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J B McCormick

Publications and source records attributed to J B McCormick.

At least 91 records · Page 5Linked to original sources
PubMed1987

A prospective study of the epidemiology and ecology of Lassa fever.

In studies of Lassa fever in Sierra Leone, the prevalence of human antibody to Lassa virus ranged from 8% to 52%. Mastomys natalensis, the reservoir of Lassa virus, constituted 50%-60% of the rodents captured in houses but only 10%-20% of those captured in surrounding agriculture and bush areas (chi 2 = 90.2, P less than 10(-6), df = 1), a finding suggesting that houses are the most-important location for transmission of Lassa virus. Viral infection of Mastomys from houses ranged from 0% to 80%. The incidence of seroconversions in susceptible persons ranged from 5% to 22% per year; the ratio of illness to infection ranged from 9% to 26%, and the proportion of febrile illness associated with seroconversion was 5%-14%. Eightfold rises in titer of antibody occurred in 1%-18% of the antibody-positive population, a result suggesting reinfection. We estimate the ratio of fatalities to infection to be 1%-2%, a rate lower than estimates based on hospitalized cases. The high incidence of Lassa fever makes it a major problem in West Africa.

Adolescent↗
PubMed1987

A case-control study of the clinical diagnosis and course of Lassa fever.

A prospective case-control study of Lassa fever was established in Sierra Leone to measure the frequency and case-fatality ratio of Lassa fever among febrile hospital admissions and to better delineate the clinical diagnosis and course of this disease. Lassa fever was responsible for 10%-16% of all adult medical admissions and for approximately 30% of adult deaths in the two hospitals studied. The case-fatality ratio for 441 hospitalized patients was 16.5%. We found the best predictor of Lassa fever to be the combination of fever, pharyngitis, retrosternal pain, and proteinuria (predictive value together, .81); of outcome, the best predictor was the combination of fever, sore throat, and vomiting (relative risk of death, 5.5). Complications included mucosal bleeding (17%), bilateral or unilateral eighth-nerve deafness (4%), and pleural (3%) or pericardial (2%) effusion. Lassa fever is endemic in this area and is a more-common cause of hospital admission and death than has previously been described; this disease must be considered when diagnosing febrile illness in West Africa.

Adolescent↗
PubMed1987

Clinical virology of Lassa fever in hospitalized patients.

We measured levels of virus in sequential specimens from 137 patients with Lassa fever. The probability of fatal disease increased significantly with the level of viremia measured either on admission or during the course of illness. The odds ratio of death in patients with viremia greater than 10 TCID50/ml was 3.7 (90% confidence interval, 1.9-7.2). The same ratio in patients with viremia greater than 10 TCID50/ml and with levels of aspartate aminotransferase greater than or equal to 150 IU/liter was 21.5 (95% confidence interval, 5.2-99.0). Virus was found in throat cultures from 39% of viremic patients, compared with 14% of nonviremic patients (P less than .002); however, the level of virus was usually less than or equal to TCID50/ml. Fewer than 3% of patients were viruric during acute illness, and virus was isolated from three of three samples of cerebrospinal fluid. On admission, 53% of patients had IgG antibodies, and 67% had IgM antibodies. Recovery was not associated with the presence of either IgG or IgM. Virus was isolated from greater than 100 serum specimens that also contained high titers of IgG. Clinical Lassa fever was shown to be a disseminated systemic, primary viral infection, with an outcome highly associated with viremia but not with development of antibody.

Adult↗
PubMed1987

Physiological and immunologic disturbances associated with shock in a primate model of Lassa fever.

The degree of cell and organ damage in clinical and histological studies of patients dying of Lassa fever has been insufficient to explain the catastrophic shock characteristic of the fatal illness. To explore this issue further, we conducted a study of the evolution of shock in three Lassa virus-infected rhesus monkeys. By the sixth day after infection, a marked, progressive reduction of in vitro platelet aggregation occurred despite normal numbers of circulating platelets and a normal platelet survival time and was accompanied by loss of prostacyclin production by postmortem endothelium. Both of these functions recovered rapidly in a surviving animal. There was no evidence of disseminated intravascular coagulation, nor were clotting factors significantly abnormal. We observed association of viral antigen with neutrophils and progressive neutrophilia. Viremia was not reduced by a brisk antibody response in our animals, and there was a general depression of response to mitogens in mixed lymphocyte stimulation assays. Our findings suggest that shock in Lassa fever is due to biochemical dysfunctions of platelets and endothelial cells and results from loss of intravascular plasma volume, effusions, and hemorrhage.

Animals↗
PubMed1987

Detection of human T cell leukemia virus type I and human immunodeficiency virus in cultured lymphocytes of a Zairian man with AIDS.

We report the detection of human T cell leukemia virus type I (HTLV-I) and human immunodeficiency virus (HIV) in the cultured lymphocytes of a 45-year-old Zairian man with AIDS. HIV was successfully isolated and analyzed by SDS-PAGE and competition radioimmunoassay. However, by the culture techniques used, HTLV-I could not be separated from the HIV. Western blot analysis of the patient's serum showed the presence of both HTLV-I- and HIV-specific antibodies. The finding of this dual infection may explain reports that greater than or equal to 30% of patients with AIDS are positive for antibodies to HTLV-I.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Antibody to hemorrhagic fever with renal syndrome viruses (Hantaviruses) in the United States.

Hantaviruses similar to those which cause hemorrhagic fever with renal syndrome have been isolated from rodents in the United States. Serologic evidence suggests that these viruses infect humans. Clinical disease has not, however, been associated with infection in the United States. To expand knowledge of the distribution of Hantaviruses in the United States and attempt to identify a clinical syndrome associated with infection, a serologic survey was undertaken of US Forestry Service personnel and US Geological Survey personnel in Mississippi, Virginia, and Alaska. In addition, sera from persons with unidentified illnesses were collected from state public health laboratories in Washington state and Virginia. One of 85 sera (1.2%) from Forestry Service personnel in Mississippi and one of 79 sera (1.3%) from Forestry Service personnel in Virginia, and nine of 360 sera (2.5%) from Forestry Service and Geological Service personnel in Alaska were tested by immunofluorescent assay and were found to have antibody to Hantaan, Tchoupitoulas, or Prospect Hill viruses, ranging in titer from 1:32 to 1:512. Those persons questioned revealed no renal disease, hemorrhagic phenomenon, or unidentified febrile illnesses. Sera from two persons in Virginia, collected at the time of an illness, had antibody titers of 1:32 and 1:64, respectively, to Prospect Hill virus. An etiologic role for Prospect Hill virus could not be confirmed. Current information would suggest that Hantaviruses do not present a public health problem in the United States.

Adolescent↗
PubMed1987

Isolation of human immune deficiency virus from African AIDS patients and from persons without AIDS or IgG antibody to human immune deficiency virus.

We previously reported a high incidence of acquired immune deficiency syndrome (AIDS) in Kinshasa, Zaire, as well as a high frequency of antibody to human immunodeficiency virus (HIV), which includes HTLV-III and LAV viruses, in persons without AIDS. In this report we assessed the frequency of HIV virus infection in persons with and without clinical AIDS and the association of virus isolation to presence of antibody. We isolated HIV from 27 (77%) of 35 patients with AIDS, and 5 of 9 patients with AIDS-related complex (ARC). Virus was also isolated from plasma and cerebrospinal fluid of patients in the study. The presence of antibody was a reliable marker for virus infection in African patients with AIDS. HIV was isolated from 5 of 27 control patients without AIDS, 3 of whom had normal T helper to T suppressor ratios and normal numbers of T helper cells. Two of these patients had no detectable antibody to HIV by ELISA or Western blot methods. In a population, such as the general heterosexual population of Kinshasa, with frequent infection by HIV and with few clearly definable risk groups, screening for antibodies to HIV may not be sufficient to identify some virus infected persons.

AIDS-Related Complex↗
PubMed1986

No evidence for increased risk of Lassa fever infection in hospital staff.

A prospective serological study was undertaken in hospital personnel who care for Lassa fever (LF) patients in an endemic region of Sierra Leone, West Africa. Among personnel from three hospitals where barrier nursing is practised, antibody prevalence and seroconversion by age and sex were consistently equal to or lower than those of persons in nearby village populations. No group among hospital personnel evaluated by age, sex, contact, or occupational exposure was at higher risk than another. Hospital staff in Sierra Leone who care for LF patients using simple barrier nursing methods have no higher risk of infection than the local population. These findings support the proposal that patients with LF in non-endemic countries need not be confined to isolators.

Adolescent↗
PubMed1986

Nucleotide sequence of the glycoprotein gene and intergenic region of the Lassa virus S genome RNA.

Two overlapping cDNA clones corresponding to the 5' region of the Lassa virus S genome RNA were isolated and their nucleotide sequences determined. Similar to Pichinde and lymphocytic choriomeningitis viruses (LCMV), Lassa virus has an ambisense S RNA. The precursor to the viral glycoproteins (GPC) is encoded in viral RNA sequence originating at position 56 and terminating at position 1529 from the 5' terminus of the S RNA. A short, noncoding, intergenic region capable of forming a hairpin structure separates the termination codons of the nucleoprotein (N) and GPC genes. Hydropathic analysis of the GPC gene product of Lassa virus indicates the presence of hydrophobic domains near the amino and carboxy termini as previously noted in the corresponding proteins of Pichinde and LCM viruses. A comparison of the nucleotide sequences on the 3' termini of the viral and viral-complimentary S RNA species of Lassa, LCM, and Pichinde viruses reveals slight sequence differences that may possibly be involved in the regulation of RNA synthesis and gene expression.

Amino Acid Sequence↗
PubMed1986

Prevalence of HTLV-III/LAV in household contacts of patients with confirmed AIDS and controls in Kinshasa, Zaire.

Household members of 46 patients with confirmed acquired immunodeficiency syndrome (AIDS) and 43 human T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV)-seronegative controls from Kinshasa, Zaire, were identified and sought for serologic testing for evidence of HTLV-III/LAV infection. Twenty (9.8%) of 204 case-household members and three (1.9%) of 155 control-household members were HTLV-III/LAV seropositive (relative risk = 5.1; 95% confidence interval, 1.7 to 15.2). Eleven (61.1%) of 18 spouses of patients with AIDS were HTLV-III/LAV seropositive, compared with one (3.7%) of 27 control spouses (relative risk = 16.5; 95% confidence interval, 3.7 to 75.0). Except for spouses, the rate of HTLV-III/LAV seropositivity did not differ significantly between case and control households. Furthermore, for adults in case households who were not spouses, the number seropositive for HTLV-III/LAV was identical to that predicted from sex- and age-specific HTLV-III/LAV seroprevalence rates. These data from Zaire confirm the results of US and European studies of household contacts of infected hemophiliacs and pediatric patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Lassa fever. Effective therapy with ribavirin.

In a study of Lassa fever in Sierra Leone, West Africa, we identified two variables associated with a high risk of death, and we evaluated the efficacy of ribavirin and Lassa virus-convalescent plasma for the treatment of Lassa fever. A serum aspartate aminotransferase level greater than or equal to 150 IU per liter at the time of hospital admission was associated with a case-fatality rate of 55 percent (33 of 60). Patients with the same risk factor who were treated for 10 days with intravenous ribavirin, begun within the first 6 days after the onset of fever, had a case-fatality rate of 5 percent (1 of 20) (P = 0.0002 by Fisher's exact test). Patients whose treatment began seven or more days after the onset of fever had a case-fatality rate of 26 percent (11 of 43) (P = 0.01). Viremia with levels greater than or equal to 10(3.6) TCID50 per milliliter on admission was associated with a case-fatality rate of 76 percent (35 of 46). Patients with this risk factor who were treated with intravenous ribavirin within the first six days after onset of fever had a case-fatality rate of 9 percent (1 of 11) (P = 0.006), whereas those treated after seven days or more of illness had a fatality rate of 47 percent (9 of 19) (P = 0.035). Oral ribavirin was also effective in patients at high risk of death. Lassa-convalescent plasma did not significantly reduce mortality in any of the high-risk groups. We conclude that ribavirin is effective in the treatment of Lassa fever and that it should be used at any point in the illness, as well as for postexposure prophylaxis.

Administration, Oral↗
PubMed1986

Therapeutic effect of the antiviral agent ribavirin in Junín virus infection of primates.

In order to assess the effect of the antiviral Ribavirin on the course of Junín virus infection in Callithrix jacchus, seven inoculated monkeys were treated with 15 mg of the drug, twice a day, starting 6 days after infection when all animals were viremic. The three untreated controls showed typical signs of Junín virus infection at 14 days pi and their mean time of death was 18 days. In contrast, no signs of illness were detected in Ribavirin-treated animals until 24 days pi, when marmosets showed signs of neurological involvement: 5 of these animals died (mean day of death: 36) but the two remaining treated monkeys improved and survived infection without sequelae. The comparison of survival rates (0% vs 28%) and the delay of the mean day of death observed indicates that the Ribavirin treatment used has therapeutic effect on Junín virus infection in vivo.

Animals↗