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Biomedical subjects

A J Shepherd

Publications and source records attributed to A J Shepherd.

57 records · Page 4Linked to original sources

The clinical pathology of Crimean-Congo hemorrhagic fever.

Observations were made of 15 fatal and 35 nonfatal Crimean-Congo hemorrhagic fever (CCHF) infections diagnosed from February 1981 to March 1987 in Kimberly and Sandringham, Republic of South Africa. Following an incubation period of 2-9 days after exposure to infection, patients had a sudden onset of disease with fever, nausea, severe headache, and myalgia. Petechial rash and hemorrhagic signs such as epistaxis, hematemesis, and melena supervened on days 3-6 of illness. Deaths occurred on days 5-14 of illness. Patients with fatal infections had thrombocytopenia and markedly elevated levels of serum aspartate and alanine aminotransaminases, gamma-glutamyltransferase, lactic dehydrogenase, creatine kinase, bilirubin, creatinine, and urea. Total protein, albumin, fibrinogen, and hemoglobin levels were depressed. Values for prothrombin ratio, activated partial thromboplastin time, thrombin time, and fibrin degradation products were grossly elevated, findings that indicate the occurrence of disseminated intravascular coagulopathy. Many of the clinical pathologic changes were evident at an early stage of the disease and had a highly predictive value for fatal outcome of infection. Changes were present but less marked in nonfatal infections.

Animals↗

Antibody response in Crimean-Congo hemorrhagic fever.

IgG and IgM antibodies became demonstrable by indirect immunofluorescence on days 7 to 9 of illness in 35 survivors of Crimean-Congo hemorrhagic fever. Maximum titers of antibody were usually attained in the second to third week of illness. Titers of IgM declined gradually thereafter and were low or negative by the fourth month. In some patients titers of IgG increased markedly between 2 and 4 months after onset of illness and remained readily demonstrable by indirect immunofluorescence 3 years after infection. Endogenous antibody response was demonstrated in only two of 15 patients who died of infection. Techniques for demonstrating antibody were (in order of decreasing sensitivity) enzyme-linked immunosorbent assay, reversed passive hemagglutination-inhibition, indirect immunofluorescence, fluorescent-focus reduction, complement-fixation, and immunodiffusion. Most patients developed relatively low levels of neutralizing antibodies (range, 1:8 to 1:32 by fluorescent-focus reduction tests), but some developed titers of 1:256 to 1:512. Plasma intended for therapeutic use should be selected on the basis of its neutralizing ability.

Antibodies, Viral↗