Malabsorption of vitamin A in preruminating calves infected with Cryptosporidium parvum

Robert E. Holland From the Departments of Large Animal Clinical Sciences (Holland, Herdt) and Pathology (Grimes) and the Animal Health Diagnostic Laboratory (Walker), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, and from the Department of Veterinary Pathobiology (Boyle), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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Stephen M. Boyle From the Departments of Large Animal Clinical Sciences (Holland, Herdt) and Pathology (Grimes) and the Animal Health Diagnostic Laboratory (Walker), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, and from the Department of Veterinary Pathobiology (Boyle), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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Thomas H. Herdt From the Departments of Large Animal Clinical Sciences (Holland, Herdt) and Pathology (Grimes) and the Animal Health Diagnostic Laboratory (Walker), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, and from the Department of Veterinary Pathobiology (Boyle), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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Sheila D. Grimes From the Departments of Large Animal Clinical Sciences (Holland, Herdt) and Pathology (Grimes) and the Animal Health Diagnostic Laboratory (Walker), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, and from the Department of Veterinary Pathobiology (Boyle), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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Robert D. Walker From the Departments of Large Animal Clinical Sciences (Holland, Herdt) and Pathology (Grimes) and the Animal Health Diagnostic Laboratory (Walker), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, and from the Department of Veterinary Pathobiology (Boyle), Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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SUMMARY

Serum retinol, retinyl palmitate, and total vitamin A concentrations, and jejunoileal 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 107 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 107 C parvum oocysts and, after the onset of diarrhea, were treated with difluoromethylornithine (dfmo, 200 mg/kg of body weight iv, q 12 h) for 6 days. Group-4 calves were naturally infected with C parvum. Jejunoileal 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 administration, water-miscible retinyl palmitate was administered orally (2,750 μg/kg) to each calf in each group. Cryptosporidium parvum infection was associated with significant (P ≤ 0.05) reduction in postadministration serum retinol, retinyl palmitate, and total vitamin A concentrations in calves of groups 2, 3, and 4. Cryptosporidium parvum infection caused significant (P ≤ 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.

SUMMARY

Serum retinol, retinyl palmitate, and total vitamin A concentrations, and jejunoileal 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 107 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 107 C parvum oocysts and, after the onset of diarrhea, were treated with difluoromethylornithine (dfmo, 200 mg/kg of body weight iv, q 12 h) for 6 days. Group-4 calves were naturally infected with C parvum. Jejunoileal 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 administration, water-miscible retinyl palmitate was administered orally (2,750 μg/kg) to each calf in each group. Cryptosporidium parvum infection was associated with significant (P ≤ 0.05) reduction in postadministration serum retinol, retinyl palmitate, and total vitamin A concentrations in calves of groups 2, 3, and 4. Cryptosporidium parvum infection caused significant (P ≤ 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.

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