Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Francis William Reitz, the second last President of the Republic of the Orange Free State, resigned his office on 16 November 1895 for health reasons. He died 39 years later at the age of 89. An analysis of this health history shows his resignation to have been caused by a symptom complex quite characteristic of endogenous depression, probably precipitated by virus hepatitis, During 1896 he recovered fully, but in 1903, as an embittered man at the end of the Anglo-Boer War, he experienced a severe recurrence of depression which lasted 18 months, despite the best therapy available in Europe at the time.
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PMID:[President F.W. Reitz and his health problem]. 36 80

Pathogenesis of tularemia in nonimmune rats given (intraperitoneal inoculation) virulent strain (SCHU S4) or vaccinal strain (LVS) of Francisella tularensis and in immune rats given SCHU S4 is described. Both LVS and SCHU S4 caused pyogranulomas in liver and spleen of nonimmune rats. Nonimmune rats given 10(4) SCHU S4 organisms did not survive beyond 72 hours, but immune rats given challenge inoculum of 10(8) SCHU S4 organisms developed lesions and survived. Larger doses of LVS resulted in earlier onset of characteristic hepatitis and splenitis in nonimmune rats. Periportal lymphocytic infiltrates were present in the liver 48 hours after SCHU S4 challenge inoculation of immune rats and 96 hours after inoculation of LVS in nonimmune rats and were associated with intense macrophage aggregation. These changes indicate that the pathogenesis of tularemia is a result of the interdependency of the dose and virulence of the causative agent with the immune status of the host and that cellular immunity has a significant role in the response of the rat to tularemia.
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PMID:Pathogenesis of tularemia in immune and nonimmune rats. 119 May 92

Drawing upon our experience with 88 cases and a survey of the English literature, we reviewed the clinical, pathophysiological, and epidemiological aspects of tularemia. Tularemia can be thought of as two syndromes--ulceroglandular and typhoidal. This dichotomy simplifies earlier nomenclature and emphasizes the obscure typhoidal presentation. Clinical manifestations suggest that the two syndromes reflect differences in host response. In ulceroglandular tularemia the pathogen appears to be well contained by a vigorous inflammatory reaction. Pneumonia is less common and the patient's prognosis is good. In typhoidal disease there are few localizing signs; pneumonia is more common; and the mortality without therapy is much higher, suggesting that the host response is somehow deficient. Francisella tularensis is an extremely virulent pathogen capable of initiating infection with as few as 10 organisms inoculated subcutaneously. During an incubation period of 3 to 6 days the host responds first with polymorphonuclear leukocytes and then macrophages. Granulocytes are unable to kill the pathogen without opsonizing antibody leaving cellular immunity to play the major role in host defense. One to 2 weeks after infection, a vigorous T-lymphocyte response can be detected in vitro with lymphocyte blast transformation assays and in vivo with an intradermal skin test, which, unfortunately, is not commercially available. Humoral immunity, often used as a diagnostic modality, appears 2 to 3 weeks into the illness. Cellular immunity is long-lasting, accounting for the common reoccurrence of localized disease upon repeated exposures to the pathogen. There are no symptoms that distinguish the ulceroglandular from the typhoidal syndrome. A pulse-temperature dissociation is seen in less than half of the patients. The location of ulcers and enlarged lymph nodes give a clue to the likely vector since lesions located on the upper extremities are more commonly associated with mammalian, and those of the head and neck and lower extremities with arthropod, vectors. Pharyngitis, pericarditis, and pneumonia can complicate both syndromes, although the latter is much more common in typhoidal disease. Hepatitis, usually of a mild degree, is common and occasionally erythema nodosum is seen. No specific laboratory tests characterize tularemia, and cultures of the pathogen are often difficult to obtain because of the special growth requirements of Francisella tularesis and the inability of many clinical laboratories to handle the dangerous pathogen.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tularemia: a 30-year experience with 88 cases. 389 22

Immunological studies were performed on Ugandan patients with hepatocellular carcinoma to test the hypothesis that the high rate of persistence of hepatitis-associated antigen in these patients is the result of defects in host immune response. The responses to 1-chloro-2,4-dinitrobenzene sensitization and to a battery of recall skin test antigens were normal, as was the humoral antibody response to tularaemia antigen. Neither hypogammaglobulinaemia nor specific immunoglobulin deficiencies were found. Thus it appears unlikely that generalized defects in host immune responses can account for the high incidence of persistent hepatitis B virus infection found in Ugandan patients with hepatocellular carcinoma.
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PMID:Immunological studies in Ugandan patients with hepatocellular carcinoma. 434 3

We report a case of tularemia in a common marmoset (Callithrix jacchus) diagnosed by determination of the isolate's 16S ribosomal RNA (rRNA) gene sequence. Pathological examination of the animal revealed a multifocal acute necrotizing hepatitis, interstitial nephritis, splenitis, and lymphangitis of the mandibular, retropharyngeal, and cervical and mesenteric lymph nodes. Moreover, multiple foci of acute necrosis were found in the epithelium of the jejunum and the interstitium of the lung. Bacteriological investigations revealed a septicemia. The isolated infectious agent was uncommon, not routinely diagnosed in our laboratory and therefore difficult to identify by conventional tools in a reasonable time and effort. thus, we decided to perform a genetic analysis based on the 16S rRNA gene sequence. Thereby, an infection with Francisella tularensis, the causative agent of tularemia, was unambiguously diagnosed. This shows the great advantage 16S rRNA gene sequencing has as a general identification approach for unusual or rare isolates.
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PMID:Tularemia in a common marmoset (Callithrix jacchus) diagnosed by 16S rRNA sequencing. 964 73

The Republic of Serbia, with WHO support, has implemented an early warning system (ALERT) for priority communicable diseases, to complement the routine surveillance system which notifies individual confirmed cases. The results of its evaluation, conducted one year after implementation is presented here. ALERT relies on notification of 11 syndromes by primary care facilities. Data is analysed weekly at district level and transmitted to national epidemiologists. ALERT is perceived to be a simple and flexible tool. Acceptability is higher at national level than at district level. Some districts perceive ALERT as a parallel system poorly connected to control measures. Sensitivity of ALERT in detecting cases of meningitis is 93%, and 37% for cases of hepatitis. Retrospective analysis of ALERT data identified 9 outbreaks, 5 of which had been recognized by epidemiologists. ALERT was the timeliest system for detecting 4 outbreaks identified by both systems. ALERT was useful for triggering timely investigation and control of outbreaks of hantavirus and salmonellosis and for detecting the start of the influenza season. However, ALERT did not detect clusters of brucellosis and tularaemia targeted by the unexplained fever syndrome. This evaluation underlined the need for a global review of surveillance activities when implementing new components such as ALERT. While control measures based on notification of individual confirmed cases are well understood and implemented, the investigation and verification process that should result from an increase in ALERT syndromes is not fully understood. Field epidemiology training programmes, such as the EPIET programme, are best suited to bring about this change of perspective.
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PMID:Strengthening early warning function of surveillance in the Republic of Serbia: lessons learned after a year of implementation. 1520 69

A cougar (Felis concolor) was diagnosed with hepatic yersiniosis by bacterial culture and histopathology. The animal had a 2-week history of anorexia and jaundice before its death. Grossly, the liver exhibited caseo-necrotic foci. Histopathologically, there was necrotizing and suppurative hepatitis, with large numbers of intralesional gram-negative coccobacilli. Additional hepatic lesions included central vein thrombosis, lymphoplasmacytic portal hepatitis, and capsulitis. Yersinia pseudotuberculosis coccobacilli were isolated in pure culture from the hepatic lesions. Because the hepatic lesions in this animal resemble those of other zoonotic diseases, such as plague and tularemia, veterinarians and laboratory personnel who handle samples should take adequate safety precautions. This report is the first to describe the pathology associated with hepatic yersiniosis in a cougar.
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PMID:Hepatic yersiniosis in a cougar (Felis concolor). 1703 28

Tularemia is a highly contagious infectious zoonosis, transmissible by inoculation, ingestion, or inhalation of the infectious agent Francisella tularensis. The disease is perpetuated by infected rodents, blood-sucking arthropods, and by contaminated water. Therefore, nonhuman primates housed outdoors may be at risk for exposure. An epizootic of F. tularensis occurred in an indoor/outdoor-housed group of cynomolgus monkeys (Macaca fascicularis) at the German Primate Center. Tularemia was diagnosed in 18 out of 35 animals within a period of 2 years. Six animals died with unspecific clinical symptoms; 12 animals developed seroconversion and were still alive. Pathologic findings were similar in all monkeys that died and resembled the clinical picture of the human disease, including an ulceroglandular syndrome with local lymphadenopathy, gingivostomatitis, and systemic spread, with manifestations such as subacute necrotizing hepatitis, granulomatous splenitis, and pneumonia. Tularemia was diagnosed by culture, real-time polymerase chain reaction, and ELISA techniques. This is the largest outbreak in nonhuman primates and the first report of tularemia in cynomolgus monkeys. An overview of the recent literature about tularemia in nonhuman primates is given.
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PMID:Epizootic of tularemia in an outdoor housed group of cynomolgus monkeys (Macaca fascicularis). 1749 Oct 74

Susceptibility and lethality studies of inhalational tularaemia were undertaken using the common marmoset (Callithrix jacchus) to determine its suitability as a non-human primate model. Pairs of marmosets were exposed to varying challenge doses of Francisella tularensis by the airborne route and monitored for up to 14 days postchallenge (p.c.). Lethal infection was achieved following a retained dose of less than 10 bacterial colony-forming units (CFU). However, precise LD(50) determination was not possible. The model was characterized using a target challenge dose of approximately 100 CFU. Increased core body temperature was the first indicator of disease, at approximately 2.5 days p.c. Overt clinical signs were first observed 12-18 h after the temperature increase. Significantly decreased activity was observed after approximately 3 days. All animals succumbed to infection between 4.5 and 7 days p.c. At postmortem examination, gross pathology was evident in the liver, spleen and lungs of all animals and high bacterial numbers were detected in all the organs assessed. Bacteraemia was demonstrated in all animals postmortem. Histopathological observations included severe suppurative bronchopneumonia, severe multifocal pyogranulomatous hepatitis, splenitis and lymphadenitis. Tularaemia disease progression in the common marmoset therefore appears to be consistent with the disease seen in humans and other animal models. The common marmoset may therefore be considered a suitable model for further studies of inhalational tularaemia.
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PMID:Establishment of lethal inhalational infection with Francisella tularensis (tularaemia) in the common marmoset (Callithrix jacchus). 1933 49

Tularemia is a severe disease caused by Francisella tularensis This bacterium has a major pathogenic potential in countless animal species as well as in humans. Despite the relatively significant body of literature available on this microorganism, many questions are still open concerning its biological cycle in the environment, the pathology and pathogenesis of the disease, the possible routes of infection in animals, and the pathologic and ecological relevance of the distinct phylogenetic clusters of F. tularensis In order to address these questions, we have thoroughly characterized the pathology and microbiology of terminally ill European brown hares (Lepus europaeus) infected with F. tularensis subsp. holarctica, collected in Switzerland from 2012 to 2014. F tularensis isolates were typed by defining their phylogenetic clusters. We showed that the pathology associated with F. tularensis subsp. holarctica belonging to the clade B.FTNF002-00 is different from that previously reported to be associated with the clade B.13. In particular, strains of the clade B.FTNF002-00 were almost invariably associated with splenitis and hepatitis and not with the polyserositis affecting pleura, pericardium, and kidney reported in the literature for infections caused by the clade B.13. We describe findings suggesting that the ports of entry for the bacteria might be the respiratory and digestive routes.
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PMID:Francisella Tularensis Clades B.FTN002-00 and B.13 Are Associated With Distinct Pathology in the European Brown Hare (Lepus europaeus). 2693 97


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