Cases reported "Rabies"

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1/14. Correlation of clinical and neuroimaging findings in a case of rabies encephalitis.

    BACKGROUND: Rabies encephalitis is a feared, virtually uniformly fatal form of central nervous system infection. The incidence of rabies encephalitis in the united states is almost certainly underestimated because of the predominance of bat-borne rabies, which can be spread without traumatic exposure. Because of its rarity in developed countries, rabies encephalitis has been seldom studied with modern imaging techniques. SETTING: University-based teaching hospital. PATIENT: A case of pathologically confirmed rabies encephalitis is presented. diagnosis of rabies was made by seroconversion testing while the patient was alive and was confirmed postmortem by the presence of rabies antigens and Negri bodies in the brain. The patient had 2 magnetic resonance studies done that showed dramatic abnormalities in the medulla and pons that correlated with features of the neurologic examination and hypothalamic-pituitary abnormalities. RESULT: The patient had a fulminant encephalitic course that ended in death. CONCLUSION: Rabies is an uncommon cause of fatal encephalitis. Anatomic imaging studies such as computed tomographic and magnetic resonance scans have generally been negative in confirmed cases of rabies. We report a case of confirmed rabies with extensive brainstem and hypothalamic-pituitary abnormalities on magnetic resonance imaging. Although these findings are nonspecific, they should raise the clinical suspicion of rabies in the setting of aggressive encephalitis of unclear cause, and appropriate diagnostic tests should be performed.
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2/14. Imaging findings in rabies encephalitis.

    SUMMARY: Rabies encephalitis is perhaps one of the few infectious diseases that command attention and fear not only from the layman but also from physicians. The unique mode of transmission, the virtually exclusive neurotransmission shown by the agent, and the complete hopelessness of the established disease sets rabies apart from other zoonoses transmitted to man. Rabies encephalitis is a fatal disease and its diagnosis is usually based on the clinical presentations and findings. Hence, imaging in rabies is seldom done, and imaging findings in rabies encephalitis have rarely been described. We present the imaging findings in two confirmed cases of rabies encephalitis in which antemortem diagnosis was obtained by corneal impression smears showing the presence of viral antigens. The differential diagnosis of the imaging findings as well as the role and the relevance of imaging in the diagnosis of this disease are discussed. The current literature on the subject is also reviewed.
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3/14. Rabies: otolaryngologic manifestations.

    Rabies is a rare, fatal viral infection, usually transmitted by the bite of an infected animal. Some 30,000 Americans are immunized annually, however, so public health considerations are common. The development of a new vaccine, grown in human diploid cell culture, is discussed. It appears to have high antigenicity with no serious morbidity. A case of a patient with fatal rabies who had fever, delirium, dysphagia, and cervical and pectoral subcutaneous emphysema is presented.
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4/14. Quantitative study of the infection in brain neurons in human rabies.

    rabies virus is a highly neuronotropic virus that causes encephalomyelitis. rabies virus infection was studied in neurons in the brain of an 8-year-old girl that died of rabies in mexico. The extent of the neuronal infection was evaluated quantitatively in neuronal cell types of the brain using histologic staining for Negri bodies and immunoperoxidase staining for rabies virus antigen in the same neurons. Quantitative image analysis was used to compare the amount of infection in five different neuronal cell types, which was expressed as a percentage of neuronal area. purkinje cells and periaqueductal gray neurons showed the largest percentage area for both Negri bodies and signal for rabies virus antigen. In general, there was a good linear relationship between the area of Negri bodies and the area of signal for rabies virus antigen. Many neurons with rabies virus antigen did not have Negri bodies, however, and some neurons with large antigen signals, especially purkinje cells and periaqueductal gray neurons, lacked Negri bodies. Formation of Negri bodies is likely influenced by factors that vary in different neuronal cell types.
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5/14. Rabies in marmosets (callithrix jacchus), Ceara, brazil.

    A new rabies virus variant, with no close antigenic or genetic relationship to any known rabies variants found in bats or terrestrial mammals in the americas, was identified in association with human rabies cases reported from the state of Ceara, brazil, from 1991 to 1998. The marmoset, callithrix jacchus acchus, was determined to be the source of exposure.
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6/14. Rabies encephalitis following fox bite--histological and immunohistochemical evaluation of lesions caused by virus.

    Rabies caused by fox bite is uncommon, most cases being caused by bite of rabid dogs (95%). We report a 45-year-old lady with rabies encephalomyelitis caused by bite of a rabid wild fox (Vulpes vulpes), a species prevalent in the Deccan plateaus of Central india. Though foxes are known to be susceptible to rabies, literature on the pathological changes caused by fox bite rabies in humans is scarce. Unlike the mild histological alterations described in canine rabies, a florid encephalitic process evolved in fox bite rabies, in our case, with intense microglial reaction, neuronophagia and perivascular inflammatory infiltrates despite clinical manifestation as a paralytic rabies. Immunostaining using polyclonal antibodies to the rabies viral nucleocapsid antigen and to the whole virion demonstrated high viral load within neurons with extensive spread along dendritic arborization and axonal tracts. Genomic sequence analysis demonstrated close homology with canine virus strain with only minor variations.
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7/14. The clinical picture of rabies in a child.

    An eight-year-old boy developed rabies 31 days after having been scratched by a dog and died 9 day later. Intensive supportive medical treatment was complicated by apnea, cardiac arrest, hypotension, increased secretion of antidiuretic hormone and severe hypoproteinemia. The treatment with intramuscular human antirabies immunoglobulin (HRIG) 2400 I.U. and intrathecal 1200 I.U. in combination with intramuscular interferon alpha 4 million I.U. was given every second day. The diagnosis of rabies was confirmed before death, on the third day of the disease, by direct fluorescent antibody staining of the saliva and cerebrospinal fluid for viral antigen. At the autopsy, the brain tissue specimens were tested for the presence of the virus by inoculation into the suckling mice brain and for the viral antigen by direct fluorescent antibody method. The brain tissue specimens collected at autopsy were also tested for virus by direct fluorescent antibody method.
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8/14. Unexplained rabies in three immigrants in the united states. A virologic investigation.

    BACKGROUND. Extensive investigation of three patients who died of rabies in the united states failed to reveal any source of exposure to the disease. The three patients had immigrated to the united states from areas in laos, the philippines, and mexico where rabies is endemic. methods. We studied rabies viruses isolated from the three patients, other patients with a known source of exposure, and animals in the united states, thailand (as a proxy for laos), the philippines, and mexico. The viruses were characterized by indirect immunofluorescence and neutralization tests according to their reactions to panels of monoclonal antibodies. Transcribed complementary dna from these isolates was amplified by the polymerase chain reaction; the dna product was then analyzed by differential digestion with restriction enzymes. RESULTS. The viral isolate from each of the three patients was a rabies variant with distinctive antigenic or genetic characteristics. For each of the three isolates, identical variants were found in specimens from rabid animals obtained from or near the country in which the patient lived before immigrating to the united states. None of these variants were found among the isolates collected from rabid animals in the united states. CONCLUSIONS. Rabies infection in these three patients did not originate in the united states but resulted from exposures in laos, the philippines, and mexico. Since the three patients had lived in the united states for 4 years, 6 years, and 11 months, our findings suggest that the onset of the clinical manifestations of rabies occurred after long incubation periods.
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9/14. Failure of interferon alfa and tribavirin in rabies encephalitis.

    OBJECTIVE--To test the effect of interferon alfa and tribavirin (ribavirin) in patients with rabies encephalitis. DESIGN--An open trial of chemotherapy and intensive care in patients with early rabies. SETTING--The intensive care unit of a Bangkok hospital. patients--Four conscious men with clinical rabies encephalitis. INTERVENTIONS--Rapid virological diagnosis of rabies. Treatment with intravenous and intraventricular injections of high doses of lymphoblastoid interferon alfa in three patients and tribavirin in one patient. intensive care was given throughout. MAIN OUTCOME MEASURES--Rabies infection confirmed by antigen detection and virus isolation. Rabies neutralising antibody and specific IgM sought in serum and cerebrospinal fluid. Interferon concentrations monitored before and during treatment in three patients. RESULTS--Interferon alfa treatment produced high concentrations in serum and cerebrospinal fluid. All four patients died after 5 1/2 to 12 1/2 days of treatment with no evidence of virostatic or clinically beneficial effects from either treatment. CONCLUSION--Interferon alfa treatment is not effective in rabies encephalitis. The use of tribavirin warrants further study, possibly combined with new therapeutic methods.
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10/14. Rabies: ocular pathology.

    Ocular pathology in the first European case of human bat-borne rabies is described. The patient was a 30-year-old bat scientist who seven weeks after bat bite developed neurological symptoms and died 23 days later. rabies virus antigens were detected in brain smears. After extensive virological studies the virus turned out to be a rabies-related virus, closely resembling the Duvenhage virus isolated from bats in south africa in 1980. By light microscopy focal chronic inflammatory infiltration of the ciliary body and of the choroid was found. PAS-positive exudate was seen in the subretinal and in the outer plexiform layers of the retina, and retinal veins showed endothelial damage and perivascular inflammation. Many of the retinal ganglion cells were destroyed. The presence of rabies-related viral antigen in the retinal ganglion cells was shown by positive cytoplasmic immunofluorescence, though electron microscopy failed to identify definite viral structures in the retina. By immunohistochemistry glial fibrillary acidic protein was observed in the Muller's cells, which are normally negative for this antigen but express it as a reactive change when the retina is damaged. synaptophysin, a constituent of presynaptic vesicles of normal retinal neurons, was not detected in the retina.
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