Yersinia enterocolitica, RovA regulates expression of the invasion factor invasin (inv), which mediates translocation across the intestinal epithelium. A Y. enterocolitica rovA mutant has a significant decrease in virulence by LD(50) analysis and an altered rate of dissemination compared with either wild type or an inv mutant, suggesting that RovA regulates multiple virulence factors. Here, we show the involvement of RovA in the virulence of Yersinia pestis, which naturally lacks a functional inv gene. A Y. pestis DeltarovA mutant is attenuated approximately 80-fold by LD(50) and is defective in dissemination/colonization of spleens and lungs after s.c. inoculation. However, the DeltarovA mutant is only slightly attenuated when given via an intranasal or i.p. route, indicating a more important role for RovA in bubonic plague than pneumonic plague or systemic infection. Microarray analysis was used to define the RovA regulon. The psa locus was among the most highly down-regulated loci in the DeltarovA mutant. A DeltapsaA mutant had a significant dissemination defect after s.c. infection but only slight attenuation by the pneumonic-disease model, closely mimicking the virulence defect seen with the DeltarovA mutant. DNA-binding studies revealed that RovA specifically interacts with the psaE and psaA promoter regions, indicating a direct role for RovA in regulating this locus. Thus, RovA appears to be a global transcription factor in Y. pestis and, through its regulatory influence on genes such as psaEFABC, contributes to the virulence of Y. pestis.

Animals↗
PubMed2000

Early diagnosis of bubonic plague using F1 antigen capture ELISA assay and rapid immunogold dipstick.

Plague is still prevalent in more than 20 countries. Two F1 antigen diagnostic assays (an immunocapture ELISA and an immunogold chromatography dipstick) were evaluated using bubo aspirates, serum and urine specimens from patients suspected with plague. The specificity of the two F1 assays was found 100%. Using bacteriology as a gold reference diagnostic assay, 52 patients were Yersinia pestis culture positive and 141 negative. The sensitivity of the F1 ELISA test was 100% in bubo, 52% in serum and 58% in urine specimens. In culture negative patients, the F1 antigen could be found in 10% bubo aspirates, 5% serum and 7% urine specimens of culture negative patients for whom a seroconversion for anti-F1 antibodies was also observed. The sensitivity of the dipstick assay was 98% on bubo aspirates specimens. Compared to the ELISA test, the agreement rate was 97.5% and the correlation coefficient tau = 0.90 (p < 10(-3)). In conclusion, the diagnosis of bubonic plague has to be performed on bubo fluid rather than on serum or urine specimens. Both the F1 ELISA and the dipstick assays are valuable tools for an early diagnosis and for the surveillance of plague.

Antibodies, Monoclonal↗
PubMed1999

The haemin storage (Hms+) phenotype of Yersinia pestis is not essential for the pathogenesis of bubonic plague in mammals.

The haemin storage (Hms+) phenotype of Yersinia pestis enables this bacillus to form greenish/brown or red colonies on haemin or Congo Red agar plates, respectively, at 26 but not 37 degrees C. Escherichia coli strains that contain mutations in genes essential for siderophore biosynthesis, porphyrin generation and/or haemin transport remain unable to utilize exogenous haemin as a nutritional iron or porphyrin source when transformed with the cloned Y. pestis hmsHFRS locus. Further physiological analysis of the Hms+ phenotype of Y. pestis strain KIM6+ suggests that the haemin and inorganic iron stored by the Hms system was not used nutritionally under subsequent iron-deficient conditions. In vitro analysis of the bactericidal effects of hydrogen peroxide, superoxide and nitric oxide showed that Hms- Y. pestis cells, in certain cases, were more susceptible than the Hms+ parent cells to these reactive oxygen species at 26 and/or 37 degrees C. In adherence assays, a higher percentage of Hms+ cells were associated with HeLa cells and normal human neutrophils, compared to Hms- cells. However, the Hms+ phenotype did not provide any additional protection against the killing effects of neutrophils. Finally, LD50 analysis in subcutaneously infected mice showed that an Hms- strain was slightly more virulent than Hms+, indicating that the Hms phenotype is not essential for the pathogenesis of bubonic plague in mammals.

Animals↗
PubMed1990

Yersinia pestis pH 6 antigen: genetic, biochemical, and virulence characterization of a protein involved in the pathogenesis of bubonic plague.

We studied a protein antigen, designated pH 6 Ag, that has the same regulation of expression as the previously described Yersinia pestis pH 6 Ag. Monospecific antiserum to this antigen recognized several proteins, ranging from 15 to over 75 kilodaltons (kDa), which were strongly expressed when Y. pestis was cultivated at 37 degrees C and pH 6 but were expressed weakly, if at all, at 37 degrees C and pH 8 and at 26 degrees C. The antigen appeared to be composed of aggregates of a 15-kDa subunit. Escherichia coli minicell analysis and Western blotting (immunoblotting) of minicell extracts containing the cloned pH 6 Ag locus revealed that a 1.7-kilobase-pair (kb) region of Y. pestis chromosomal DNA produced 16- and 15-kDa immunoreactive proteins. We used transposon mutagenesis of the pH 6 Ag-coding region to demonstrate that the 16- and 15-kDa polypeptides were produced by the same cistron. The pH 6 Ag structural gene, psaA, was located within a 0.5-kb region of DNA. A Tn10lacZ transposon insertion 1.2 kb upstream of the psaA locus but outside the psaA transcriptional unit caused decreased expression of pH 6 Ag in both E. coli and Y. pestis and defined the psaE locus necessary for maximum pH 6 Ag expression. This locus itself was not regulated by temperature or pH. However, psaA remained responsive to both of these environmental signals in a Y. pestis psaE mutant. Mutation of either psaE or psaA resulted in at least a 100-fold reduction in the intravenous 50% lethal dose of Y. pestis in mice. Accordingly, pH 6 Ag is involved in the pathogenesis of bubonic plague.

Animals↗
PubMed1996

Recombinant V antigen protects mice against pneumonic and bubonic plague caused by F1-capsule-positive and -negative strains of Yersinia pestis.

The purified recombinant V antigen from Yersinia pestis, expressed in Escherichia coli and adsorbed to aluminum hydroxide, an adjuvant approved for human use, was used to immunize outbred Hsd:ND4 mice subcutaneously. Immunization protected mice from lethal bubonic and pneumonic plague caused by CO92, a wild-type F1+ strain, or by the isogenic F1- strain C12. This work demonstrates that a subunit plague vaccine formulated for human use provides significant protection against bubonic plague caused by an F1- strain (C12) or against substantial aerosol challenges from either F1+ (CO92) or F1-(C12) Y. pestis.

Animals↗
PubMed1999

Yersinia outer proteins (YOPS) E, K and N are antigenic but non-protective compared to V antigen, in a murine model of bubonic plague.

The pathogenic Yersiniae produce a range of virulence proteins, encoded by a 70 kb plasmid, which are essential for infection, and also form part of a contact-dependent virulence mechanism. One of these proteins, V antigen, has been shown to confer a high level of protection against parenteral infection with Y. pestis in murine models, and is considered to be a protective antigen. In this study, the protective efficacy of V antigen has been compared in the same model with that of other proteins (YopE, YopK and YopN), which are part of the contact-dependent virulence mechanism. Mice immunised with two intraperitoneal doses of V antigen or each of the Yops, administered with either Alhydrogel or interleukin-12, produced high antigen-specific serum IgG titres. As shown in previous studies, V+Alhydrogel was fully protective, and 5/5 mice survived a subcutaneous challenge with 90 or 9x10(3) LD50's of Y. pestis GB. In addition, these preliminary studies also showed that V+IL-12 was partially protective: 4/5 or 3/5 mice survived a challenge with 90 or 9x10(3) LD50's, respectively. In contrast, none of the mice immunised with the Yops survived the challenges, and there was no significant delay in the mean time to death compared to mice receiving a control protein. These results show that using two different vaccine regimens, Yops E, K and N, failed to elicit protective immune responses in a murine model of plague, whereas under the same conditions, V antigen was fully or partially protective.

Animals↗
PubMed1986

Multiple lung cavities in a 12-year-old girl with bubonic plague, sepsis, and secondary pneumonia.

After one week of nonspecific symptoms, pneumonia and an extremely tender and enlarged cervical lymph node developed in a 12-year-old girl who lived in an area of New Mexico known to have plague-infected rodents. Cultures from an aspirate of the node, her sputum, and blood all showed growth of Yersinia pestis. She was treated successfully with aminoglycosides and tetracycline. As the pneumonia resolved, areas of consolidation were replaced by cavitary lesions.

Child↗