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PubMed1995

[Standardization of conditions for the evaluation of effectiveness of antibacterial drugs in pneumonic plague in sacred baboons].

The signs of pneumonic plague in sacred baboons infected by aerosol are: fever, hurried breathing, depression and constantly increasing bacteremia. Some infected animals isolate the plague microbes while coughing and thus could be a source of the infection. By the clinical and pathomorphological signs, pneumonic plague in sacred baboons is similar to that in humans which makes it possible to use the animals in the development of schemes for special prophylaxis and treatment of the disease. In efficacy estimation of antibacterial drugs sacred baboons should be infected by aerosol by highly virulent strains of Y. pestis in doses of 1.10(4)-1.10(5) live microbes. The treatment of the animals should be started from the moment of the rectal temperature increase to 39.5 degrees C or higher after collecting the blood specimens for the bacteriological tests. It was shown that a two-day course of the treatment with antibacterial drugs was not efficient in the animals with pneumonic plague. The use of streptomycin, gentamicin, netilmicin or ciprofloxacin for 7 days cured all the infected animals. The use of streptomycin in the therapeutic doses was not efficient in the animals whose blood specimens of 1 cm3 contained 4.10(4) or more plague microbes by the moment when the treatment was started.

Animals↗
PubMed1997

Hepatic hemosiderosis in common marmosets, Callithrix jacchus: effect of diet on incidence and severity.

We examined the effect of dietary iron concentration on the incidence of hepatic hemosiderosis in common marmosets (Callithrix jacchus) and assessed the impact of hemosiderosis on animal health. Thirteen young adult common marmosets were fed nutritionally balanced natural-ingredient diets formulated to contain either 100 or 500 ppm of iron. Six were fed the low-iron and seven received the high-iron diet. Baseline blood values and liver iron content were determined for each animal. Animals were weighted monthly, blood work (hematologic analysis, serum iron concentration, total iron-binding capacity, percent of transferrin saturation) was performed semi-annually, and liver biopsies for iron analysis were obtained after marmosets had consumed the test diets for 13 months or at necropsy. Midway in study, the high-iron diet was reformulated to contain 350 ppm of iron because of the death of a male which had consumed that diet for 7 months. Four of seven marmosets fed the high-iron diet died during the first year of the study, compared with one death in the low-iron cohort. The mean increase in liver iron content of the marmosets fed the high-iron diet was 6,371 micrograms/g, dry weight analysis. In contrast the low-iron cohort had a mean decrease of 621.5 micrograms/g. These results indicate that liver iron content can be affected by dietary iron intake. The increased mortality in the marmosets fed the high-iron diet also suggests that hepatic hemosiderosis can be detrimental to marmoset health.

Animals↗
PubMed1980

Experimental pelvic inflammatory disease provoked by Chlamydia trachomatis and Mycoplasma hominis in grivet monkeys.

Pelvic inflammatory disease was produced by inoculation with Mycoplasma hominis and Chlamydia trachomatis directly into the fallopian tubes of grivet monkeys. The effects of various routes of infection were examined. The method of inoculation with the infecting agent influenced the resulting clinical spectrum. In these monkeys significant changes in humoral antibodies occurred with inflammation caused by both M. hominis and C. trachomatis. Development of cellular antibodies against M. hominis could be demonstrated in all experimentally infected monkeys, whereas no such antibodies could be detected in monkeys with chlamydia salpingitis. M. hominis in female grivet monkeys may spread from the cervix or the uterine cavity, probably via blood vessels and lymphatics, producing parametritis and "exosalpingitis." C. trachomatis may spread from the cervix via the uterine mucosa, producing endosalpingitis with destruction of the epithelium. The infection caused by M. hominis in the genital tract of female grivet monkeys resembles "nongonococcal" salpingitis while C. trachomatis produces infection resembling "gonococcal" salpingitis.

Animals↗
PubMed1985

Aging in the musculoskeletal system of rhesus monkeys: II. Degenerative joint disease.

In order to discuss the rate and onset of adult aging in rhesus monkeys, 55 adult animals from the Wisconsin Regional Primate Research Center and the University of Wisconsin Psychology Primate Laboratory were examined. Degenerative joint disease (DJD) at the hip and spine was scored, and loss of passive joint mobility at the hip was measured. Development of DJD at both the hip and spine was significantly and positively correlated with age. Spinal changes, especially at the thoraco/lumbar intervertebral symphyses, appeared to develop somewhat more rapidly than hip degeneration. In some individuals, DJD was observed soon after the completion of growth, but pronounced changes seldom occurred before the middle of the second decade of life. Similarly, age-dependent losses of passive joint mobility appeared to begin early in ontogeny and to become increasingly pronounced in the aging adult. Although interspecific comparisons are difficult due to intraspecies and intraindividual variation, the timing of musculoskeletal aging in the rhesus spine and hip differs from that observed in humans in a way that parallels previously documented species differences in patterns of musculoskeletal growth. These observations and data on age-related change in other systems, suggest that rates and durations of many ontogenetic processes in rhesus monkeys are approximately three times as fast and one-third as long as those of the corresponding human processes. Importantly, differences in the timing of reproduction do not appear to follow the same scaling factor observed in other systems. Although reproduction may, therefore, be under separate control, the consistent pattern observed in other aspects of somatic growth and aging supports the hypothesis (Cutler, 1976; Sacher, 1978) that evolutionary changes in ontogeny have resulted from selection acting upon a few genes with widespread regulatory effects.

Aging↗
PubMed1997

Mononeuropathy multiplex in rhesus monkeys with chronic Lyme disease.

Peripheral neuropathy is a recognized but poorly understood manifestation of Lyme disease. We performed serial electrophysiological studies on 8 rhesus monkeys chronically infected with the JD1 strain of Borrelia burgdorferi and compared the results with those of similar studies on 10 uninfected control monkeys. Four infected and 2 uninfected animals underwent sural nerve biopsy. Five of the infected and 1 of the uninfected animals also had postmortem neuropathological examinations. Altogether, 5 of the infected monkeys demonstrated primarily axonal-loss-variety multifocal neuropathies. Only one nerve lesion exhibited findings compatible with demyelination. Pathologically, peripheral nerve specimens showed multifocal axonal degeneration and regeneration and occasional perivascular inflammatory cellular infiltrates without vessel wall necrosis. Free spirochetal structures were not seen, but several macrophages exhibited positive immunostaining with a highly specific anti-B. burgdorferi, 7.5-kd lipoprotein monoclonal antibody. In the infected animals, serial analysis of serum antibodies to B. burgdorferi showed increasing numbers of IgG specificities and new IgM specificities, suggesting persistent infection. Thus, peripheral neuropathy in the form of a mononeuropathy multiplex develops frequently in rhesus monkeys chronically infected with B. burgdorferi. The pathogenesis of these nerve lesions is not yet known, but our studies suggest an immune-mediated process perhaps driven by persistent infection with B. burgdorferi.

Animals↗
PubMed2005

Echocardiographic diagnosis of muscular ventricular septal defect in a cynomolgus monkey (Macaca fascicularis).

There have been only a few case reports of heart disease in monkeys. In the case we present, a cardiac murmur was auscultated in a 26-month-old male cynomolgus monkey during a routine physical examination. Echocardiography of this monkey revealed features indicating blood flow from the left ventricle to the right ventricle through the ventricular septum. These findings clarified that the animal had a muscular interventricular septal defect.

Animals↗
PubMed1987

Development of adult T-cell leukemia-like disease in African green monkey associated with clonal integration of simian T-cell leukemia virus type I.

Proviral integration of a simian retrovirus highly homologous to human T-cell leukemia virus type I was examined in cellular DNAs extracted from primary peripheral blood lymphocytes of 31 adult African green monkeys (Cercopithecus aethiops) that were seropositive for simian T-cell leukemia virus type I (STLV-I). Among these monkeys, one case with overt leukemia, showing pleomorphic leukemia cells similar to those in human adult T-cell leukemia (ATL), and five cases in a preleukemic state of ATL-like disease were found. Judging from the integration site of the provirus genome, primary lymphocytes of these leukemic or preleukemic cases contained monoclonally proliferated STLV-I-infected cells, whereas lymphocytes of other seropositive monkeys without hematological abnormalities were polyclonal, and those of seronegative monkeys did not contain the provirus. The restriction patterns with PstI ans SstI of most STLV-I proviruses were identical to those of the previous isolate from this species, but in three monkeys there was a deletion of one PstI site. From the correlation of the development of simian ATL-like disease with the monoclonal integration of the STLV-I provirus genome, it should be indicated that STLV-I has similar leukemogenicity to human T-cell leukemia virus type I, and so STLV-I infection in African green monkeys will be useful as an animal model of human ATL.

Animals↗
PubMed1990

Mechanisms for reduced total lung capacity at birth and during hyaline membrane disease in premature newborn monkeys.

To determine whether the cause of reduced total lung capacity (TLC) in hyaline membrane disease (HMD) is due to alveolar collapse, alveolar edema, or both, TLC was measured by N2-washout in premature Macaca nemestrina monkeys during the first 3 h of life. The TLC of animals with HMD was only one-third that of healthy premature monkeys over the first 3 h of life (p less than 0.01). At 3.5 h, lung tissue was rapidly frozen in situ during lung inflation to TLC. Samples of frozen lung tissue were freeze dried, embedded, sectioned, and examined by point counting. Animals with HMD had alveolar saccules filled with the residue of proteinaceous fluid, but little alveolar collapse was noted. The proportion of points falling on empty alveolar spaces was 74% in the healthy animals but only 18% in animals with HMD (p less than 0.01); there was a 70-fold increase in the residue present in alveoli of animals with HMD (p less than 0.05). In a separate experiment, rapid serial measurements of TLC by N2-washout showed that healthy premature monkeys, but not those with HMD, have a steady increase in TLC during the first few minutes of life, presumably due to clearance of lung liquid. Although the initial cause of reduced TLC in HMD appears to be inadequate clearance of fetal lung liquid, by 3 h of age proteinaceous alveolar edema is primarily responsible.

Animals↗
PubMed1993

Early and early disseminated phases of Lyme disease in the rhesus monkey: a model for infection in humans.

We demonstrate that Borrelia burgdorferi infection in the rhesus monkey mimics the early and early disseminated phases of human Lyme disease. Clinical, bacteriological, immunological, and pathological signs of infection were investigated during 13 weeks after inoculation of the spirochete. Three animals were given B. burgdorferi (strain JD1) by needle inoculations, six animals were exposed to the bite of B. burgdorferi-infected Ixodes dammini ticks, and three animals were uninfected controls. B. burgdorferi could be recovered from all animals that were given the spirochete. Bacteria were detectable until week 6 postinoculation (p.i.) in blood, until week 8 p.i. in skin biopsies, and at 10 weeks p.i. in the conjunctiva of one of two animals which developed conjunctivitis. Erythema migrans (EM) appeared in one of the three animals infected by needle inoculation and in five of the six animals infected by ticks. Deep dermal perivascular lymphocytic infiltrations (characteristic of human EM) were observed in all animals showing EM clinically. Both EM and conjunctivitis were documented concomitantly with the presence of the spirochete. Lethargy, splenomegaly, and cerebrospinal fluid pleocytosis were also noted in some animals, but the direct connection of these signs with the infection was not shown. The appearance rate of immunoglobulin M and immunoglobulin G antibodies to B. burgdorferi, as well as the antigen spectra recognized, were remarkably similar to those seen in humans. Serum antibodies from infected animals were able to kill B. burgdorferi in vitro in the presence of rhesus complement. The rhesus monkey model appears to be useful for the investigation of the immunology and pathogenesis of Lyme disease and for the development of immunoprophylactic, diagnostic, and chemotherapeutic protocols.

Animals↗