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H L Amyx

Publications and source records attributed to H L Amyx.

35 records · Page 2Linked to original sources

Evidence for an unconventional virus in mouse-adapted Creutzfeldt-Jakob disease.

Homogenates of a human brain from a case of Creutzfeldt-Jakob disease and a homogenate of mouse brains from mouse passage 1 of the disease in mice contained no detectable conventional viruses. Both human material and mouse-passaged material were inoculated into nude mice, and the mouse-passaged material was also inoculated into eight different tissue culture lines. The tissue cultures showed no cytopathic changes or hemadsorption and failed to produce an increased amount of reverse transcriptase. The nude mice inoculated with human brain suspensions developed a disease identical to that in immunocompetent mice, with a nearly identical incubation period of 9 to 13 months. The incubation period of the disease in mice was under host genetic control and was, additionally, directly related to the inoculum size. The agent was resistant to 10% Formalin, 5% deoxycholate, 1% Triton X-100, and 5% glutaraldehyde; however, glutaraldehyde treatment resulted in a significant loss of infectivity. Approximately 1 log of infectivity was lost by heating brain suspensions to 80 degrees C for 15 min, with no additional loss upon further incubation up to 45 min. Heating at 100 degrees C for 15 min led to a 3-log loss of infectivity.

Animals↗

Indirect immunofluorescence tests in Korean hemorrhagic fever and epidemic (endemic) nephropathia: treatment at low pH for removal of 'nonspecific' fluorescence in tissues from immunocompetent hosts.

A 'nonspecific' fluorescence probably caused by immunocomplexes appears in the lung tissue of immunocompetent hosts infected with Korean hemorrhagic fever (KHF) or epidemic nephropathy (EN) viruses. Indirect immunofluorescence tests with such KHF- or EN-infected tissue as antigen are unsatisfactory for the detection of low-titer antibody or the reading of titer endpoints. Treatment of acetone-fixed lung sections at pH 3.0 followed by washing with 0.01 M phosphate-buffered saline and distilled water apparently dissolves the immunocomplexes, resulting in an effective removal of the 'nonspecific' fluorescence while the viral antigens are not significantly impaired. Lung sections of KHF-infected Apodemus agrarius coreae and EN-infected Clethrionomys glareolus, acetone-fixed and treated at pH 3.0, were used for the antigenic differentiation of the EN and KHF viruses.

Animals↗

Propagation of Korean hemorrhagic fever virus in laboratory rats.

Korean hemorrhagic fever virus (KHFV) has been adapted to the Wistar and Fisher strains of rats. Infection was detected by the appearance of specific antigen in the lung tissue of the infected rats at 14 to 64 days after inoculation and by the appearance of circulating antibodies in ther serum which reacted specifically with KHFV antigen in the lungs of infected Apodemus agrarius subsp. coreae 3 weeks after inoculation. Distribution of antigen in rat tissues as determined by immunofluorescent staining was the same as that in Apodemus mice except that antigen was present in the spleens of rats. Adaptation of KHFV to the laboratory rat provides an animal model that is free of wild rodent viruses and is readily available for use in studies on the characterization of KHFV.

Animals↗

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

Animals↗

Persistent shedding of adenovirus in urine of chimpanzees.

A new adenovirus, designated Pan 11, was isolated repeatedly from the urine of several chimpanzees for more than 1 year. One chimpanzee had chronic interstitial nephritis; the others were healthy. Most chimpanzees tested had neutralizing antibodies to Pan 11 virus in the serum; three people who worked with chimpanzees also acquired antibodies. Transplantable rhabdomyosarcomas developed in hamsters inoculated as newborns with Pan 11 virus.

Adenoviridae↗

Antibodies in urine of chimpanzees with chronic adenoviral viruria.

Many chimpanzees have naturally occurring chronic intermittent viruria with an adenovirus of a new type called Pan 11. Small amounts of neutralizing antibodies to Pan 11 adenovirus were found in the urine of chimpanzees. Urinary antibodies to adenovirus were mainly of the immunoglobulin G (IgG) class with some IgA antibodies also present. There was no neutralizing activity in urine against another adenovirus, Pan 9, which has been isolated from lymph nodes, but not from urine, of chimpanzees; however, sera of all chimpanzees had neutralizing antibodies to Pan 9 virus, some with titers similar to those of antibodies against Pan 11 virus. Antibodies reacting with simian cytomegalovirus by indirect immunofluorescence were found in sera of all chimpanzees tested and in two of six urines. There was no correlation between levels of antiviral IgG antibodies in serum and urine by immunofluorescence. These findings suggest that both IgG and IgA antibodies may be locally produced in response to viral infection of the urinary tract in primates.

Adenoviridae Infections↗

Hepatic amebiasis in spider monkeys.

In the past, investigators have been able to produce hepatic amebiasis in laboratory animals only by direct introduction of parasites into the liver or its vasculature, or by other artificial manipulations. A natural model of human visceral amebiasis has been lacking. We document an extensive outbreak of amebic dystentery which took place in a colony of spider monkeys; severe hepatic abscesses occurred in many animals. The spider monkey is highly susceptible to infection with Entamoeba histolytica and could provide a valuable model for the study of the pathogenesis of invasive amebiasis.

Animals↗

Transmission of Ehrlichia canis to dogs by ticks (Rhipicephalus sanguineus).

Two strains of Rhipicephalus sanguineus acquired Ehrlichia canis by feeding as either larvae or nymphs on acutely infected dogs and, in subsequent instars, transmitted the agent to normal dogs. Three strains of R sanguineus transmitted E canis as adults after their larval and nymphal stages fed on infected dogs. More than 400 adult female ticks were fed on infected dogs as larvae or nymphs or both, but none transmitted E canis transovarially.

Alanine Transaminase↗

Epizootiology of tropical canine pancytopenia.

Tropical canine pancytopenia (TCP) is a newly recognized infectious disease of dogs in diverse tropical and subtropical areas. The disease is characterized by hemorrhage, pancytopenia, severe emaciation and persistent infection. Dogs with TCP are often presented with epistaxis, which is the most dramatic sign of the disease; however, a large number of affected dogs develop severe pancytopenia and die without manifesting clinical signs of hemorrhage. The disease has been reported most frequently in the German Shepherd. Pathological findings consist of petechial and ecchymotic hemorrhages on serosal and mucosal surfaces of numerous organs. The most prominent histological finding is a perivascular plasma cell infiltrate in most organs. Disease, indistinguishable from the natural disease, has been produced in laboratory dogs inoculated with whole blood from affected dogs. Ehrlichia canis has been consistently recovered from all experimentally infected dogs. Attempts to transmit the disease to other laboratory animals and to propagate the agent in cell cultures and embryonating eggs have been unsuccessful. The tick is the probable vector of the disease.

Animals↗