Protein deficiency in primates. IV. Pregnant rhesus monkey.

Young adult female rhesus monkeys, maintained in a seminatural environment, when pregnant 30 days were fed a balanced semisynthetic diet containing 15.3 percent casein (13.4 percent protein) or 0.5, or 0.25 that amount for the remainder of thir pregnancy. The diets, made isocaloric by the addition of carbohydrates to replace the missing casein, supplied 4, 2, or 1 g protein/kg per day if the animals ate 120 kcal/kg per day, an assumption that was reasonably accurate. We studied the responses of monkeys delivering normal young at term. All monkeys were clinically healthy during the experiment. All reduced their total plasma protein concentration, principally by decreasing their albumin concentration. Greatest loss occurred in the low-protein group. Albuminuria was a common finding in all groups. Food consumption though varying throughout pregnancy, remained fairly comparable from group to group. Weight gain of the highest protein group was greatest; that for the lowest protein group barely covered the weight of the products of conception. Blood pressure declined during pregnancy while blood glucose rose. There were no morphologic changes in hair bulbs and only suggestive changes in liver cells that pointed to increased vacuolation. Increased metabolic efficiency during pregnancy enables the mother to safely pass through a long pregnancy during most of which she is fed a low-protein diet. Nonpregnant aminals suffer more under the same circumstances.

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.

Dermatophilosis in a titi monkey (Callicebus moloch).

The occurrence of dermatophilosis in the titi monkey is reported. Lesions were principally in the epidermis of the skin and were characterized by parakeratosis, necrosis, abscess formation, acanthosis, and hyperkeratosis. The cause, Dermatophilus congolensis, was demonstrated as a gram-positive filamentous organism with both horizontal and vertical septums.

Naturally occurring and experimentally induced eastern encephalomyelitis in calves.

Eastern encephalomyelitis virus was isolated from the brain of 2 calves with encephalomyelitis. Using the isolant from 1 of these calves, the disease was reproduced in a clinically normal calf. Histopathologic features conformed with those described for eastern encephalomyelitis in the horse.

The response of colostrum-deprived, specific pathogen-free pigs to experimental infection with Teschen disease virus.

The clinical response to Teschen disease and the excretion and rate of virus distribution in tissues of colostrum-deprived, specific pathogenfree pigs was determined. Severe, mild, and clinically inapparent responses to the disease were noticed following simultaneous intracranial and intranasal infections. Fourteen-day-old pigs reacted more severely to infection than 21-day-old pigs. The virus was detected in feces 2-3 days following infection but not in stools of surviving pigs 30 days after infection. The highest concentration of virus occurred during the incubation period and before onset of paralysis; the lowest concentrations were found during terminal disease stages. In tissues collected before or immediately after death of pigs, Teschen disease virus was found in several visceral organs but not in blood, urine or urinary bladder tissue. Virus yield was highest in brain and spinal cord tissues. Highest virus concentration was found in the cervical thoracic portions of the spinal cord, thalamus and cerebellum. Other aspects of the clinical disease are discussed.