Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SWINE DISEASES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed1969

An attempt to experimentally produce edema disease in swine by oral administration of escherichia coli serotype O139:K82:H1.

Diarrhea, reduced appetite, and nervousness were observed following oral exposure of six pigs to freeze-thaw extract and living culture of E. coli strain 0139:K82:H1. The most significance gross change was the appearance of subserosal edema of the mesentry, especially of the mesocolon. Histological findings included perivascular edema of the brain and reticulum cells as well as lymphocytic aggregates in the renal cortex simulating early neoplasia. Edema of the submucosa of gallbladder, the duodenum, the spiral colon and the fundic stomach as well as the lymph nodes was also observed. The syndrome which was produced resembled, in many aspects, edema disease although some complicating factors were ob-

Animals↗
PubMedDate not supplied

Treatment and prophylaxis of some infectious diseases of swine and cattle using of natural alpha-interferons.

On the basis of experimental studies which proved stimulating action on absorbing and bactericidal function of blood phagocytes and antibody genesis the methods of therapy and prophylaxis of wide spread infections in modern live-stock (transmissive gastroenteritis of pigs, parainfluenza of calves, colibacteriosis of swine and cattle) were created. It was established, that optimal one-time therapeutical dose of homologous alpha-IFN for intramuscular administration to new-born pigs was 2000-4000 IU per head, prophylactic dose was 1000-2000 IU. Therapeutical doses of alpha-IFN for calves did not exceed 4000-6000 IU, prophylactic--4000 IU. As a rule, it is necessary to introduce the preparation three times with 48 h intervals. With the account of these data the large-scale commissional trials of these preparations were carried out.

Animals↗
PubMed1974

Experimental edema disease of swine (E. coli enterotoxemia). 3. Pathology and pathogenesis.

Experimental colibacillary (Escherichia coli) enterotoxemia as described in this report mimics natural edema disease both clinically and in gross pathology. The histopathology is characterized by accumulations of non-inflammatory edema and by arteriopathy. The smaller arterial and arteriolar changes recorded here are similar to those described in natural edema disease. The vascular changes described in recovered cases of experimental colibacillary enterotoxemia concur with those reported in so-called subacute and chronic edema disease. The arteriolar changes that occur in colibacillary enterotoxemia of swine are comparable to those associated with hypertension. Thin sections of cerebral cortex from four pigs with acute experimental edema disease were examined by electron microscopy in an attempt to demonstrate brain edema. Sections from one pig taken during the convulsive phase of disease revealed dilatation of perivascular glial processes. However, examination of sections taken from three other pigs during an earlier phase of the neurological disturbance revealed no significant lesions. We were unable to ascertain the role of brain edema in the pathogenesis of the nervous system disturbance in these experiments.

Animals↗
PubMed1996

Vaccination with genetically modified Shiga-like toxin IIe prevents edema disease in swine.

Escherichia coli strains producing Shiga-like toxin II variant (SLT-IIe, formerly called SLT-IIv) cause edema disease in weaned pigs. Vaccination of pigs with a genetically modified form of Shiga-like toxin IIe, SLT-IIe(E167Q), has been previously shown to be nontoxic and to induce antibodies to SLT-IIe (V.M. Gordon. S.C. Whipp, H.W. Moon, A.D. O'Brien, and J.E. Samuel, Infect, Immun. 60:485-502, 1992). Fifty micrograms of SLT-IIe(E167Q) toxin was used to vaccinate suckling pigs at 1 and 2 weeks of age. Both vaccinated and nonvaccinated pigs were orally inoculated with an SLT-IIe-producing strain of E. coli after weaning (3 to 4 weeks of age). Pigs fed a low-protein diet that were not vaccinated with SLT-IIe(E167Q) developed subclinical edema disease, histologically evident as vascular necrosis. Pigs fed a high-protein diet that were not vaccinated with SLT-IIe(E167Q) developed clinical edema disease manifested as vascular necrosis, reduced weight gain, ataxia, palpebral edema, lateral recumbency, and death. Pigs vaccinated with SLT-IIe(E167Q) had a reduction in the incidence of subclinical edema disease and never developed clinical edema disease. These data demonstrate that vaccination with a genetically modified form of SLT-IIe prevents edema disease and are consistent with the notion that diet influences susceptibility to edema disease.

Animals↗
PubMed1997

The public health risks associated with wild and feral swine.

Wild swine populations (Sus scrofa) are present in many regions of the world. Large feral populations in North America and Australia are principally derived from introduced domestic pigs. In Europe, most wild boar are found in Germany and Poland. While wild swine are certainly a significant reservoir of infection for domestic swine diseases (for example, African swine fever virus in wild boar in Sardinia), these swine generally do not constitute a major public health risk. Brucella suis infections and trichinellosis are the most important zoonotic threats to public health.

Animals↗
PubMed1991

Reproduction of edema disease of swine with purified Shiga-like toxin-II variant.

Twenty-one weaned Yorkshire-Landrace pigs were injected intravenously with graded doses of purified Shiga-like toxin-II variant (edema disease toxin). In a preliminary study, three pigs (Nos. 1, 2, 3) were injected with 48, 24, and 12 ng, respectively, of SLT-IIv/kg of body weight. Subsequently, three groups (Nos. 4, 5, 6) of six pigs each were injected with 6, 3, and 1.5 ng, respectively, of SLT-IIv/kg of body weight. Severe clinical signs and histologic lesions characteristic of edema disease developed in pigs Nos. 1, 2, and 3, and all six pigs in group No. 4. Eight of these pigs were euthanatized in extremis (mean time to death was 34 hours) and one died of the disease (52 hours). Moderate signs and lesions of edema disease were observed in all pigs in group No. 5, and three pigs were euthanatized (mean time to euthanasia was 42 hours). Mild signs and lesions were observed in three pigs in group No. 6. The most common gross pathologic changes were edema of the eyelids, submucosa of the stomach, and mesentery of the spiral colon and hemorrhage of the colon and cerebellum. Microscopic lesions were associated with vascular injury and included vessel necrosis, perivascular edema and hemorrhage, and superficial colonic and cecal erosions. The vascular lesions were observed in the cerebellar folia, submucosa and mucosa of the stomach, cecum, colon, and sporadically in the retina. None of the clinical signs associated with endotoxin were observed.

Animals↗