Acetaminophen is widely used in human beings for analgesic purposes, but is one of the most frequent causes of poisoning in cats. Acetaminophen-poisoned cats develop methemoglobinemia and sometimes hepatic failure. To determine the benefit of using methylene blue, a treatment for methemoglobinemia, along with N-acetylcysteine (NAC), the recommended treatment for acetaminophen-poisoned cats, groups of 3 male and 3 female cats each were given methylene blue NAC, or both after administration of acetaminophen (120 mg/kg of body weight, PO). Male cats seemed more susceptible than female cats to acetaminophen toxicosis, because 3 males died of hepatic failure (2 cats given acetaminophen/methylene blue and 1 given acetaminophen/NAC/methylene blue). Although NAC alone seemed to elicit the best overall response, methylene blue, alone or in combination with NAC, may be useful in female cats.

The hypothalamic-pituitary-adrenocortical (HPA) axis was studied in 8 healthy cats after administration of supraphysiologic doses of methylprednisolone (MP). Ovine corticotropin-releasing hormone (oCRH) administration increased cortisol and adrenocorticotropic hormone (ACTH) concentrations. Significant (P < 0.05) suppression of cortisol and a trend toward suppression of ACTH was observed after 1 week of MP administration. The HPA axis quickly recovered from suppressive effects of MP 1 week after administration of the steroid was discontinued. Side effects of oCRH administration were minimal in 7 cats; however, 1 cat had a severe hypotensive reaction. Clinical abnormalities were not associated with MP administration. The HPA axis was suppressed by supraphysiologic doses of MP in all treated cats that lacked clinical signs consistent with iatrogenic HPA axis suppression. Despite the relatively active pars intermedia in cats, compared with human beings and dogs, feedback of MP on the HPA axis resulted in similar trends in oCRH-stimulated ACTH and cortisol concentrations as observed in human beings and dogs. Lack of consistent correlation between ACTH and cortisol concentrations was observed in 3 cats and possibly was related to the active pars intermedia in the cat.

Zoometric measurements and bioelectrical impedance analysis were evaluated as methods of body composition determination in healthy cats. Zoometric and impedance measurements were taken on 22 anesthetized adult cats of various ages, genders, breeds, and body weights. The cats were then euthanatized. The bodies were processed through a tissue homogenizer and free-catch specimens were taken, freeze-dried, and analyzed for total body water, protein, fat, potassium, and ash content. Stepwise regression analysis was implemented to identify statistically significant relationships between the chemically determined dependent variables (total body water, protein, potassium, fat-free mass, fat mass, and percent body fat) and the zoometric measurements, with or without bioelectrical impedance analysis. Statistical analysis revealed high correlations between the dependent variables and the corresponding predicted values of those variables. Body weight alone was a poor predictor of body composition in these cats. On the basis of these findings, we suggest that zoometric and bioelectrical impedance measurements may serve as practical, noninvasive, simple, and accurate methods for estimating body composition in domestic cats.

Concentrations of total, free, and esterified carnitine were determined in plasma, liver, and skeletal muscle from cats with idiopathic hepatic lipidosis and compared with values from healthy cats. The mean concentrations of plasma, liver, and skeletal muscle total carnitine; plasma and skeletal muscle free carnitine; and plasma and liver esterified carnitine were greater (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. The mean for the ratio of free/total carnitine in plasma and liver was lower (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. These data suggest that carnitine deficiency does not contribute to the pathogenesis of feline idiopathic hepatic lipidosis.

An experimental model of keratoconjunctivitis sicca (KCS) was produced by removing the lacrimal gland and the gland of the third eyelid from the left eye of 6 cats. The right eye of each cat was left intact and used as a control. After 2 weeks, cats were euthanatized and the central portion of the upper eyelid from both eyes of each cat was excised. Histologic sections were stained with either hematoxylin and eosin or with a battery of biotinylated lectins including concanavalin A (conA), soybean agglutinin (SBA), wheat germ agglutinin (WGA), succinylated wheat germ agglutinin (S-WGA), Ulex europaeus agglutinin I (UEA), Dolichos biflorus agglutinin (DBA), Ricinus communis agglutinin (RCA), peanut agglutinin (PNA), and PNA pretreated with neuraminidase. Consistent differences in histologic features were not observed between conjunctivas with KCS and control conjunctivas. A variable degree of mononuclear cell infiltration of the substantia propria was observed in control conjunctivas and those with KCS. In both groups, conjunctival goblet cell density decreased and epithelial stratification increased as the degree of submucosal inflammatory cell infiltration increased. Lectin binding sites for DBA, WGA, S-WGA, UEA, PNA, and PNA pretreated with neuraminidase were detected on conjunctival goblet cells of conjunctivas with KCS and control conjunctivas. The mucus/glycocalyx layer of conjunctival epithelial cells in both groups of conjunctivas bound lectins RCA, WGA, UEA, and conA, but inconsistently bound S-WGA. In both groups, DBA principally bound to the mucus layer overlying normal epithelium, whereas PNA pretreated with neuraminidase consistently bound to the mucus layer of stratified epithelial surfaces free of goblet cells. Binding of SBA to goblet cells and the mucus/glycocalyx layer was variable.

Eight adult cats were inoculated IV (n = 6) or SC (n = 2) with Ehrlichia risticii-infected P388Dl (continuous murine macrophage) cells or with E risticii released from P388D1 cells. Three additional cats were inoculated with organism-free P388D1 cultured monocytes, and 1 cat, which served as a medium control, was inoculated with balanced salt solution. Clinical signs of illness were observed in the IV inoculated cats from which E risticii was isolated. One cat developed intermittent diarrhea between postinoculation days (PID) 8 and 18, and the other cat developed lymphadenopathy, acute depression, and anorexia between PID 20 and 24. Ehrlichia risticii was isolated in cultures from 2 of 6 IV inoculated cats on PID 6, 10, and 17. Both cats were inoculated with E risticii released from the P388D1 cells. Ehrlichia risticii was not isolated from SC inoculated cats or from control cats. All 8 cats inoculated with E risticii seroconverted between PID 10 and 23. A pony inoculated with E risticii isolated from 1 of the inoculated cats developed clinical signs of equine monocytic ehrlichiosis including fever, anorexia, depression, and mild colic. Ehrlichia risticii was isolated from the blood of this pony on PID 7, 9, 11, and 16.