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Results for “MONKEY DISEASES”

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At least 253 records · Page 14Linked to original sources
PubMed1971

Respiratory pathogens in monkeys.

Respiratory disease in a dynamic colony of nonhuman primates during a 4-year period was due primarily to infections caused by Klebsiella pneumoniae, Diplococcus pneumoniae, Bordetella bronchiseptica, Pasteurella multocida, and Haemophilus influenzae. The principal secondary invaders were Escherichia coli, Staphylococcus aureus, and streptococci. A high fatality rate was associated with infections caused by each of the primary pathogens, and females appeared to be more susceptible than males. Incidence of respiratory disease was greatest in the fall and early winter; however, at all times newly colonized monkeys had a higher infection rate than conditioned monkeys. Infections were occasionally confined only to the lungs and were sometimes present without grossly observable lung lesions. The information given on susceptibility of 10 species of nonhuman primates to respiratory infections provides a basis for developing disease models.

Journal Article↗
PubMed1988

Invasive amebiasis in naturally infected New World and Old World monkeys with and without clinical disease.

Histopathological preparations of cecum and colon from monkeys naturally infected with invasive Entamoeba histolytica were examined to determine the distribution of amebae in the tissues and the types of lesions, if any, associated with them. Infections were studied in 3 New World species (10 Callicebus moloch, 1 C. torquatus, and 2 Aotus trivirgatus) and 3 Old World species (8 Macaca mulatta, 6 Erythrocebus patas, and 1 Cercopithecus aethiops). Amebiasis was recorded as the principal or a contributing cause of death of all of the 13 New World monkeys and in 6 of the 15 Old World monkeys; amebiasis was detected in the rest of the monkeys only after tissues were re-examined specifically for amebae. Amebae causing no apparent damage were found in the lamina propriae, mainly at the muscularis mucosae. Most frequent were colonies or aggregates of amebae in the crypts between the epithelium and basement membrane, causing either no evident necrosis or changes ranging from necrosis and disarrangement of adjacent cells to complete destruction of the epithelium and reduction of the cells to pyknotic bodies. A lesion interpreted as possibly characteristic of carrier-state invasive amebiasis was destruction of the epithelium in patches of mucosal crypts, not leading to ulceration. Uncommon but present in both New and Old World monkeys were typical areas of surface erosion and classical flask-shaped ulcers. The observations show that in some species of Old World monkeys amebiasis can be invasive without causing clinical disease.

Amebiasis↗
PubMed1982

Experimental hyaline membrane disease in the premature monkey: effects of antenatal dexamethasone.

A blind, randomized trial of antenatal glucocorticoid treatment was conducted using the premature monkey (Macaca nemestrina) model of hyaline membrane disease (HMD). Twelve dams received dexamethasone (2 mg/dose) 72, 48, and 24 h before abdominal delivery at 135 +/- 1 days of gestation. Twelve control animals received saline. Infants of dexamethasone-treated dams had significantly lower incidence and severity of HMD than did infants of control animals (50 versus 92%, p less than 0.05). Improvement with treatment was markedly greater for males than for females. Differences in volume-pressure behavior of the excised lungs included greater distensibility in the infants from dexamethasone-treated dams (20.6 +/- 7.1 ml/g dry lung versus 14.7 +/- 6.1, p less than 0.05) and enhanced deflation stability with treatment. Accelerated production of surface active material (SAM) phospholipids in infants from dexamethasone-treated dams was indicated by increases in total lung phospholipid (84.5 +/- 8.1 mg/g dry lung versus 75.1 +/- 9.9, p less than 0.025), alveolar lavage fluid phospholipid (5.65 +/- 3.33 mg/g dry lung versus 3.01 +/- 1.84, p less than 0.05), and alveolar lavage fluid disaturated phosphatidylcholine (DPC) (2.47 +/- 1.84 mg/g dry lung versus 1.06 +/- 1.05, p less than 0.05). Incorporation of 14C-palmitate into lung lipid was not influenced by dexamethasone, but a significantly greater portion of the label appeared in the DPC fraction with treatment. Antenatal dexamethasone treatment was successful in reducing the incidence and severity of experimental HMD in this animal model; the beneficial effects of treatment were associated with accelerated maturation of fetal pulmonary functions, including, but not limited to, synthetic metabolism of SAM phospholipid.

Animals↗
PubMed1997

Protective effect of encapsulated cells producing neurotrophic factor CNTF in a monkey model of Huntington's disease.

Huntington's disease is a genetic disorder that results from degeneration of striatal neurons, particularly those containing GABA (gamma-aminobutyric acid). There is no effective treatment for preventing or slowing this neuronal degeneration. Ciliary neurotrophic factor (CNTF) is a trophic factor for striatal neurons and therefore a potential therapeutic agent for Huntington's disease. Here we evaluate CNTF as a neuroprotective agent in a nonhuman primate model of Huntington's disease. We gave cynomolgus monkeys intrastriatal implants of polymer-encapsulated baby hamster kidney fibroblasts that had been genetically modified to secrete human CNTF. One week later, monkeys received unilateral injections of quinolinic acid into the previously implanted striatum to reproduce the neuropathology seen in Huntington's disease. Human CNTF was found to exert a neuroprotective effect on several populations of striatal cells, including GABAergic, cholinergic and diaphorase-positive neurons which were all destined to die following administration of quinolinic acid. Human CNTF also prevented the retrograde atrophy of layer V neurons in motor cortex and exerted a significant protective effect on the GABAergic innervation of the two important target fields of the striatal output neurons (the globus pallidus and pars reticulata of the substantia nigra). Our results show that human CNTF has a trophic influence on degenerating striatal neurons as well as on critical non-striatal regions such as the cerebral cortex, supporting the idea that human CNTF may help to prevent the degeneration of vulnerable striatal populations and cortical-striatal basal ganglia circuits in Huntington's disease.

Animals↗
PubMed1981

Abnormal behavior patterns in rhesus monkeys: symptoms of mental disease.

This paper describes the morphology of abnormal behavior of rhesus monkeys which had experienced a certain degree of social isolation. Analysis of the morphology of the behavior starts from the hypothesis that abnormal activities should preferably be interpreted as distortions of normal behavior. The results indicate that all abnormal activities seemed to be symptoms of one social deprivation syndrome, because all activities could tentatively be interpreted as more or less idiosyncratically distorted, often self-directed forms of normally social behavior. The results also illustrate that abnormal behavior patterns can be considered at different levels of integration which should be clearly distinguished in comparative studies. Similarities to the behavior of human mental patients suggest that social deprivation is a prominent factor in a wide variety of mental diseases.

Animals↗
PubMed1985

Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans.

Thiamine deficiency in the monkey is the animal counterpart of Wernicke's disease in humans. In the present study, thiamine deficiency was induced in 11 monkeys while three monkeys were given paired feedings supplemented by thiamine hydrochloride and three monkeys were maintained on regular chow. The typical clinical symptoms were apathy, inattention to peripheral stimuli, ataxia, ptosis, mydriasis progressing to pupillary areflexia, nystagmus, and ophthalmoparesis progressing to total ophthalmoplegia. With thiamine treatment, recovery was prompt and complete in mild to moderate cases but delayed and incomplete in severe cases. The animals were killed six or more months after discontinuance of the experiments to determine the chronic effects of treated thiamine deficiency. The significant abnormalities in the brain stem were symmetric gliosis and neuronal loss in the inferior colliculi, the regions of the third and sixth nerve nuclei, and the medial vestibular nuclei. White matter was characteristically spared. With the exception of the inferior colliculi, the target sites for neuropathologic changes were the centers for ocular motor control.

Animals↗