Malabsorption of vitamin A in preruminating calves infected with Cryptosporidium parvum
Holland, R.E.; Boyle, S.M.; Herdt, T.H.; Grimes, S.D.; Walker, R.D.
American Journal of Veterinary Research 53(10): 1947-1952
1992
ISSN/ISBN: 0002-9645 PMID: 1456546 Document Number: 393914
Serum retinol, retinyl palmitate, and total vitamin A concentrations, and jejunoilea morphology were examined in neonatal calves infected with Cryptosporidium parvum. Group-1 calves served as noninfected controls and, after an adjustment period, were given 50 ml of saline solution IV every 12 hours for 6 days. Group-2 calves were inoculated with 10-7 C. parvum oocysts and, after the onset of diarrhea, were given 50 ml of saline solution IV every 12 hours for 6 days. Group-3 calves were inoculated with 10-7 C. parvumoocysts and, after the onset of diarrhea, were treated with difluromethylornithine (DFMO, 200 mg/kg of body weight IV, q 12 h) for 6 days. Group-4 calves were naturally infected with C. parvum. Jejuno-ileal biopsy specimens were excised from calves of groups 1-3 at 3 and again at 15 to 16 days of age. During the course of diarrhea and 3 days after saline or DFMO admininstration, water-miscible retinyl palmitate was administered orally (2,750 mu-g/kg) to each calif in each group. Cryptosporidium parvum infection was associated with significant (P ltoreq 0.05) reduction in postadministration serum retinol, retinyl palmitate, and total vitamin A concentrations in calves of groups 2, 3, adn 4. Cryptosporidium parvum infection caused significant (P ltoreq 0.05) reduction in villus height. Decreased villus height, villus blunting and fusion, and attenuation of the intestinal mucosa were associated with reduced absorption of vitamin A, as indicated by lower peak postadministration retinyl palmitate concentration in C. parvum-infected calves. Intravenous administration of DFMO to group-3 calves did not improve retinol absorption. Vitamin A should be provided parenterally to young calves with enteric cryptosporidiosis in an attempt to avoid depletion of concurrent low liver vitamin A reserves.