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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Yersinia pestis appears to be a good candidate agent for a bioterrorist attack. The use of an aerosolised form of this agent could cause an explosive outbreak of primary plague pneumonia. The bacteria could be used also to infect the rodent population and then spread to humans. Most of the therapeutic guidelines suggest using gentamicin or streptomycin as first line therapy with ciprofloxacin as optional treatment. Persons who come in contact with patients with pneumonic plague should receive antibiotic prophylaxis with doxycycline or ciprofloxacin for 7 days. Prevention of human-to-human transmission via patients with plague pneumonia can be achieved by implementing standard isolation procedures until at least 4 days of antibiotic treatment have been administered. For the other clinical types of the disease, patients should be isolated for the first 48 hours after the initiation of treatment.
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PMID:Bichat guidelines for the clinical management of plague and bioterrorism-related plague. 1567 47

In the United States, there is currently a major gap in the diagnostic capabilities with regard to plague. To address this, we developed an antigen capture assay using an essential virulence factor secreted by Yersinia spp., LcrV, as the target antigen. We generated anti-LcrV monoclonal antibodies (MAbs) and screened them for the ability to bind bacterially secreted native Yersinia pestis LcrV. Anti-LcrV MAb 19.31 was used as a capture antibody, and biotinylated MAb 40.1 was used for detection. The detection limit of this highly sensitive Yersinia LcrV capture enzyme-linked immunosorbent assay is 0.1 ng/ml. The assay detected LcrV from human sputum and blood samples treated with concentrations as low as 0.5 ng/ml of bacterially secreted native Y. pestis LcrV. This assay could be used as a tool to help confirm the diagnosis of plague in patients presenting with pneumonia.
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PMID:LcrV capture enzyme-linked immunosorbent assay for detection of Yersinia pestis from human samples. 1569 31

The authors report a rare case of Yersinia enterocolitica O:3 pneumonia in an immunocompetent 70-year old man. There was no evidence of acute gastrointestinal disease. Diagnosis was confirmed by blood cultures. He responded with resolution of the infection after 21 days of therapy with a third-generation cephalosporin then by cotrimoxazole. Only 15 cases have been reported so far. Most of the patients were immunocompromised. This is the first case in France.
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PMID:[Bacteremia and pneumonia due to Yersinia enterocolitica serotype O:3 in an immunocompetent patient]. 1598 46

A study was undertaken to indicate the importance of different causes of death in goats and to investigate the management factors which influence these problems. Over a 15 month period, 324 dead goats were received from 67 farms in the Horowhenua, Wairarapa, Wanganui and Wellington regions. Although a wide range of diseases was encountered in the study, the major causes of mortality could be divided into 4 groups: problems directly related to management, microbial diseases, nematode parasitism, and trace element related deficiencies and toxicities. The highest proportion of deaths related directly to management problems and included deaths from hypothermia, mismothering, premature birth, ruminal acidosis, pregnancy toxaemia, trauma, and plant and chemical toxicities. In larger flocks, microbial diseases including Pasteurella pneumonia and yersiniosis were major problems. Deaths from nematode parasitism were predominantly observed in goats 12 months of age and older. White muscle disease (selenium/vitamin E deficiency) was the major trace element deficiency causing death in goats. The influence of factors including age of goat, flock size and management practices on the major causes of death are discussed.
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PMID:A goat mortality study in the southern North Island. 1603 83

Mice were vaccinated with a recombinant fusion protein, rF1-V, by an intramuscular prime followed by an intranasal boost, to evaluate protection against pneumonic plague. Forty-two days after the intranasal boost, the mice were challenged by aerosol exposure to Yersinia pestis. Survival after exposure depended upon the dose of rF1-V given i.n. with > or = 80% survival in the highest dose groups. Pulmonary and serum antibody titers to V were the best predictors of outcome. For vaccinated mice that succumbed to the infection, death was delayed by 1-2 days compared to sham-inoculated controls. Weight loss early after exposure correlated with outcome. Pathology studies indicated a severe, necrotizing bronchopneumonia in vaccinated mice that succumbed to the infection, compatible with a prolonged disease course, while the lungs of sham-inoculated mice had only mild pneumonia, which is compatible with a more rapid disease course. Immunity in the respiratory tract appears to be critical for protection against primary pneumonia caused by Y. pestis.
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PMID:Respiratory immunity is an important component of protection elicited by subunit vaccination against pneumonic plague. 1637 37

A localized outbreak of bubonic plague occurred in village Dangud (population 332), district Uttar Kashi, Uttaranchal, India in the second week of October 2004. 8 cases were considered outbreak associated based on their clinical and epidemiological characteristics; 3 (27.3%) of them died within 48 hours of developing illness. All the 3 fatal cases and five surviving cases had enlargement of inguinal lymph nodes. None of them had pneumonia. The age of the cases ranged from 23-70 years and both sexes were affected. No such illness was reported from adjoining villages. The outbreak was fully contained within two weeks of its onset by supervised comprehensive chemoprophylaxis using tetracycline. A total of approximately 1250 persons were given chemoprophylaxis in three villages. There was no clear history of rat fall in the village. No flea was found on rodents or animals. 16 animal serum samples were found to be negative for antibodies against F-1 antigen of Y. pestis. However, Y. pestis was isolated from two rodents (Rattus rattus and Mus musculus) trapped in the village. One case and three animal sera showed borderline sero-positivity against rickettsial infection. The diagnosis of plague was confirmed by detection of four fold rise of antibody titre against F-1 antigen of Yersinia pestis in paired sera of three cases (one of the WHO approved criteria of diagnosis of confirmed plague). This outbreak and the occurrence of earlier outbreaks of plague in Surat (Gujarat) and Beed (Maharashtra) in 1994 and in district Shimla (Himachal Pradesh) in 2002 confirm that plague infection continue to exist in sylvatic foci in many parts of India which is transmitted to humans occasionally. Thus, there is a strong need for the States to monitor the plague activity in known sylvatic foci regularly and have a system of surveillance to facilitate prompt diagnosis and treatment of cases to control the disease. This investigation highlights that with high index of suspicion the disease can be diagnosed early and mounting of supervised comprehensive response can prevent the disease to proceed to pneumonic stage where man to man transmission gets established and outbreak assumes larger dimensions.
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PMID:Quick control of bubonic plague outbreak in Uttar Kashi, India. 1650 45

Plague is a zoonotic disease caused by the bacterium Yersinia pestis. In 2006, a total of 13 human plague cases have been reported among residents of four states: New Mexico (seven cases), Colorado (three cases), California (two cases), and Texas (one case). This is the largest number of cases reported in a single year in the United States since 1994. Dates of illness onset ranged from February 16 to August 14; two (15%) cases were fatal. The median age of patients was 43 years (range: 13-79 years); eight (62%) patients were female. Five (38%) patients had primary septicemic plague, and the remaining eight (62%) had bubonic plague. Two (15%) patients developed secondary plague pneumonia, leading to administration of antibiotic prophylaxis to their health-care providers. This report summarizes six of the 13 cases, highlighting the severity and diverse clinical presentations of plague and underscoring the need for prompt diagnosis and treatment when plague is suspected.
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PMID:Human plague--four states, 2006. 1694 64

Yersinia pseudotuberculosis infects many mammals and birds including humans, livestock, and wild rodents and can be recovered from the lungs of infected animals. To determine the Y. pseudotuberculosis factors important for growth during lung infection, we developed an intranasal model of infection in mice. Following intranasal inoculation, we monitored both bacterial growth in lungs and dissemination to systemic tissues. Intranasal inoculation with as few as 18 CFU of Y. pseudotuberculosis caused a lethal lung infection in some mice. Over the course of 7 days, wild-type Y. pseudotuberculosis replicated to nearly 1 x 10(8) CFU/g of lung in BALB/c mice, induced histopathology in lungs consistent with pneumonia, but disseminated sporadically to other tissues. In contrast, a Delta yopB deletion strain was attenuated in this model, indicating that translocation of Yersinia outer proteins (Yops) is essential for virulence. Additionally, a Delta yopH null mutant failed to grow to wild-type levels by 4 days postintranasal inoculation, but deletions of any other single effector YOP did not attenuate lung colonization 4 days postinfection. Strains with deletions in yopH and any one of the other known effector yop genes were more attenuated that the Delta yopH strain, indicating a unique role for yopH in lungs. In summary, we have characterized the progression of a lung infection with an enteric Yersinia pathogen and shown that YopB and YopH are important in lung colonization and dissemination. Furthermore, this lung infection model with Y. pseudotuberculosis can be used to test potential therapeutics against Yersinia and other gram-negative infections in lungs.
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PMID:Intranasal inoculation of mice with Yersinia pseudotuberculosis causes a lethal lung infection that is dependent on Yersinia outer proteins and PhoP. 1707 49

Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses the innate immune response to infection. Therefore, the early host response during the course of primary pneumonic plague was investigated in two mouse strains, the outbred strain CD1 and the inbred strain C57BL/6. A comparative analysis of the course of disease in these two strains of mice indicated that they are susceptible to intranasal Y. pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect to colonization of the lung, liver, and spleen. Significantly, in both strains of mice, robust neutrophil recruitment to the lungs was not observed until 48 h after infection, suggesting that there was a delay in inflammatory cell recruitment to the site of infection. In addition, proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha, gamma interferon, IL-12p70, monocyte chemoattractant protein 1) and chemokines (KC, MIP-2) in the bronchoalveolar lavage fluids were not readily detected until 48 h after infection, which coincided with the increase in polymorphonuclear leukocyte (PMN) recruitment to the lungs. In comparison, CD1 mice with gram-negative pneumonia caused by Klebsiella pneumoniae exhibited strong inflammatory responses early in infection, with PMNs comprising the majority of the cells in the bronchoalveolar lavage fluid 24 h postinfection, indicating that PMN recruitment to the lungs could occur earlier in this infection than in Y. pestis infection. Together, our results indicate that there is a delay in the recruitment of neutrophils to the lungs in the mouse model of primary plague pneumonia that correlates with delayed expression of proinflammatory cytokines and chemokines in both outbred and inbred mice.
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PMID:Delayed inflammatory response to primary pneumonic plague occurs in both outbred and inbred mice. 1710 42

Primary pneumonic plague is transmitted easily, progresses rapidly, and causes high mortality, but the mechanisms by which Yersinia pestis overwhelms the lungs are largely unknown. We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective.
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PMID:A plasminogen-activating protease specifically controls the development of primary pneumonic plague. 1725 10


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