Heinz body formation was examined in kittens, in response to consumption of a variety of diets. A commercial salmon-based diet containing 16.5 mg of nitrite, 39 mg of histamine, and 210,000 IU of vitamin A/kg of diet (dry-matter basis) was found to induce Heinz body formation. Purified experimental diets--containing nitrite up to 405 mg/kg; histamine, 50 mg/kg; histamine, 50 mg/kg plus nitrite, 45 mg/kg; or vitamin A, 250,000 IU/kg--failed to induce Heinz body formation. The effect of propylene glycol (PG) on Heinz body formation was examined by giving groups of 6 kittens purified diets containing 5 or 10% PG for 12 weeks. Two additional kittens were fed a commercial soft-moist diet containing PG for 12 weeks. All kittens fed PG developed Heinz bodies, with peak values for erythrocytes containing Heinz bodies being: 28% for kittens of the 10% PG group; 20% for kittens of the 5% PG group; and 36% for kittens of the soft-moist diet group. Kittens did not develop anemia or methemoglobinemia. Heinz body percentage required 6 to 8 weeks to decrease to the pretreatment value of < 1% after diets containing PG were discontinued. 51Chromium-labeled erythrocytes were used to evaluate erythrocyte survival in 4 kittens of the 10% PG-fed group and in 4 control kittens. Kittens with Heinz body formation induced by 10% PG had significantly (P < 0.001) decreased erythrocyte survival, compared with that for controls, with half-life of 8.3 days for kittens of the PG group, compared with 12.6 days for kittens of the control group.

Avian influenza outbreaks have occurred during winter months, and effective disinfection of poultry premises at freezing temperatures is needed. The commercial disinfectants Virkon and Accel, supplemented with an antifreeze agent [propylene glycol (PG), methanol (MeOH), or calcium chloride (CaCl2)], were evaluated for their effectiveness in killing avian influenza virus (AIV) at −20°C or 21°C. An AIV suspension was applied to stainless steel disks, air-dried, and covered with a disinfectant or antifreeze agent for 5 to 30 min. Virkon (2%) and Accel (6.25%) with 30% PG, 20% MeOH, or 20% CaCl2 inactivated 6 log10 AIV within 5 min at −20°C and 21°C. At these temperatures PG and MeOH alone did not kill AIV, but the 20% CaCl2 solution alone inactivated 5 log10 AIV within 10 min. The results suggested that CaCl2 is potentially useful to enhance the effectiveness of disinfection of poultry facilities after outbreaks of AIV infection in warm and cold seasons.

Cat foods containing propylene glycol (PG) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary PG, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0, 6, or 12% PG on a dry-weight basis. Cats fed PG had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in PCV, hemoglobin concentration, and RBC count, punctate reticulocytes were significantly increased in the group fed 12% PG. Mean RBC survival was decreased in the groups fed 6 or 12% PG by 30 and 55%, respectively, compared with the control group. These data indicate that PG-containing diets cause a dose-dependent erythrocyte destruction, even when fed at concentrations as low as 6%.

Objective: To develop in genetically engineered mice an alternative screening method for evaluation of P-glycoprotein substrate toxicosis in ivermectin-sensitive Collies. Animals: 14 wild-type C57BL/6J mice (controls) and 21 genetically engineered mice in which the abcb1a and abcb1b genes were disrupted and the mutated canine ABCB1 gene was inserted. Procedures: Mice were allocated to receive 10 mg of ivermectin/kg via SC injection (n = 30) or a vehicle-only formulation of propylene glycol and glycerol formal (5). Each was observed for clinical signs of toxic effects from 0 to 7 hours following drug administration. Results: After ivermectin administration, considerable differences were observed in drug sensitivity between the 2 types of mice. The genetically engineered mice with the mutated canine ABCB1 gene had signs of severe sensitivity to ivermectin, characterized by progressive lethargy, ataxia, and tremors, whereas the wild-type control mice developed no remarkable effects related to the ivermectin. Conclusions and Clinical Relevance: The ivermectin sensitivity modeled in the transgenic mice closely resembled the lethargy, stupor, disorientation, and loss of coordination observed in ivermectin-sensitive Collies with the ABCB1–1Δ mutation. As such, the model has the potential to facilitate toxicity assessments of certain drugs for dogs that are P-glycoprotein substrates, and it may serve to reduce the use of dogs in avermectin derivative safety studies that are part of the new animal drug approval process.