Domestic poultry is a natural reservoir of Campylobacter, the host–pathogen interaction being predominantly asymptomatic. This study investigated whether chickens remain asymptomatic partly because of lactic acid bacteria (LAB). Campylobacter spp. and LAB were isolated from the gut of poultry chickens using enrichment and screening assays and were identified via rDNA sequencing. The C. jejuni DC3 isolate was grown in different cell-free supernatants (CFS) generated from a priority LAB isolate. An in vivo challenge involving the C. jejuni and LAB isolates using a chicken model was performed to confirm the in vitro findings. Twelve presumptive LAB isolates had anti-C. jejuni activity based on cross-streak and agar plug assays, with Lactobacillus sakei L14 isolate exhibiting the highest activity. Inhibition by L. sakei L14 CFS of the growth of C. jejuni occurred in a dose-dependent manner. Campylobacter jejuni DC3 inhibition was most evident in CFS harvested at 72 h and produced by co-culture with the pathogen. Neutralisation of the CFS abrogated the observed inhibition. Co-infection with C. jejuni DC3 and L. sakei L14 in vivo, however, failed to inhibit C. jejuni colonisation in chickens. The results suggest that the anti-C. jejuni effect of L. sakei L14 in chickens may be due to mechanisms other than direct inhibition of growth.

This project investigated the use of ultrasonography at first diagnosis of presumptive early bovine respiratory disease (BRD) in feedlot cattle from western Canada. One hundred seventy-four cattle (116 cases and 58 controls) at high risk of developing BRD were enrolled in a prospective longitudinal study over 2 y (2006-2007). Cattle with clinical signs relating to the respiratory system and assessed as sick at the time of feedlot arrival (arrival fever cases) or assessed as sick in the pen 3 to 30 d post-arrival (post-arrival fever cases, post-arrival no fevers cases) were eligible for enrollment. Control animals were identified at the time of case enrollments. Ultrasonography was done using a 3.5 sector transducer at enrollment and at 2, 4, and 6 wk post-enrollment. Lung lesions were identified at least 1 time over the course of the trial in 32/116 (28%) cases and 9/58 (16%) controls. At enrollment, lung lesions were identified in 20/115 (17%) cases and 2/55 (4%) controls (data unreadable n = 4). Post-arrival fever cases (14/48) were the most likely to have a lesion identified using ultrasound. In arrival fever cases, average daily gain (enrollment to last ultrasound, average 34 d) was improved (P = 0.007) in cattle identified with a lesion at enrollment using ultrasound compared with those not identified with a lesion at that time, potentially demonstrating the effects of gut fill at arrival weighing, as these sicker animals may have eaten less prior to arrival and, therefore, had more room for improvement in weight over time due to restoration of normal gut fill. None of the ultrasound time points explored (enrollment, 2, 4, or 6 wk post-enrollment) were associated with the animal health outcomes of interest (subsequent treatment, chronicity, wastage, or mortality) for cattle enrolled at arrival or post-arrival.

Twelve Holstein calves mere used to determine the prophylactic efficacy of ivermectin against challenge exposure with gastrointestinal and pulmonary nematodes. Two groups of 6 calves (mean body weight, 205 kg) each were formed by restricted randomization according to body weight. Group-l calves served as nonmedicated controls. Each calf of group 2 was orally given one prototype sustained-release bolus designed to deliver ivermectin at a continuous daily dose of 8 mg. Third-stage nematode infective larvae were given to the calves on posttreatment days 28 and 42. The calves were euthanatized 77 or 78 days after treatment. Ivermectin was 100% effective (P < 0.05) in preventing the establishment of infection by Haemonchus placei, Ostertagia ostertagi, Cooperia spp (C punctata, C oncophora, C surnabada), Nematodirus helvetianus, Oesophagostomum radiatum, and Dictyocaulus viviparus and was > 99% effective against Trichostrongylus axei. Incidental infection by Trichuris spp was reduced by 94% (P = 0.08).

In rats infected with the cestode Taenia taeniaeformis, hepatomegaly results from development of parasitic cysts in the liver. Diffuse nodular mucosal hyperplasia in the glandular region (corpus and antrum) of the stomach, and gross thickening of the intestinal mucosa also result. Between postinfection days (PID) 21 and 84, radiologic observations were made after oral administration of a barium sulfate suspension in T taeniaeformis-infected rats and in age/sex-matched controls. There was radiographic evidence of hepatic enlargement at PID 21. Enlargement of the gastric folds was first observed along the greater curvature of the stomach at PID 35. Fimbriation of small intestinal mucosal surfaces resulted from thickening of the intestinal villi and was observed in the duodenum at PID 21. Intestinal motility was assessed, and contractions were counted, using image intensification fluoroscopy, then were recorded on videotape. There were no significant differences between control and infected rats for gastric emptying time, intestinal transit time, and number of intestinal contractions per minute. Barium contrast radiography clearly indicated large gastric folds, thickening of the small intestinal villi, and hepatic enlargement, and was useful for assessing gastrointestinal motility.

Development of the rickettsia, Anaplasma marginale, salivary glands of male Dermacentor andersoni exposed as nymphs or adult ticks, was studied indirectly by inoculation of susceptible calves with homogenates and directly by examination, using light microscopy and a DNA probe; some unfed ticks were incubated before tissues were collected. Salivary gland homogenates made from ticks in every treatment group caused anaplasmosis when injected into susceptible calves; prepatent periods decreased as the time that ticks had fed increased. Colonies of A marginale were seen only in salivary glands of ticks exposed as adults and not in those exposed as nymphs; the percentage of salivary gland acini infected in these ticks increased linearly with feeding time. However, the probe detected A marginale DNA in salivary glands of ticks from both groups; the amount of DNA detected increased as feeding time was extended. The amount of A marginale DNA appeared to remain constant in gut tissues, but to increase in salivary glands. Salivary glands of adult-infected male ticks that were incubated, but did not feed a second time, became infected with A marginale, and the pattern of infection of acini varied with incubation temperature. Development of A marginale in salivary glands appears to be coordinated with the tick feeding cycle; highest infection rate was observed in ticks exposed as adults.

Chicken egg yolk IgG can be absorbed and transferred as efficiently as colostral antibodies in the blood of neonatal pigs. Egg yolk IgG has a half-life of 1.85 days in newborn pig serum. This is shorter than the reported half-life (12 to 14 days) of homologous IgG in serum of pigs. Similar to colostral antibodies, egg yolk IgG absorption from intestine ceased at about 34 hours of age, after a logarithmic decrease in absorption rate from birth. Egg yolk IgG absorption inhibition time in the gastrointestinal tract took 1.73 hours to decrease by half. Egg yolk IgG was protective against experimentally induced diarrhea in pigs when it was administered at high dose, and multiple dosing was instituted. Adverse effects were not observed when chicken egg yolk IgG was administered orally to pigs.

Experiments were conducted to establish a persistent Salmonella typhimurium infection in convalescent swine, and to determine rate of shedding and distribution of the organism in internal organs. Naturally farrowed Salmonella-free pigs (n = 37) were orally exposed to S typhimurium when 7 to 8 weeks old. Fecal samples, tonsillar scrapings, and rectal swab specimens were examined bacteriologically for S typhimurium at weekly intervals after exposure until necropsy (maximum of 28 weeks after exposure). Necropsies of 1 to 4 randomly selected pigs were conducted at 2, 4, and 7 days and at 2, 4, 6, 8, 12, 16, 20, 24, and 28 weeks after exposure. The following internal organs were examined bacteriologically for S typhimurium: liver, spleen, kidney, gallbladder, heart, lung, and stomach; segments of the intestinal tract with corresponding lymph nodes; lymph nodes from lymphocenters of the head and neck, thoracic and abdominal cavities, pelvic wall, and thoracic and pelvic limbs. Fecal samples were 83 to 100% culture-positive up to postexposure (PE) week 22, then varied from 14 to 67% positive until PE week 28. At least 60% of tonsillar swab specimens and 50% of rectal swab specimens were culture-positive up to PE week 20, after which they varied from 0 to 70% positive until PE week 28. At necropsy, S typhimurium was recovered most freguently from tonsils (93.5% positive), followed by segments of the intestinal tract from caudal portion of jejunum to rectum (71% recovery from cecum), and mandibular (54.8%) and ileocolic (45.2%) lymph nodes. The organism generally did not persist beyond PE week 2 in other lymph nodes of the head and neck, lymph nodes of the abdominal wall, thoracic cavity, or limbs, or in heart, liver, or spleen. The gallbladder, kidney, and lungs of all pigs were culture-negative.

A controlled test was performed to titrate the anthelmintic dosage of dienbendazole in 24 mixed-breed ponies naturally infected with Strongylus vulgaris, S edentatus, and small strongyle species, as determined by parasitic egg and larval counts in feces. Comparison of results of treatment was made among 3 dienbendazole dosages--2.5, 5, and 10 mg/kg of body weight-and a gum (excipient) mixture given by nasogastric intubation. All ponies were euthanatized and necropsied at 7 or 8 days after treatment. Trichostrongylus axei, Habronema muscae, S vulgaris, S edentatus, small strongyles, and Oxyuris equi were efficaciously eliminated in response to all doses of dienbendazole; Gasterophilus spp were not affected by any dose. There were not sufficient numbers of Draschia megastoma, Anoplocephala spp, or Parascaris equorum in the ponies to evaluate drug effect. Changes in the appearance of the intestinal lining were dose-dependent; in the ponies treated with 5 and 10 mg of dienbendazole/kg, the mucosa appeared clean and smooth, though in ponies given 2.5 mg/kg, it appeared clean, but was nodular and moderately reactive to embedded immature small strongyles. In the gum mixture-treated ponies, the large intestinal mucosa was inflamed, with edematous areas, in response to infections caused by large and small strongyles. A limited clinical titration was done in 12 ponies that were fecal culture negative for S vulgaris larvae, although other strongyles were detected. Two ponies in each of 6 groups were given the following dosages: 0 (gum mixture only), 0.5, 1, 2.5, and 5 mg of dienbendazole/kg. One group of 2 ponies was given 5 mg of fenbendazole/kg as a standard treatment control. On the basis of pre- and posttreatment fecal examinations (for egg and larval counts), dienbendazole at dosages that ranged from 1 to 5 mg/kg was highly effective and as effective as fenbendazole given at a dosage of 5 mg/kg. Small strongyles were most responsive to fenbendazole and dienbendazole at all dosages. Egg production by S edentatus was eliminated by administration of fenbendazole and dienbendazole (at dosages of 2.5 and 5 mg/kg). Administration of dienbendazole at a dosage of 1 mg/kg resulted in partial elimination of S edentatus egg production. Trichostrongylus axei egg production was eliminated by administration of dienbendazole at dosages of 2.5 and 5 mg/kg, but not by the administration of 1 mg/kg. Parascaris equorum egg production was eliminated from the single infected pony given dienbendazole at a dosage of 5 mg/kg.