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A method to cryopreserve semen from the Vervet monkey (Cercopithecus aethiops) has been developed, yielding a mean post thaw recovery of 63.60% of pre-freeze progressive motility. The extender contained a TES-TRIS buffer, egg yolk, dextrose, streptomycin, penicillin, and glycerol as cryoprotectant. The pH ranged from 7.10-7.18 and the osmolality was 330-345 mOsmol/L.
Previous studies have identified the monkey as an animal model for the genetic polymorphism affecting human hepatic cytochrome P450 2D6 enzyme. However, contrary to an earlier in vivo observation, the present study failed to find evidence of polymorphism of this enzyme activity in liver preparations of 84 African green (Cercopithecus aethiops) monkeys. The kinetics of dextromethorphan O-demethylation were similar in liver microsomes from African green (n = 21) and Crab eater (Macaca fascicularis, n = 7) monkeys (Km = 1.1 +/- 0.07 and 1.7 +/- 0.27 microM; Vmax = 215 +/- 71.7 and 152 +/- 21.1 nmol/mg/h, respectively). These Km values were lower and less variable than those in liver microsomes from 10 human extensive metabolizers (5.3 +/- 2.43 microM). Furthermore, the Vmax of the reaction in human liver microsomes was significantly lower (32 +/- 15.7 nmol/mg/h; P < .001). Inhibitor constants (Ki values) determined in monkey and human liver microsomes were highly correlated (r = 0.97), but two high-affinity inhibitors of the human enzyme (quinidine and lobeline) were approximately 40-fold less potent in monkey livers than in human livers. These data show that the monkey enzyme is functionally homologous, but is not identical to human hepatic cytochrome P450 2D6. Failure to observe poor metabolizer monkeys does not preclude their potential usefulness in evaluating the role of human hepatic cytochrome P450 2D6 activity in drug addiction and neurotoxicity because of the possibility of producing poor metabolizer phenocopies by potent hepatic cytochrome P450 2D6-like enzyme inhibitors in monkeys.
In dyslipidemic or hyperlipidemic patients etofibrate (CAS 31637-97-5, active principle of Lipo-Merz-retard) improves plasma lipoprotein profiles by reducing low density lipoprotein cholesterol and triglycerides. Experimentally, it also promotes fibrinolysis and thrombolysis and reduces the susceptibility of lipoproteins to oxidative stress. In order to investigate the possible efficacy of etofibrate on atherosclerosis, a study in African Green Monkeys was performed. To accelerate atherogenesis, balanced groups of adult male Vervetes (Cercopithecus aethiops) were fed an atherogenic diet, with and without etofibrate, while negative controls received a prudent diet. Total dietary risk exposure was 38 months, with etofibrate treatment during the final 27 months. The etofibrate dose achieved plasma concentrations of clofibric acid comparable to the one achieved clinically. Necropsy demonstrated lesions equivalent to human atherosclerosis types I-VII, which were compared between treatments both macroscopically and microscopically. Peripheral atherosclerosis was significantly less frequent after etofibrate treatment than in positive controls. In aortas, etofibrate probably ameliorated atherogenesis, as defined by proliferation of smooth muscle and foam cells, and accumulation of cholesterol crystals. Effective reduction of plasma cholesterol by etofibrate was confirmed. In conclusion, anti-atherogenic efficacy of etofibrate was demonstrated in a non-human primate model of accelerated atherogenesis. The results on peripheral atherosclerosis confirm the preliminary clinical data in patients suffering from peripheral vascular occlusion.
As a model for AIDS, experimental infections of old-world monkeys with various simian immunodeficiency viruses (SIV) are frequently carried out to study mechanisms of pathogenicity. For example, SIVsmmPBj14 was isolated from a pig-tailed macaque (Macaca nemestrina) suffering from acute viral disease. The molecular virus clone SIVsmmPBj1.9, which displays close genetic homology to other related SIVs, was shown to induce an acute viral disease in vivo after infection of pig-tailed and rhesus macaques. The acute pathogenicity of SIVsmmPBj1.9 was correlated with its unique ability to replicate in non-stimulated peripheral blood mononuclear cells from pig-tailed macaques. We have exploited this in vitro assay to resolve putative pathogenic genetic determinants of another SIV, namelySIVagm3, isolated from African green monkeys (Cercopithecus aethiops). Hybrid viruses encompassing subgenomic regions of SVsmmPBj1.9 in place of comparable regions of molecular virus clone SIVagm3mc were constructed and tested for their ability to replicate in non-stimulated PBMC from pig-tailed macaques and African green monkeys. Only those hybrid viruses comprising the U3 region of the viral LTR of SIVsmmPBj1.9 replicated in non-stimulated peripheral blood mononuclear cells. This in vitro assay will be used to determine the potential of SIV and of hybrid viruses between different SIVs to induce acute viral disease in vivo. It will help to avoid excessive experimental infections of monkeys with respective hybrid viruses for determining genetic determinants of acute pathogenicity of immunodeficiency viruses.
An outbreak of septicemia caused by S. zooepidemicus in representatives of 5 species of lower monkeys, viz. Macaca mulatta (5), Macaca nemestrina (1), Macaca fascicularis (2), Cercopithecus aethiops (2), Mandrillus sphinx (1), is described. The disease was accompanied by the symptoms of enteric infection and well responded to etiotropic therapy with antibiotics of the penicillin row. The source of this infection was not established. Until now it is one of few descriptions of enteric infection in lower monkeys caused by S.zooepidemicus.
In 1978-1991 the USSR-Guinea Virological and Microbiological Laboratory functioned in Kindia, the Republic of Guinea. Arbovirus activity in this country was studied by a number of virologists and other specialists. Their personal contribution and achievements in this collaboration are reflected in the present paper. About 74,000 mosquitoes, 100,000 Ixodidae ticks, 1,500 wild birds, 2,700 bats, 106 monkeys, and 308 other mammals, 927 blood samples collected from febrile patients were examined in 1978-1989, using inoculation of new-born white mice. As a result of this work 127 strains of the following arboviruses were isolated: Chikungunia (1 strain), Dengue 2 (4), Saboya (7), Wesselsbron (1), Bunyamwera (4), M'Poko (5), Rift Valley Fever (6), CHF-Congo (9), Dugbe (22), Bhanja (6), Forecariah (2), Jos (26), Abadina (15), Kindia (2), Ark 6956 (1), Fomede (2), Bluetongue (9), Mossuril (2), AnK 6009 (1), and Kolente (2). Dengue 2, Wesselsbron, Bunyamwera, M'Poko, Kindia, Mossuril viruses were isolated from mosquitoes. Ixodidae ticks were sources for isolation of Chikungunia, Saboya, CCHF, Dugbe, Bhanja, Forecaciah, Jos, Abadina, Kindia, Ark 6956, Fomede, Bluetongue, and Kolente viruses. Saboya, RVF, Fomede, Kolente, AnK 6909 were isolated from bats (Chiroptera); Saboya, Abadina, and Bluetongue viruses from birds. One strain of Dugbe virus was originated from the brain of Cercopithecus patas. Bunyamwera and Abadina viruses were isolated from the blood of two febrile patients. Serological identification of many strains was kindly conducted at the Pasteur Institute, Dakar (J. P.Digoutte) and some at the YARU, USA (R. Shope). Kindia and Ark 6956 (Reovirus, gr. Palyam), Fomede (gr. Chobar Gorge), Forecariah (Bunyavirus, gr. Bhanja), Kolente (Rhabdovirus) were identified as an original type of Lagos bat virus. The results of seroepidemiological surveys are also presented.
Endocrine cells in the duodenal mucosa of some primates (Cercopithecus aetiops, Macaca cinomolgus-nemestrina and Macaca rhesus) have been studied with immunohistochemical methods for chromogranins. Material sampling immediately after death (by carotid bleeding concomitantly with formalin 10% perfusion) was helpful in the study of endocrine cells. The location and number of endocrine cells of the duodenal mucosa of the primates under study are generally similar to those of humans. The use of an antibody cocktail against all three Cgs/Sgs appears to be the method of choice to identify neuroendocrine granule-containing cells. When comparing the results of this study with those obtained by us in a previous work by silver staining, the Grimelius technique is recommended together with the immunohistochemical techniques for chromogranins in the practice of the usual diagnosis of the endocrine pathology.
Cultural strains of hepatitis A virus (HAV) have been isolated from spontaneously infected Macaca mulatta (HAV-MM), Papio hamadryas (HAV-PH), African green monkeys Cercopithecus aethiops (HAV-CA), and patients (HAV-H). The strains replicate in continuous cells lines AGMK, 4647, Vero, and FRhk-4. AGMK and 4647 cells are the most permissive at 32 degrees C. Virus propagation was not associated with the cytopathic effect and could be detected by enzyme immunoassay (EIA), immune electron microscopy (IEM), and molecular hybridization method (MHM). The morphological and antigenic properties of the above monkey and human strains did not differ in EIA and IEM with polyclonal antibodies and for one most conservative genome sites in the VP1 domain. Cultural strains retained their pathogenicity for monkeys. HAV strains are proposed to be used as HAV antigen in immunological tests and for hepatitis A induction in monkeys.
The prevalence of Herpesvirus papio 2 (HVP2) in several groups of captive and wild-caught baboons was determined by detection of anti-HVP2 antibodies in 133 sera of adult baboons. Over 90% of newly imported (wild-caught) adult olive baboons (Papio anubis) from Kenya and chacma baboons (P. ursinus) from South Africa were found to have anti-HVP2 titers. Similarly, approximately 85% of captive breeding colony baboons (P. anubis and P. cynocephalus) were seropositive for HVP2. Infected animals were generally easily identifiable by enzyme-linked immunosorbent assay because anti-HVP2 IgG titers in immune animals were usually high (16,000 to 64,000). There was little variation in the relative reactivity patterns of individual HVP2-immune sera when tested against herpes simplex viruses 1 and 2, monkey B virus, H. cercopithecus 2, and HVP2, or against different HVP2 strains. Also, differences were not detected between reactivity of olive and chacma baboon immune sera. Analysis of the polypeptide specificity of immune sera by western blot identified four viral antigens that were consistent targets of immune sera. These antigens were the gB glycoprotein, a pair of unidentified glycoproteins of 80 to 100 kDa, the gD glycoprotein, and a series of smaller capsid proteins. Additional viral proteins were variably recognized by individual immune sera. The results of this study indicate that HVP2 is a common infection of baboons; there is little antigenic variation among HVP2 strains; and there are several HVP2 antigens that represent consistent targets of the anti-HVP2 immune response of baboons.
BACKGROUND: Ebola virus has been responsible for explosive lethal outbreaks of hemorrhagic fever in both humans and nonhuman primates. Previous studies showed a predilection of Ebola virus for cells of the mononuclear phagocyte system and endothelial cells. OBJECTIVE: To examine the distribution of lesions and Ebola virus antigen in the tissues of six adult male African green monkeys (Cercopithecus aethiops) that died 6 to 7 days after intraperitoneal inoculation of Ebola-Zaire (Mayinga) virus. METHODS: Tissues were examined histologically, immunohistochemically, and ultrastructurally. RESULTS: A major novel finding of this study was that fibroblastic reticular cells were immunohistochemically and ultrastructurally identified as targets of Ebola virus infection. CONCLUSIONS: The role of Ebola virus-infected fibroblastic reticular cells in the pathogenesis of Ebola hemorrhagic fever warrants further investigation. This is especially important because of recent observations indicating that fibroblastic reticular cells, along with the reticular fibers they produce, maximize the efficiency of the immune response.
In this work the experimental model of hepatitis A on monkeys, adequate to human hepatitis A, was used. Ten monkeys (6 Macaca mulatta and 4 Cercopithecus aethiops) were reinfected with different doses of hepatitis A virus (HAV) a year after recovery from spontaneous and experimental hepatitis A. The monkeys were completely resistant to the inoculation of the virus in moderate doses (10(3) ID50). The inoculation of HAV in large doses (10(4)-10(5) ID50) induced a mild form of this infection in the animals with a transient rise in the level of serum alanin aminotransferase and HAV shedding in feces, but in the absence of morphological changes in the liver. It should be specially pointed out that after the reinfection of monkeys virus shedding in feces was observed, which may be of great epidemiological importance. After reinfection the absence of IgM and a pronounced rise in the titers of IgC antibodies were observed.
Melarsoprol has remained the chosen drug for the late-stage treatment of human African trypanosomiasis (HAT) due both to Trypanosoma brucei (T.b.) gambiense and T.b. rhodesiense; however, arsenical encephalopathies, which are often fatal, occur in 5-10% of the treated cases. To date, two major problems have not been solved. The first one is the precise diagnosis of early involvement of the central nervous system (CNS) which determines the therapeutics to be administered. The second one is linked to the lack of data on in vivo efficacy of products which are effective in vitro against trypanosomes. Answers have to be provided by experimental animal models of HAT. Such models would allow for better studies of the pathology and pathogenesis of the disease, as well as therapeutic trials of potentially effective new drugs or combinations. We have developed acute and chronic murine and sheep experimental animal models of HAT infected by T. b. brucei. Meningoencephalitis and neurological signs are relatively difficult to obtain in murine models and require artificial means, such as suramin treatment on day 21 after-infection. The chronic murine model has demonstrated CNS involvement with meningitis, followed by meningoencephalitis with progressive astrocytosis. The sheep model develops a disease with CNS complications and cerebrospinal fluid can be collected. In the sheep model, we have described anti-galactocerebrosides antibodies, which represent major components of myelin, which may indicate an autoimmune process in the CNS. We then described these antibodies in the cerebrospinal fluids and sera from patients at a late-stage of the disease. From a therapeutic point of view, we have cured mice or sheep with low doses of melarsoprol, or with the nitroimidazole derivatives Ro 15-0216 and megazol, alone or combined with suramin. Further studies of these nitroimidazole compounds, which could be proposed for human use, have to be carried out on a-primate model infected by T.b. gambiense. To our knowledge, this primate model is not available. This is why we have recently developed a T. b. gambiense primate model of HAT on Cercopithecus aethiops.
Necropsies performed between 1989 and 1995 on 15 African rope squirrels (Funisciurus substriatus) and 20 African ground squirrels (Xerus erythropus) from the Baltimore Zoo revealed 13 cases of gongylonemiasis. Nematodes were embedded in the epithelium of the esophagus, pharynx, buccal mucosa, and tongue, resulting in varying degrees of esophagitis, pharyngitis, stomatitis, and glossitis, respectively. Routine fecal examinations were negative, and the nematodes appeared to be unaffected by repeated treatments with ivermectin. Most of the affected animals had shown clinical signs of dyspnea and/or inanition and emaciation. Suppurative rhinitis was also a frequent finding at necropsy and was associated with the presence of the nematodes in eight animals. Dissection of whole nematodes from formalin-fixed specimens revealed morphologic features consistent with Gongylonema macrogubernaculum, a species previously only reported in nonhuman primates. The squirrels were housed in the same building with numerous primate species, and a review of pathology records revealed esophageal gongylonemiasis in three lion-tailed macaques (Macaca silenus), lingual gongylonemiasis in a spotnose monkey (Cercopithecus buettikoferi), and buccal gongylonemiasis in a brown-headed tamarin (Saguinus fuscicollis). Examination of whole nematodes dissected from one of the lion-tailed macaques also demonstrated the unique morphology of G. macrogubernaculum. Nematodes belonging to the species Gongylonema are acquired by ingestion of the intermediate host, the cockroach. This is the first report of G. macrogubernaculum in a nonprimate species and suggests that captive African squirrels can serve as reservoir hosts for this parasite in a zoo environment.
This study demonstrates that monkey esophagus is a more sensitive substrate than guinea pig esophagus for the demonstration of serum antibodies, in patients with pemphigus vulgaris. In this study, for example, five patients with active pemphigus who had demonstrable pemphigus antibodies on monkey esophagus substrate failed to demonstrate pemphigus antibody activity when guinea pig esophagus was employed as a substrate. Furthermore, pemphigus antibody titers determined on monkey esophagus substrate frequently exceeded, by several dilutions, titers detected with guinea pig esophagus. By contrast, in no instance did we detect pemphigus antibody titer activity on guinea pig esophagus in excess of the pemphigus antibody activity detected on monkey esophagus. The reason for the disparity in the sensitivity of the guinea pig and monkey esophagus substrates is unknown.
Colloid solutions of technetium Tc 99m and india ink injected into the retrobulbar space of the cynomolgus monkey outside the extraocular muscle cone were removed from the orbit by the lymphatic vessels of the conjunctiva and eyelids and were then concentrated within the lymph nodes that drained the conjunctival and eyelid areas. Colloid solutions injected into the retrobulbar space inside the extraocular muscle cone did not reach the conjunctiva and did not collect in any lymph nodes over a 24-hour period. Within the orbit, the injected colloids spread along the planes of the connective-tissue septa. No lymphatic vessels were identified within the orbits posterior to the conjunctiva. Small amounts of india ink left the posterior orbit and ultimately entered the contralateral orbit. This posterior pathway did not lead to lymphatic vessels or lymph nodes and therefore does not appear to represent a prelymphatic pathway.
Hyperopic hydrogel intracorneal lenses were successfully implanted into 27 of 33 primate eyes. All eyes were evaluated preoperatively and postoperatively at monthly intervals for clinical appearance and refractive alteration. In a preliminary surgical series, several factors, such as tight sutures and implant design, resulted in a poor refractive yield. The final surgical series used a microkeratome with a pediatric microkeratome ring for smooth interface cuts, interrupted suturing with sufficient tension to align the wound without compression, a suture through the lens to prevent its dislocation, and intraoperative keratometry to reduce postoperative cylinder. The predicted vs measured refractive alteration for a range of 6 to 20 diopters had a correlation coefficient of .95. Keratometry changes correlated to the refractive changes with a coefficient of .97 but understand the change in refraction created by the surgery.
Dominant male adult vervet monkeys have whole-blood serotonin concentrations approximately twice those of subordinate adult males. We examined the effects of spontaneous and induced changes in social status, temporary isolation from the social group, and membership in single male groups on whole-blood serotonin concentrations. We found that in male vervet monkeys, elevated blood serotonin concentration is a state-dependent consequence of active occupation of the dominant male social position, and we believe that a reinterpretation of the significance of hyperserotonemia in humans may be warranted.
This study investigates subadult growth spurts in a large sample of anthropoid primates, including humans. Analyses of body mass growth curves show that humans are not unique in the expression of female and male body mass growth spurts. Subadult growth spurts are observed in both New World and Old World anthropoid primates and are more common in males than in females. Allometric analyses of growth spurts indicate that many aspects of primate growth spurts are strongly correlated with species size. Small species tend not to exhibit growth spurts. Although male and female scaling patterns for velocity and size measures are comparable, scaling relations of variables that measure the timing of growth spurts differ by sex. These patterns can be related to sexual differences in life histories. Scaling analyses further show that humans do not depart substantially from patterns that describe other anthropoid primates. Thus, in relative terms, human growth spurts are not exceptional compared to this sample of primates. The long absolute delay in the initiation of the human growth spurt may be of substantial evolutionary importance and serves to distinguish humans from other primates. In essence, humans exhibit growth spurts that are comparable to other primates in many respects. However, human growth spurts are shifted to very late absolute ages.