Mycoplasma meleagridis-induced lesions in the tarsometatarsal joints of turkey embryos.

Mycoplasma meleagridis (MM) has the ability to cause bone deformity in turkey poults. However, few pathological lesions have been described and no evidence of MM-induced damage to the bones has been shown. In this study, 17-day-old turkey embryos were inoculated with MM into the allantoic cavity.

Interactions between the membranes of turkey cells and Mycoplasma meleagridis.

We used Myoplsma meleagridis (MM) to infect the RP-9 cells and the eggshell membranes and scanning electron microscopy (SEM) and confocal microscopy to study the interactions between the organisms and the cell surfaces. The surface of the RP-9 cells contained numerous projections. After 24 hr of infection with MM, those projections were either lost or aggregated to the side; MM-like particles could be seen on the surface of the cells, and surface fluorescence could be detected by confocal microscopy.

Infection of the turkey embryonic trachea with Mycoplasma meleagridis.

Mycoplasma meleagridis was used to infect turkey embryos and tracheal explants. In the embryonic trachea, there was a decrease in the number of cilia and the sloughing of epithelial cells. In the tracheal explants, the deciliation was more severe and erosion of the tracheal surface was also evident; additionally, the cells of the trachea showed prominent perforation.

Chemotactic response of lymphocytes in chicken embryos infected with Mycoplasma gallisepticum.

A prominent feature of Mycoplasma gallisepticum (MG) infection is a lymphoproliferative response at the site of infection. In this study, artificial air cells (AACs) were made in eggs containing 16-day old chicken embryos. An MG culture and supernates from MG-infected RP-9 cells, HD-11 cells and monocytes were separately deposited on the membranes of the AAC.

Mycoplasma gallisepticum -induced release of macrophage inflammatory protein-1 beta from chicken monocytes-macrophages.

Chicken monocytes and a macrophage-like cell line were used to determine the presence of macrophage inflammatory protein-1 beta (MIP-1 beta). RNA was extracted from these cells and subjected to reverse transcription with an anti-sense primer specific for the whole length of the MIP-1 beta cDNA. After a polymerase chain reaction to amplify the cDNA, a 200 bp gene product was detected, which corresponded to the molecular weight of the MIP-1 beta.

A pathological and immunohistochemical study of goat kids undergoing septicaemic disease caused by Mycoplasma capricolum subsp. capricolum, Mycoplasma mycoides subsp. capri and Mycoplasma mycoides subsp. mycoides (large colony type).

This paper studies the pathological and immunohistochemical findings in 12 kids experimentally infected with Mycoplasma capricolum subsp. capricolum (Mcc), M. mycoides subsp.

Polymerase chain reaction and restriction endonuclease digestion for selected members of the "Mycoplasma mycoides cluster" and Mycoplasma putrefaciens.

A specific diagnostic method using the polymerase chain reaction, together with restriction endonuclease digestion patterns, was developed for members of the "Mycoplasma mycoides cluster" that normally occur in the United States (i.e., Mycoplasma mycoides subsp.

Immunohistochemical and ultrastructural characteristics of Mycoplasma capricolum subsp. capricolum in caprine abortion: a case report.

Described in this study are the immunohistochemical and ultrastructural findings in a case of caprine abortion due to the experimental infection of the dam with strain GM13 of Mycoplasma capricolum subsp. capricolum. Mycoplasma antigens were seen mainly in choriallantoic trophoblasts and in the lumen of blood vessels in the allantoic membrane.

Experimental reproduction of Mycoplasma gallisepticum disease in chukar partridges (Alectoris graeca).

An outbreak of conjunctivitis and severe respiratory disease occurred in an integrated chukar partridge (Alectoris graeca) operation that involved about 8000 birds. The main clinical features were conjunctivitis and sinusitis and frequent mouth breathing, but almost no gasping or coughing. In 1000 breeders, egg production declined from 73% to 20%.

DNA diversity among isolates of Campylobacter jejuni detected by PCR-based RAPD fingerprinting.

A PCR-based randomly amplified polymorphic DNA method was used to amplify Campylobacter jejuni DNA using a single oligonucleotide primer derived from either a homologous source or from Mycoplasma gallisepticum. The method was able to detect the heterogeneity of amplified DNA from human, chicken and turkey sources and can be used as a tool to study the epidemiology of Campylobacter jejuni infection.

In ovo pathogenicity of Mycoplasma iners strain Oz.

Embryonating chicken eggs were inoculated with the type strain (PG30) of Mycoplasma iners and with an additional strain of this species designated Oz. Marked gross and histopathologic lesions were observed in the embryos inoculated with strain Oz but not in those infected with strain PG30. Gross lesions were manifested by an enlargement of one or more joints that often contained a caseous exudate, both in the joint space and periarticularly.

Mycoplasma infection in a commercial goat dairy caused by Mycoplasma agalactiae and Mycoplasma mycoides subsp. mycoides (caprine biotype).

A commercial dairy goat herd of 600 animals experienced sudden onset of arthritis/polyarthritis, clinical mastitis, and sudden death in does. The offending infectious agents were Mycoplasma agalactiae and M. mycoides subsp.

Mycoplasma auris sp. nov., Mycoplasma cottewii sp. nov., and Mycoplasma yeatsii sp. nov., new sterol-requiring mollicutes from the external ear canals of goats.

Three mycoplasma strains, designated GIHT (T = type strain), UIAT, and VIST, were isolated from the external ear canals of goats and were shown to be serologically distinct from each other and from previously described Acholeplasma, Entomoplasma, Mesoplasma, and Mycoplasma species. Using light and transmission electron microscopy, we showed that the cells of these organisms were small, pleomorphic, coccoid, nonmotile, and nonhelical and that each cell was surrounded by a single cytoplasmic membrane. There was no evidence of a cell wall, and the organisms grew freely in media containing penicillin at concentrations of 1,000 U/ml or more and thallous acetate (final concentration, 1:4,000) and produced the "fried-egg" morphology typical of most mollicutes.

Pathogenicity of Campylobacter jejuni for turkeys and chickens.

A Campylobacter jejuni isolate obtained from a turkey liver, designated C101, and a C. jejuni isolate obtained from the feces of a chicken, designated C111, were used to inoculate their respective hosts. Isolate C101 depressed weight gain by 20% when inoculated into newly hatched poults or 4-day-old poults.

Characteristics of an unusual mycoplasma isolated from a case of caprine mastitis and arthritis with possible systemic manifestations.

A mycoplasma designated strain GM790A was isolated from milk and internal organs of 2 lactating goats showing mastitis and arthritis. The isolate was not related serologically to any of the currently known ovine-caprine mycoplasmas, except an isolate designated Mycoplasma sp. G, first recorded from the external ear canal of clinically normal goats in Australia.

Comparison of caprine mycoplasmosis caused by Mycoplasma capricolum, Mycoplasma mycoides subsp. mycoides, and Mycoplasma putrefaciens.

We reviewed the disease process in goats caused by Mycoplasma capricolum, M. mycoides subsp. mycoides, and M.

Taxonomy of the Mycoplasma mycoides cluster.

Some of the mycoplasmas found in diseases of ruminants, Mycoplasma capricolum, M. mycoides subsp. capri (PG3), bovine group 7 (PG50), strain F38 and strain Y goat show various degrees of relationship to M.

Caprine mycoplasmosis: an outbreak of mastitis and arthritis requiring the destruction of 700 goats.

An acute outbreak of mastitis and arthritis in a herd of 700 goats required the destruction of all but the few animals that were held for observation. The milk of nearly all of about 400 lactating does contained almost pure cultures of Mycoplasma putrefaciens with counts in 150 samples up to 1 X 10(9) colony forming units/ml. At post mortem examination the joints of both the adults and kids contained a fibrinopurulent discharge.

Induction of mycoplasmosis in goat kids by oral inoculation with Mycoplasma mycoides subspecies mycoides.

A one-time, orally administered dose of greater than or equal to 1 X 10(6) colony-forming units of Mycoplasma mycoides subspecies mycoides was sufficient to induce clinical mycoplasmosis (n = 37) terminating in fatal mycoplasmemia in 73% (37 of 51) of the clinically affected kids. The pathogen was isolated from the blood samples as early as 24 hours after oral inoculation; hot, swollen joints frequently were evident by 4 or 5 days after exposure. Pyrexia (to 42.

Pathogenicity of Mycoplasma capricolum and Mycoplasma putrefaciens.

Mycoplasma capricolum causes high morbidity and mortality in goats. Young kids fed a one-time oral dose of greater than or equal to 1 X 10(5) colony-forming units of the GM13 isolate usually died during the septicemic phase. The cardinal lesions were a fibrinopurulent polyarthritis and an acute, diffuse interstitial pneumonia.