The present study assessed the association of tail-biting lesions in ϐinishing pigs with weight gain, occurrence of locomotion or respiratory disorders and abscesses during ϐi-nishing period, and carcass condemnation at slaughter. The study was carried out on 4 different farms. For each animal with a tail biting lesion, two control pigs were selected. The total number of animals in the study was 312, with 104 of them being tail-bitten. Tail lesions were classiϐied according to the degree of severity into four scores: score 0 -normal tail withou lesion; score 1-3 -increasing lesion severity, and score 4 -healed lesions. Overall, the occurrence of severe tail lesions (score 3) varied from 55 to 73% of tail-bitten pigs among farms. On all farms, healing of tail lesions was observed in 95% to 100% of the animals at the evaluation performed within 41-43 days after the commencement of the study. In two out of the four evaluated farms, pigs with score of 3 showed lower weight gain (P<0.05) compared with score 0 pigs. Before slaughter, the occurrence of locomotion problems and nodules/abscesses was associated (P<0.05) with the presence of tail-biting lesions. At slaughter, tail-biting lesions were associated (P<0.05) with the presence of abscesses, lung lesions (pleuritis and embolic pneumonia) or arthritis in carcasses. Carcass condemnation was associated with the presence of tail-biting lesions (P<0.05). Overall, carcass condemnation rate was 21.4%, of which animals with tail-biting lesions accounted for 66.7% of condemnations. Among the animals diagnosed with cannibalism at farm level, only two had not healed their lesions at slaughter. The fact that there were a lot of carcass condemnations, despite the fact that tail-bitten animals had no more active lesions, suggests that different situations may be observed between the ϐield and slaughter, reinforcing the need to analyze pigs both at farm and slaughter to allow proper assessment of losses related to tail biting. Collectively, the observations of the present study show that complications associated with tail-biting found in slaughterhouses are probably underestimating ϐield prevalence.

A case-control study was carried out in litters of 1 to 7-day-old piglets to identify the main infectious agents involved with neonatal diarrhea in pigs. Fecal samples (n=276) from piglets were collected on pig farms in the State of Rio Grande do Sul, Brazil, from May to September 2007. Litters with diarrhea were considered cases (n=129) and normal litters (n=147) controls. The samples were examined by latex agglutination test, PAGE, conventional isolating techniques, ELISA, PCR, and microscopic methods in order to detect rotavirus, bacterial pathogens (Escherichia coli, Clostridium perfringens type A and C, and Clostridium difficile), and parasites (Coccidian and Cryptosporidium spp.). Outbreaks of diarrhea were not observed during sampling. At least one agent was detected in fecal samples on 25 out of 28 farms (89.3%) and in 16 farms (57.1%) more than one agent was found. The main agents diagnosed were Coccidia (42.86%) and rotavirus (39.29%). The main agents identified in litters with diarrhea were Clostridium difficile (10.6%), Clostridium perfringens type A (8.8%) and rotavirus (7.5%); in control litters, Clostridium difficile (16.6%) and Coccidian (8.5%). Beta hemolytic Escherichia coli and Clostridium perfringens type C were not detected. When compared with controls, no agent was significantly associated with diarrhea in case litters. These findings stress the need for caution in the interpretation of laboratorial diagnosis of mild diarrhea in neonatal pigs, as the sole detection of an agent does not necessarily indicate that it is the cause of the problem. dos surtos e a diarréia, quando presente, apresentou-se leve. Pelo menos um agente foi identificado nas amostras fecais de 25 entre 28 granjas (89,3%) analisadas e em 16 granjas (57,1%) mais de um agente foi detectado. Os principais agentes encontrados nas granjas foram coccídeos (42,86%) e rotavírus (39,29%). Os principais agentes detectados nas leitegadas com diarreia foram Clostridium difficile (10,6%), Clostridium perfringens tipo A (8,8%) e rotavírus (7,5%). Por outro lado, nas leitegadas controle os agentes mais prevalentes foram Clostridium difficile (16,6%) e coccídeos (8,5%). E. coli Beta hemolítica e Clostridium perfringens tipo C não foram detectados. O presente estudo de caso-controle demonstrou que nenhum agente infeccioso esteve associado significativamente com diarreia (p>0.05). Esses achados reforçam a necessidade de que haja cuidado na interpretação de resultados de exames laboratoriais em materiais coletados de leitões com diarreia neonatal leve, pois a detecção isolada de um agente infeccioso não indica necessariamente que o mesmo seja a causa do problema.

Pesq. Vet. Bras. 34 (7) The objective of the study was to identify the frequency of macroscopic and microscopic lesions and bacterial agents involved with pericarditis in slaughter pigs in the State of Rio Grande do Sul, Brazil. The samples were collected in slaughterhouses with Federal Inspection Service (SIF) between February and October, 2010. Condemnation due to pericarditis in the examined animals was 3.9% (299/7,571). Ninety one cases of pericarditis were examined and by histopathology 89% were chronic and 47% of the corresponding lungs showed chronic pleuritis, but there was no significant association between both lesions. The bacterial agents isolated from the hearts were Streptococcus spp., Pasteurella multocida, Haemophilus parasuis and Streptococcus suis. Bacterial DNA from Mycoplasma hyopneumoniae and Actinobacillus pleuropneumoniae were the most frequently detected by PCR. There was significant association between isolation of P. multocida and Streptococcus spp. in the hearts and corresponding lungs. The results suggest that lung infection could act as a port of entry to the colonization of the adjacent pericardium. In spite of the fact that M. hyopneumoniae was the agent more frequently identified by PCR in the heart and corresponding lung, there was no significant association of the agent in the organs. This suggests that the infections were independent events. The other agents investigated did not show significant association between isolation or DNA detection in heart and corresponding lungs. Another important finding was the presence of coinfection between bacterial agents in 2% of the hearts and by PCR were identified bacterial DNA of two or more agents in 16.5% of the hearts. These results suggest that coinfections in cases of pericarditis need further investigation.

In this study, we determined whether vaccination with Duramune DAPPi+LC containing canine parvovirus (CPV) type 2b protects against challenge with virulent CPV antigenic type 2c. Seven healthy dogs, seronegative for CPV2, were enrolled into two treatment groups; five were vaccinated twice, 21 days apart, with minimum titre vaccine, and two were given saline. Dogs were challenged with CPV 2c three weeks later. Clinical observations, body weight and rectal temperature measurements, blood samples for serology and white blood cell counts and faecal samples for virus excretion were collected. Control dogs remained seronegative until challenge; vaccinated dogs seroconverted and were positive for antibodies to CPV2 from day 21. Four days after challenge, clinical signs associated with parvovirus infection (vomiting, paroxysmal shivering, depression, loose stools) were observed in the control dogs. Both animals were withdrawn from the study for welfare reasons one day later. On day 47, leucopenia was observed in controls, with white blood cell counts less than 50 per cent prechallenge values. No specific clinical sign of parvovirus infection were observed in the vaccinated dogs, nor was (detectable) challenge virus shed in faeces suggesting that antibodies generated contributed sterilising immunity. We conclude that vaccination of dogs with Duramune DAPPi+LC protects against challenge with a virulent field strain of CPV 2c.

Our objective was to evaluate experimental induction of empyema in rats by intrapleural inoculation of Staphylococcus aureus by means of thoracentesis with pleural pressure monitoring. Forty female albino Wistar rats, anesthetized with droperidol and fentanyl, underwent intrapleural inoculation of a 0.2-ml solution. Group I ( N=25) received 10(10) colony-forming units/ml of Staphylococcus aureus cultivated in brain-heart infusion agar (BHI); group II (N = 15), the control group, received sterile BHI agar. Rats were inoculated after right hemithorax thoracentesis with a needle connected to an oscilloscope for pressure monitoring to confirm that the needle was inside the pleural space. Animals were killed after 3 (groups Ia and IIa) to 5 (groups Ib and IIb) days with sodium pentobarbital. The macroscopic changes, amount of pleural fluid, and anatomopathological aspects of pleura and lungs were recorded, as well as death causes and bacteriological findings of pleural fluid for animals that died before the time established for euthanasia. In group I, three animals died of thoracentesis complications, and five others died in the first 24 h due to septicemia; blood and spleen cultures isolated the bacteria previously inoculated. In group II, there was one death of unknown cause. Of the 17 rats inoculated with bacteria, nine (group Ia) were killed on the 3rd day; all had bacteria in pleural fluid (volume 0.5-3.8 ml). The other eight rats (group Ib) were killed on the 5th day; three (39.5%) had pleural fluid with bacteria (0.5-1.5 ml), and five (60.5%) had no pleural fluid. Rats from group II killed on the 3rd (group IIa) and 5th (group IIb) days had no pleural fluid. Pathologic examination revealed inflammatory infiltrate (93.75%) and fibrin (18.75%) in pleura, and inflammatory interstitial infiltrate (12.5%) in the right lung in group I; no changes were observed in 93.3% of the lungs in group II. Macroscopic examination revealed only turbid and bloody pleural fluid (class I) without pleural adhesions. Pleural inflammatory infiltrate was found in rats that received the bacteria but had no fluid at necropsy (class 0). One control rat, although with no clinical signs of disease or pleural fluid, had signs of pleural and pulmonary infection at necropsy. We conclude that empyema may be induced in rats by the inoculation of Staphylococcus aureus by means of thoracentesis with pleural pressure monitoring. The highest amount of pleural fluid was observed 3 days after bacterial inoculation.