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[Pasteurella multocida infections--10 years' experience].

Dog and cat bites are commonly seen at emergency rooms, but have been inadequately characterized. This study attempted to characterize the clinical features of 10 patients from whom P. multocida was cultured. During the past 10 years, 108 patients have been hospitalized for pet bites, at a rate of 3.4/10,000 hospitalizations. Five patients had a documented exposure to cats, 3 to dogs, and two had an unknown exposure. The mean age was 50.8 years (+/- 20.5) and 80% were men. An average delay of 5.7 days was noted from exposure to hospitalization, and additional 4.4 days until P. multocida was characterized. P. multocida was cultured from wounds in six patients, and three patients had bacteremia; another patient had septic arthritis. Six patients needed debridement and the average hospital stay was 11.7 days (3 times our hospital's average). Animal bites may take a complicated course. Our findings call for reassessment of the need for prophylaxis in animal bites.

Animals↗

Further investigations on Pasteurella multocida infections in feral birds injured by cats.

A total of 64 Pasteurella multocida strains (46 out of 11 different feral bird species, partly injured by cat bites, and 18 strains originating from clinically healthy cats) were biochemically differentiated. As a result, 67.4% of the strains from feral birds and 61.1% from the cats were classified as the subspecies multocida, whilst 21.7% and 27.8% were identified as the subspecies septica. The percentage of frequency for both the subspecies was of a comparable order of magnitude from the birds injured by cat bites and from cats (58.6% and 61.1%, 24.1% and 27.8% resp.), whereas the frequency from other feral birds differed considerably (82.4% and 17.6%). Maltose-positive strains were only demonstrable in birds with wounds inflicted by cats. To date, maltose-positive strains have only been obtained from one cat and one human being with an injury caused by a cat. The results of this investigation confirm the possibility of the direct transmission of Pasteurella multocida via cat bites. 19 strains from feral birds and 15 strains from cats were tested for their capability to produce toxins. The results of these tests were negative. The present paper also describes the pathologic-anatomical and histopathological lesions caused by the infection in feral birds.

Animals↗

Effect of pituitary adrenocorticotropic and growth hormones on the resistance of rats infected with Pasteurella pestis.

The influence of highly purified pituitary adrenocorticotropic (ACTH) and growth (somatotropic, STH) hormones on resistance of normal, young adult rats infected with Pasteurella pestis organisms (EV 76) has been studied. The daily dosage of ACTH was 0.1 mg. (25 I.U per mg.) and that of STH was 1.0 mg. When these hormones were administered for 3 days prior to infection (1 LD(50)) and for 4 days thereafter, ACTH treatment resulted in a significant depression of resistance (p = < 0.001). The simultaneous administration of STH not only resulted in a definite counteraction of the depression (p = < 0.001), but resistance was increased to a level significantly above that of the non-hormone treated controls (p = < 0.001). Treatment with STH alone also showed a significantly higher protection when compared to the same controls (p = < 0.05). The results of experiments in which the challenge dose was 1 LD(50) suggested that greater alterations in resistance, whether it be a depression or enhancement, could be obtained by continuing hormone treatment after challenge instead of discontinuing on the day prior to challenge. When animals were treated with a relatively high daily dose (1.0 mg.) of ACTH and challenged with only (1/4) of an LD(50) of organisms, the majority of animals died within 4 to 7 days, whereas either the ACTH treatment or the bacterial dose alone resulted in no deaths. If the hormones were administered for 2 weeks prior to challenge with a high, toxic dose of organisms (4 LD(50)), and discontinued thereafter, there were significant differences in mortality in the various groups during the first 24 hours post challenge. The ACTH treated group showed a marked drop in resistance (p = < 0.001). STH, when given alone, exercised a significant protection (p = < 0.02), and in combination with ACTH, effectively counteracted the depression of resistance to acute, toxic deaths induced by the latter hormone (p = < 0.001). In this particular experiment, practically all animals died within 4 to 5 days, owing to the high challenge dose; the few survivors were in the group that had been pretreated with growth hormone. The maximal loss in body weight following an LD(50) challenge dose occurred by the 3rd day post challenge in all groups except in the ACTH-treated animals. At this time the LD(50) control group had lost an average of 14 gm. per rat, the STH group only 3 gm. per rat, whereas the group receiving both hormones lost an average of 7.5 gm. per rat. The ACTH-treated animals showed the greatest weight loss on the 4th day. Thus, under the conditions of the experiment, the beneficial effect of STH on the maintenance of body weight was demonstrated during the period of acute infection. The peak incidence of death in controls or hormone-treated animals following infection with 1 LD(50) of living organisms occurred on the 4th to 5th day post challenge; the earliest deaths occurred on the 3rd day, while the latest occurred on the 7th day. The peak incidence of death after the 4 LD(50) challenge dose occurred earlier, falling on the 2nd to 3rd day. Death was always accompanied by the characteristic gross pathology which results from infection with Pasteurella pestis organisms, particularly in the animals which succumbed after the 3rd day. Bacterial cultures usually revealed the presence of numerous Pasteurella pestis organisms in the spleen and heart blood at the time of death.

Adrenocorticotropic Hormone↗

[Pasteurella multocida: infections in man].

The literature data on human infection due to a representative of the genus Pasteurella, i.e. P. multocida are reviewed: the main clinical forms and signs of pasteurellosis, the results of the studies on susceptibility of P. multocida to antibiotics and chemotherapeutics and the results of their use in the treatment of the infection.

Anti-Bacterial Agents↗

Malignant rabbit fibroma virus: observations on the culture and histopathologic characteristics of a new virus-induced rabbit tumor.

The clinical, histopathologic, and cultural characteristics of a newly isolated poxvirus, malignant rabbit fibroma virus (MV), were investigated. MV was isolated from tumors induced by an uncloned stock of Shope fibroma virus (SFV). MV, SFV, and rabbit myxoma virus were compared. Similarly to myxoma virus, MV grew to higher titer in vitro than did SFV and produced plaques rather than foci on rabbit kidney cell monolayers. Unlike the local, self-limited fibroblastic proliferations observed in SFV recipients, MV and myxoma caused a fulminant clinical syndrome characterized by malignant histology, metastases, and supervening fatal gram-negative infection with Pasteurella multocida. MV induced a large, protuberant local tumor and discrete metastases histologically resembling myxosarcomas. Draining lymph nodes contained metastases and showed diffuse cortical hyperplasia. Kupffer's cells were prominent in the liver, and macrophages were abundant in the splenic sinusoids. The lungs and trachea were spared, but the conjunctiva and nasal mucosa showed squamous metaplasia and atypia, with overlying Pasteurella infection and underlying tumor. Myxoma virus infection produced similar mucosal changes, but both of these as well as the epidermis overlying the myxomas showed cytoplasmic virus inclusions. Neither the skin nor the epithelial surfaces overlying MV-induced tumors nor the tumors themselves contained virus inclusions. Thus the tumor syndrome caused by MV differed from other known rabbit tumors. Endonuclease restriction digests showed that the MV genome resembled, but was distinct from, rabbit myxoma virus. Opportunistic infection associated with MV-induced disseminated tumor may be an experimental model for the infectious complications that often supervene in host-tumor relationships.

Animals↗

Dermal necrosis caused by Pasteurella multocida infection in turkeys.

Severe dermal necrosis caused by Pasteurella multocida Serotype 1 was diagnosed in three dressed turkey carcasses and two live turkeys from a commercial flock. The dressed carcasses were among several condemned at a processing plant. The isolate, P. multocida Serotype 1, produced progressive dermal necrosis when experimentally inoculated into injured skin of turkeys. The organism was reisolated from the dermal lesions. The turkey houses were found to be infested by mice; the skin injury and infection with P. multocida probably originated from mouse bites.

Animals↗

Lesions associated with Pasteurella multocida infection in raptors.

Several case reports attest to the pathogenicity of Pasteurella multocida in raptors; however, the pathologic syndromes have not been fully described. We describe here the lesions encountered in 22 avian cholera cases in raptors. Besides septicemia-related lesions, a unique syndrome of esophageal abscesses was noted in 8 of the 11 (73%) Buteo hawks that succumbed to avian cholera. Esophageal abscesses were not noted in birds belonging to the order Strigiformes (owls) or family Falconidae (falcons and their relatives). Thus, the presence of white plaques in both the oropharynx and esophagus of Buteo hawks may indicate a possible P. multocida infection and should be considered in the differential diagnosis. This study also documents the first cases of avian cholera in a rough-legged hawk (Buteo lagopus) and a flammulated owl (Otus flammeolus).

Abscess↗

Lymphocyte subpopulations in peripheral blood of lambs experimentally infected with Pasteurella haemolytica.

The lymphocyte subpopulations in peripheral blood obtained from eleven lambs experimentally infected with Pasteurella haemolytica were compared with those obtained from eight control lambs by flow cytometry, using a panel of monoclonal antibodies against specific lymphocyte epitopes. Experimental infection with P. haemolytica was characterized by a transient but significant reduction in SBU-T1+ (CD5+) T cells and SBU-T4+ (CD4+ or helper) T lymphocytes (P less than 0.05) and a significant rise in lymphocytes which did not express the LCA p220 epitope and the pan T cell surface marker (CD5-LCA p220-) ("null"). The reductions in CD5+ and CD4+ lymphocytes occurred 24 h after experimental infection, returning to preinoculation levels 5 days post inoculation (DPI). Five to 9 days after experimental infection, there was a significant increase in the number of lymphocytes, which expresses the pan T cell surface marker (CD5+) but which were CD4-CD8-. Lymphocyte transformation responses to the mitogen phytohaemagglutinin (PHA) were significantly reduced 24 h after experimental infection with P. haemolytica (P less than 0.05).

Animals↗

[Experimental Pasteurella multocida infection of swine. A contribution to the etiology of enzootic porcine pneumonia].

Pasteurella can be isolated from about 50 per cent of pneumonically changed pig lungs. Isolation, however, is possible also from intact lungs of conventional or secondary SPF animals. The authors of this paper used the positive hyaluronidase test and identified exclusively Pasteurella multocida, with predominance of capsular type A. Most of the Pasteurella strains tested in this context caused pneumonia in SPF animals, particularly, following intratracheal application. No correlations were found to exist with murine virulence, the serological type or the origin of the strains from affected or intact lungs. Apart from virulence differences between the strains, host reactivity was found to depend primarily on high germ counts and, under natural conditions, on environmental stresses. Pasteurella multocida, hence, can be considered as one of the potential pathogens of porcine pneumonia. Pneumonia foci with transduced localised fibrinous pleuritis are characteristic and constitute a process of purulent inflammation with early involvement of fibrin.

Animals↗

Effect of Pasteurella haemolytica infection on the distribution of sulfadiazine and trimethoprim into tissue chambers implanted subcutaneously in cattle.

A study was designed to determine the effect of Pasteurella haemolytica infection on the rate and extent of penetration of sulfadiazine and trimethoprim into tissue chambers implanted SC in cattle. Thermoplastic tissue chambers were implanted SC in 6 calves. At 35 days after implantation, sulfadiazine (25 mg/kg of body weight) and trimethoprim (5 mg/kg) were administered IV to 5 of the calves. Chamber fluid and blood samples were collected from each animal at various time intervals for 24 hours after administration. Ten days later, all chambers were inoculated with P haemolytica serotype 1. At 36 hours after inoculation, a second pharmacokinetic study was conducted, using sulfadiazine and trimethoprim. Drug doses and sampling schedules were identical to those used prior to inoculation. A histologic study of infected chamber tissue was conducted, using the calf not included in the pharmacokinetic studies. Disposition curves of antimicrobials in serum and chamber fluid were well described by 2-compartment and 1-compartment pharmacokinetic models, respectively. Inoculation of P haemolytica into tissue chambers was accompanied by marked changes in the composition of chamber fluid. Increased total protein and albumin concentrations, decreased pH, and disruption of chamber tissue vasculature were associated with a significant increase in the penetration of sulfadiazine and trimethoprim into infected tissue chambers, compared with that in noninfected chambers. This increased penetration was accompanied by increases in the apparent volume of distribution for sulfadiazine and trimethoprim.

Animals↗

[Abdominal infection by Pasteurella spp. A report of 3 cases].

Pasteurella spp. is a gram-negative coccobacillary micro-organism which is a common cause of soft-tissue infections caused by animal bite or scratch and more uncommonly at another locations. We report here the clinical and evolutive characteristics of three patients with different varieties of intra-abdominal infection caused by the microorganism as well as the potential exposure to pet animals.

Abdomen↗