Relationship to growth performance of pneumonia and atrophic rhinitis lesions detected in pigs at slaughter among four seasons.

A commercial swine herd was selected for study, because pigs at slaughter repeatedly had lung lesions consistent with enzootic pneumonia and had snout lesions typical of atrophic rhinitis. Pigs born during various seasons of the year were allotted to 4 investigations and were evaluated from birth to slaughter. Individual lungs and snouts were identified and collected at the slaughter plant and later examined for gross lesions of bronchopneumonia and atrophic rhinitis, respectively. Each lesion was scored, and the following comparisons were made within investigations: prevalence and mean scores for lung lesions; prevalence and mean grades for snout lesions; correlations between lung lesion scores and growth indicators; correlations between snout lesion grades and growth indicators; and correlations between lung lesion scores and snout grade scores. Included in the growth indicators were average daily gain during the growing phase, average daily gain during the finishing phase, average daily gain during growing and finishing phases, and days to attain 104.5 kg of body weight. Prevalence of lung or snout lesions, mean values for lung lesion scores, mean values for snout lesion grades, and mean values for the various growth indicators were tested for statistical differences among the 4 investigations. Prevalence of lung lesions was highest (96%) for winter-slaughtered and lowest (81%) for autumn-slaughtered pigs. Mean scores for lung lesions were 7% (summer), 5% (autumn), 9% (winter), and 16% (spring). Prevalence of snout lesions was highest (85%) for spring-slaughtered pigs and lowest (42%) for autumn-slaughtered pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathologic response of the lung to irritant gases.

The pathologic response of the lung to irritant gases ranges from the acute exudative phase through the subacute proliferative phase to the chronic fibrosing phase. These responses are based on damage to the Type I cells, and possibly endothelial cells, and the subsequent proliferative and repair processes in the surviving animals. Responses to high dose exposures appear at the microscopic level as exudation of protein rich fluids into alveoli (alveolar edema) and subsequent death due to anoxia. Physiologically, this could be described as a mismatch of ventilation with perfusion, resulting in impaired gas exchange. Animals surviving this acute exudative phase resolve the alveolar edema to fibrin, and Type II cells become hypertrophic and hyperplastic in the process of replacing the damaged Type I cells. The acute and subacute responses also elicit inflammatory changes in the interstitium of the lung that may progress to fibrosis in the chronic stage of a survivable exposure. Diagnostic cases in livestock involving irritant gases reflect similar toxic injuries to the lung.

Relationship of growth performance to pneumonia and atrophic rhinitis detected in pigs at slaughter.

Three commercial swine herds were selected for study, because pigs at slaughter consistently had lung lesions typical of bronchopneumonia and snout lesions consistent with atrophic rhinitis. Pigs were reared in the conventional system for each herd except that they were identified at birth and weighted at various intervals. At slaughter, individual pig lungs and snout were examined for lesions of pneumonia and atrophic rhinitis, respectively. Lesions were scored and correlated with growth indicators for each pig. Included in the growth indicators were: average daily gain (growing phase), average daily gain (finishing phase), average daily gain (total), and days to reach 104.5-kg body weight. Additionally, for each pig, scores for lung lesions were correlated to grades for snout lesions. Three correlation coefficients for measurements of pigs within herd B were significant and included days to 104.5-kg body weight and grades for snout lesions, -0.15 (P less than 0.02); average daily gain (finishing) and grades for snout lesions, 0.17 (P less than 0.01); and average daily gain (total) and grades for snout lesions, 0.16 (P less than 0.01). Contrary to findings in other investigations, pigs that attained market weight at the youngest age did not have the lowest score for lung lesions, the lowest grade for snout lesions, or the least extensive or severe lesions. Combining data from all 3 herds, the mean scores for lung lesions and mean grades for snout lesions decreased significantly (P less than 0.05) as the age of pigs at slaughter increased. All other statistical correlations were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E.

Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-vitamin E preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (vitamin E)/kg, IM; (ii) vitamin E only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of criteria for the postmortem diagnosis of mycoplasmal pneumonia of swine.

Ten swine from each of five herds believed to be affected with mycoplasmal pneumonia of swine and ten swine from each of five herds believed to be mycoplasmal pneumonia-free were selected for postmortem study. Lungs from the 100 swine were examined; grossly and microscopically for lesions typical of mycoplasmal pneumonia of swine and culturally and by an indirect immunofluorescent procedure for the presence of Mycoplasma hyopneumoniae. Nineteen of the lungs had both gross and microscopic lesions typical of mycoplasmal pneumonia of swine and 13 (68%) of these were infected, i.e. were culturally and/or indirect immunofluorescent positive. Absence of gross lesions did not prove freedom from mycoplasmal pneumonia, 14 of 73 (19%) grossly normal lungs were found to be infected with M. hyopneumoniae. Comparison of the indirect immunofluorescent and cultural examination, as methods of diagnosing mycoplasma pneumonia, revealed that neither procedure alone was reliable in the case of negative results. Ten lungs were indirect immunofluorescent negative and culturally positive and seven were culturally negative and indirect immunofluorescent positive (11 lungs were positive by both procedures). It was concluded that a definitive diagnosis of mycoplasmal pneumonia of swine requires that M. hyopneumoniae be visualized in indirect immunofluorescent stained lung sections or that it be recovered culturally.

Comparison of the enzyme-linked immunosorbent assay and the indirect hemagglutination and complement fixation tests for detecting antibodies to Mycoplasma hyopneumoniae.

Caesarean-derived, colostrum-deprived swine were exposed to a broth culture of a low passage field isolate of Mycoplasma hyopneumoniae by intranasal inoculation. The intranasal-inoculated swine subsequently were commingled with their litter-mates to effect transmission via contact-exposure. Sera were collected from the swine at two to four week intervals for approximately one year postexposure and evaluated by the enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination and complement fixation tests. The intranasal-exposed swine seroconverted earlier, developed higher titers and remained indirect hemagglutination and complement fixation positive longer than the contact-exposed swine. It was concluded that the antibody response of intranasal-exposed swine was artificially high and that sera from such swine were not suitable for evaluating the sensitivity of mycoplasmal pneumonia of swine serodiagnostic tests. The indirect hemagglutination test was relatively insensitive and technically cumbersome and the least promising as a practical field test. The complement fixation test appeared to be slightly more sensitive in detecting early antibody production (especially in contact-exposed swine) but it was the least sensitive in detecting late antibodies. The ELISA was generally the most sensitive procedure. Individual high ELISA titers were from ten to 32 times greater than maximum complement fixation and indirect hemagglutination titers. The most striking difference among the three tests was the persistence of high ELISA titers late in the study. All swine were ELISA positive at necropsy approximately one year postexposure despite the fact that lungs were devoid of lesions and culturally and immunofluorescent negative for M. hyopneumoniae.

Pseudorabies virus, porcine parvovirus, and porcine enterovirus interactions with the zona pellucida of the porcine embryo.

Porcine embryos (n = 93) were incubated on cell monolayers that had been previously inoculated with pseudorabies virus, porcine parvovirus (PPV), or each of 2 porcine enteroviruses. After 2, 24, or 48 hours of incubation, the embryos were fixed in glutaraldehyde and examined by electron microscopic procedures. It was found that pseudorabies virus adsorbed to the zona pellucida (ZP) and entered sperm tracks in the ZP. The PPV and both enteroviruses entered pores in the ZP and were associated with sperm that were at or near the outer surface of the ZP. In addition, PPV was seen enmeshed in cellular debris on the outer surface of the ZP. Evidence of a productive viral infection of the blastomeres of the embryos was not found.

Equine granulosa cell tumors.

Unilateral ovariectomy was performed on 3 mares affected with granulosa cell tumors. Tumor fluid in each mare was found to contain estrogen, testosterone, and progesterone. In 2 mares, preoperative blood plasma concentrations of these hormones were comparable to those of a series of clinically normal mares. The other mare, which had a history of aggressive, masculine behavior, had higher testosterone content in the tumor fluid and in the preoperative blood sample. After surgical removal of the tumors, each mare developed follicles and ovulated with the remaining ovary. Each was eventually bred and 2 conceived. The probability of metastasis of these tumors in mares appears uncertain. Data from other species suggests a guarded long-term prognosis may be justified.