SummaryImmunoglobulin E (IgE)-mediated late-phase reactions can be induced in atopic humans by intradermal injection of relevant allergens or anti-IgE antibodies. The histology of these reactions resembles that of naturally occurring atopic dermatitis. Strikingly similar responses can be induced in dogs, suggesting that a canine model could prove valuable for preclinical investigation of drugs targeting late-phase reactions. This study was designed to characterize the cellular, cytokine and chemokine responses after intradermal anti-IgE injection in untreated and prednisolone-treated dogs. Normal beagles were untreated or treated with prednisolone before intradermal injection of polyclonal rabbit anti-canine IgE or normal rabbit IgG. Biopsies were taken before injection and 6, 24 and 48 hr after injection. Samples were evaluated by histological and immunohistochemical staining, as well as by real-time quantitative polymerase chain reaction analysis. Dermal eosinophil and neutrophil numbers increased dramatically within 6 hr after injection of rabbit anti-canine IgE, and remained moderately elevated at 48 hr. The numbers of CD1c + and CD3 + mononuclear cells were also increased at 6 hr. The real-time quantitative polymerase chain reaction demonstrated marked increases in mRNA expression for interleukin-13 (IL-13), CCL2, CCL5 and CCL17. Levels of mRNA for IL-2, IL-4, IL-6 and IFN-c did not change within the limits of detection. Prednisolone administration suppressed the influx of neutrophils, eosinophils, CD1c + and CD3 + cells, as well as expression of IL-13, CCL2, CCL5 and CCL17. These data document the cytokine and chemokine responses to anti-IgE injection in canine skin, and they demonstrate the ability of the model to characterize the anti-inflammatory effects of a known therapeutic agent.

Twenty-eight horses with the diagnosis of an intestinal disorder requiring surgical intervention were randomly assigned to lidocaine (n ϭ 13) or saline (control, n ϭ 15) treatment groups. After induction of anesthesia, treated horses received a loading dose of 2% lidocaine (0.65 mg/kg) intravenously, followed by a continuous rate of infusion of 1% lidocaine (0.025 mg/kg/min) until the discontinuation of anesthesia. Upon recovery from anesthesia, a 2nd loading dose of 2% lidocaine (1.3 mg/kg) was administered, followed by an infusion of 1% lidocaine (0.05 mg/kg/min) for 24 hours postoperatively. The control group received equivalent volumes of saline. Lidocaine-treated horses had significantly better minimum jejunal cross-sectional area scores (P ϭ .011), minimum jejunal diameter scores (P ϭ .002), and intestinal ultrasound index (IUI) (P ϭ .007). Peritoneal fluid was detected by percutaneous ultrasound examination in 8 of the 15 control animals but in none of the treated animals (P ϭ .003). Failure to obtain fluid via abdominocentesis was significantly more frequent for lidocaine-treated horses (P ϭ .025). No significant differences between the groups were found in the presence of gastrointestinal sounds, time to passage of 1st feces, number of defecations in the 1st 24 hours, presence of gastric reflux, duodenal or jejunal wall thickness, maximum duodenal or jejunal diameter or crosssectional area, minimum duodenal diameter or cross-sectional area, duodenal and jejunal intraluminal echogenicity, small-intestinal contractions per minute, rate of complications, or outcome. On the basis of this study, lidocaine infusion may have some desirable effects on jejunal distension and peritoneal fluid accumulation and was well tolerated perioperatively in horses with colic. The low incidence of small-intestinal lesions and gastric reflux in the study makes it difficult to assess the use of lidocaine in the prevention of postoperative ileus (POI).

Summary A hypercoagulable condition and poor perfusion to distal extremities might occur during equine endotoxaemic or septic shock, which could cause thrombosis of limb arteries. In our review, thrombosis occurred in neonatal foals in association with Gram‐negative bacteraemia. In 3 olderfoals and adults, thrombosis was associated with inflammatory bowel disease, diarrhoea and toxaemia. All patients had been treated with broad‐spectrum antibiotics, nonsteroidal anti‐inflammatory drugs and i.v. crystalloid solutions. Two horses received i.v. hyperimmune plasma. A generalised coagulopathy was not suspected prior to clinical signs of distal limb necrosis, although thrombocytopenia occurred in 4 of the 5 cases at the time of, or shortly before, thrombosis. Thrombocytopenia, possibly due to platelets adherence to exposed subendothelial collagen, which induces contact activation of the intrinsic coagulation pathway, has been described in endotoxaemic horses and foals with gastrointestinal infectious or inflammatory diseases and disseminated intravascular coagulation. Activation of procoagulants by endotoxins, decreased blood flow to the limbs and endothelial damage, may have been responsible for a hypercoagulable condition leading to thrombosis in these 5 cases. The 3 enterocolitis patients may have had increased risk of thrombosis because of loss of antithrombin III, haemoconcentration and acidosis.

During the last few years, reports have appeared claiming that lufenuron diminished or even cured dermatophyte infections in cats and dogs. As these observations have a rather anecdotal character leading to some ambiguity in the literature, it was decided to test lufenuron in a generally accepted animal model for dermatomycotic infection. The test was carried out in guinea pigs artificially infected with Microsporum canis on scarified dorsal skin and orally treated with lufenuron (Programä). The efficacy of up to five doses of 80 mg/kg was assessed 7 and 14 days after the start of treatment. All animals failed to show any improvement in skin lesions as compared to the vehicle-only treated animals. Clinical symptoms taken into account were scaling, crust formation, erythema, and exudation. Neither the number of treatments (one or five) nor the dose range (40 or 80 mg/ kg) made any difference. Itraconazole, tested earlier under identical circumstances, resulted in a clear and consistent improvement at day 7 of the infection at a dose of 15 mg/kg, given either in one dose or spread over several days. The absence of antimycotic activity of lufenuron in this established animal model constitutes a significant element in the discussion on the antifungal potency of lufenuron and supports the fact that there is, as yet, no evidence that benzoylphenyl urea derivative compounds have an effect on chitin synthesis in fungi.

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