Infection of a canine macrophage cell line with leishmania infantum: determination of nitric oxide production and anti-leishmanial activity

We have previously shown that resistance to Leishmania infantum in dogs is associated with a Th1 type of immune response. In this study, we use a canine macrophage cell line (030-D) that can readily be infected with this protozoan parasite. Our aim is to further characterize the effector mechanisms involved in killing of Leishmania parasite in dogs. We observed that activation of 030-D cells by incubation with a supernatant derived from a Leishmania-specific T cell line containing IFN-gamma, TNF-alpha and interleukin-2 (IL-2) resulted in enhanced nitric oxide (NO) production by these cells. In addition, we observed enhanced anti-leishmanial activity of infected 030-cells after activation. Both, NO production and anti-leishmanial activity were abrogated by addition of L-N(G)-nitroargininemethyl ester (L-NAME), an analogue of L-arginine. Thus, NO play an important role in the anti-leishmanial activity of these canine macrophages. We propose the infection of the 030-D cell line as a good in vitro model to further investigate parasite-host cell interactions in dogs, a natural host of Leishmania parasites.     

Flystrike prevention on Merino lambs with the insect growth regulator dicyclanil

The efficacy of a ready-to-use 5% dicyclanil pour-on formulation as a preventative of natural flystrike on Merino lambs was investigated in a field trial involving 5 sites in the southern Cape Province. A total of 1,804 lambs treated with dicyclanil were compared with 882 untreated control lambs for up to 25 weeks after treatment. Efficacy was assessed by calculating the weekly cumulative strike rate at each site and aggregated for all sites, as well as by calculating the percentage reduction achieved in treated lambs. Cumulative strike rates for the untreated controls aggregated for all sites at Weeks 9,14 and 19 after treatment reached 6.2, 12.8 and 17.8%, respectively, compared with 0.4, 1.7 and 3.6% for the dicyclanil treated lambs. Percentage control aggregated for all sites at Weeks 9,14 and 19 after treatment was 93, 87 and 80%, respectively. Heavy rains during the 1st half of the trial did not substantially reduce the efficacy of the product.     

Regulation of atrial fibrillation in horses with oral quinidine sulfate. Discussion of the disease picture in a typical case

Atrial fibrillation is a disorder of cardiac rhythmicity, and its importance in the horse depends on the underlying cause and the function of the horse. Before the decision is taken to start treatment, it has first to be ascertained whether treatment is worthwhile and whether the horse is an appropriate candidate for treatment. This article gives a short overview of current opinion on the cause and treatment of atrial fibrillation in the horse. The most used treatment at the moment, oral chinidine sulphate, is discussed. The hemodynamic consequences of atrial fibrillation and the response of a patient to treatment with chinidine sulphate are also discussed.     

Leukoencephalomalacia in a horse induced by fumonisin B1 isolated from Fusarium moniliforme

Each of two horses was dosed by stomach tube with culture material on maize of Fusarium moniliforme MRC 826. One horse developed severe hepatosis and mild oedema of the brain after 6 doses of 2.5 g of culture material/kg body mass/day in 7 days. The second horse, in a similar experiment but at a dosage rate of 1.25 g/kg/day, developed mild hepatosis and moderate oedema of the brain. In both animals the brain oedema was particularly noticeable in the medulla oblongata. The mycotoxin fumonisin B1 was extracted and purified from the culture material of F. moniliforme MRC, 826 which contained approximately 1 g/kg of this compound. A horse was injected intravenously 7 times from Day 0-Day 9 with 0.125 mg of fumonisin B1/kg body mass/day. Clinical signs of neurotoxicosis, which appeared on Day 8, included nervousness followed by apathy, a wide-based stance, trembling, ataxia, reluctance to move, paresis of the lower lip and tongue, and an inability to eat or drink. Euthanasia was performed on the horse on Day 10 while the animal was in a tetanic convulsion. The principal lesions were severe oedema of the brain and early, bilaterally symmetrical, focal necrosis in the medulla oblongata. This report provides experimental evidence that fumonisin B1, produced by F. moniliforme, causes equine leukoencephalomalacia.     

Thymic hyperplasia causing right ventricular outflow tract compression following treatment for oesophageal rupture in an Arabian colt

True thymic hyperplasia has been reported sporadically in the human literature as an immunological rebound phenomenon following immunosuppressive treatment or disease. There are limited accounts in domestic species, mainly following vaccination, and thymic hyperplasia has not been a recognised condition in the horse to date. This report details a case of true thymic hyperplasia in a 10-week-old Arabian colt diagnosed by histopathology of core biopsy samples. The colt developed pulmonary stenosis caused by compression due to a space occupying lesion in the cranial mediastinum following a 3-month history of hospitalisation for treatment of traumatic oesophageal rupture with perioesophageal abscess formation. Diagnostic imaging of the cranial mediastinum was indicative of a thymic mass, and histopathology confirmed the mass was normal (hyperplastic) thymic tissue. The colt was treated with a tapering dose of corticosteroids, which led to involution of the hyperplastic tissue and resolution of pulmonary artery compression. Thymic hyperplasia may be an unrecognised sequela to chronic inflammation in horses and was only identified in this case when the size was sufficient to compress right cardiac outflow.     

Acute toxoplasmosis in squirrel monkeys (Saimiri sciureus) in Mexico

Toxoplasma gondii causes fatal multisystemic disease in New World primates, with respiratory failure and multifocal necrotic lesions. Although cases and outbreaks of toxoplasmosis have been described, there are few genotyping studies and none has included parasite load quantification. In this article, we describe two cases of lethal acute toxoplasmosis in squirrel monkeys (Saimiri sciureus) of Mexico city. The main pathological findings included pulmonary edema, interstitial pneumonia, hepatitis and necrotizing lymphadenitis, and structures similar to T. gondii tachyzoites observed by histopathology in these organs. Diagnosis was confirmed by immunohistochemistry, transmission electron microscopy and both end point and real time PCR. The load was between <14 and 23 parasites/mg tissue. Digestion of the SAG3 gene amplicon showed similar bands to type I reference strains. These are the first cases of toxoplasmosis in primates studied in Mexico, with clinical features similar to others reported in Israel and French Guiana, although apparently caused by a different T. gondii variant.     

Quantification of melamine absorption, distribution to tissues, and excretion by sheep

Eight D?hne Merino rams were used to quantify apparent absorption, distribution to tissues, and excretion of dietary melamine in sheep. Two batches of concentrate pellets were made; one (CON) contained corn gluten meal with no detectable melamine and the other (MEL) contained corn gluten meal that was previously found to be highly contaminated with melamine at 15,117 mg/kg. The MEL pellets contained 1,149 mg/kg of melamine. During a 10-d adaptation period, all the animals received a forage-based diet supplemented with 600 g/d of the CON pellets. This was followed by an 8-d collection period during which 6 of the animals received MEL pellets and 2 received CON pellets. Melamine intake of sheep that received MEL pellets was 0.69 g/d. Blood samples were taken before first ingestion of MEL pellets on d 1 and again on d 3, 6, and 8 of the collection period for melamine and serum creatinine analyses. Feces and urine were collected quantitatively over the 8 d for proximate and melamine analyses. All the animals were slaughtered at the end of the trial, and samples of the LM, liver, kidneys, and abdominal fat were taken for melamine analysis. Data of the 2 sheep that received CON pellets for the duration of the trial confirmed that no melamine was detected in any of the samples, and no statistical analyses were performed on these data. The apparent digestibility or efficiency of absorption of ingested melamine was 76.7%. Melamine was detected in the urine, blood, muscle (LM), and fat tissue of all the sheep that received MEL pellets. Serum melamine concentrations reached 5.4 mg/kg on d 8 of the collection period, and the meat (LM) contained 9.6 mg/kg of melamine. Calculations on the partitioning of ingested melamine suggested that urine is the major excretion route accounting for 53.2%, whereas feces accounted for 23.3% of ingested melamine. Approximately 3.5% of the ingested melamine was detected in muscle. It was concluded that ingested melamine is highly absorbable from the small intestine and that a pathway exists for the distribution of dietary melamine to meat.     

Ciclosporin A therapy is associated with disturbances in glucose metabolism in dogs with atopic dermatitis

The effect of ciclosporin A (CsA) on glucose homeostasis was investigated in 16 dogs with atopic dermatitis by determining plasma glucose, serum fructosamine and insulin concentrations, and serial insulin and glucose concentrations following a glucagon stimulation test, before and 6 weeks after CsA therapy at 5 mg/kg once daily. All dogs completed the study. Following CsA treatment, the median serum fructosamine concentrations were significantly higher (pretreatment 227.5 μmol/L; post-treatment 246.5 μmol/L; P = 0.001; reference range 162-310 μmol/L). Based on analyses of the areas under concentration-time curves (AUC) pre- and post-CsA treatment, plasma glucose concentrations were significantly higher (AUC without baseline correction 31.0 mmol/L/min greater; P = 0.021) and serum insulin concentrations were significantly lower (AUC without baseline correction 217.1 μIU/mL/min lower; P = 0.044) following CsA treatment. Peak glucose concentrations after glucagon stimulation test were significantly higher following CsA treatment (10.75 versus 12.05 mmol/L; P = 0.021), but there was no significant difference in peak serum insulin (52.0 versus 35.0 μIU/mL; P = 0.052). There was a negative correlation between baseline uncorrected insulin AUC and trough serum log CsA concentrations (r = -0.70, P = 0.005). The administration of CsA to dogs with atopic dermatitis leads to disturbances in glucose homeostasis. The clinical significance of this is unclear, but it should be taken into account when considering CsA treatment in dogs that already have such impairments.     

Tepoxalin reduces pruritus and modified CADESI-01 scores in dogs with atopic dermatitis: a prospective, randomized, double-blinded, placebo-controlled, cross-over study

Thirty dogs with atopic dermatitis were given tepoxalin (Zubrin®, Intervet/Schering-Plough Animal Health, Boxmeer, the Netherlands) or placebo once daily for 4 weeks, followed by a wash-out period of 1 week before reversing the treatments. Pruritus was scored by the owners using the Edinburgh Pruritus Scale and one investigator employed a modification of the Canine Atopic Dermatitis Extent and Severity Index-01 (mCADESI-01) to score the physical lesions. After administration of tepoxalin there was a ≥ 50% reduction in pruritus and mCADESI-01 scores in 36% and 25% of the dogs, respectively, whereas following administration of the placebo there was a ≥ 50% reduction in pruritus and mCADESI-01 scores in only 25% and 16% of the dogs, respectively. Analysis of pooled data indicated that tepoxalin resulted in a significant reduction in pruritus ( P  = 0.012) and mCADESI-01 ( P  = 0.002) scores but there was no significant change after placebo. The median pruritus scores before and after tepoxalin were 2 (range 1–5) and 1 (range 0–5), respectively, and before and after placebo were 2 (range 0–4) and 2 (range 0–4), respectively. The median mCADESI scores before and after tepoxalin were 23 (range 0–68) and 16 (range 0–72), respectively, and before and after placebo were 18 (range 3–79) and 24 (range 0–65), respectively. At the dose used in this study (10.0–19.1 mg kg⁻¹), tepoxalin was well-tolerated and no adverse effects were noted.