IMMUNIZATION OF CATTLE AGAINST SHIPPING FEVER: EXPERIMENTAL EXPOSURE.
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The susceptibility of homozygous BSVS mice to acute disseminated encephalomyelitis (ADE) has been found to be nutritionally dependent. On a laboratory stock regimen of commercial fox chow pellets, whole wheat bread, and milk this genotype is 100 per cent susceptible to the disease. On a "synthetic" diet, containing a minimal list of vitamins adequate for growth and maintenance, susceptibility was found to be reduced to 15 per cent. Supplementation of the "synthetic" diet with biotin, folic acid, and vitamin B(12) restored susceptibility to a frequency of 70 per cent. Increasing the supplements tenfold had no further effect in restoring susceptibility frequencies to the 100 per cent level. In the restoration of susceptibility, folic acid and vitamin B(12) were equally effective as single supplements and equivalent to the triple vitamin supplement. The effect of single biotin supplementation was less. An outbreak of fatal pasteurellosis among BSVS mice latently infected with Pasteurella and used in an ADE susceptibility test has been described. The fatal pasteurellosis has been ascribed to a constellation of determinants including (a) diet, (b) sex, (c) inoculation events, and (d) latent infection with Pasteurella. With males the susceptible sex it was possible to avert the fatal pasteurellosis and continue the nutritional experiments by using females exclusively.
The authors report a case of pasteurellosis with abscess of the brain consecutive to a bronchopulmonary infection in a woman with old-standing bilateral bronchiectasis. The prevalence of respiratory infections caused by Pasteurella multocida is low, but it is certainly underestimated. Bronchial and/or pleuro-pulmonary infections occur in subjects with reduced local and/or systemic defences. The respiratory system is colonized by direct or indirect contagion, usually in contact with pet animals carrying the organism.
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Nonpesticinogenic Pasteurella pestis, which is also negative for coagulase and fibrinolytic activities and therefore referred to as (PI-C-F)(-), was investigated to determine whether greatly reduced and erratic lethal responses observed in mice and guinea pigs might be due to inability of the inoculum to establish infection and multiply in survivors. Immunity of survivors was regarded as an indication of previous infection, and, in the case of guinea pigs infected intradermally, appearance of a local lesion and bubo were also noted. Evidence of infection was obtained in most mice and guinea pigs surviving injection of (PI-C-F)(-) strains G-32 and Dodson, suggesting that the virulence determinant (PI-C-F) is related to lethality rather than to infectivity.
An outbreak of Pasteurella multocida infection, involving seven patients on two adjacent wards, has been observed. All seven patients were debilitated and had underlying chronic neuromuscular and/or pulmonary disease and had a tracheostomy tube in situ. The isolates of P. multocida were of the same biotype and serotype, and had an identical antibiogram. Epidemiological studies failed to determine the source of these infections.
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Atrophic rhinitis in swine is presented by means of recently published research work. Thereby it is emphasized as a significant forensic matter, that a reliable diagnosis could only be produced by combined application of clinical, pathoanatomical and bacteriological investigations and that the isolation of toxin-producing strains of Pasteurella multocida in a herd without clinical symptoms of atrophic rhinitis is to be considered as a proof of latent atrophic rhinitis.
Mallards (Anas platyrhynchos platyrhynchos) and white pekin ducks (Anas platyrhynchos domesticus) were infected with duck plague virus and challenged with LD20's of Pasteurella multocida and P. anatipestifer. There was no difference between mortality rates of duck plague-infected ducks and controls, suggesting that these organisms do not act synergistically under the conditions of our experiments. There was a difference of about 500-fold between the LD20 of P. multocida for mallards and that for white pekin ducks, indicating that mallards are much more susceptible to avian cholera than white pekin ducks.
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Lung lavage fluids of 23 young pigs were investigated prior to and after experimental infection with Pasteurella multocida. Comparison of the phospholipid patterns showed an increase in the relative concentration of phosphatidylinositol and a decrease in that of phosphatidylglycerol in the diseased animals. The phosphatidylcholine-to-phosphatidylinositol and phosphatidylglycerol-to-phosphatidylethanolamine ratios were used as parameters to characterize the changing patterns. The reductions in these ratios following infection were found to be useful indicators of bacterial pneumonia. Immunization did not affect the characteristic variations. A rapid screening procedure involving solid-phase extraction, one-dimensional thin-layer chromatography and densitometric scanning of the plates was used.
INTRODUCTION: Healthy pets contact are able to induce unusual and severe diseases. CLINICAL CASE: This case reports the medical history of a dorsal spondylodiscitis in a diabetic patient admitted for a chronic wound of his toes. He had a long-standing history of regular consumption of alcohol and tobacco. Blood bottles and biopsy of intervertebral disc infected discovered Pasteurella dagmatis, commonly colonizing the oropharynx of healthy dogs and cats. In this case, licking of his injured toe by his dog was the likely source of entry of the organism. DISCUSSION: We found no identical cases in the medical literature. Diabetes mellitus and other immunocompromised disorders justify to change behaviours toward domestic animals.
Prior attempts to create an animal model of empyema by direct inoculation of bacteria alone into the pleural space have been unsuccessful. The animals either died of overwhelming sepsis or cleared the infection from the pleural space without development of an empyema. We hypothesized that injection of bacteria with a nutrient agar into the pleural space would allow the bacteria to remain in the pleural space for an extended time period, permitting an empyema to develop. The bacterium Pasteurella multocida in brain heart infusion (BHI) agar was injected into the right hemithorax of 12 New Zealand white male rabbits. Our preliminary studies showed that the animals died in less than 7 days if they were not given parenteral antibiotics. For this reason, the rabbits were given penicillin, 200,000 U, IM, every 24 h starting 24 h after bacterial injection. Pleural fluid was sampled by thoracentesis at 12, 24, 48, 72, and 96 h after bacterial injection. Pleural fluid pH, glucose, lactate dehydrogenase (LDH), leukocyte count, and Gram's stain and culture (in one half of the animals) were obtained at each time point. Pleural biopsy specimens were obtained at autopsy after 96 h. The mean pleural fluid pH reached a nadir of 7.01 at 24 h and remained less than 7.1 throughout the experiment. The mean pleural fluid glucose level reached a nadir of 10 mg/dL at 24 h. The mean pleural fluid LDH peaked at 21,000 IU/L at 24 h and the mean pleural fluid leukocyte count peaked at 12 h with a value of 67,000 cells per cubic millimeter. Gram's stains revealed organisms and cultures were positive for growth in all animals at 12 and 24 h. Some animals had positive Gram's stains and growth on cultures up to 72 h after bacterial injection. At autopsy, all rabbits injected with bacteria had gross pus in the right pleural space and had developed a thick pleural peel. Microscopic specimens of the pleura revealed large numbers of leukocytes (primarily polymorphonuclear lymphocytes) with invasion of the adjacent lung and chest wall. In conclusion, this model more closely mimics the empyema that occurs in humans, relative to previous animal models. This model appears appropriate for additional randomized studies in which different methods for the treatment of empyema can be evaluated.
Vascular cell adhesion molecule-1 (VCAM-1) is expressed by endothelial cells in a variety of inflammatory conditions in experimental animals and humans. It is increased in rabbit endothelium after the intravenous administration of endotoxin, after cholesterol feeding, in regeneration after injury, and in alloxan-induced diabetes mellitus. The effect of a respiratory tract infection with Pasteurella multocida, a common laboratory pathogen in rabbits, on VCAM-1 expression by aortic endothelial cells and on the endothelial ultrastructure was examined in specific-pathogen-free (SPF) New Zealand White rabbits infected by the instillation of a suspension of live organisms into the nose and in conventionally raised rabbits with naturally acquired P. multocida infection. Age-matched SPF rabbits maintained in a disease-free environment were controls. Rabbits were euthanized 50 days after infection, the aorta was excised, and the endothelial cells expressing VCAM-1 were identified by immunohistochemistry. Perfusion-fixed aortas from infected and SPF rabbits were prepared for examination by electron microscopy. All infected animals had pneumonitis and leukocytosis. In SPF rabbits the total leukocyte count was highest at postinfection day 25. There was a significant (P < 0.05) increase in the number of VCAM-1-positive aortic endothelial cells in infected SPF rabbits (34 +/- 4/10(4) endothelial cells; n = 5) and rabbits with naturally acquired infection (57 +/- 14/10(4) endothelial cells; n = 5) compared with control animals (12 +/- 3 per 10(4) endothelial cells; n = 4). The endothelium of infected rabbits had morphologic alterations consistent with injury. Thus infection at remote sites can activate arterial endothelium and induce the expression of VCAM-1.