Cases reported "Hepatitis A"

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1/10. Hepatitis A outbreak in an institution.

    In February 1996, four serologically confirmed cases of hepatitis a virus (HAV) occurred in one household. Investigation showed that the source was a family member with sub-clinical HAV who attended a Unit for learning Disabilities. Reports of two further cases in the institution followed and control measures were instigated. Contacts were unwilling to accept human normal immunoglobulin (HNIG). Following salivary antibody and serological testing, hepatitis A vaccine was offered to the non-immune. An investigation found that sub-clinical infection was significantly associated with being less than 5 years old (RR = 6.07, p < 0.005) and being in one particular classroom (RR = 6.21, p < 0.0005). None of the staff in the institution became infected. In all, 31 cases of hepatitis A (18 clinical and 13 subclinical cases) occurred. This paper (a) describes an outbreak of hepatitis A (b) refers to the use of a salivary antibody test (assay performance to be published elsewhere) (c) identifies factors associated with the acquisition of HAV and (d) endeavours to assess the effectiveness of the vaccine to contain the outbreak.
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2/10. Presence of oligoclonal T cells in cerebrospinal fluid of a child with multiphasic disseminated encephalomyelitis following hepatitis a virus infection.

    We have investigated the clonality of beta-chain T-cell receptor (TCR) transcripts from the cerebrospinal fluid (CSF) and peripheral blood from a 7-year old child who developed a multiphasic disseminated encephalomyelitis following an infection with hepatitis a virus. We amplified beta-chain TCR transcripts by nonpalindromic adaptor (NPA)-PCR-Vbeta-specific PCR. TCR transcripts from only five Vbeta families (Vbeta13, Vbeta3, Vbeta17, Vbeta8, and Vbeta20) were detected in CSF. The amplified products were combined, cloned, and sequenced. sequence analysis revealed in the CSF substantial proportions of identical beta-chain of TCR transcripts, demonstrating oligoclonal populations of T cells. Seventeen of 35 (48%) transcripts were 100% identical, demonstrating a major Vbeta13.3 Dbeta2.1 Jbeta1.3 clonal expansion. Six of 35 (17%) transcripts were also 100% identical, revealing a second Vbeta13 clonal expansion (Vbeta13.1 Dbeta2.1 Jbeta1.2). Clonal expansions were also found within the Vbeta3 family (transcript Vbeta3.1 Dbeta2.1 Jbeta1.5 accounted for 5 of 35 transcripts [14%]) and within the Vbeta20 family (transcript Vbeta20.1 Dbeta1.1 Jbeta2.4 accounted for 3 of 35 transcripts [8%]). These results demonstrate the presence of T-cell oligoclonal expansions in the CSF of this patient following infection with hepatitis a virus. Analysis of the CDR3 motifs revealed that two of the clonally expanded T-cell clones exhibited substantial homology to myelin basic protein-reactive T-cell clones. In contrast, all Vbeta TCR families were expressed in peripheral blood lymphocytes. Oligoclonal expansions of T cells were not detected in the peripheral blood of this patient. It remains to be determined whether these clonally expanded T cells are specific for hepatitis A viral antigen(s) or host central nervous system antigen(s) and whether molecular mimicry between hepatitis A viral protein and a host protein is responsible for demyelinating disease in this patient.
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keywords = family
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3/10. Transfusion-acquired hepatitis A.

    An outbreak of hepatitis A in a neonatal intensive care unit was apparently attributable to blood transfusion. Several infants received aliquots from a single unit of packed red blood cells donated by an individual who subsequently became ill with hepatitis A. Although none of the infants became symptomatic, there was serologic evidence of recent exposure in four. Several staff and family members exposed to these infants became symptomatic. An adult patient who received platelets from this same unit developed elevated liver enzymes and his wife also showed serologic evidence of hepatitis A. These are the first reported cases of hepatitis A associated with a blood transfusion since implementation of alanine aminotransferase testing.
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4/10. Sequentially-occurring transmission of hepatitis A in a family.

    Most hepatitis A infections are acquired through sporadic transmission and it has been suggested that the intrafamilial spread of HAV is important in most sporadic outbreaks. An intra-household outbreak of hepatitis A involving three cases occurring sequentially is reported.
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keywords = family
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5/10. Reiter's syndrome following shigella flexneri 2a: a sequel to traveler's diarrhea. Report of a case with hepatitis.

    shigella flexneri 2a was isolated from a patient with Reiter's syndrome (RS) following a family outbreak of traveler's diarrhea. Among 3 members at risk, only the patient was positive for HLA-B27. Data from 3 similar families support the hypothesis that susceptibility to RS is genetically transmitted. It is urged that every effort be made to culture and subtype Shigella and other enteric pathogens in RS following diarrhea. Concurrently, the patient had hepatitis, interpreted as a parallel enteric infection.
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6/10. Nosocomial transmission of hepatitis A in an adult population.

    Nosocomial transmission of hepatitis A from patients to staff members is an unusual event. Recently, several cases of occupational transmission of hepatitis A to health care workers have been reported in the literature. Most of these have occurred as a result of transmission from an infected child to a staff member involved in his or her care. We report an additional case of transmission of hepatitis A from an infected adult to a staff member and review the literature regarding nosocomial hepatitis A transmission. The review emphasizes several points that nearly all instances of nosocomial transmission of hepatitis A have in common, including the role of asymptomatic infection, the timing of hospitalization, and the fact that index patients often have an underlying illness that obscures the early diagnosis of hepatitis A. In addition, several other areas of controversy with respect to hepatitis A are discussed.
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7/10. Maternal transmission of hepatocellular carcinoma.

    A family in which four members have died of hepatocellular carcinoma is presented. hepatitis b surface antigen was present in both cases in which it was sought and also present in nine of ten surviving siblings in the second generation. Maternal transmission of hepatitis b surface antigen and susceptibility to hepatocellular carcinoma is postulated.
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8/10. Nosocomial transmission of hepatitis A from a hospital-acquired case.

    An outbreak of hepatitis A occurred in a pediatric hospital in texas. The index case had been admitted during the incubation period for cardiac surgery and developed symptoms while hospitalized. A child in a nearby bed acquired hepatitis A, as did three staff members. The second child was still hospitalized when she developed symptoms and infected 12 nurses, 3 physicians, 2 medical students, 2 patients and 1 respiratory therapist. Children with diarrhea can effectively disseminate this virus even when normal hospital routines and rules of hygiene are observed.
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9/10. Autoimmune hepatitis following hepatitis a virus infection.

    A 7-year-old patient is reported who suffered from fatigue and jaundice due to chronic hepatitis. He had acquired hepatitis a virus infection in his community and communicated the disease to his German family 4 weeks later. While the other family members recovered from acute viral hepatitis A, the patient presented 10 weeks after the onset of hyperbilirubinemia (12 mg/dl) with the histology of chronic hepatitis, absence of markers for viral persistence, presence of autoantibodies against smooth muscle (1:320) and the asialoglycoprotein receptor (1:600), and marked hypergammaglobulinemia (3700 mg/dl), leading to the diagnosis of autoimmune hepatitis. The patient received immunosuppressive therapy, symptoms of liver disease disappeared, and autoantibodies cleared from circulation. The case is discussed in the context of a putative virus-induced autoimmune hepatitis in childhood. Autoimmune hepatitis may be induced by an external trigger. hepatitis a virus infection is one of probably several triggers that may induce autoimmune hepatitis in predisposed individuals.
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keywords = family, member
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10/10. pregnancy in hepatitis b antigen positive cirrhosis.

    Two pregnant women with chronic active viral hepatitis (HBs Ag ) and cirrhosis are described. In the first patient, maternal death occurred postpartum due to bleeding esophageal varices and liver and renal failure. Postmortem examination revealed advanced nodular cirrhosis and thrombosis of the splenic and portal veins. The infant was premature but did well and did not become infected despite the detection of HBsAg in the cord blood. Nine members of the patient's immediate family were tested; the blood of one sibling of the patient was found to be HBsAg and samples from 5 other members were found to be anti-HBs . In the second patient, death due to liver failure occurred in the seventh month of pregnancy and postmortem examination revealed advanced nodular cirrhosis. Examination of multiple fluids from the mother and fetus were negative for HBsAg. In contrast to the apparent lack of effect of pregnancy on cirrhosis of the liver in general, the possibility of an adverse effect in this particular type(HBs Ag ) should be considered.
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