Experimental scoliosis in primates: a neurological cause.

Although a variety of techniques have been used with varying success to induce scoliosis in animals, primates have rarely been used. A series of monkeys is presented where scoliosis developed incidentally during the routine virulence testing of live, attenuated, oral poliomyelitis vaccines by intraspinal injection. The site and extent of histological damage in the different anatomical areas of the spinal cord were examined in 25 scoliotic monkeys and 25 matched controls. Analysis of the data demonstrated that there was significantly greater damage on the convex side of the spinal cords of the scoliotic animals, particularly in the sensory areas-the posterior horn and Clarke's column. Scoliosis was not thought to be caused by clinical poliomyelitis as the involvement of the anterior horn was not significantly greater than in the scoliotic animals than in the controls. These observations are taken to support the view that scoliosis may develop as a result of asymmetrical weakness of the paraspinal muscles due to the loss of proprioceptive innervation.

Scoliosis caused by section of dorsal spinal nerve roots.

Experimental evidence has accumulated in recent years to suggest that scoliosis can be caused by asymmetrical spinal muscle weakness due to sensorineural loss, though this suggestion has not achieved universal acceptance. The evidence is supported by histopathological observations on cases of clinical idiopathic scoliosis. A study is presented in which cynomolgus monkeys had one, two or three dorsal spinal nerve roots cut. Scoliosis developed, convex to the damaged side; its severity was dependent on the number of nerve roots cut. Section of the first lumbar dorsal spinal nerve root had a marked tendency to cause scoliosis. The study supports the view that scoliosis may be caused by asymmetrical paraspinal muscle weakness acting through loss of proprioception.

Red-bellied tamarins (Saguinus labiatus): Hematologic reference values and hemopathologic responses.

Hematologic reference values have been established for captive adult red-bellied tamarins (Saguinus labiatus) by carrying out full blood counts and fibrinogen estimations on 25 clinically normal animals. The only significant sex difference detected was in the reticulocyte count which was higher in females than in males. The reference values were used to identify abnormal changes in the blood of nine clinical cases. Hypochromic anemia, neutrophilia, and raised fibrinogen levels were found in animals with self-inflicted injuries, dermatitis, and ileocecal intussusception. Target cells and jaundiced plasma were noted in a case of yersiniosis. Two animals in which generalized muscle wasting was the main abnormal clinical sign were severely anemic, and in one of these cases a significant number of Heinz bodies was present. The findings in these two animals were compared with those in common marmosets (Callithrix jacchus) with possible wasting marmoset syndrome.

Pinworm infections in laboratory rodents: a review.

The important and common oxyurids which affect laboratory rodents- Syphacia spp., Aspiculuris tetraptera and Passalurus ambiguus-are discussed and reviewed. Their life histories, pathogenicity and immunity are examined, and mention is made of the influence of age, sex, strain and host status on infection. The importance of using worm-free animals in experimental work is stressed, and guidance is given on diagnosis and control.

An outbreak of Yersinia pseudotuberculosis infection in a small indoor breeding colony of red-bellied (Saguinus labiatus) tamarins.

A spontaneous outbreak of yersiniosis caused by Yersinia pseudotuberculosis serotype IIB occurred in a small indoor breeding colony of red-bellied tamarins (Saguinus labiatus) during the winter of 1981. Of 35 monkeys at risk 6 died of an acute or subacute infection over a period of 23 days. Clinical signs were anorexia, weakness, listlessness and depression. The disease was characterized by focal necrosis of the liver, spleen, mesenteric lymph nodes, ulcerative enteritis, and the presence of colonies of Gram-negative bacilli in the lesions. Y. pseudotuberculosis was isolated from the liver, spleen, mesenteric lymph nodes and kidney but not from the blood, lung or intestine. Contaminated food was believed to be the source of infection.

Susceptibility of tamarin (Saguinus labiatus) red blood cell membrane lipids to oxidative stress: implications for wasting marmoset syndrome.

Captive Callitrichids frequently suffer a fatal wasting disease, wasting marmoset syndrome (WMS), of unexplained cause. This paper describes studies on the erythrocytes from animals in a breeding colony of tamarins (Saguinus labiatus), in which deaths from anaemia and wasting were occurring, to seek evidence for biochemical changes which could lead to oxidative damage and premature cell lysis. In only one animal of 33 studied did the red blood cell lipids show an increased susceptibility to oxidative damage. This animal, with some degree of certainty, could be diagnosed as having WMS. It was concluded that evidence for a primary deficiency of antioxidants as a cause of unexplained deaths, or WMS, in the colony could not at present be substantiated.

Hypersensitivity to some nematode antigens.

Immediate and delayed skin reactions to antigens derived from Ascaris suum, Necator americanus, and Toxocara canis are described in three subjects and related to eosinophil counts and serum IgE levels. One, who had laboratory contact with ascarides but no known infection, gave positive immediate reactions to all three antigens. Another, following repeated experimental infection with necator, gave positive immediate reactions to all three antigens and a delayed reaction to necator alone. The third, following a single recent infection with necator, gave no immediate or delayed reaction.