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Biomedical subjects

J C Morrill

Publications and source records attributed to J C Morrill.

At least 19 recordsLinked to original sources
PubMed1994

Serum levels of alpha and gamma interferons in hemorrhagic fever with renal syndrome.

Hemorrhagic fever with renal syndrome is an acute viral disease caused by Hantavirus. On the basis of clinical observation, the illness is divided into five sequential stages: febrile, hypotensive, oliguric, diuretic, and convalescent. Because interferons can be induced by viruses, and because their stimulating effects on immune cells can alter the course of viral infections, we examined the presence of alpha interferon (IFN-alpha) and gamma interferon (IFN-gamma) in 276 serum samples collected from 110 patients during the Korean Conflict. We tested these sera for IFN-alpha by bioassay with bovine kidney MDBK cells, and for IFN-gamma by a sandwich ELISA with antibodies specific for human IFN-gamma. We found variable, but persistently elevated levels of IFN-gamma throughout the various phases of the disease, which suggested persistent immune activation through convalescence. Moderate levels of IFN-alpha were found in all stages of infection.

Animals↗
PubMed1993

Recurrence of Rift Valley fever in Egypt.

Rift Valley fever (RVF) has been recorded in man and in domestic animals in Egypt after a 12-year absence. Human infections were first noted in the Aswan Governorate in late May, 1993. Only cases of ocular disease, an infrequent and late manifestation, were reported. Of 41 cases, 35 were tested serologically and 27 (77%) had RVF virus-specific IgM antibodies. An estimated 600-1500 infections occurred in the region. Abortions in cattle and buffalo were seen concurrently and antibodies to RVFV were present in 39% of domestic livestock, presumably unvaccinated. RVFV was isolated from an aborted water buffalo fetus.

Abortion, Veterinary↗
PubMed1992

Rift Valley fever virus-induced encephalomyelitis and hepatitis in calves.

Three calves (Nos. 1, 2 = 7 days old; No. 3 = 21 days old) were inoculated subcutaneously with virulent Rift Valley fever (RVF) virus. All calves became viremic and clinically ill, but the two 7-day-old calves were moribund and were euthanatized subsequently on post-inoculation day (PID) 3. Highest viral titers were measured in the serum, with lesser concentrations in the brain, heart, spleen, and liver of these animals. Viral antigens were detected by immunohistochemical analysis only in the livers, where positive staining was localized in coalescing foci of hepatocellular necrosis. The 21-day-old calf appeared to recover after viremia and pyrexia but became lethargic and ataxic and was euthanatized on PID 9. The calf was no longer viremic, and RVF virus was isolated only from the brain. Microscopic examination of the central nervous system revealed diffuse perivascular infiltrates of lymphocytes and macrophages, multifocal meningitis, and focal areas of neuronal necrosis and aggregates of macrophages, lymphocytes, and neutrophils throughout all regions of the brain and cervical spinal cord. There was positive immunohistochemical staining for viral antigens within the cytoplasm of neurons and glial cells throughout the central nervous system. Thus, RVF virus can cause encephalomyelitis in calves, and the specific virologic diagnosis can be made by immunohistochemical localization of viral antigens in formalin-fixed tissues.

Animals↗
PubMed1991

Further evaluation of a mutagen-attenuated Rift Valley fever vaccine in sheep.

A previous study demonstrated that a mutagen-attenuated Rift Valley fever virus (RVFV) vaccine, RVF MP-12, was immunogenic and non-abortogenic when ewes, 90-110 days pregnant, were inoculated with 5 x 10(5) plaque-forming units (p.f.u.) of the virus strain. The ewes delivered live, healthy lambs that had no neutralizing antibody to RVFV until after they had ingested colostrum. To assess further the safety and protective capability of this candidate vaccine, six pregnant ewes were inoculated with 5 x 10(3) p.f.u. of RVF MP-12 and challenged with 5 x 10(5) p.f.u. of virulent ZH-501 strain of RVFV 30 days later. No viraemia was detected after vaccination or challenge and all six ewes delivered live, healthy lambs. Those lambs tested before their nursing did not have neutralizing antibody to RVFV but quickly acquired antibody titres of 1:320 to greater than or equal to 1:10,240 after ingesting colostrum. To test the safety of the RVF MP-12 immunogen in neonates, lambs less than or equal to 7 days old, born to unvaccinated ewes, were inoculated with 5 x 10(5) p.f.u. of RVF MP-12. With the exception of brief pyrexia in 18 of 26 lambs, and a transient low-titred viraemia in 16 of 26 lambs after inoculation, no untoward effects were observed. Serum-neutralizing antibody to RVFV was detected 5-7 days after inoculation. Lambs vaccinated with either 5 x 10(5) or 5 x 10(3) p.f.u. of RVF MP-12 were protected against virulent RVFV challenge at 14 days postvaccination.

Animals↗
PubMed1991

Recombinant human interferon-gamma modulates Rift Valley fever virus infection in the rhesus monkey.

Prophylactic treatment of rhesus macaques with 10(4)-10(6) U/kg of recombinant human interferon-gamma (rHuIFN-gamma) modulated Rift Valley fever (RVF) virus infection. IFN was given intramuscularly at 24 h prior to infection and daily thereafter for a total of five doses. After infection, treated monkeys showed no evidence of clinical disease; some had no detectable viremia; when viremia was observed, peak virus titers were decreased compared to control infected monkeys; and only minor and transient perturbations in hematologic and clinical chemistry values were seen. Untreated infected control monkeys developed high-titered viremia, mild to severe clinical disease, and moderate to severe changes in hemostatic parameters and clinical laboratory measurements. No evidence of synergism was noted when RVF virus-infected monkeys were treated prophylactically with combined low doses of rHuIFN-gamma and rHuIFN-alpha A.

Animals↗
PubMed1991

Serological evidence of arboviral infections among humans of coastal Kenya.

A serosurvey was conducted during September 1987 for evidence of human arboviral infections in the Coast Province of Kenya. Sera were collected from 1624 outpatients at three hospitals and tested for antibody to eight arboviruses by the indirect immunofluorescent antibody technique. Antibody prevalence rates were: Rift Valley fever, 2.8%; Sindbis, 2.6%; dugbe, 2.1%; dengue-2, 1.0%; West Nile, 0.9%; chikungunya, 0.7% and Nairobi sheep disease, 0.3%. Evidence of Crimean-Congo haemorrhagic fever viral antibody was not detected. The data suggested low arbovirus activity since 1982, when an epidemic of dengue occurred in this region, and revealed the first evidence of dugbe viral infection among humans in Kenya.

Adolescent↗
PubMed1990

Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response.

Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12 h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.

Analysis of Variance↗
PubMed1990

Serological evidence of Crimean-Congo haemorrhagic fever viral infection among camels imported into Egypt.

A serosurvey was conducted during 1986-87 to determine evidence of prior Crimean-Congo haemorrhagic fever (CCHF) viral infection among camels imported into Egypt from Sudan and Kenya. Sera obtained from camesl arriving at the Aswan quarantine station, southern Egypt, were tested for CCHF antibody by the agar gel diffusion (AGD) and the indirect fluorescent antibody (IFA) techniques. CCHF viral antibody was demonstrated in 14% (600/4301) of the camels, with both techniques yielding similar results. CCHF viral antibody prevalence among camels imported from Sudan was lower (12%) than among camels imported from Kenya (26%). Ganjam and Qalyub viral antibody was not detected among the 600 CCHF viral antibody positive sera, but 7% (44/600) were positive for Dugbe viral antibody. CCHF viral antibody was not demonstrated in 400 sheep and 200 cows of native animals. These data indicate that camels imported from Sudan and Kenya had previous CCHF viral infection, but evidence of transmission to animals of Egypt was not obtained. Further studies are needed to assess the possible role of imported animals in the ecology and epidemiology of CCHF virus in Egypt.

Animals↗
PubMed1989

Epidemiology of hepatitis B in eastern Kenya.

A cross-sectional survey of outpatients attending the three distinct hospitals in the towns of Mombasa, Kilifi, and Malindi was conducted to determine the patterns of hepatitis B transmission in eastern Kenya. Of 1,533 study subjects (mean age 21.9 +/- 13.2 years; range, 4 months to 80 years), 11.4% were positive for HBsAg and 56.2% were seropositive for at least one hepatitis B marker (HBsAg, anti-HBs, or anti-HBc). Anti-delta antibody was found in 1.2% of HBsAg-positive samples. HBeAg was found in 36.0% of HBsAg-positive samples obtained from women of childbearing age. The prevalence of seropositivity for hepatitis B markers was positively correlated with age, increasing from 20% in subjects less than 4 years old to more than 80% in study subjects greater than 40 years old. On multivariate analysis, male sex was found to be associated with HBsAg positivity, and age and previous deliveries of children were associated with seropositivity for any hepatitis marker (HBsAg, anti-HBs, or anti-HBc). An effective hepatitis B immunization strategy in this region of Kenya would require vaccination early in life because a major portion of hepatitis B transmission occurs in childhood.

Adolescent↗
PubMed1989

Seroprevalence of Rickettsia typhi and Rickettsia conorii infection among rodents and dogs in Egypt.

A serological survey of 1813 rodent and 549 dog sera, collected from 1979 to 1986 from animals in 16 Egyptian Governorates were tested for antibody to Rickettsia typhi and Rickettsia conorii by the indirect fluorescent antibody test. Only three of 82 (4%) sera from Rattus rattus collected near Aswan had antibody to R. conorii. The prevalence of R. typhi antibody in dog sera was only 0.4% (n = 549) while 25% (n = 547) of Rattus norvegicus and 11% (n = 1138) of R. rattus had measurable antibodies. Among the other rodents, antibody was demonstrated in only 2% (n = 45) of Arvicanthis spp., and 1% (n = 83) of Acomys spp. Collectively, rodents captured in the Nile Delta had a higher prevalence (mean 24% (n = 787] than those captured in the Nile Valley (mean 4% (n = 650]. Antibody to R. typhi was detected in rodents collected in all port cities: ismailiya, 13%; Port Said, 9%; Suez, 9%; Safaga, 16%; Quseir, 32% and Alexandria, 34%. These data showed evidence of R. typhi infection among rodents in widespread geographic localities of Egypt and suggested that infected rodents may be a source of human infections.

Animals↗
PubMed1989

Seroprevalence of murine typhus and fièvre boutonneuse in certain human populations in Egypt.

A study was conducted between 1984 and 1987 to determine the prevalence of Rickettsia typhi and Rickettsia conorii infections among humans residing in the Nile Delta, Suez Canal area and Nile Valley of Egypt. Serum specimens were obtained from garbage and rodent control workers, other unclassified occupational workers, and from patients with fever of undetermined aetiology. All sera were assayed for IgA + IgM + IgG (IgAMG) antibody mixture and if positive, reassayed for specific IgM antibody to rickettsia by the indirect fluorescent antibody technique. R. typhi antibody was found in 19% (33/178) of the garbage collectors, whereas only 1% (2/178) had demonstrable antibody to R. conorii. Among those with other occupations, R. typhi antibody was detected in 0.7% (2/295) and none had R. conorii antibody. The antibody prevalence rate for R. typhi among patients with febrile illness ranged from 25 to 41%, and from 2 to 15% for R. conorii, at three different locations in Egypt. In addition, IgM antibody to R. typhi was demonstrated in some patients showing symptoms compatible with rickettsial disease and in some patients who seroconverted, indicating that R. typhi was the cause of illness among some of these patients. These findings support previous observations that R. typhi and R. conorii are the causes of human rickettsial disease in Egypt, and that humans are commonly infected with R. typhi.

Adult↗
PubMed1989

AIDS: the situation in Mogadishu during spring 1987.

To determine if AIDS was present in Mogadishu during spring 1987, we screened hospital patients for the presence of diseases compatible with acquired immunodeficiency. Twenty-nine such patients were identified and had their serum tested for antibodies to HIV by standard serologic techniques. All these sera were negative for HIV antibodies. During the same time, at the Mogadishu clinic for sexually transmitted diseases, 48 individuals were examined for evidence of HIV infection. No patient had clinical signs compatible with AIDS, but one serum was anti-HIV antibodies positive in both the ELISA and western blot assay. We conclude that there was no clinical AIDS in Mogadishu in early 1987 and that prevalence of HIV infection in high risk individuals was very low.

Acquired Immunodeficiency Syndrome↗
PubMed1988

A study of viral and rickettsial exposure and causes of fever in Juba, southern Sudan.

Patients presenting at the Juba Teaching Hospital, either with fever of undetermined origin or with a clinical cause of fever, gave evidence of exposure to a wide range of viral and rickettsial agents. Serological tests showed high antibody levels to flaviviruses (56.9%) and alphaviruses (29.2%), with lesser levels of bunyamweraviruses (3.8%), Rift Valley fever (2.3%), and sandfly fever (0.75%). Flavivirus exposure was significantly associated with clinical evidence of liver disease; repeated exposure to flaviviruses was particularly prevalent in those with poor sanitation and who had received previous injections. A significant focus of Ebola and Marburg exposure in Juba has been identified. Clinical evidence of liver disease was evident in 37% of patients studied, and 24.6% were HBsAg positive. The first 2 HIV-positive individuals from the southern Sudan are reported, including one with clinical AIDS. A high prevalence of positive antibodies to Rickettsia typhi in the population indicated that murine typhus was common locally. This study indicates the need for further public health measures in the southern Sudan to control the spread of these infections.

Adolescent↗
PubMed1988

Solid-phase immunosorbent technique for rapid detection of Rift Valley fever virus immunoglobulin M by hemagglutination inhibition.

A solid-phase immunosorbent technique (SPIT) was adapted to detect Rift Valley fever (RVF) virus-specific immunoglobulin M (IgM) in serum samples from humans vaccinated with Formalin-inactivated RVF vaccine. Microdilution plates coated with goat anti-human IgM were successively incubated with serum samples from human vaccinees, RVF virus hemagglutinating antigen, and goose erythrocytes. The RVF virus-specific IgM in the serum samples from vaccinees bound to the RVF virus antigen and inhibited hemagglutination of goose erythrocytes. SPIT was compared to the IgM capture enzyme linked immunosorbent assay (ELISA) and the indirect immunofluorescent-antibody (IFA) assay and was found to be sensitive in detecting RVF virus-specific IgM antibody, with high correlations between SPIT and the other two tests (Pearson's correlation coefficient [r] = 0.9 and 0.6, respectively). Results of SPIT were obtained within 5 h, offering speed over ELISA (8 h). In addition, SPIT does not require sophisticated equipment or expensive reagents. Serum rheumatoid factor did not produce false-positive reactions in SPIT as in the indirect immunofluorescent-antibody assay and IgM capture ELISA.

Antibodies, Viral↗