Caecal disease in equids

Objective To review the breed, age, gender, clinical and laboratory findings, treatment and outcome of horses with caecal disease presented to a referral centre. Design Retrospective study of 96 cases. Procedure The breed, age, and gender of the study population were compared with the corresponding hospital population for the same period. The means (± SD) for clinical and laboratory findings were recorded for each caecal disorder. Treatment was categorised as medical or surgical, and outcome was recorded. Results Caecal diseases included impaction (40% of total cases), rupture associated with concurrent unrelated disease (13%), rupture with parturition (9%), rupture with no associated disease (5%), infarction (11%), torsion (9%), abscess or adhesion (7%), tumour (3%), and miscellaneous conditions (3%). The breed or gender of affected horses did not differ from the hospital population, although horses > 15 years were more frequently represented (P < 0.05). This age group was specifically more predisposed to caecal impaction (P < 0.05), as were Arabian, Morgan, and Appaloosa breeds (P < 0.05). In horses with caecal impaction transrectal examination was the most useful diagnostic procedure; 90% of affected horses treated medically were discharged while horses treated by typhlotomy alone, or typhlotomy and blind end ileocolostomy, had survival rates to discharge of 71% and 86%, respectively. Horses with caecal rupture associated with concurrent un-related disease showed no signs of impending rupture; all were receiving phenylbutazone, all were euthanased, and 50% had caecal ulceration at necropsy. Of horses with caecal rupture with parturition 56% had prior dystocia; in two-thirds the site of rupture was the ileocaecal junction and all were euthanased. Horses with caecal rupture with no associated disease died or were euthanased; rupture was idiopathic. Horses with caecal infarction usually had signs of abdominal pain and abdominal fluid changes consistent with peritonitis; transrectal examination was nonspecific, and typhlectomy was successful in seven of eight horses. Horses with caecal torsion had signs of severe, acute abdominal pain and typhlectomy was successful in three of five horses. Diagnosis of caecal adhesion or abscess was assisted by transrectal palpation in two of seven horses and surgical treatment was successful in two of five horses. A caecal tumour was diagnosed in three horses aged 20 years or older that presented with chronic weight loss. Other caecal diseases were uncommon. Conclusion Caecal disease is uncommon in equids but some specific features of the history and physical findings can alert the veterinarian to the possibility of caecal involvement in horses with gastrointestinal dysfunction. Medical or surgical therapy can be effective in horses where caecal rupture has not occurred.     

Response of Thawed Epidi dymal Red Deer Spermatozoa to Increasing Concentrations of Hydrogen Peroxide,and Importance of Individual Male Variability

Oxidative stress represents a challenge during sperm manipulation. We have tested the effect of increasing hydrogen peroxide (H₂O₂) levels on red deer spermatozoa after cryopreservation, and the role of male‐to‐male variation in that response. In a first experiment, eight thawed samples were submitted to 0, 25, 50, 100 and 200 μm H₂O₂ for 2 h at 37°C. Intracellular reactive oxygen species (H₂DCFDA‐CM) increased with H₂O₂ concentration, but we only detected a decrease in sperm function (motility by CASA and chromatin damage by sperm chromatin structure assay) with 200 μm . Lipoperoxidation assessed by the thiobarbituric acid reactive substance (TBARS) method increased slightly with 50 μm H₂O₂ and above. In a second experiment, samples from seven males were submitted to 0 and 200 μm H₂O₂ for 2 h, triplicating the experiment within each male. Males differed at thawing and regarding their response to incubation and H₂O₂ presence. We found that the kinematic parameters reflected male‐to‐male variability, whereas the response of the different males was similar for lipid peroxidation and viability. A multiparametric analysis showed that males grouped differently if samples were assessed after thawing, after incubation without H₂O₂ or after incubation with H₂O₂. Red deer spermatozoa are relatively resilient to H₂O₂ after thawing, but it seems to be a great male‐to‐male variability regarding the response to oxidative stress. The acknowledgement of this individual variability might improve the development of optimized sperm work protocols.     

Effects of an insecticidal dip containing d-limonene in the cat

A study was undertaken to determine the effects of a single dermal application of a commercial insecticidal dip containing 78.2% d-limonene in cats. At the manufacturer's recommended concentration of 1.5 oz/gal of water, no clinical signs or lesions of toxicosis were seen. At 5 times the recommended concentration, clinical signs were mild and consisted of hypersalivation of short duration, ataxia, and muscle tremors resembling shivering. At 15 times the recommended concentration, clinical signs included hypersalivation lasting 15 to 30 minutes, moderate-to-severe ataxia lasting 1 to 5 hours, muscle tremors resembling shivering lasting 1 to 4 hours, and severe hypothermia beginning soon after treatment and lasting 5 hours. Gross lesions were confined to excoriation of the scrotal and perineal areas of the treated male cats at the 15 X concentration. No deaths or other lasting effects were seen at any dosage.     

Toxicity of microcystin LR, a cyclic heptapeptide hepatotoxin from Microcystis aeruginosa, to rats and mice

Rats (Sprague-Dawley) and mice (Balb/c) were given microcystin LR intraperitoneally and were killed at intervals up to 24 hr (rats) or 90 min (mice) and necropsied. The lowest consistently lethal dose was 160 micrograms/kg in rats and 100 micrograms/kg in mice. Rats that were clinically unaffected had no lesion. All clinically affected rats in all dose groups died (from 20 to 32 hr after toxin) and had similar hepatic lesions. Livers were enlarged and dark red beginning 40 to 60 min after toxin. Mild disassociation and rounding of centrilobular hepatocytes developed within 20 min. By 60 min after toxin, degeneration and necrosis of hepatocytes involved most of the lobules except for small periportal zones. Weights of livers and kidneys were significantly increased. Eosinophilic fibrillar material filled renal glomerular capillaries as early as 9 hr after toxin. At 18 to 24 hr there was moderate vacuolation of proximal tubular epithelium with mild tubular dilatation. Beginning at 1 hr, intact hepatocytes and hepatic debris were present in pulmonary vessels. Analysis of serum revealed an increase in alanine aminotransferase 40 min after toxin; at 6 to 12 hr there were significant increases in alkaline phosphatase, total bilirubin, blood urea nitrogen, and creatinine. Mice survived only 60 to 90 min after toxin. Hepatic lesions were similar to those in rats, but renal and pulmonary lesions were not seen.