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)

Q fever is a worldwide zoonosis with many acute and chronic manifestations caused by the pathogen Coxiella burnetii. Farm animals and pets are the main reservoirs of infection, and transmission to human beings is mainly accomplished through inhalation of contaminated aerosols. Persons at greatest risk are those in contact with farm animals and include farmers, abattoir workers, and veterinarians. The organs most commonly affected during Q fever are the heart, the arteries, the bones and the liver. The most common clinical presentation is an influenza-like illness with varying degrees of pneumonia and hepatitis. Although acute disease is usually self-limiting, people do occasionally die from this condition. Endocarditis is the most serious and most frequent clinical presentation of chronic Q fever. Vascular infection is the second most frequent presentation of Q fever. The diagnosis of Q fever is based on a significant increase in serum antibody titers. The treatment is effective and well tolerated, but must be adapted to the acute or chronic pattern with the tetracyclines to be considered the mainstay of antibiotic therapy. For the treatment of Q fever during pregnancy the use of long-term cotrimoxazole therapy is proposed.
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PMID:Emergence of q Fever. 2311 81

Inoculation with the neurotropic JHM strain of mouse hepatitis virus (MHV) into the central nervous system (CNS) of susceptible strains of mice results in an acute encephalomyelitis in which virus preferentially replicates within glial cells while excluding neurons. Control of viral replication during acute disease is mediated by infiltrating virus-specific T cells via cytokine secretion and cytolytic activity, however sterile immunity is not achieved and virus persists resulting in chronic neuroinflammation associated with demyelination. CXCR2 is a chemokine receptor that upon binding to specific ligands promotes host defense through recruitment of myeloid cells to the CNS as well as protecting oligodendroglia from cytokine-mediated death in response to MHV infection. These findings highlight growing evidence of the diverse and important role of CXCR2 in regulating neuroinflammatory diseases.
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PMID:The chemokine receptor CXCR2 and coronavirus-induced neurologic disease. 2321 21

The detrimental effects of West Nile virus (WNV) have been well characterized in several taxonomic groups of North American birds, such as corvids and raptors. Relatively less is known about the virus' effects in waterfowl species, many of which are abundant in North America and occupy habitats, for example wetlands and marshes, likely to harbour dense mosquito populations. In two successive years, outbreaks of WNV-associated disease were observed in waterfowl at a rehabilitation centre. In the present report, clinical and pathological findings are provided for seven mallards (Anas platyrhynchos) and one Canada goose (Branta canadensis) that developed acute disease and either died or were killed humanely. The most severe and consistent microscopic lesion in mallards was myocardial degeneration and coagulative necrosis consistent with acute heart failure. The Canada goose had necrotizing myocarditis. Other lesions included pulmonary perivascular oedema, lymphoplasmacytic hepatitis, and splenic and bursal lymphoid depletion. WNV infection was confirmed using reverse transcriptase-polymerase chain reaction and immunohistochemical staining. Myofibres within all cardiac muscle layers had positive immunohistochemical staining, as did blood vessel walls in the heart and spleen. These results suggest that juvenile mallards are highly susceptible to fatal WNV-associated cardiac failure, and confirm that adult Canada geese are susceptible to fatal WNV-associated disease. The synchronous timing of clinical disease and death in these waterfowl are consistent with WNV mosquito-borne infections within a WNV transmission focus during the summer (July and August) of 2012 and 2013.
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PMID:Outbreaks of West Nile virus in captive waterfowl in Ontario, Canada. 2563 41

Q fever, caused by Coxiella burnetii, can present as an outbreak of acute disease ranging from asymptomatic disease, pneumonia, hepatitis or fever of unknown origin, which can progress to a chronic disease, most frequently endocarditis. The occurrence of Q fever within families is rarely described, and in most cases presents with uniform acute disease manifestations. Here we present a familial cluster of Q fever presenting as highly variable synchronous manifestations in four of five family members, including prolonged fever of unknown origin, asymptomatic carrier state, hepatitis, and chronic endocarditis developing in the absence of previous symptoms. This case series highlights the possibility of Q fever developing in cohabitated individuals with highly variable symptoms masking the common disease etiology. Screening of all exposed individuals, even those not clinically suspected to be infected, may enable to better identify, treat and prevent progression to chronic disease.
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PMID:Familial Q fever clustering with variable manifestations imitating infectious and autoimmune disease. 2577 Jul 47

Q fever is a worldwide distributed zoonotic disease with a mostly benign course, which regularly reoccurs in Germany. This report is about a patient with sporadic serologically proven Q fever, which also showed typical histopathological findings with nonspecific granulomatous hepatitis, usually seen in acute disease. The bone marrow biopsy revealed so-called doughnut granulomas, which are not pathognomonic but a typical finding in Q fever. This case report impressively underlines that the histomorphological findings can make a decisive contribution to the clarification by extended differential diagnostics, even though it plays a subordinate role in the routine diagnostics of disseminated Q fever.
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PMID:[Q fever : A rare differential diagnosis of granulomatous disease]. 2691 49

Inclusion body hepatitis is an acute disease of chickens ascribed to viruses of the genus Aviadenovirus and referred to as fowl adenovirus (FAdV). There are 12 FAdV types (FAdV1to FAdV8a and FAdV8b to FAdV11), classified into five species based on their genotype (designated FAdVA to FAdVE). A total of 218 000 chickens, 2-29 days of age, were affected over a 1-year period, all testing positive by microscopy, virus isolation and confirmation with polymerase chain reaction (PCR). Affected birds were depressed, lost body weight,were weak and had watery droppings. Pathological changes observed during necropsy indicated consistent changes in the liver, characterised by hepatomegaly, cholestasis and hepatitis. Lesions were also discernible in the spleen, kidney and gizzard wall and were characterised by splenomegaly, pinpoint haemorrhages, nephritis with haemorrhage,visceral gout and serosal ecchymosis of the gizzard wall. Histopathological lesions were most consistently observed in the liver but could also be seen in renal and splenic tissue. Virus isolation was achieved in embryonated eggs and most embryos revealed multifocalto diffuse hepatic necrosis, with a mixed cellular infiltrate of macrophages and heterophils(necro-granulomas), even in the absence of macroscopic pathology. Virus isolation results were verified by histopathology and PCR on embryonic material and further characterised by nucleotide sequence analysis. Two infectious bursal disease virus isolates were also made from the Klerksdorp flock. Nucleotide sequence analysis of the L1 hexon loop of all the FAdV isolates indicated homology (99%) with prototype strains P7-A for FAdV-2, as well as for FAdV-8b.
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PMID:Inclusion body hepatitis associated with an outbreak of fowl adenovirus type 2 and type 8b in broiler flocks in South Africa. 2747 9

Q fever is a zoonosis caused by the intracellular bacterium Coxiella burnetii. While it is mostly an asymptomatic infection, acute disease can manifest as fever associated with signs of pneumonia or hepatitis. Chronic Q fever develops in 1-5% of infected persons. Patients with a history of cardiac valve surgery, vascular prosthesis or vascular aneurysm, and to a lesser extent patients with pre-existing valvular disease, immune deficiencies, or renal insufficiency, are at highest risk. Most common manifestations are Q fever endocarditis and Q fever vascular infection. We present a case of chronic Q fever, followed by a summary of available literature.
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PMID:A case of recurrent fever in an older man caused by Coxiella burnetii. 2749 24

Q fever is a worldwide zoonotic infection caused by the obligate intracellular bacterium Coxiella burnetii that can course with acute or chronic disease. This series describes 7 cases of acute Q fever admitted in a Portuguese University Hospital between 2014 and 2015. All cases presented with hepatitis and had epidemiological history. Diagnosis was done by PCR on majority (5) and by serology and PCR in only 2. Serological tests can be negative in the initial period of the disease. Molecular biology methods by polymerase chain-reaction are extremely important in acute disease, allowing timely diagnosis and treatment.
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PMID:Presentation and diagnosis of acute Q fever in Portugal - A case series. 2807 Apr 91

Sequence-based typing of Francisella tularensis has led to insights in the evolutionary developments of tularemia. In Europe, two major basal clades of F. tularensis subsp. holarctica exist, with a distinct geographical distribution. Basal clade B.6 is primarily found in Western Europe, while basal clade B.12 occurs predominantly in the central and eastern parts of Europe. There are indications that tularemia is geographically expanding and that strains from the two clades might differ in pathogenicity, with basal clade B.6 strains being potentially more virulent than basal clade B.12. This study provides information on genotypes detected in the Netherlands during 2011-2017. Data are presented for seven autochthonous human cases and for 29 European brown hares (Lepus europaeus) with laboratory confirmed tularemia. Associated disease patterns are described for 25 European brown hares which underwent post-mortem examination. The basal clades B.6 and B.12 are present both in humans and in European brown hares in the Netherlands, with a patchy geographical distribution. For both genotypes the main pathological findings in hares associated with tularemia were severe (sub)acute necrotizing hepatitis and splenitis as well as necrotizing lesions and hemorrhages in several other organs. Pneumonia was significantly more common in the B.6 than in the B.12 cases. In conclusion, the two major basal clades present in different parts in Europe are both present in the Netherlands. In hares found dead, both genotypes were associated with severe acute disease affecting multiple organs. Hepatitis and splenitis were common pathological findings in hares infected with either genotype, but pneumonia occurred significantly more frequently in hares infected with the B.6 genotype compared to hares infected with the B.12 genotype.
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PMID:Phylogeographic Distribution of Human and Hare Francisella Tularensis Subsp. Holarctica Strains in the Netherlands and Its Pathology in European Brown Hares (Lepus Europaeus). 3080 12


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