S6 Strain Of Mycoplasma Gallisepticum Research Articles

Effects of S6-Strain Mycoplasma gallisepticum Inoculation at Ten, Twenty-Two, or Forty-Five Weeks of Age on the Blood Characteristics of Commercial Egg-Laying Hens ,

In 2 consecutive trials of the current study, the effect of the age of application of S6-strain Mycoplasma gallisepticum (S6MG) inoculation on the blood characteristics of commercial layers housed and maintained under controlled conditions was determined. The ages of inoculation compared were those before lay at 10 wk of age, during onset of lay at 22 wk of age, and during postpeak lay at 45 wk of age. In each trial, hematocrit, plasma protein, and serum cholesterol, triglycerides, and Ca were determined at 20, 24, 32, 43, 47, and 58 wk of age. The data from both trials were pooled then analyzed together, whereas, data from wk 20 (effect of 10-wk S6MG inoculation); data from wk 24, 32, and 43 (effects of 10- and 22-wk S6MG inoculations); and data from wk 47 and 58 (effects of 10-, 22-, and 45-wk S6MG inoculations) were analyzed separately. At wk 20, hematocrit was higher in birds inoculated with S6MG at 10 wk compared with sham-inoculated birds, and across wk 24, 32, and 43, serum Ca was higher in birds inoculated with S6MG at 10 or 22 wk compared with those that were sham-inoculated. Serum Ca level across wk 47 and 58 was higher in birds inoculated with S6MG at 10 wk compared with sham-inoculated controls and birds inoculated with S6MG at 22 wk, with 45-wk S6MG-inoculated birds being intermediate. The response of serum cholesterol level at 47 wk to S6MG inoculation at either 10, 22, or 45 wk compared with controls was nearly opposite to that of the response observed at 58 wk. However, serum triglycerides were depressed only at wk 47 due to the 45-wk S6MG inoculation compared with all other treatments. Variable post-peak alterations in serum Ca and lipids occur in response to the timing of S6MG inoculation in layers housed under controlled conditions.

Effects of S6-Strain Mycoplasma gallisepticum Inoculation at Ten, Twenty-Two, or Forty-Five Weeks of Age on the Egg Yolk Composition of Commercial Egg-Laying Hens

Commercial laying hens maintained under controlled conditions were experimentally inoculated with the S6 strain of Mycoplasma gallisepticum (S6MG) at 45 wk of age. This resulted in depressed liver lipid concentration, and inoculations at 20 and 45 wk affected the size of various portions of the reproductive tract. In 2 consecutive trials of the current study, the effect of age of application of S6MG inoculation on the egg yolk characteristics of commercial layers similarly housed and maintained under controlled conditions was determined. The ages of inoculation compared were prior to lay at 10 wk of age, during onset of lay at 22 wk of age, and during postpeak lay at 45 wk of age. In each trial, yolk moisture and total lipid content were determined at 24, 32, 43, 47, and 58 wk of age. Yolk cholesterol concentration and yolk fatty acid profiles at wk 47 and 58 were also examined. Data from wk 24, 32, and 43 (effects of S6MG inoculations at 10 and 22 wk) and data from wk 47 and 58 (effects of S6MG inoculations at 10, 22, and 45 wk) were analyzed separately. The data of both trials were pooled then analyzed together. Across wk 47 and 58, percentage yolk lipid was significantly lower in eggs laid by birds inoculated at 10 wk compared with those inoculated at 45 wk. Sham-inoculated control and 22-wk inoculated groups had intermediate percentage yolk lipids. Compared with sham-control and 10-wk S6MG inoculation groups across wk 47 and 58, yolk myristic, oleic, and linolenic acid concentrations were reduced, whereas yolk stearic and arachidonic acid levels were increased by either 22- or 45-wk S6MG inoculations. In comparison with all other treatment groups at wk 47, yolk linoleic acid concentration was reduced by S6MG inoculation at 45 wk. Variable postpeak alterations in yolk total lipid and fatty acid content occur in response to the timing of S6MG inoculation in layers housed under controlled conditions.

Effects of S6-Strain Mycoplasma gallisepticum Inoculation at 10, 22, or 45 Weeks of Age on the Digestive and Reproductive Organ Characteristics of Commercial Egg-Laying Hens

Experimental inoculation of commercial laying hens with the S6-strain of Mycoplasma gallisepticum (S6MG) at 20 wk of age, while being maintained under ideal conditions, has previously been shown to affect the lengths and weights of various portions of the reproductive tract. Two trials were conducted in the current study to compare the effects of S6MG inoculation prior to lay at 10 wk of age, during onset of lay at 22 wk of age, and during lay at 45 wk of age on the digestive and reproductive organs of commercial layers similarly housed and maintained under ideal conditions. In each trial, liver weight, liver moisture and lipid concentration, incidence of fatty liver hemorrhagic syndrome, ovary weight, ovarian mature follicle numbers, weights and lengths of the oviduct and oviductal regions, and weights and lengths of the small intestine and small intestinal regions were examined at 60 wk of hen age. At 60 wk, liver lipid concentration was depressed, and isthmus weight, as a percentage of total oviduct weight, was increased in birds that had been inoculated with S6MG at 45 wk. Alterations in liver lipid content and weight of the isthmal portion of the oviduct may occur in response to S6MG inoculation during the later stages of production in layers housed under ideal conditions.

Effects of S6-strain Mycoplasma gallisepticum inoculation at ten, twenty-two, or forty-five weeks of age on the performance characteristics of commercial egg laying hens

Experimental inoculation of commercial laying hens, maintained under controlled conditions, with the S6-strain of Mycoplasma gallisepticum (S6MG) at 10 wk of age has previously been shown to affect the lengths and weights of various portions of the reproductive tract without affecting subsequent performance. Two trials were conducted to compare the effects of S6MG inoculation at 10 wk of age (prior to lay), 22 wk of age (onset of lay), and 45 wk of age (during lay) on performance characteristics in commercial layers housed and maintained under controlled conditions, as in previous studies. In each trial, BW, mortality, egg production, egg weight, eggshell weight per unit of surface area, percentage eggshell weight, percentage albumen weight, percentage yolk weight, and yolk weight per albumen weight ratio were examined at various ages throughout an entire laying cycle. Across wk 47 and 58 (age periods after the last 45 wk inoculation), eggshell weight per unit of surface area and percentage eggshell weight were significantly reduced in birds that had received an S6MG inoculation at 45 wk of age when compared with birds that had not received an S6MG inoculation or had been inoculated with S6MG at either 10 or 22 wk of age. Alterations in eggshell quality in response to S6MG may become evident only in older birds that are experiencing declines in production when housed under controlled conditions.

Effects of an S6 Strain of Mycoplasma gallisepticum Inoculation Before Beginning of Lay on the Leukocytic Characteristics of Commercial Layers

A clinical study was conducted on commercial layers housed in biological isolation units, within which exogenous stress factors potentially affecting bird performance were minimized. This set-up was devised in order to assess how a pre-lay inoculation of S6 strain Mycoplasma gallisepticum affects the leukocytic properties of laying chickens. Previous studies have demonstrated relative decreases in lymphocyte and relative increases in heterophil percentages in birds infected with other strains of Mycoplasma gallisepticum. However, current results showed that the differential percentages of lymphocytes were decreased, whereas those of heterophils were increased, in both sham-inoculated control birds and birds inoculated with S6 Mycoplasma gallisepticum between 19 and 26 wk of age. This study clearly shows that a pre-lay inoculation of S6 Mycoplasma gallisepticum alone had no apparent effect on the leukocyte profile of commercial layers housed in biological isolation units.

Effects of cyclosporin A on the immune responses and pathogenesis of a virulent strain of Mycoplasma gallisepticum in chickens

Immune responses to the virulent S6 strain of Mycoplasma gallisepticum in immunocompetent and cyclosporin A (CsA)-treated specific pathogen free chickens were investigated, and pathogenesis of the M. gallisepticum strain was also examined. Ten-day-old specific pathogen free chickens were inoculated by eye-drop with M. gallisepticum, and a control uninfected group was inoculated with mycoplasma broth. Blood was collected weekly for 4 weeks from five birds in each group and whole blood lymphocyte transformation assayed against concanavalin A and lipopolysaccharide. Blood samples were also collected at intervals for serological assays. Live body weight, clinical signs and lesions were monitored, and recovery of M. gallisepticum was attempted from choanal cleft of live birds and also from various sites at necropsy. In parallel to the aforementioned groups, another set of two groups of chicks treated with CsA was infected with M. gallisepticum S6 or mycoplasma broth. These groups were subjected to the same experimental procedures. In the immunocompetent chickens, M. gallisepticum caused temporary T-cell suppression at 2 weeks post-infection. Comparison of the clinical signs and macroscopic lesions produced in immunocompetent and CsA-treated chickens indicated that T cells may not play an active role in disease development. The percentage of birds with mycoplasma isolation and the load of mycoplasmas suggested that T cells may have some role in resisting mycoplasma colonization or in the elimination of the infection.

Effects of an S6 strain of Mycoplasma gallisepticum challenge at onset of lay on digestive and reproductive tract characteristics in commercial layers.

Mycoplasma gallisepticum (MG), a reproductive/respiratory pathogen in poultry, has been implicated in suboptimum egg production and decreased hatchability. Commercial layer hens raised in a controlled environment were inoculated with the S6 strain of MG at 20 wk of age. The S6 inoculation had no effect on bird weight, egg production, digestive tract weight and length, or histopathologic lesion scores, although significant differences were noted in the lengths and weights of various portions of the reproductive tract. This study shows that S6MG inoculation does not detrimentally affect layer hen performance when in the absence of environmental stressors customary to a caged layer facility.

Effects of an S6 strain of Mycoplasma gallisepticum challenge before beginning of lay on various egg characteristics in commercial layers.

Mycoplasma gallisepticum (MG) is a reproductive/respiratory disease in poultry implicated in suboptimum egg production and decreased hatchability. Commercial layer hens raised in a controlled environment were inoculated with the S6 strain of MG at 10 wk of age. Egg production and selected egg and egg quality parameters were quantitated over the entire lay cycle for inoculated and control birds. The S6 inoculation had no effect on bird weight, egg production, associated egg quality parameters, or histopathologic lesion scores. This study shows that in the absence of environmental stressors a prelay S6 MG inoculation does not produce detrimental effects on layer hen performance.

Natural case of salpingitis apparently caused by Mycoplasma gallisepticum in chickens

Summary A natural case of salpingitis, apparently caused by Mycoplasma gallisepticum (MG), in layer chickens is described. In the flock from which the chickens originated, there was a 3 to 4% drop in egg production per month around 250 days old. The production was reduced 70% at 400 days of age, which was 77% of the predisease level. Salpingitis was characterized by marked thickening of the oviductal mucosa due to epithelial hyperplasia and marked lymphoplasmacytic infiltration. Colonization of MG on the epithelial surface was evidenced by electron microscopy and immunohistochemistry using rabbit hyperimmune serum against the S6 strain of MG. Antibodies to MG were detected in all the chickens examined..

Occurrence of keratoconjunctivitis apparently caused by Mycoplasma gallisepticum in layer chickens.

Natural cases of keratoconjunctivitis, apparently caused by Mycoplasma gallisepticum (MG), in layer chickens are described. The disease occurred in a commercial flock consisting of 36,000 pullets (Babcock), first appearing around 30 days of age. Clinically, affected chickens showed unilateral or bilateral swelling of the facial skin and the eyelids, increased lacrimation, congestion of conjunctival vessels, and respiratory rales. Some of the severely affected chickens closed their eyes. The morbidity reached 27.8%, and it was estimated that approximately 10% died from reduced feed intake due to impaired vision. Ten 70-day-old chickens with clinical diseases were examined for lesions. There was acute to subacute keratoconjunctivitis in all of the chickens, and some exhibited laryngitis. Adherence of mycoplasma organisms to epithelial cells of the conjunctiva, cornea, and larynx was frequently observed. These organisms had an ultrastructure characteristic of MG and showed a positive reaction with rabbit polyclonal antibodies against the S6 strain of MG by immunohistochemical analysis. MG was isolated from tissue homogenates of the eyelids and tracheas of the affected chickens. Many of the chickens had atrophic bursae, and infectious bursal disease virus antigens were detected in necrotic bursal follicles by immunostaining. Therefore, immunosuppression due to infectious bursal disease was implicated in the pathogenesis of keratoconjunctivitis in the present cases.

Delineation of the Lateral Spread of Mycoplasma gallisepticum Infection in Chickens

Lateral spread of S6 strain Mycoplasma gallisepticum (MG) was studied in small populations of chickens. One experimentally exposed bird served as the source of infection, and the presence of MG-agglutinating antibody was evidence of infection in individuals. The results were subjected to survival data analysis. In the seven experiments, four similar but not identical phases of lateral spread were observed: phase 1, a generally long latent phase (median 15, range 12-21 days) before antibody was first detected in the MG-inoculated bird; phase 2, a generally short period (median 1, range 1-21 days) in which infection gradually appeared in 5-10% of the population; phase 3, a fairly constant characteristic phase (median 24, range 7-32 days) in which 90-95% of the remaining population developed MG antibody; phase 4, a generally short terminal phase (median 4, range 3-19 days) in which the remainder of the population became positive. Increasing the population density increased the rate at which lateral spread occurred.

A Mycoplasma gallisepticum Strain-Specific DNA Probe

Total DNA from the vaccine F strain (K810) and the reference S6-strain of Mycoplasma gallisepticum (MG) was cloned in Escherichia coli using the plasmid pUC8. A 6-kilobase fragment, specific for the vaccine strain, was identified by colony dot and Southern hybridization analyses. When labeled and used as a probe, this fragment hybridized with the homologous and one other vaccine F-strain (F2F10), but it did not hybridize with other MG strains (Fg38, S6, A5969, V503) or with three other species of avian mycoplasmas.

Vaccination of Turkeys against Air-Sac Infection with a Temperature-Sensitive Mutant of Mycoplasma gallisepticum

Turkeys were vaccinated with temperature-sensitive (TS) mutants of Mycoplasma gallisepticum (MG) to determine pathogenicity and immunogenicity. TS 37 was apathogenic yet immunogenic to turkeys, TS 100 was highly pathogenic, and TS 102 was slightly pathogenic and nonimmunogenic. Five or 7 weeks after intranasal vaccination of turkeys with the TS 37 mutant, a highly statistically significant resistance against intra-air-sac challenge with the S6 strain of MG was observed.

Resistance of chickens immunized against Mycoplasma gallisepticum is mediated by bursal dependent lymphoid cells

Newly hatched chickens were significantly protected against challenge by the virulent S6 strain of Mycoplasma gallisepticum after vaccination with the TS 100 mutant. Removal of the thymus did not abolish the protective effect of the vaccine, but removal of the bursa of Fabricius did. The results suggest that the resistance induced by vaccine is mediated by the bursal-dependent lymphoid cells.

Immunization of Chickens with Temperature-Sensitive Mutants of Mycoplasma gallisepticum

Temperature-sensitive (TS) mutants of the S6 strain of Mycoplasma gallisepticum (MG) were used to immunize newly hatched chickens. Immunized chickens developed antibodies to the wild-type (WT) S6 strain as demonstrated by serologic tests. MG was recovered from nasal cavities but not from the lower respiratory tract of the immunized chicks. Three weeks after intranasal immunization, chickens were challenged via the air sacs with the virulent S6 strain. Immunized chickens were significantly better protected from development of air-sac lesions than were controls.

Experimental Infection of Ducks with Mycoplasma gallisepticum

Specific-pathogen-free ducks 24 and 180 days old were inoculated intranasally with the S6 strain of Mycoplasma gallisepticum (MG). No significant gross lesions were found in trachea, lung or air sacs at 7 or 28 days postinfection (PI). MG was recovered from the infraorbital sinus and trachea but not from the air sacs 7 and 28 days PI. A few ducks responded serologically by developing agglutinating antibody. MG multiplied in embryonated duck eggs but to lower titers than in embryonated chicken eggs.

Summary of Discussion

DR. THOMAS: We have been interested in the possible implication of Mycoplasma in human diseases other than primary atypical pneumonia, partly because it seems unreasonable for this ubiquitous class of microbes, known to be related causally to such a wide variety of diseases elsewhere in the animal and the plant kingdoms, to be responsible for only one or perhaps two varieties of human disease. Because of this special interest, the model originally uncovered by Henry Adler and associates seems particularly useful even though it involves turkeys and chickens, at first blush a long distance from human pathology. There are two reasons for interest in Adler's model. One is that it is possible with the S6 strain of Mycoplasma gallisepticum to produce lesions that resemble quite closely those that characterize human disease ascribed either to systemic hypersensitivity reactions or lesions of autoimmunity: to wit, polyarteritis nodosa, which the S6 strain produces with extraordinary reproducibility in virtually all of the arteries of the central nervous system, and a variety of arthritis that Adler and associates have recently described in detail, which is, like rheumatoid arthritis, regularly associated with the occurrence of polyarteritis with fibrinoid necrosis in the walls of arteries in the periarticular tissue and, by and large, only in those environments. It is true that chickens given a large enough dose of the S6 strain will also undergo arteritis in the central nervous system, but by far the most frequently involved arteries are those in the periarticular tissues. The arthritis itself is a spectacular lesion that is characteristically progressive and can become a chronic destructive disease. There is another reason for interest in the lesions produced by M. gallisepticum in the consideration of their possible relationship to human disease. This is that all of the lesions, the polyarteritis and the arthritis, are prevented or can be cured by treatment of the animals with gold salts. It has long been a source of puzzlement to students of human arthritis that while other proposed remedies for arthritis have come and gone down the decades, only two pharmaceutical agents seem generally accepted as being significantly effective against this disease in man. One of these is aspirin (and drugs related to aspirin), which at best has some kind of palliative effect and some effect generally described by the term antiinflammatory, that has little meaning but makes patients with arthritis feel better. The other drug is gold. You may be interested in knowing, as I certainly was, something of the story of how gold came into the armamentarium of rheumatology. It is a rather typical story about medicine. Sometime in the 1920's efforts were being made by Forrester and others to discover better pharmacologic agents for the management of pulmonary tuberculosis. At that time the realization had just dawned that metals were good for certain diseases, particularly syphilis, and, therefore, a study was begun involving treatment in large numbers of cases of pulmonary tuberculosis with every available metal that could be dissolved and injected, and among these was gold. Gold, and, indeed, all of the other metals tested, had no beneficial effect on pulmonary tuberculosis, but the clinicians involved in this study noticed that several patients with rheumatoid arthritis who had been included along with the tuberculous patients seemed to recover from their arthritis, and this was reported. Subsequently others confirmed the observation and since that time, to my knowledge, no one has failed (and many studies have been undertaken) to confirm the original observation that treatment with gold salts will, in a significant number of the patients with active intractable rheumatoid arthritis, bring about subsidence of all manifestations of the disease and in some cases, what appears to be a cure.

Metabolic and growth inhibition of Mycoplasma gallisepticum by antiserum.

SUMMARY: Chicken antisera to the s6 strain of Mycoplasma gallisepticum were used to study the mechanism of metabolic inhibition and growth inhibition by specific antibody. In high dilutions of antiserum the lag phase of growth was significantly prolonged, but eventually growth commenced and proceeded normally. In low dilutions of antiserum, growth was permanently inhibited. The prolongation of the lag phase was greater in a medium containing 10% horse serum than in 10% swine serum; with chicken serum in the medium the lag phase was of normal duration. The results correlated with the observation that the metabolic inhibition (m.i.) titres of antisera were higher when the test was conducted in horse serum than in swine or chicken serum. The antigens on the organism associated with the inhibition of growth by antiserum appeared to be essential physiologically active receptors. Antisera to growth medium caused agglutination of the organism, but did not inhibit growth or metabolism.