A reproducible model of postweaning colibacillosis was obtained by controlling management and environmental variables to simulate conditions often seen at weaning. Suckling pigs were exposed briefly to starter diet at 1 week of age, weaned at 3 weeks of age, held at an ambient temperature of 20 +/- 2 C, again given the starter diet. One day after weaning, each pig was given 10(10) colony-forming units of enterotoxigenic Escherichia coli strain M1823B (0157:K88ac:H43-LT+ STb+) in broth containing 1.2% sodium bicarbonate via stomach tube. In vitro adhesion by strain M1823B to isolated intestinal branch borders was used to tst pigs for susceptibility to K88. In this model, 3 syndromes were induced in susceptible pigs: (1) peracute fatal diarrhea; (2) moderate diarrhea, weight loss, and fecal shedding of the inoculum strain; and (3) no diarrhea, weight loss, and fecal shedding of the inoculum strain. Rotavirus particles were not found in fecal specimens of pigs with diarrhea. The K88-susceptible, noninoculated control pigs remained clinically normal. It was concluded that susceptibility to adhesion by K88+ enterotoxigenic Escherichia coli was a requirement for the production of disease in this model; inoculation with rotavirus was not necessary.

The feasibility of renal arterial infusion of nonbiodegradable microspheres as a model of chronic renal disease in dogs was evaluated. Resin-coated, styrene-divinyl benzene copolymer microspheres were infused into the kidneys of healthy adult Beagles by direct injections of both renal arteries in a single surgical procedure. Injections of 25-micrometer diameter microspheres had minimal effect on either the clinical status or serum values of the dogs. Histologic examination revealed the majority of the microspheres lodged within the capillary beds of the glomeruli, and little change to the kidneys. However, injections of 50-micrometer diameter microspheres caused significant increases in serum concentrations of urea nitrogen and creatinine. Histologically, the larger microspheres obstructed afferent arterioles and small arteries, which caused diffuse glomerular necrosis and nephron damage. With doses ranging from 1 to 3 million microspheres/dog, a correlation between the quantity of microspheres injected and severity of renal damage was observed. The optimal dose for producing a model of moderate renal disease was determined to be 1.8 million microspheres/dog (0.9 million microspheres/kidney). During long-term studies, microsphere-injected dogs fed a moderately restricted protein ration remained relatively azotemic, compared with control dogs on the identical ration. During the 5-month postsurgical period, the serum urea nitrogen concentration averaged 18.41 +/- 1.59 mg/dl (mean +/- SE) for the microsphere-injected dogs vs 9.31 +/-0.38 for the control dogs (P < 0.001). Similarly, the mean serum creatinine value was significantly higher (P = 0.020) for the microsphere-injected dogs, compared with the controls (1.23 +/- 0.12 mg/dl vs 0.94 +/- 0.03). In addition, the difference in mean endogenous creatinine clearance rates was statistically significant (microsphere-injected 1.02 0.05 ml/min/kg, vs control 1.53 +/- 0.06, P < 0.001).

Uveitis was induced in dogs by intracameral injection of canine lens protein. The lipoxygenase inhibitors phenidone and norhydroguaiaretic acid, and dimethyl sulfoxide decreased fibrin production at 0.5 and 1 hour after induction uveitis. Phenidone and norhydroguaiaretic acid also inhibited the initial increase intraocular pressure early in the course of inflammation. Leukotriene B4 in the aqueous was measured by use of radioimmunoassay at 1 hour after inflammation. In control dogs, 230 to 1,700 pg of leukotriene B4/ml was measured; in dogs treated with phenidone, leukotriene, B4 was not measured.

The in vivo effects of a single prophylactic dose of recombinant bovine interferon (rBoIFN)-alphaI1 in calves with salmonellosis were investigated, using a Salmonella typhimurium infection model. Treatment with rBoIFN-alphaI1 reduced the degree of septicemia compared with that in control groups, and, in one experiment, using disease of reduced severity, body temperature was lower in treated calves than in controls.

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.

Cryptosporidium infection is one of the most common causes of parasitic diarrhoea worldwide in cattle and humans. In developing countries, human cryptosporidiosis is most prevalent during early childhood and links between zoonotic infection and animal related activities have been demonstrated. This study investigated the prevalence and species/genotype distribution of Cryptosporidium among children (< 5 years) and calves (< 6 months) living in a rural farming area adjacent to the Kruger National Park in South Africa, where interactions between humans and wild and domestic animals are known to occur. Cryptosporidium oocysts were detected in 8/143 stool samples of children recruited within the hospital system (5.6%; 95% CI 2.4%, 10.7%) and in 2/352 faecal samples of calves (0.6%; 95% CI 0.1%, 2.0%) using the modified Ziehl–Neelsen (MZN) staining technique. Microscopy positive samples from children were further analysed by PCR targeting the 18S rRNA gene and identified as Cryptosporidium hominis (3/4) and Cryptosporidium meleagridis (1/4). Regardless of the microscopy outcome, randomly selected samples (n = 36) from calves 0–4 months of age were amplified and sequenced at the 18S rRNA gene using nested PCR. Two calves tested positive (5.6%; 95% CI 1.7%, 18.7%), and revealed the presence of Cryptosporidium parvum and Cryptosporidium bovis. The detection of only two zoonotic species (C. parvum in one calf and C. meleagridis in one child) suggests that zoonotic cryptosporidiosis is not currently widespread in our study area; however, the potential exists for amplification of transmission in an immunocompromised population. (Résumé d'auteur)

The article reviews the outbreaks and distribution of African swine fever (ASF) in South Africa since the first probable outbreak that occurred in the Koedoesrand Ward in 1926. Retrospective data on the ASF outbreaks in South Africa were obtained from the World Organisation for Animal Health (OIE) disease database and the South African veterinary services annual reports in addition to published articles and online sources. South Africa has experienced many outbreaks that can be divided into 2 time periods: the period before the development of the OIE diseases database (1993) and the period after. More than 141 outbreaks of ASF were reported during the first period. Since the development of OIE disease database, 72 outbreaks directly involving 2968 cases, 2187 dead and 2358 killed pigs mainly in smallholder pig farms were reported. The median number of cases for a given ASF outbreak is 17, but in 50% of outbreaks no pigs were killed for prevention. The most important ASF outbreak was reported in April 2014 in the Greater Zeerust district (North West province) involving 326 cases and 1462 killed pigs. However, the outbreak with highest mortality involving 250 pigs was reported in 2016 (Free State province). According to phylogenetic analysis, nine p72 genotypes (I, III, IV, VII, VIII, XIX, XX, XXI and XXII) have been identified in South Africa. Season-wise, more outbreaks were recorded during summer. It was also observed that the OIE disease database could contain errors that would have been introduced through compiled forms at country level. Spatiotemporal studies on ASF outbreaks in South Africa are therefore required in order to assess statistically and quantitatively the clustering of outbreaks over space and time.

Peste des petits ruminants (PPR) is a highly contagious viral disease that mainly affects goats and sheep in Asia, Africa and the Middle East, and threatens Europe [R.E.1]. The disease is endemic on the African continent, particularly in West Africa, and is a major factor driving food insecurity in low-income populations. The aim of this research study was to carry out surveillance, genetic characterisation and isolation of recently circulating PPR viruses (PPRV) in sheep and goats from the six agro-ecological zones of Nigeria. A total of 268 post-mortem tissue samples of lung and mesenteric ganglia were collected from clinically suspected sheep and goats in 18 different states, of which five never previously sampled. The presence of PPRV was confirmed using a reverse-transcription coupled with a polymerase chain reaction (RT-PCR) assay. A total of 72 samples, 17 sheep (6%) and 55 goats (21%), were found to be PPR positive. Positive samples were distributed in almost all states, except Kano, where PPR was detected in previous studies. The PPRV-positive samples were further confirmed by sequencing or virus isolation in areas where the infection had never previously been detected. These results confirm the active circulation of PPRV across all six agro-ecological zones of Nigeria, and consequently, the need for introducing strict measures for the control and prevention of the disease in the country.