Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diplococcous infection was observed in 15 calves aged 3 to 30 days. Diplococcous pneumoniae was isolated from synovial fluid and parenchymal organs in affected joints of dead calves. Clinically and morphologically the disease had an active course in calves aged up to 20 days, while in the older ones a subacute or chronic course of the disease was observed. The morphological changes depended on the type of infection. In acute infections a septic course of the disease, including hemorrhagic diathesis, enlarged spleen, myocarditis, hyperaemia, oedema and isolated hemorrhages of the brain meninges was observed, while in the chronic cases pneumonia, pleutisy, pericarditis, arthritis of the knee, elbow, dorsal and carpal joints and ofien suppurative meningoencephalitis were encountered.
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PMID:[Morphological changes in diplococcosis in calves]. 54 5

33 children (22 girls) with brucellosis seen between 1972-1988 were studied retrospectively. All but 1 were Bedouins. The mean age at diagnosis was 9.8 years (range: 17 months-17 years). Duration of illness prior to diagnosis was less than 1 week in 13 (39%), 1-4 weeks in 8 (24%) and 1-3 months in 10 (30%). In 2 cases the symptoms lasted 6 and 8 months, respectively, before diagnosis. Presenting symptoms included fever (85%), articular involvement (65%), hepatomegaly (45%) and splenomegaly (33%). Less common manifestations were anorexia (30%) and weight loss (15%) cases. Meningoencephalitis developed in 2 patients and uveitis and glomerulonephritis in 1 each. Diagnosis was based on positive agglutination titers (greater than 160), which were found in all. Brucella melitensis was isolated in blood cultures in 8 of the 33. 18 were treated with tetracycline and 9 with tetracycline and streptomycin, all of whom responded well. 3 of the 6 treated with trimethoprimsulphamethoxazole were only cured when therapy was changed to tetracycline in 2 and tetracycline plus streptomycin in 1. All patients recovered without sequelae. We conclude that brucellosis due to Brucella melitensis is endemic among the Bedouin of the Negev. An increased incidence of brucellosis among hospitalized children has been noted in the past 2 years, indicating the need for diagnostic awareness.
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PMID:[Childhood brucellosis in the Negev]. 228 18

A 44-year-old man had several episodes of tingling sensation in his lower extremities, head and face over 1 year and presented mental disturbance 2 months prior to admission. He additionally suffered from dysuria and acute onset of gait disturbance 18 days before admission. Physical and neurological examination revealed marked splenomegaly, stupor, abnormal behavior, spastic tetraparesis and sphincter disturbances, and meningoencephalitis was suspected. There was lymphocytosis in peripheral blood, some of which showed atypical morphology. CSF examination revealed increased protein content and mononuclear pleocytosis. The titers of antibodies against E-B virus were elevated as follows; VCA IgM (X320), VCA IgG (X20,480), EA (X10,240) and EBNA (X10) in serum, and VCA IgM (X4), VCA IgG (X160), EA (X40) and EBNA (less than 1) in CSF. CT and MRI examination revealed ring enhanced lesion adjacent to left lateral ventricle with surrounding diffuse edema. Administration of intravenous glycerol and oral prednisolone induced substantial improvement in sensory, mental and sphincter disturbances and brain CT findings but not in splenomegaly and pyramidal tract signs. Antibody titer against VCA IgM also decreased. After withdrawal of prednisolone, CSF and CT findings worsened, and the antibody titer became elevated again, and CSF and CT findings improved by readministration of prednisolone. From the above signs and laboratory data, especially continuous elevation of antibody titer against E-B VCA IgM for as long as 1 year, this case was considered to be a meningoencephalitis caused by persistent E-B virus infection.
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PMID:[A case of meningoencephalitis caused by persistent Epstein-Barr (E-B) virus infection]. 254 1

Gross and microscopic lesions associated with Bolivan hemorrhagic fever virus infection in the rhesus monkey were studied in 10 animals which died following inoculation. Gross lesions included skin rash, lymphadenopathy, splenomegaly, meningeal edema, hydropericardium and enlarged friable livers. Hemorrhagic manifestations of the infection were not consistently observed, but hemorrhages were present in the skin, heart, brain and nares in some monkeys. Histopathologic lesions were fairly consistent. Hepatic necrosis with the presence of acidophilic hyaline bodies, necrotizing enteritis, epithelial necrosis and adrenal cortical necrosis were present in all monkeys. Those monkeys which died after the seventeenth day of infection had nonsupurative meningoencephalitis; lymphoid necrosis was present in 3 monkeys that died after day 18. Other microscopic lesions included myocardial degeneration, lymphoid and reticuloendothelial cell hyperplasia and lymphoid depletion. Most of the histopathologic lesions described in human autopsy material were reproduced; however, the necrosis in the skin and oral mucosa, mucosa of the gastrointestinal tract and the adrenal cortex have not been described in man. Despite these apparent discrepancies the results of this investigation indicate that the rhesus monkey is a good experimental model for the study of Bolivian hemorrhagic fever infection.
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PMID:Pathology of Bolivian hemorrhagic fever in the rhesus monkey. 420 35

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

West Nile fever caused fatal disease in humans, horses, and birds in the northeastern United States during 1999. We studied birds from two wildlife facilities in New York City, New York, that died or were euthanatized and were suspected to have West Nile virus infections. Using standard histologic and ultrastructural methods, virus isolation, immunohistochemistry, in situ hybridization and reverse-transcriptase polymerase chain reaction, we identified West Nile virus as the cause of clinical disease, severe pathologic changes, and death in 27 birds representing eight orders and 14 species. Virus was detected in 23/26 brains (88%), 24/ 25 hearts (96%), 15/18 spleens (83%), 14/20 livers (70%), 20/20 kidneys (100%), 10/13 adrenals (77%), 13/ 14 intestines (93%), 10/12 pancreata (83%), 5/12 lungs (42%), and 4/8 ovaries (50%) by one or more methods. Cellular targets included neurons and glial cells in the brain, spinal cord, and peripheral ganglia; myocardial fibers; macrophages and blood monocytes; renal tubular epithelium; adrenal cortical cells; pancreatic acinar cells and islet cells; intestinal crypt epithelium; oocytes; and fibroblasts and smooth muscle cells. Purkinje cells were especially targeted, except in crows and magpies. Gross hemorrhage of the brain, splenomegaly, meningoencephalitis, and myocarditis were the most prominent lesions. Immunohistochemistry was an efficient and reliable method for identifying infected cases, but the polyclonal antibody cross-reacted with St. Louis encephalitis virus and other flaviviruses. In contrast, the in situ hybridization probe pWNV-E (WN-USAMRIID99) reacted only with West Nile virus. These methods should aid diagnosticians faced with the emergence of West Nile virus in the United States.
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PMID:Pathology of fatal West Nile virus infections in native and exotic birds during the 1999 outbreak in New York City, New York. 1081 Sep 85

We report a retrospective study of 115 hospitalized non-immunocompromised adults with proved or presumed diagnosis of cytomegalovirus infection. Clinical symptoms were fever (95%), constitutive symptoms (80%), joint and muscle pain (41%), shivering (32%), abdominal pain (26%), non-productive cough (20%), cutaneous eruption (20%), and diarrhea (10%). Examination found hepatomegaly (25%), splenomegaly (23%), cutaneous rash (20%), adenopathy (19%), pharyngitis (9%), jaundice (3%) or signs of meningeal irritation (1%). Seventeen patients had a gastrointestinal form (hepatitis, jaundice, colitis, antral gastritis or cholecystitis), eight had a pattern of hemopathy, two interstitial pneumonitis, two pericarditis, two immune thrombocytopenic purpura, two a polymyalgia rheumatica-like pattern, one thrombotic thrombocytopenic purpura, one cutaneous vasculitis and one meningoencephalitis. Sixty-four percent of the patients had atypical lymphocytosis. Hepatocellular injury occurred in 90% of the patients. Nineteen of the patients had biological immune abnormalities. Cytomegalovirus infection should be mainly suspected in any patient with persistent fever, isolated or associated with signs of poor specificity, or in some patients with visceral manifestations of initially unknown origin.
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PMID:Clinical and laboratory findings of cytomegalovirus infection in 115 hospitalized non-immunocompromised adults. 1147 69

The H5N1 type A influenza viruses that emerged in Hong Kong in 1997 are a unique lineage of type A influenza viruses with the capacity to transmit directly from chickens to humans and produce significant disease and mortality in both of these hosts. The objective of this study was to ascertain the susceptibility of emus (Dramaius novaehollandiae), domestic geese (Anser anser domesticus), domestic ducks (Anas platyrhynchos), and pigeons (Columba livia) to intranasal (i.n.) inoculation with the A/chicken/Hong Kong/220/97 (H5N1) highly pathogenic avian influenza virus. No mortality occurred within 10 days postinoculation (DPI) in the four species investigated, and clinical disease, evident as neurologic dysfunction, was observed exclusively in emus and geese. Grossly, pancreatic mottling and splenomegaly were identified in these two species. In addition, the geese had cerebral malacia and thymic and bursal atrophy. Histologically, both the emus and geese developed pancreatitis, meningoencephalitis, and mild myocarditis. Influenza viral antigen was demonstrated in areas with histologic lesions up to 10 DPI in the geese. Virus was reisolated from oropharyngeal and cloacal swabs and from the lung, brain, and kidney of the emus and geese. Moderate splenomegaly was observed grossly in the ducks. Viral infection of the ducks was pneumotropic, as evidenced by mild inflammatory lesions in the respiratory tract and virus reisolation from oropharyngeal swabs and from a lung. Pigeons were resistant to HK/220 infection, lacking gross and histologic lesions, viral antigen, and reisolation of virus. These results imply that emus and geese are susceptible to i.n. inoculation with the HK/220 virus, whereas ducks and pigeons are more resistant. These latter two species probably played a minimal epidemiologic role in the perpetuation of the H5N1 Hong Kong-origin influenza viruses.
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PMID:Pathogenicity of a Hong Kong-origin H5N1 highly pathogenic avian influenza virus for emus, geese, ducks, and pigeons. 1192 3

Immunodeficient CD8 knockout mice were infected with Sarcocystis neurona merozoites, in order to determine the role of CD8 cells in protective immunity. Using a direct agglutination test, all infected mice seroconverted by selected time points. Infected mice developed splenomegaly and bilateral lymphadenopathy. Histological changes included marked follicular development in the spleen, endothelitis and moderate perivascular inflammation in the liver, and meningoencephalitis in the brain. Infected brains were positive for S. neurona by polymerase chain reaction. Corresponding to histopathological changes, there were decreased numbers of B-cells in the spleen. The mice did not have significant memory (CD44hi/CD4) or effector (CD45RBhi/CD4) populations present at the time of euthanasia. Flow cytometry confirmed the lack of CD8 cells. Taken together, these data support previous studies suggesting a critical role for CD8 cells in the prevention of menigoencephalitis in S. neurona-infected mice.
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PMID:Prevention of meningo/encephalomyelitis due to Sarcocystis neurona infection in mice is mediated by CD8 cells. 1561 22

The present study reports the clinical, virological and pathological findings observed in a natural outbreak of highly pathogenic avian influenza in farmed commercial ducks. The ducks developed clinical signs, including mild respiratory distress, depression, mild diarrhoea, loss of appetite and increasing mortality (up to 12%). At necropsy, multifocal mottled necrosis was commonly found in the pancreas with splenomegaly, hepatomegaly, and swollen kidneys. Microscopically, there was necrotized pancreatitis and hepatitis, and lymphocytic meningoencephalitis and myocarditis. Influenza viral antigen was demonstrated in areas closely associated with histopathological lesion. Avian influenza virus was isolated from the caecal tonsil, faeces, and kidney of the domestic ducks. The isolated virus was identified as a highly pathogenic H5N1, with a haemagglutinin proteolytic cleavage site deduced amino acid sequence of ... QREKRKKR/GLFGAIAG ... In order to determine the pathogenicity of the isolate, eight 6-week-old specific pathogen free chickens were inoculated intravenously with the virus, and all birds died within 24 h after inoculation. This is the first report of an outbreak of highly pathogenic avian influenza with clinical signs in commercial domestic ducks in South Korea.
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PMID:Highly pathogenic avian influenza (H5N1) in the commercial domestic ducks of South Korea. 1614 75


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