Experimental ocular herpesvirus infection in the cat. Sites of virus replication, clinical features and effects of corticosteroid administration.

Experimentally induced ocular feline herpesvirus 1 (FHV-1) infection was studied in 30 specific pathogen-free cats. In ten cats, the ability of five field isolates of FHV-1 to replicate in the epithelium and substantia propria of cornea and conjunctiva was demonstrated by histochemical techniques. Feline herpesvirus 1 was found to preferentially infect and induce necrosis of conjunctival epithelium. Although significant histologic lesions were not induced, all FHV-1 strains were observed to replicate in corneal epithelium; minimal viral antigen was detected in the corneal stroma. The course and clinical features of ocular FHV-1 infection were then studied over a period of 60 days in two groups of ten cats: in one group, infection was preceded by administration of subconjunctival betamethasone. In each of these groups, a distinct clinical syndrome developed. In cats not receiving corticosteroids, a course of epithelial keratitis, characterized by the formation of punctate and dendritic epithelial lesions, persisted for up to 24 days postinfection. In the corticosteroid treated group, a chronic (greater than 60 days) stromal keratitis developed, characterized by geographic epithelial ulceration, interstitial edema and deep vascularization. Other complications observed in corticosteroid-treated animals included decreased tear production, calcific-band keratopathy and a unique stromal disorder of cats termed corneal sequestration. The results of this study indicate that while epithelial keratitis may occur during primary infection, stromal keratitis does not, unless immune responsiveness to FHV-1 is concomitantly suppressed. This feature is similar to naturally occurring HSV-1 keratitis of humans, but contrasts to other animal model systems in which stromal keratitis predictably occurs during primary infection. Study of this animal model, therefore, may allow unique insights into the events preceding the establishment of stromal keratitis.

Effect of 2,3-diphosphoglycerate concentration on the alkaline fragility of phosphofructokinase-deficient canine erythrocytes.

1. Erythrocytes in whole blood samples from dogs with phosphofructokinase (PFK) deficiency had lower 2,3-diphosphoglycerate (2,3-DPG) concentrations, higher ATP concentrations, and were more alkaline fragile than normal canine erythrocytes. 2. Reticulocytes from a PFK-deficient dog contained nearly three times the ATP concentration of normal canine erythrocytes, and had 2,3-DPG concentrations similar to normal canine erythrocytes. 3. PFK-deficient reticulocytes are not alkaline fragile. 4. The erythrocyte 2,3-DPG concentration in whole blood samples from PFK-deficient dogs was increased to normal by in vitro incubation with dihydroxyacetone, pyruvate and phosphate. This incubation resulted in only a slight increase in ATP concentration. 5. The alkaline fragility of these 2,3-DPG replenished PFK-deficient erythrocytes was normal. 6. Findings in this study indicate that the increased alkaline fragility of canine PFK-deficient erythrocytes is the result of decreased intracellular 2,3-DPG concentration.

Serum ferritin, serum iron, and erythrocyte values in foals.

Twenty-one healthy Thoroughbred and Quarter Horse foals were studied from birth until 1 year of age. Foals had access to an iron-supplemented creep feed before weaning and were fed an iron-supplemented concentrate as part of their diet after weaning at 4 months of age. Initial blood samples were taken before foals were allowed to nurse. Serum iron concentration, total iron-binding capacity, and PCV decreased during the foal's first 24 hours of life. Serum iron concentration decreased rapidly from 446 +/- 16 micrograms/dl (mean +/- SE) at birth to 105 +/- 11 micrograms/dl at 3 days of age. Serum ferritin concentration increased from a mean of 85 +/- 8 ng/ml at birth to 159 +/- 11 ng/ml at 1 day of age. Thereafter, ferritin concentration decreased gradually to a minimum of 61 +/- 6 ng/ml at 3 weeks of age, and then at 6 months increased to values similar to those from reference adult horses. The ferritin concentration in colostrum at birth was 354 +/- 42 ng/ml, compared with 25 +/- 2 ng/ml in milk 1 day later. The decrease and then increase in serum ferritin concentration occurred concomitantly with opposite changes in serum total iron-binding capacity. The mean PCV decreased gradually to a minimum at 3 months of age. This decrease was associated with an increasing number of microcytes, as determined with a cell-size distribution analyzer.