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At least 631 records · Page 35Linked to original sources
PubMed1992

Epizootic of Yersinia pseudotuberculosis in a wildlife park.

An epizootic attributable to Yersinia pseudotuberculosis infection was confirmed in captive ruminants in a wildlife park by microbiologic and histologic findings. An epornitic of Y pseudotuberculosis infection was identified at the same period in a vicinity near the ruminant deaths. Yersinia pseudotuberculosis can infect human beings and cause acute enteritis and mesenteric lymphadenitis. People in contact with infected animals should use extreme caution and use good sanitary precautions to preclude transmission of this agent.

Animals↗
PubMed1978

Spontaneous colonic adenocarcinoma in marmosets.

We find that colonic adenocarcinoma, which is an extremely rare neoplasm of all animals except man and carcinogen-treated rodents, occurs spontaneously in some marmosets. The cotton-topped Saguinus oedipus oedipus is particularly prone to develop it, but we have found it also at necropsy in Callimico goeldii (Goeldi's marmoset). Numerous metastases to regional lymph nodes develop. The cancers arise de novo in the mucosa and early invade the submucosa and lymphatic apparatus and paracolonic lymph nodes. These findings and the continuing occurrence of this cancer in our colony suggests that the marmoset may be the long-sought primate model for experimental intestinal carcinogenesis.

Adenocarcinoma↗
PubMed1997

SIV/HIV-1 chimeric viruses having HIV-1 env gene: a new animal model and a candidate for attenuated live vaccine.

In order to generate an HIV-1, which is infectious to and induces AIDS-like disease in monkeys, an SIVmac/HIV-1 chimeric virus, designated NM-3rN, which was replication-competent in monkeys, was constructed by recombination between HIV-1 and SIV mac genomes. The NM-3rN enabled to evaluate the efficacy of HIV-1 Env-directed vaccines using macaque monkeys instead of chimpanzees, because NM-3rN had HIV-1 derived Env. Other NM-3rN-derivative chimeric viruses, designated NM-3 and NM-3n, which had defective vpr (plus nef for NM-3) genes, induced long-term persistent infection in monkeys having long-lasting humoral and cell-mediated immune reactions without manifesting the disease. The challenge inoculation with NM-3rN to these defective chimeric virus-infected monkeys resulted in protection. Furthermore, these protected monkeys were also resistant to challenge with another chimeric virus having different antigenicity in V3 loop from that of NM-3 and NM-3n. These results indicate that SIV/HIV-1 chimeric viruses may be a potential candidate for development of anti-AIDS live attenuated vaccines.

AIDS Vaccines↗
PubMed1987

Immunogenetic studies of maternal-fetal relationships: a review: why newborn rhesus monkeys don't get hemolytic disease.

The discovery of the Rh blood group factor in humans was made using the red blood cells of rhesus monkeys. Because of its importance to human medicine and immunogenetics, this finding contributed greatly to the appreciation of the importance of nonhuman primates in research. It is now widely recognized that blood group incompatibility between mother and fetus can lead to differential fertility, fetal death, and hemolytic disease of the newborn (HDN). The blood group systems of several nonhuman primate species have been studied in detail and found to be analogous, although not identical, to those of humans. It is therefore surprising that HDN has been reported in only four nonhuman primate species--marmosets, sacred baboons, chimpanzees, and orangutans. Maternal-fetal blood group incompatibility and its consequences have been extensively studied in rhesus monkeys, and these macaques may well be representative of many nonhuman primates. Rhesus monkeys exhibit all five of the conditions that lead to HDN in humans: (1) blood group incompatible matings; (2) transplacental hemorrhage; (3) maternal immunization to blood group alloantigens on fetal erythrocytes; (4) transplacental transfer of maternal antibodies; and (5) coating of the newborn's erythrocytes. Yet, newborns show no clinical or hematological evidence of HDN. We have shown that the rhesus alloantibodies engendered by transplacental immunization do not mediate immune elimination of the newborn's erythrocytes. Evaluation of the maternal antibodies demonstrated that they have low titers and low avidities and perhaps belong to IgG subclasses that do not bind effectively to receptors on phagocytic cells of the rhesus reticuloendothelial system. The newborn's genotype may also affect the expression of allogeneic blood group antigens and thereby help protect the newborn's cells from destruction. These factors together undoubtedly play a major role in the survival of the antibody-coated newborn's RBC and are thus able to account for the absence of HDN in this species.

Animals↗
PubMed1996

Experimental infection of cynomolgus macaques with Ebola-Reston filoviruses from the 1989-1990 U.S. epizootic.

This study describes the pathogenesis of the Ebola-Reston (EBO-R) subtype of Ebola virus for experimentally infected cynomolgus monkeys. The disease course of EBO-R in macaques was very similar to human disease and to experimental diseases in macaques following EBO-Zaire and EBO-Sudan infections. Cynomolgus monkeys infected with EBO-R in this experiment developed anorexia, occasional nasal discharge, and splenomegaly, petechial facial hemorrhages and severe subcutaneous hemorrhages in venipuncture sites, similar to human Ebola fever. Five of the six EBO-R infected monkeys died, 8 to 14 days after inoculation. One survived and developed high titered neutralizing antibodies specific for EBO-R. The five acutely ill monkeys shed infectious virus in various bodily secretions. Further, abundant virus was visualized in alveolar interstitial cells and free in the alveoli suggesting the potential for generating infectious aerosols. Thus, taking precautions against aerosol exposures to filovirus infected primates, including humans, seems prudent. This experiment demonstrated that EBO-R was lethal for macaques and was capable of initiating and sustaining the monkey epizootic. Further investigation of this animal model should facilitate development of effective immunization, treatment, and control strategies for Ebola hemorrhagic fever.

Animals↗
PubMed1990

Galanin-like immunoreactivity within the primate basal forebrain: differential staining patterns between humans and monkeys.

Galanin-like immunoreactivity (GAL-ir) was examined within the basal forebrain and adjacent regions of eight young adult New World monkeys (Cebus apella), one aged Old World monkey (Macaca mulatta), and eight humans without clinical or pathological evidence of neurological disease. All monkeys demonstrated similar patterns of immunoreactive profiles characterized by a continuum of GAL-ir magnocellular neurons located within the medial septum, diagonal band nuclei, and nucleus basalis. Colocalization experiments revealed that most (greater than 90%) of GAL-ir basal forebrain neurons also expressed the receptor for nerve growth factor (NGFR), an excellent marker for primate cholinergic basal forebrain neurons. A few smaller parvicellular GAL-ir neurons were also observed within the monkey basal forebrain. In contrast, identical cytochemical experiments revealed that virtually none of the magnocellular neurons within the basal forebrain of humans were GAL-ir. Rather, a network of GAL-containing fibers and terminal-like profiles were observed encompassing the magnocellular cholinergic neurons in humans. This immunohistochemical species difference does not appear to be mediated by procedural or technical factors since human brains contained numerous GAL-ir perikarya and fibers within adjacent regions including the bed nucleus of the stria terminalis and medial hypothalamus. These data demonstrate that there is a prominent phylogenetic transformation in primates with respect to the processing of GAL-mediated information. This species difference potentially relates to the severe basal forebrain degeneration reported in human dementias and illustrates the possible need for a reevaluation of the use of monkeys as an animal model of human basal forebrain-related cognitive dysfunction.

Aged↗
PubMed1977

Preparation and evaluation of a noninfectious monkey pox virus vaccine.

Monkey pox virus was mechanically disrupted by low temperature and high pressure into soluble and insoluble fractions. Soluble fractions elicited virus-neutralizing antibodies (1:20 to 1:160) in rabbits, whereas the insoluble (in saline) fractions did not (less than 1:5). No infectious virus was detected after the disruption procedure. Rhesus monkeys immunized with the soluble fraction elicited virus-neutralizing (1:1,200), complement-fixing (1:16), and hemagglutinating-inhibiting (1:80 to 1:160) antibody titers and were completely protected against monkey pox virus-induced disease. This model of monkey pox virus subunit vaccine preparation may prove to be useful in developing an efficacious noninfectious vaccinia vaccine for use in high-risk individuals.

Animals↗
PubMed2003

Antibody-dependent enhancement, a possible mechanism in augmented pulmonary disease of respiratory syncytial virus in the Bonnet monkey model.

Bonnet monkeys develop an enhanced disease after immunization with the formalin-inactivated (FI) respiratory syncytial virus (RSV) vaccine that is characterized by increased viral replication in perivascular sites of the lung. These sites contain many mononuclear cells, which are known to be permissive for RSV replication. To test the hypothesis that FI-RSV vaccine stimulates the production of enhancing antibodies that serve to increase the replication of RSV in macrophages, in vitro studies were done. Antibody-dependent enhancement was observed in animals immunized with FI-RSV but not in control animals with primary and tertiary infections or those immunized with FI-Vero cell culture. In the presence of serum samples from animals immunized with FI-RSV, an increased number of U937 cells was infected. The enhancement index correlated positively with the pathologic scores of the FI-RSV-vaccinated monkeys.

Animals↗