Effects Of Certain Organisms Associated With Chronic Respiratory Disease On Spf And Conventional Rats

Bell, Deirdre P.; Elmes, P. C.

doi:10.1099/00222615-2-4-511

Cited by 15 publications

(5 citation statements)

References 2 publications

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“…Bell (1967) also considered M. pulmonis to be merely a secondary organism in chronic respiratory disease of the rat. This view was supported by later work (Bell & Elmes, 1969) in which only minor lung changes were induced in rats by the intranasal inoculation of either M. pulmonis alone or M. pulmonis in combination with Streptobacillus moniliformis. Nevertheless, lung lesions developed in rats inoculated intranasally with lung homogenates from rats with chronic respiratory disease; the responsible pneumonia-inducing agent was not identified.…”

Section: Introductionmentioning

confidence: 71%

“…Complement-fixing antibody to M. pulmonis was demonstrated in the sera of naturally and experimentally infected rats (Lemcke, 1961); its presence correlated with the demonstration of the mycoplasma by cultural methods. However, Bell & Elmes (1969) were unable to correlate titres of specific complement-fixing antibody with the presence of M. pulmonis in conventional rats with chronic respiratory disease or in specific pathogen-free rats inoculated with lung homogenates from rats with chronic respiratory disease. Only one animal with chronic respiratory disease gave a titre as high as 16 and most were less than 4.…”

Section: Introductionmentioning

confidence: 91%

“…(1971) appeared not to be pathogenic by the intranasal route. Bell & Elmes (1969) did not produce chronic respiratory disease or CF antibody response using intranasal infection of rats; they called their organism M. pulmonis, but did not provide evidence of its identity. The unidentified mycoplasmas inoculated into rats by Pankevicius, Wilson & Farber (1957) and Joshi, Dale & Blackwood (1965) also failed to produce pathological changes in the lungs.…”

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confidence: 99%

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Respiratory disease in a colony of rats. II. Isolation ofMycoplasma pulmonisfrom the natural disease, and the experimental disease induced with a cloned culture of this organism

Whittlestone

Lemcke

Olds

1972

J. Hyg.

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SUMMARYMycoplasma pulmonis was isolated from the pneumonic lung of a rat. Two groups of mycoplasma-free rats were inoculated, one with a culture of the M. pulmonis strain which had been cloned four times (group A) and the other with a lung homogenate of the rat from which the strain had been isolated (group B). A third group (C) consisted of uninoculated control animals. Each group was kept in strict isolation and allowed to breed so that the progeny was naturally exposed to any pathogens present in the inoculated animals. After different periods of exposure, rats were autopsied, respiratory tracts and inner ears were cultured for mycoplasmas and bacteria, and sera were tested for complement-fixing antibodies to murine mycoplasmas.In group-A rats, M. pulmonis was consistently isolated from the inner ears or lungs from 50 to 715 days after exposure. Complement-fixing antibody to M. pulmonis was detected 20 days after inoculation, but in the naturally exposed progeny antibody took longer than 50 days to develop. Antibodies to the other known mycoplasmas of murine origin, M. arthritidis and M. neurolyticum, were never found. Purulent otitis interna was consistently found from day 55 onwards, while lung lesions were first observed at 85 days and persisted to 715 days. Pulmonary lesions developed more slowly in inoculated parents than in exposed progeny. Similar results were found in group-B rats, which were examined up to 441 days after inoculation. Uninoculated group-C rats were examined up to 768 days of age, but M. pulmonis was not recovered; of the 54 animals whose serum was tested all were negative to the three species of mycoplasmas, except one which had a titre of 16 with M. pulmonis. Pneumonia, bronchiectasis or lymphoreticular hyperplasia were not seen in any of these control rats. Bacterial respiratory pathogens were not isolated from rats in any of the groups, nor was antibody to Sendai virus detected.The results suggest that M. pulmonis alone can cause pneumonia and bronchiec-25 HYG 70P. WHITTLESTONE AND OTHERS tasis in rats since mechanical carry-over of another pathogen with the initial cloned inoculum is very unlikely and there was no evidence for the participation of any other rat pathogen. The respiratory disease induced by the cloned culture was comparable with that induced by the lung homogenate, and with the well-known syndrome of chronic respiratory disease and bronchiectasis in the rat.

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Section: Introductionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 91%

mentioning

confidence: 99%

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Respiratory disease in a colony of rats. II. Isolation ofMycoplasma pulmonisfrom the natural disease, and the experimental disease induced with a cloned culture of this organism

Whittlestone

Lemcke

Olds

1972

J. Hyg.

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“…Nevertheless, agglutinating antibodies were also used early in taxonomic studies to type S. moniliformis strains. 125 A complement fixation test 74,129,130 and an indirect immunofluorescence assay (IFA) 11,27,75 have been employed in intravenously infected mice. The latter was prepared by using air-dried and heat fixed bacterial suspensions with an OD of 0.2 on IFA slides as antigen.…”

Section: Indirect Techniques For Detection Of Infectionmentioning

confidence: 99%

Approved and novel strategies in diagnostics of rat bite fever and otherStreptobacillusinfections in humans and animals

Eisenberg¹,

Ewers

Rau

et al. 2016

Virulence

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Rat bite fever (RBF), a worldwide occurring and most likely under-diagnosed zoonosis caused by Streptobacillus moniliformis, represents the most prominent disease of Streptobacillus infections. Recently, novel members have been described, from which a reservoir in rats and other animal species and a zoonotic potential can be assumed. Despite regularly published case reports, diagnostics of RBF continues to represent a 'diagnostic dilemma', because the mostly applied 16S rRNA sequence analysis may be uncertain for proper pathogen identification. Virtually nothing is known regarding prevalence in humans and animal reservoirs. For a realistic assessment of the pathogen's spread, epidemiology and virulence traits, future studies should focus on the genomic background of Streptobacillus. Full genome sequence analyses of a representative collection of strains might facilitate to unequivocally identify and type isolates. Prevalence studies using selective enrichment mechanisms may also enable the isolation of novel strains and candidate species of this neglected group of microorganisms.

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“…Although numerous reports [3] have been published on the isolation of the organisms from the respiratory system of rats and mice, distribution of the organisms in other sites of the hosts has not been extensively examined. In rats, isolation of the organisms from the nasopharynx [2,10], inner and middle ears [8,10,11,13,24] and female genital tract [8], as well as from the respiratory tract [3] has been described and Juhr [9] found that M. pulmonis were located in the epithelial cells of the urogenital, intestinal and respiratory tracts for a long time after mono-contamination of germf ree rats.…”

Section: Localizationmentioning

confidence: 99%

Localization of <I>Mycoplasma pulmonis</I> in Mice

Saito

Nakayama

Nakagawa

1976

EXPERIMENTAL ANIMALS

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Localization of Myco plasma pulmonis was examined in mice infected by direct contact with previously infected mice. After contact with infected animals, the organisms were shown to become detectable first in the nasal and oral cavities and trachea on the next day, and then they were recovered from the middle ear and brain after 3 and 4 days, respectively. After 7 days of contact, isolation rates retained to be 100% in the nasal, oral and tracheal cavities, while 95% in the middle ear and brain, 25% in the lung and 200 in the vagina and uterus. The number of colonies was the most numerous from the nasal, uterine and vaginal cavities, followed by the trachea, middle ear, oral cavity, brain and lung in this order, except for a few mice having pneumonic lesions giving a large number of the organisms.The isolation rates with these organs were not changed even after 6 weeks of contact and organisms were never detected from the liver, spleen, kidney and heart.Mice from a naturally infected breeding colony showed similar finding to those sacrificed after 6 weeks of experimental contact.

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Effects Of Certain Organisms Associated With Chronic Respiratory Disease On Spf And Conventional Rats

Cited by 15 publications

References 2 publications

Respiratory disease in a colony of rats. II. Isolation ofMycoplasma pulmonisfrom the natural disease, and the experimental disease induced with a cloned culture of this organism

Respiratory disease in a colony of rats. II. Isolation ofMycoplasma pulmonisfrom the natural disease, and the experimental disease induced with a cloned culture of this organism

Approved and novel strategies in diagnostics of rat bite fever and otherStreptobacillusinfections in humans and animals

Localization of <I>Mycoplasma pulmonis</I> in Mice

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