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

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

As part of a species recovery program, 129 Canada lynx (Lynx canadensis) originating from British Columbia, the Yukon, Manitoba, and Quebec, Canada, and Alaska, USA, were reintroduced to southwestern Colorado, USA, from 1999 to 2003. Of 52 lynx mortalities documented by October 2003, six lynx, including a female and her 5-mo-old kitten, had evidence of Yersinia pestis infection as determined by fluorescent antibody test and/or culture. Postmortem findings in these lynx were characterized by pneumonia, ranging from acute suppurative pneumonia, to multifocal necrotizing pneumonia, to fibrinous bronchopneumonia. Histopathologic examination of lung revealed multiple areas of inflammation and consolidation, areas of edema and hemorrhage, and bacteria surrounded by extensive inflammation. Spleens had severe lymphoid depletion and hypocellular red pulp. Lymphadenomegaly was observed in only one plague-affected lynx. We hypothesize that these Canada lynx were exposed to Y. pestis by infected prey, and these are the first reports of plague in this species.
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PMID:Plague as a mortality factor in Canada lynx (Lynx canadensis) reintroduced to Colorado. 1709 96

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

Febrile respiratory illnesses with respiratory failure are one of the most common reasons for admission to the intensive care unit. Most causes of febrile respiratory illness are bacterial and viral agents of community-acquired pneumonia. However, a small number of rare and highly contagious agents can initially present as febrile respiratory illnesses, which can lead to an epidemic that can greatly impact the health care system. This impact includes sustained mass critical care, with potential scarcity of critical resources (eg, positive-pressure ventilators), spread of disease to health care workers, sustained spread within the community, and extensive morbidity and mortality. The main agents of febrile respiratory illness that would lead to an epidemic include influenza, the coronavirus that causes severe acute respiratory syndrome, smallpox, viral hemorrhagic fever, plague, tularemia, and anthrax. Recognition of these agents occurs largely based on epidemiological clues, and management consists of antibiotics, antivirals, supportive care, and positive-pressure ventilation. Acute respiratory failure and acute respiratory distress syndrome occur with these agents, so a lung-protective (low tidal volume) ventilation strategy is indicated. Additional respiratory care measures, such as nebulized medications, bronchoscopy, humidified oxygen, and airway suctioning, potentiate aerosolization of the virus or bacteria and increase the risk of transmission to health care workers and patients. Thus, appropriate personal protective equipment, including an N95 mask or powered air-purifying respirator, is indicated. A basic understanding of the epidemiology, clinical findings, diagnosis, and treatment of these agents will provide a foundation for early isolation, evaluation, infection control, and public health involvement and response in cases of a febrile respiratory illness that causes respiratory failure.
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PMID:Severe febrile respiratory illnesses as a cause of mass critical care. 1817 59

The action of mustard gas on six animal, one plant, and two bacterial viruses; also on bacteria, yeast, and the pneumococcus-transforming principle has been studied. The viruses include Newcastle's disease of chickens, equine encephalomyelitis (Eastern strain), feline pneumonitis (Baker), rabbit papilloma (Shope), fixed rabies, rabbit myxoma, tobacco mosaic, T(2)r(+) phage of E. coli B, and a Staphylococcus muscae phage. The cells include bakers' yeast, E. coli B, Staphylococcus muscae, and swine plague bacillus. The rates of inactivation of the viruses and cells were of the same order of magnitude and faster than those of enzymes. Of the viruses examined those containing desoxyribose nucleic acid were inactivated faster than those containing ribosenucleic acid. Preparations of the pneumococcus-transforming principle which were largely desoxyribose nucleic acid have shown the greatest sensitivity to mustard gas of all systems examined. An expression was derived describing the inactivation rate when mustard gas decreases during the experiment.
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PMID:Inactivation of viruses and cells by mustard gas. 1889 Nov 48

The Brown Norway rat was recently described as a bubonic plague model that closely mimics human disease. We therefore evaluated the Brown Norway rat as an alternative small animal model for pneumonic plague and characterized both the efficacy and potency of vaccine candidates. When infected by intranasal instillation, these rats rapidly developed fatal pneumonic plague within 2 to 4 days of infection. Plague disease was characterized by severe alveolar edema and vascular hemorrhage in the lung in addition to fulminant necrotizing pneumonia caused by massive bacterial replication and inflammation. Twenty-four hours before death, animals developed systemic disease with an apparent delayed inflammatory response. We evaluated the ability of the protective antigen, LcrV, and a mutant derivative, V10, to protect these rats from pneumonic plague. Both were highly effective vaccines because complete protection was observed at challenge doses of 7500 LD(50). Antibody analyses suggested stronger potency of V10 immune sera compared with LcrV in the passive transfer of immunity to bubonic plague, with multiple neutralizing epitopes in LcrV. Taken together, these data demonstrate the effectiveness of inhibiting type III secretion in the prevention of pneumonic plague in rats and reveal critical contributions from both the cellular and humoral immune systems. Thus, the Brown Norway rat is an appealing alternative small animal model for the study of pneumonic plague pathogenesis and immunity.
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PMID:Pneumonic plague pathogenesis and immunity in Brown Norway rats. 1916 5

Presently there is a significant effort to develop and evaluate vaccines and antibiotics against the potential bioterrorism agent Yersinia pestis. The animal models used to test these countermeasures involve the deposition of small particles within the lung. However, deliberate aerosol release of Y. pestis will generate both small and large inhalable particles. We report in this study that the pathogenesis patterns of plague infections caused by the deposition of 1- and 12-microm-particle aerosols of Y. pestis in the lower and upper respiratory tracts (URTs) of mice are different. The median lethal dose for 12-mum particles was 4.9-fold greater than that for 1-microm particles. The 12-microm-particle infection resulted in the degradation of the nasal mucosa and nasal-associated lymphoid tissue (NALT) plus cervical lymphadenopathy prior to bacteremic dissemination. Lung involvement was limited to secondary pneumonia. In contrast, the 1-microm-particle infection resulted in primary pneumonia; in 40% of mice, the involvement of NALT and cervical lymphadenopathy were observed, indicating entry via both URT lymphoid tissues and lungs. Despite bacterial deposition in the gastrointestinal tract, the involvement of Peyer's patches was not observed in either infection. Although there were major differences in pathogenesis, the recombinant F1 and V antigen vaccine and ciprofloxacin protected against plague infections caused by small- and large-particle aerosols.
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PMID:Different pathologies but equal levels of responsiveness to the recombinant F1 and V antigen vaccine and ciprofloxacin in a murine model of plague caused by small- and large-particle aerosols. 1918 59

Yersinia pestis causes pneumonic plague, a necrotic pneumonia that rapidly progresses to death without early treatment. Antibodies to the protective antigen LcrV are thought to neutralize its essential function in the type III secretion system (TTSS) and by themselves are capable of inducing immunity to plague in mouse models. To develop multivalent LcrV antibodies as a therapeutic treatment option, we screened for monoclonal antibodies (MAbs) to LcrV that could prevent its function in the TTSS. Although we were able to identify single and combination MAbs that provided the high-level inhibition of the TTSS, these did not promote phagocytosis in vitro and were only weakly protective in a mouse pneumonic plague model. Only one MAb, BA5, was able to protect mice from pneumonic plague. In vitro, MAb BA5 blocked the TTSS with efficiency equal to or even less than that of other MAbs as single agents or as combinations, but its activity led to increased phagocytic uptake. Polyclonal anti-LcrV was superior to BA5 in promoting phagocytosis and also was more efficient in protecting mice from pneumonic plague. Taken together, the data support a hypothesis whereby the pulmonary clearance of Y. pestis by antibodies requires both the neutralization of the TTSS and the simultaneous stimulation of innate signaling pathways used by phagocytic cells to destroy pathogens.
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PMID:Dual-function antibodies to Yersinia pestis LcrV required for pulmonary clearance of plague. 1982 67

In this paper we have attempted to describe the manner of spread of an endemic, native, respiratory infection and a method for its control. The essential factor determining the prevalence of such an endemic disease is, we believe, host susceptibility, which is controlled by hereditary and environmental influences. Furthermore, it seems probable that the amount of this population susceptibility determines the dosage of specific microbes available to the population. An increase in dosage in the herd is followed by an increase in the spread and severity of the infection, and a decrease by a corresponding alleviation. Hence, two methods for the prevention of epidemics are available: (1) an enhancement of population resistance, and (2) the reduction to a minimum of available dosage. These procedures have proved successful for 3 years in maintaining a population of breeding rabbits, in the midst of a badly infected community, entirely free from Bact. lepisepticum infection. Confirmation of the above conclusions has been gained from other studies in the field of experimental epidemiology. Dr. D. T. Smith (2), at Saranac, New York, found that changes in population susceptibility were responsible for a severe outbreak of Bact. lepisepticum infection and septicemia. Freund (3), at Berlin, has just published an interesting account of respiratory epidemics of rabbits and guinea pigs, apparently brought about by sudden changes in temperature and housing conditions. Pneumonia and Pasteurella infection, endemic in the population, increased suddenly in extent and severity. Nevertheless, neither endemic nor epidemic strains of the microorganisms were found to be especially virulent. Dr. Theobald Smith (4), in a study of paratyphoid epidemics of guinea pigs, has made similar observations. He noted that pregnant females acted as the foci of infection, and that from these individuals, presumably of lessened resistance, the bacteria were given off and infection was spread. The studies in experimental epidemiology are rapidly reaching a stage where they may be applied to the problems of human disease. Indeed, more recent observations of the mode of spread of pneumonia (5-7), scarlet fever (8), typhoid (9, 10), plague (11), diphtheria (12-14), measles (15), and tuberculosis (16-18) increasingly show a tendency to discard the theory of fluctuating microbic virulence and to emphasize the importance of the host factors.
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PMID:BACTERIUM LEPISEPTICUM INFECTION : ITS MODE OF SPREAD AND CONTROL. 1986 98

Vaccines against primary pneumonic plague, a potential bioweapon, must be tested for efficacy in well-characterized nonhuman primate models. Telemetered cynomolgus macaques (Macaca fascicularis) were challenged by the aerosol route with doses equivalent to approximately 100 50% effective doses of Yersinia pestis strain CO92 and necropsied at 24-h intervals postexposure (p.e.). Data for telemetered heart rates, respiratory rates, and increases in the temperature greater than the diurnal baseline values identified the onset of the systemic response at 55 to 60 h p.e. in all animals observed for at least 70 h p.e. Bacteremia was detected at 72 h p.e. by a Yersinia 16S rRNA-specific quantitative reverse transcription-PCR and was detected later by the culture method at the time of moribund necropsy. By 72 h p.e. multilobar pneumonia with diffuse septal inflammation consistent with early bacteremia was established, and all lung tissues had a high bacterial burden. The levels of cytokines or chemokines in serum were not significantly elevated at any time, and only the interleukin-1beta, CCL2, and CCL3 levels were elevated in lung tissue. Inhalational plague in the cynomolgus macaque inoculated by the aerosol route produces most clinical features of the human disease, and in addition the disease progression mimics the disease progression from the anti-inflammatory phase to the proinflammatory phase described for the murine model. Defined milestones of disease progression, particularly the onset of fever, tachypnea, and bacteremia, should be useful for evaluating the efficacy of candidate vaccines.
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PMID:Milestones in progression of primary pneumonic plague in cynomolgus macaques. 2038 51


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