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PubMed2004

Brain virus burden and indoleamine-2,3-dioxygenase expression during lentiviral infection of rhesus monkey are concomitantly lowered by 6-chloro-2',3'-dideoxyguanosine.

Increased kynurenine pathway metabolism has been implicated in the aetiology of lentiviral encephalopathy. Indoleamine-2,3-dioxygenase (IDO) initiates the increased production of kynurenine pathway metabolites like quinolinic acid (QUIN). QUIN itself is elevated in AIDS-diseased monkey and human brain parenchyma and cerebrospinal fluid at levels excitotoxic for neurons in vitro. This study investigates the cellular origin of IDO biosynthesis in the brain of rhesus monkeys infected with simian immunodeficiency virus (SIV) and explores the effects of CNS-permeant antiretroviral treatment. IDO transcript and protein were absent from the brain of non-infected and SIV-infected asymptomatic monkeys. IDO biosynthesis was induced in the brain of monkeys exhibiting AIDS. Nodule and multinucleated giant cell-forming macrophages were the main sources of IDO synthesis. Treatment with the lipophilic 6-chloro-2',3'-dideoxyguanosine suppressed IDO expression in the brain of AIDS-diseased monkeys. The effectiveness of this treatment was confirmed by the reduction of virus burden and SIV-induced perivascular infiltrates, mononuclear nodules and multinucleated giant cells. Our data demonstrate that brain IDO biosynthesis is induced in a subset of monocyte-derived cells, depends on viral burden and is susceptible to antiretroviral treatment. Thus, IDO induction is associated with reversible overt inflammatory events localized to areas of active viral replication in the SIV-infected brain.

Animals↗
PubMed1989

Natural infection with canine distemper virus in a Japanese monkey (Macaca fuscata).

A case of encephalitis in a Japanese monkey (Macaca fuscata) was examined histopathologically and serologically. The animal had brain lesions consisting of perivascular cuffs, malacia, inclusion bodies and giant cells. Monoclonal antibody to the nucleoprotein of canine distemper virus (CDV) stained the inclusions, and the distribution of the virus antigen was closely associated with that of the histological lesions. Serologically, all the 22 monkeys in the same group as the diseased monkey had relatively high titers of neutralizing antibody to CDV, but not to measles virus (MV). The pattern of the antibody titers to CDV and MV closely resembled that of cynomolgus monkeys experimentally inoculated with CDV, but differed from that of monkeys inoculated with MV. These findings suggest that an epidemic of CDV occurred in these Japanese monkeys, associated with one case of fatal viral encephalitis. This is believed to be the first report of a natural infection by CDV in non-human primates.

Animals↗
PubMed1986

Polymyositis in an immunodeficiency disease in monkeys induced by a type D retrovirus.

Fifty percent of primates with acquired immunodeficiency caused by a well-characterized type D retrovirus (SAIDS D) developed clinical, laboratory, and histologic features of polymyositis. By use of specific antisera and immunochemical techniques, we found the virus in the lymphoid cells surrounding muscle fibers and invading the endomysia septa. SAIDS D virus was isolated from the involved muscles and infected myotubes of normal muscle in tissue culture. These results suggest that retroviruses, a group of viruses increasingly associated with human diseases, can cause polymyositis with immunodeficiency in nonhuman primates and could play a role in human polymyositis.

Acquired Immunodeficiency Syndrome↗
PubMed1982

[Characteristics of Escherichia serogroup O132:K isolated in intestinal diseases in monkeys].

The results obtained in the study of the main biological characteristics of 22 Escherichia strains, serogroup O132: K ., isolated from monkeys in the Sukhumi reserve are presented. For the first time Escherichia belonging to serovar O132: K .: H- have been detected; these organisms, in contrast to reference strain O132: K .: H28, possess a number of Shigella-like characteristics and are capable of intraepithelial parasitism in Shereny's test, which impedes their primary identification. The isolation of the above-mentioned cultures from live and dead monkeys with the clinical and pathologic diagnosis of catarrhal enteritis, colitis, enterocolitis, ulcerous colitis with unknown etiology, dysentery, from monkeys having had contacts with sick monkeys at the focus of clinical dysentery and in the process of prophylactic examination, as well as the pathogenicity of these strains for guinea pigs, as determined in Shigella-induced keratoconjunctivitis used as model infection, have allowed the authors to consider Escherichia, serovar O132: K .: H-, to be the etiological factor of E. coli infection in monkeys and to regard them as enteropathogenic. In this connection further research is necessary to find out the role of these microorganisms in the etiology of intestinal infections in animals; for this reason it is expedient to produce diagnostic agglutinating serum on an industrial scale.

Animals↗
PubMedDate not supplied

[Certain pathogenetic characteristics of a disease in monkeys in infected with the Marburg virus by an airborne route].

Time course of Marburg virus (strain Popp) accumulation and changes in hematological parameters were studied in aerosol infected M.rhesus monkeys. The lungs were the first organ in which the virus was detected after respiratory infection of monkeys. Four days after inoculation the virus was detected in the liver, spleen, blood, and thymus. Six days after inoculation the virus was present in virtually all organs and secretions. The period of fever was associated with manifest leukopenia in primates. Blood clotting time drastically increased by the moment of animal death.

Air Microbiology↗
PubMed1993

Experimental Parkinson's disease in monkeys. Effect of ergot alkaloid derivative on lipid peroxidation in different brain areas.

The effects of the Parkinsonism induced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were evaluated in four different monkey brain areas (frontal and occipital cortex, caudate putamen, substantia nigra). The basal and stimulated lipid peroxidation and the reduced glutathione (GSH) concentration were evaluated in three groups of male Macaca fascicularis monkeys (6 animals/group): (a) controls; (b) MPTP-treated animals; (c) animals treated with MPTP and alpha-dihydroergocryptine (DEK; ergot alkaloid characterized by a dopaminergic agonist action). In MPTP-treated animals the GSH concentration was unchanged or decreased in a non-significant way in the frontal and occipital cortex, and in substantia nigra. The basal thiobabituric acid reactive substance (TBARS) concentrations were significantly higher in the caudate putamen and substantia nigra of MPTP-treated animals. In the MPTP-treated monkeys the DEK administration induced a restoration of basal TBARS values to nearly normal ones. By incubating tissue from different brain areas with FeSO4 plus ascorbic acid, the stimulation of lipid peroxidation decreased the TBARS production in the substantia nigra of the MPTP-treated animals. These results, taken together, may indicate that an increased lipid peroxidation could possibly play a role in producing the Parkinson-like syndrome by MPTP and that a free radical excess could be responsible for the degeneration of the substantia nigra. The treatment with an ergot alkaloid (i.e., alpha-dihydroergocryptine) partially antagonizes the MPTP-induced increase in basal TBARS concentration in caudate putamen.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMedDate not supplied

Pathogenicity of a poliomyelitis-like disease in monkeys infected orally with enterovirus 71: a model for human infection.

Ten cynomolgus monkeys were given enterovirus 71 (E71) by mouth. Clinically, only one monkey showed weakness of the lower extremities. Histopathologically, vascular lesions of variable intensity, perivascular cuffing, degeneration and necrosis of the neurons and neuronophagia were observed in the CNS of 7 monkeys. E71 was recovered from the CNS and specific immunofluorescence was detected in the neurons and in associated macrophages in the CNS. Serum neutralizing antibody titres rose from 14 to 21 days. These monkeys are as susceptible to E71 infection by the oral route as by the subcutaneous route as previously shown, and its neuronal virulence was confirmed by its producing CNS lesions after oral infection. The orally infected monkey with E71 appears to provide an excellent model for infection by this agent in man.

Animals↗
PubMed1992

Medical management of inflammatory bowel disease in a spider monkey.

Inflammatory bowel disease was diagnosed in a 3-year-old, captive-born, hand-raised, female spider monkey (Ateles geoffroyi). The diagnosis was based on clinical signs, positive-contrast radiographic series, endoscopy, histologic appearance of intestinal biopsy specimens, and the monkey's response to treatment. Treatment consisted of oral administration of prednisone, sulfasalazine, and trimethoprim-sulfamethoxazole. Supportive care included a bland diet and an electrolyte solution given free choice. Although several infective agents were considered, this case illustrates that recurrent enteritis in primates may be noninfectious and may respond to anti-inflammatory agents.

Animals↗
PubMedDate not supplied

Experimental Chagas' disease in rhesus monkeys. I. Clinical, parasitological, hematological and anatomo-pathological studies in the acute and indeterminate phase of the disease.

Rhesus monkeys (Macaca mulatta) were infected subcutaneously with 1.0 x 10(4) to 1.5 x 10(4) metacyclic trypomastigotes of Trypanosoma cruzi (Colombian strain). Parasitological and immunological parameters were evaluated in these animals for periods of 1 month to over 3 years. A chagoma was observed between the 3rd and the 13th day after infection (a.i.) and patent parasitaemia between the 13th and 59th day a.i.. Thereafter, parasites were demonstrated only by haemoculture and/or xenodiagnosis. Circulating specific IgM and IgG antibodies were observed as early as in the 2nd week a.i. IgG levels persisted until the end of the experiment, but IgM antibodies were detectable nine months a.i. Haematological alterations comprised leucocytosis and lymphocytosis. Electrocardiographic alterations were minor and transient, similar to those observed in non-lethal human acute Chagas' myocarditis. Myocarditis and myositis, characterized by multiple foci of lympho-histiocyte inflammatory infiltrate, were present in monkeys sacrificed on the 41st, 70th and 76th day but not in the animal sacrificed 3 years and 3 months a. i.. The results suggest that Chagas' disease in rhesus monkeys reproduces the acute and indeterminate phases of human Chagas' disease.

Animals↗
PubMedDate not supplied

[Relationship between the level of specific antibodies with disease outcome in Cercopithecus aethiops monkeys in experimental Marburg disease].

The level of specific antibodies in the blood of Cercopithecus aethiops monkeys with experimental Marburg hemorrhagic fever appreciably affects the incidence of lethal outcomes in immunized animals infected with Marburg virus. This effect manifests starting from the titers as low as just 1:100. The level of humoral immunity with the specific antibody titer of at least 1:100 depends on the method of antigen preparation. Humoral response was higher upon challenge with formalin-inactivated virus isolated from the blood plasma of infected guinea pigs.

Animals↗
PubMed1988

Simian immunodeficiency virus/delta-induced immunodeficiency disease in rhesus monkeys: relation of antibody response and antigenemia.

Infection of the rhesus macaque (Macaca mulatta) with simian immunodeficiency virus (SIV) induces a disease similar to AIDS. We compared SIV-specific antibody and antigenemia with the progression of disease in monkeys experimentally infected with SIV/Delta isolates that varied in pathogenicity. Western blot, immunoprecipitation, and sandwich enzyme-linked immunosorbent assay of serial sera from macaques infected with attenuated virus revealed a persistent antibody response and no evidence of SIV antigenemia. Immunosuppressed macaques without central nervous system (CNS) infections responded similarly to initial infection, but antibody specific for gag or, less frequently, to gag and env determinants declined predictably before clinical disease. Monkeys with CNS infections, however, had little, if any, detectable antibody to either envelope or gag proteins, regardless of the duration of survival. SIV/Delta-specific antigenemia, evident only in immunodeficient monkeys, fluctuated reciprocally with antibody. Our data suggest that SIV/Delta-induced disease is dependent upon antigenemic episodes that, particularly in animals with CNS infection, appear coincident with diminished antibody.

Animals↗