Isolation of Campylobacter sputorum ssp. mucosalis from proliferative hemorrhagic enteropathy in pig.
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Rare cases of thymic granulomatous lesions were found in pigs. The lesions consisted of epithelioid cells, multinucleated giant cells, and lymphocytes. Such lesions also were observed in the mesenteric lymph nodes, spleen, kidney, and stomach. The cytoplasm of the majority of giant cells and some epithlioid cells was periodic acid-Schiff (PAS) positive. All cells were positive for vimentin, lysozyme, and desmin. Ultrastructurally, the giant cells were rich in organella and attached to adjacent epithelioid cells by membrane interdigitation. The cells included numerous coated vesicles and granules. No etiologic pathogen, including porcine circovirus type 2, was detected in the lesions. This is the rare case of idiopathic thymic granulomatous lesion in pigs.
The prevalence of gastric Helicobacter infection in finishing pigs and the influence of this infection on gastric lesions was studied. Stomachs of 89 finishing pigs from 27 randomly selected herds were sampled at the slaughterhouse. Forty cases (Group A) were selected based upon the presence of gross pathological lesions in the pars oesophagea, and further 49 cases were obtained at random (Group B). Three samples of gastric tissue (junction of pars oesophagea and pars cardiaca, fundic area, and pyloric area) were collected from each stomach for histological and immunohistochemical examination. Helicobacter antigen was detected in 76 cases (85.4%). No association was found between the presence of Helicobacter in the stomach and the occurrence of gross pathological lesions in the pars oesophagea or gastritis detected on histological examination. However, a significant association was found between the occurrence of Helicobacter in the pyloric area and the presence of erosions/ulcers in the pars oesophagea (OR: 7.01, p = 0.022) in Group B. A significant association was also evident between the presence of Helicobacter and glandular lesions (dilatation of the glands + glandular abscess + degeneration of glandular epithelial cells). In conclusion, Helicobacter infection seems to be a contributing factor to pathological changes in the stomach of finishing pigs.
This paper presents a review of Leptospira infection in farm animals in Portugal which is based mainly on serological results obtained in the National Veterinary Research Laboratory between January 1987 and December 1993. Serum samples were tested by the microscopic agglutination test, at a minimum dilution of 1:100. Positive titres were obtained in 15.3% of the 9,543 bovine samples examined. Sejroe, Pomona, Hebdomadis, Tarassovi and Icterohaemorrhagiae were the principal serogroups which reacted in the tests. A total of 3,195 pigs were tested, of which 20.2% showed positive reactions. The main serogroups which reacted were Australis, Pomona, Cynopteri, Icterohaemorrhagiae and Autumnalis. Field observations on outbreaks of leptospirosis in pigs, along with data obtained from an experimental infection with serovar mozdok in pregnant gilts suggest that this serovar, rather than serovar pomona, may be causing Pomona group infections in pigs. Serum samples from 5,298 sheep were tested and 3.3% gave positive results. The predominant serogroups involved were Canicola, Pomona, Cynopteri, Sejroe and Icterohaemorrhagiae. From the 1,631 goats examined serologically, 5.0% gave positive results, mainly to serogroups Grippotyphosa, Canicola, Pomona, Icterohaemorrhagiae and Pyrogenes. Only 83 serum samples from horses were obtained, of which 43.4% showed positive titres. Serogroups Australis, Autumnalis, Cynopteri and Pyrogenes were those most commonly found. Serological evidence of leptospirosis in farm animals is widespread in Portugal, particularly in cattle and pigs. Leptospirosis in horses needs to be studied further. In an attempt to provide a general view on the occurrence of leptospirosis in these animal species in Portugal, the present results are compared with results obtained in previous studies and are complemented with both previous and recent bacteriological findings.
Taipei China had been free from foot and mouth disease (FMD) over 68 years before the disease occurred in March 1997. The first suspected case was recorded on a pig farm in the Hsinchu Prefecture on 14 March 1997. Based on clinical signs, gross histopathological findings, and results of enzyme-linked immunosorbent assays and reverse-transcriptase polymerase chain reaction tests, diagnosis of FMD was confirmed by the Taiwan Animal Health Research Institute on 19 March 1997 and was reconfirmed by the FMD World Reference Laboratory in Pirbright (United Kingdom), on 25 March 1997. By the end of July 1997, 6,147 pig farms (about a quarter of the pig farms in Taipei China), were affected. The disease was well under control within two months by means of stamping-out and blanket vaccination. The Government purchased 21 million doses of inactivated oil-adjuvant FMD vaccine, which allowed for two injections per pig and one injection of other cloven-hoofed animals. Before the vaccine was used, the stamping-out policy was implemented, ensuring that all pigs in the affected farms were destroyed. After blanket vaccination, a partial stamping-out policy was adopted, i.e. only pigs showing clinical signs were destroyed.
An outbreak of foot and mouth disease (FMD) was recorded in Japan in the spring of 2000, the first for ninety-two years. Between 25 March and 11 May, four farms were infected. However, the disease was eradicated without resorting to vaccination, through a campaign of culling, movement control of cloven-hoofed animals in areas surrounding infected premises, and intensive clinical and serological surveillance. Japan regained FMD-free status by the end of September 2000. The authors describe the nature of the outbreaks, the eradication measures implemented, and the clinical and serological surveillance methods used. The possible sources of infection are also examined. Finally, the direct and indirect economic losses are presented.
Pigs and poultry in the United Kingdom have undeniably been exposed to the bovine spongiform encephalopathy (BSE) agent. They consumed the same ruminant protein that gave rise to the BSE epidemic in cattle, but there has been no evidence of an epidemic in these species. Experimental investigations have shown pigs to be susceptible to infection by multiple parenteral challenge, but resistant to oral exposure with BSE-infected cattle brain. Current but incomplete evidence suggests that they are also resistant to oral challenge with sheep scrapie. Studies in domestic chickens indicate that they are resistant to both parenteral and oral challenge. Unfortunately, no published data exists on the susceptibility of fish to infection. Incidental findings in the brains of unexposed pigs are described that could otherwise give rise to concerns aboutthe presence of a transmissible spongiform encephalopathy in pig populations around the world.
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Obese and crossbred (X-Bred) pigs were removed from sows at 14 d of age and given ad libitum access to a high-fat, milk-based diet. A subset of pigs fed this diet were killed at 28 and 49 d of age. At 28 d, another subset of pigs was given ad libitum access to a low-fat, grain-based diet and were killed at 31, 35, and 49 d of age (nutritionally weaned for 3, 7, and 21 d, respectively). Dorsal subcutaneous adipose tissue was obtained at death and adipocytes were prepared by incubation with collagenase. A portion of the cells was fixed with osmium to determine size and number; remaining cells were lysed in hypotonic media and centrifuged to yield a crude membrane fraction. The beta-adrenergic receptor (beta-AR) and A1 adenosine receptor (A1R) affinity and number were measured in the membranes by equilibrium saturation ligand binding. Obese pigs had a lower body weight than X-Bred pigs at all ages (P < .05). Obese pigs tended (P for volume > .1 but < .2) to have larger adipocytes than X-Bred pigs. The beta-AR affinity did not differ between obese and X-Bred pigs. There were fewer beta-AR per milligram of membrane protein in obese than in X-Bred pigs at 28 and 49 d of age when fed the high-fat, milk-based diet (P < .01). However, beta-AR number expressed per cell or unit cell surface area did not differ between genetic groups. As pigs of either genetic group continued to be fed the low-fat, grain-based diet, the beta-AR decreased when expressed per milligram of protein or unit cell surface area (P < .05) and tended to decrease when expressed per cell. Obese and X-Bred pigs fed the high-fat, milk-based diet had more beta-AR than respective pigs fed the low-fat, grain-based diet when data were expressed per milligram of protein (P < .01) but not when expressed per cell or unit surface area. The A1R were only detectable in 2 of 16 X-Bred litters but were more developed in adipocytes of obese pigs, being measurable in 8 of 14 litters. The A1R number, expressed per milligram of protein, was lower in obese pigs fed the milk-based diet than in those fed the grain-based diet (P < .05). These findings suggest the decreased beta-AR number after nutritional weaning, or the transition from a high-fat to low-fat diet, may contribute to fat accretion in pigs. Furthermore, the lower number of beta-AR in obese than in X-Bred pigs may contribute to the obesity.
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Certain birth defects in livestock induced by poisonous plants possess clinical similarities to congenital deformities in humans. They meet some criteria as models for those corresponding human conditions. They are induced by several plants, including members of the Astragalus, Lupinus, Conium, Nicotiana and Veratrum genera. The terata expressions include effects in bone and soft tissue, particularly in the limbs, spinal cord and cephalic regions. Whether these livestock conditions become extensively used as models of human terata will be determined by how well they meet the criteria sought in good models. These prospective models have many favorable characteristics; however, being large domestic livestock, they have certain logistic disadvantages compared with small rodents as models.
From August 1976 to July 1977, all faecal specimens (3298) sent to the Enteric Department of the Institute of Medical and Veterinary Science, Adelaide were selectively cultured for Yersinia enterocolitica. Yersinia enterocolitica was isolated from three patients with diarrhoea, one of whom acquired her infection overseas. These organisms were not isolated from faecal or lymph node material collected from a limited number of sheep and pigs found to have enteritis at the time of slaughter. Enteric infection due to Yersinia enterocolitica does not appear to be common in Australia and selective culture methods using cold enrichment techniques do not appear to be justified especially in laboratories handling specimens derived mainly from adults.
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