NUTRITIONAL AND METABOLIC DISEASES Main
I. Hypovitaminosis C (Scurvy) I. Hypovitaminosis C (Scurvy)
II. Pregnancy ToxemiaA. Etiology: Guinea pigs lack the hepatic enzyme 1-gulonolactone oxidase, which is essential for the conversion of glucose to ascorbic acid. Vitamin C is involved in many biochemical processes in the body including the synthesis of collagen and of intracellular ground substance. If vitamin C is not supplemented in the diet or if the animal is anorexic, scorbutic lesions will rapidly develop.
B. Clinical signs: Scurvy is characterized by frequent vocalizations, weakness, anorexia, diarrhea, flaky to ulcerative skin lesions, stiffness, reluctance to move, petechia of the mucous membranes, subcutaneous hemorrhages and death in two to three weeks due to starvation or secondary infection. Other nonspecific but suspicious signs may include rough hair coat, delayed wound healing, teeth grinding, inactivity, stillbirths, and chronic disease.
C. Pathology: Necropsy findings may include fascial and articular cartilage hemorrhages, petechial and ecchymotic bleeding on periosteum, muscle, and gingiva.
D. Diagnosis: A diagnosis can be made by dietary history, gross pathology, and serum ascorbate levels.
E. Treatment: Severely affected animals can be treated with 25-50 mg vitamin C IP s.i.d. until improvement is noted. Guinea pigs can then be given oral supplemental levels until the animal has recovered.
F. Control: Daily requirement of ascorbic acid is 15 mg/day, and this amount can be provided through supplemental feeding of a handful of cabbage or kale, a green pepper, a quarter of an orange, etc. Pregnant females should receive 30 mg/day. Vitamin C supplemented pellet research diets have an average shelf life of 6 months from the milling date when stored in a cool, dry place; shelf life can be prolonged by storage in a freezer. Commercial pet diets may have a shorter storage life of about 90 days after milling. If the vitamin is to be supplied in the water, a new solution at a dose of 200 to 400 mg/l drinking water should be mixed fresh daily due to instability of the vitamin in the presence of light and chlorine.
A. Etiology: Pregnancy toxemia is a syndrome that occurs in late gestation or in the immediate postpartum period. Two causes have been identified: 1) pre-eclampsia or the circulatory form with uteroplacental ischemia, and 2) fasting ketosis or the nutritional form with hypoglycemia and hyperlipidemia. It typically occurs in multiparous females. Predisposing factors include obesity, large fetal loads, sudden dietary changes, lack of exercise, and environmental stress. Obese, aged males may develop a similar toxemia.
B. Clinical Signs: The syndrome usually starts during the last two weeks of gestation or the first week post-partum. When not immediately fatal, clinical signs may include depression, lassitude, anorexia, dyspnea, convulsions, and stillbirths. The urine becomes clear, has a pH of 5 to 6, and contains high levels of ketone and protein. Hematologic abnormalities consist of hypocalcemia, hyperphosphatemia, elevated BUN, and hypoglycemia.
C. Pathology and Diagnosis: On necropsy, the stomach is empty, the liver and kidneys are quite fatty, the uterus may contain near-term fetae along with varying amounts of hemorrhage, and ample fat stores are visible throughout the abdomen. Diagnosis is based upon history, clinical signs, urinalysis, and necropsy.
D. Treatment and Control: The condition offers a poor prognosis. Therapy with glucose in fluids (1 ml 50% glucose in 3 to 5 ml Lactated Ringers IV or IP) plus a corticosteroid (cortisone at 0.25 - 1.25 mg/day delivered subQ, IM or PO) may be attempted. The condition is best prevented by supplying an adequate amount of digestible energy during late gestation and lactation, and maintaining animals in a non-obese condition. A commercial producer will not keep any female offspring as replacement breeders if they were produced by a sow that developed pregnancy ketosis.
Back to Disease Categories