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Biomedical subjects

J E Dohms

Publications and source records attributed to J E Dohms.

At least 19 recordsLinked to original sources

Characterization of MGC2, a Mycoplasma gallisepticum cytadhesin with homology to the Mycoplasma pneumoniae 30-kilodalton protein P30 and Mycoplasma genitalium P32.

A second cytadhesin-like protein, MGC2, was identified in the avian respiratory pathogen Mycoplasma gallisepticum. The 912-nucleotide mgc2 gene encodes a 32.6-kDa protein with 40.9 and 31.4% identity with the M. pneumoniae P30 and M. genitalium P32 cytadhesins, respectively. Functional studies with reverse transcription-PCR, immunoblotting, double-sided immunogold labeling, and attachment inhibition assays demonstrated homology to the human mycoplasmal P30 and P32 cytadhesins. These findings suggest that there is a family of cytadhesin genes conserved among pathogenic mycoplasmas infecting widely divergent hosts.

Adhesins, Bacterial↗

Cloning and characterization of a putative cytadhesin gene (mgc1) from Mycoplasma gallisepticum.

A 150-kDa cytadhesin-like protein from Mycoplasma gallisepticum has been identified. A previously described 583-bp fragment (J.E. Dohms, L.L. Hnatow, P. Whetzel, R. Morgan and C.L. Keeler, Jr., Avian Dis. 37:380-388, 1993) was used to probe a genomic library of M. gallisepticum DNA. An 8.0-kb SacI fragment was identified, cloned, and partially sequenced. Analysis of the resulting 3,750-bp sequence revealed the presence of a 3,366-nucleotide open reading frame, mgc1. The 1,122-amino-acid protein encoded by this open reading frame, MGC1, has characteristics of a class I membrane protein and has homology with the MgPa cytadhesin of Mycoplasma genitalium (26.3%) and the P1 cytadhesin of Mycoplasma pneumoniae (28.7%). A portion of MGC1 was expressed as a glutathione S-transferase fusion protein and used to produce antiserum in rabbits. The antiserum recognizes a 150-kDa protein from M. gallisepticum. The protein is sensitive to trypsin, confirming that it is surface exposed. Primer extension analysis indicates that the mgc1 RNA starts within an upstream open reading frame, suggesting complex control of its expression. This is the first description of a functional gene from M. gallisepticum showing homology to cytadhesin genes from human mycoplasmas.

Adhesins, Bacterial↗

Mechanisms of immunosuppression.

Immunosuppresive disease is a major economic concern in domestic poultry production. Although many immunosuppressive agents have been described, mechanisms of how infectious and noninfectious agents compromise the immune system are poorly understood in avian species. Two categories, generalized and antigen-specific immunosuppression have been described in mammals. Generalized immunosuppression produces overall reduced responsiveness and increased susceptibility to a wide variety of infectious and neoplastic diseases. The best characterized immunosuppressive mechanisms are described in HIV-1 infections that lead to acquired immune deficiency syndrome (AIDS) in humans. In contrast, the antigen-specific suppression observed in human leprosy illustrates how an infecting agent selectively suppresses host responses against itself favoring bacterial spread. Both diseases have well-defined clinical staging classifications that correlate with specific immunological defects. An approach to studying immunosuppressive mechanisms in the avian suggests the need for relating pathogenesis with tests of immune responsiveness using a series of increasingly more specific immunological assays to pinpoint defects.

Animals↗

Stress--mechanisms of immunosuppression.

Stress, a term commonly used to describe varied phenomena, should be restricted to describe an adaptive response by an animal to threats to homeostasis. The threats to homeostasis are called stressors. Stressors include a variety of physical, psychological, chemical, or infectious causes that are modified by intrinsic and extrinsic factors. Examples of modifiers include stressor severity, duration, novelty, host genetics and immune status. What may be a stressor to an animal in one situation, when modified, may not be a stressor in another situation. Mechanisms of stress once thought to involve a single pathway described by Seyle as the General Adaptation Syndrome, have been rejected. Four pathways, some incompletely defined, have been implicated in modulation of the immune system. They include autonomic nervous system, the hypothalamic adrenal axis, extra-adrenal pathways involving neuropeptides and neurotransmitters and neuroimmunological mediators. The mechanisms of stress-induced immunosuppression resistance are poorly defined in domestic fowl and will require careful experimentation linking defined stressors with altered physiological responses that affect specific immune function and result in increased disease susceptibility.

Adaptation, Physiological↗

Studies on metabolism and concentrations of immunoglobulin G in the newly hatched turkey poult.

Persistence of maternal IgG in the hatched turkey poult was studied using 125I-labeled egg yolk IgG injected at hatching. Determinations were made of the half-life of IgG in the total plasma pool, and results indicated half-life for IgG of 4.08 +/- 0.33 days. Elimination of the injected IgG (comparable with maternal IgG) was described as the percentage of the injected dose remaining in the plasma with 30.53%, 10.31%, and 3.48% of the injected dose at 7, 14, and 21 days, respectively, after injection.

Animals↗

Metabolism and passive transfer of immunoglobulins in the turkey hen.

Aspects of the metabolism and passive transfer of radioactive 125I-labeled IgG, IgM, and IgA from the turkey hen to the egg were studied. The half-life of 125I-labeled IgG in plasma was calculated to be 5.91 +/- 0.81 days, and the time of maximal passage of radioactivity from hen into eggs was 6.5 +/- 1.3 days. The following IgG determinations were made: plasma concentration (8.54 +/- 1.2 mg/ml), total plasma pool (0.518 +/- 0.07 g/kg), total turnover rate (0.062 +/- 0.01 g/kg/day), or 11.92 +/- 0.01% of the plasma pool per day. The overall passage of IgG into sequentially laid eggs of individual hens was at a constant rate over an observation period of 46 days; loss to egg yolks accounts for less than 1% of total daily irreversible loss of IgG from the hen's body. The IgG concentrations in egg yolks assayed in 3 hens ranged from 72.1 +/- 6.7 to 104.5 +/- 6.9 mg/yolk, with significant (P less than or equal to 0.01) differences observed between birds not accounted for by differences in egg weights. The IgG was detectable in egg whites, but at a low concentration. The biological importance of egg white IgG is questionable. In 2 hens examined, 125I-labeled IgM had a half-life of 2.69 and 2.74 days, with fractional turnovers of 25.76% and 25.29% of the plasma pool/day. The IgM-associated radioactivity in egg material was considered unimportant in overall immunoglobulin transfer into eggs. In 2 hens examined, 125I-labeled IgA (biliary) had a half-life of 1.92 and 1.68 days, with fractional turnovers of 36.09% and 41.25% of the plasma pool per day. Like IgM, IgA-associated radioactivity in egg material was considered unimportant in overall immunoglobulin passage into eggs.

Animals↗

Comparative pathogenesis of serotype 1 and variant serotype 1 isolates of infectious bursal disease virus and their effect on humoral and cellular immune competence of specific-pathogen-free chickens.

Specific-pathogen-free chickens inoculated with isolate VA (variant A) or isolate IM of infectious bursal disease virus (IBDV) were examined for mitogenic response to T-cell mitogens, primary and secondary antibody response to sheep erythrocytes and Brucella abortus, and gross and histologic lesions in thymus and bursa. Both isolates induced comparable depression in the mitogenic and antibody response, and both caused extensive gross and histologic lesions in the bursa of Fabricius. However, bursal necrosis induced by the IM isolate was accompanied by an inflammatory response, whereas the inflammatory component was lacking in the lesion induced by the VA isolate. Furthermore, the IM isolate induced extensive lesions in the thymus, but the VA isolate did not.

Animals↗

Protection afforded infectious bronchitis virus-vaccinated sentinel chickens raised in a commercial environment.

The protective efficacy of three infectious bronchitis virus (IBV) vaccines for sentinel chickens raised with commercial Delmarva broiler chickens was evaluated during winter 1987. Specific-pathogen-free leghorn sentinel chickens were vaccinated with Massachusetts (Mass) alone, Mass and JMK, or Mass and Arkansas (Ark) combination live vaccines, or they remained unvaccinated. Four weeks post-vaccination, sentinels were placed on broiler farms at weekly intervals for 3 weeks corresponding to weeks 4, 5, and 6 of the broiler growing cycle. Vaccine efficacy was evaluated based on IBV reisolation attempts from tracheal swabbings following a 1-week field exposure period. Sentinel chickens vaccinated with Mass and Ark combination vaccine were best protected against IBV field challenge. Only four IBV isolations were made out of a 3-week total of 36 attempts, for an 11% isolation rate. IBV vaccines containing either Mass alone or Mass and JMK offered much lower levels of protection.

Animal Husbandry↗

Plasma cell quantitation in the gland of Harder during infectious bursal disease virus infection of 3-week-old broiler chickens.

Histopathologic changes in the gland of Harder (GH) and bursa of Fabricius (BF) were studied during and after infection of 3-week-old broiler chickens with a pathogenic strain of infectious bursal disease virus (IBDV). Plasma cell (PC) necrosis in the GH was seen from 5 to 14 days postinoculation (PI), BF follicular necrosis was observed from 1 to 7 days PI. PC numbers within the GH, counted for 28 days after inoculation, declined and were reduced (P less than 0.01) by 51% at 7 days after inoculation, which coincided with PC necrosis and heterophil infiltration. After 14 days PI, however, PC numbers were equal to those in uninfected controls. Since the GH is a major antibody-producing site in the paraocular area, the reduction in PC number at 7 days PI might indicate compromise of local immunity in the paraocular region and upper respiratory tract associated with IBD.

Animals↗

The effect of infectious bursal disease virus infection on local and systemic antibody responses following infection of 3-week-old broiler chickens.

Broiler chickens infected at 3 weeks of age with infectious bursal disease virus (IBDV) were given Brucella abortus (BA) or sheep red blood cell (SRBC) antigens before, during, and after the acute phase of the infection. Gland of Harder (GH) extracts and serum samples were used to assay local and systemic antibody titer to each antigen 7 days after antigen was administered. Antibody titers to both BA and SRBC antigens were lower (P less than 0.05) in GH extracts and serum of IBDV-infected broilers than uninfected controls. The responses to BA, a thymus-independent antigen, took longer to become depressed than the responses to SRBC, a thymus-dependent antigen. The depression of antibody titers following IBDV inoculation suggests compromise of both local and systemic immune function, a finding of importance to the broiler industry.

Agglutination Tests↗

Infectious bursal disease virus infection in the quail-chicken hybrid.

Hybrids produced from crossing Cornell K-strain white leghorn chickens and Line II Japanese quails were studied for susceptibility to infection with infectious bursal disease virus (IBDV). Quail-chicken hybrids were infected successfully following inoculation with IBDV at 14, 21, or 52 days of age. In most cases, precipitating antibodies were detected in serum by 10 days postinoculation (PI). Although no clinical signs or gross lesions were evident in the bursa of Fabricius of hybrids, histologic changes in the bursa were detected upon microscopic examination using hematoxylin and eosin staining. Chickens were successfully infected also; they had gross and microscopic lesions in the bursa and produced precipitating antibodies. In addition, staining of bursal sections with low concentrations of peroxidase-conjugated concanavalin A revealed a rearrangement of a leukocyte cell type (probably macrophages) in infected chickens and hybrids. Japanese quails were refractory to infection; they showed no bursal changes and did not form precipitating antibodies.

Animals↗

Isolation of turkey immunoglobulin-A.

Trukey biliary and gut IgA were isolated and monospecific antisera were prepared in rabbits. Isolation was accomplished by filtration of precipitated globulins on Sephadex G-200 followed by step-wise-elution DEAE ion-exchange chromatography. Using an immunodiffusion procedure, IgA was detected in turkey serum, saliva, lacrimal secretions, bile, gut washings, and tracheal washings. No IgA was detected in hatching-poult serum, egg white, or yolk. Two forms of IgA (high and low molecular weight) were detected in different body fluids.

Animals↗

Plasma cell changes in the gland of Harder following infectious bursal disease virus infection of the chicken.

Tissue changes in the gland of Harder (GH) were studied following infection of day-old chicks with infectious bursal disease virus (IBDV). Broiler chicks that lacked maternal antibody to IBDV were inoculated with IBDV at 1 day of age and were maintained segregated from uninoculated controls. Plasma cell (PC) content of the GH was lowered among infected chickens from 1 to 7 weeks postinoculation. Since the GH in uninoculated control birds was not densely populated with PCs until 3 weeks of age, the PC depletion found in young chickens infected with IBDV became more clear with age. After the chickens were 3 weeks old, fewer (P less than .01) plasma cells were observed in the GH of IBDV-infected chicks than in uninoculated controls. Lymphoid follicles and heterophil populations in the GH did not appear to be affected by IBDV infection, nor could necrotic or degenerative changes be found in the acini or excretory ducts. The observation of fewer PCs suggests that a major lymphoid tissue of the upper respiratory tract is comprised by IBDV infection of day-old chicks.U

Animals↗

Cases of type C botulism in broiler chickens.

Twenty-seven cases of type C botulism were studied in integrated broiler operations on the Delmarva Peninsula. Single and repeated outbreaks in broiler flocks were observed. No botulinum toxin was found in litter and feed samples despite repeated testing. Clostridium botulinum type C was cultured from litter, feed, and tissues of morbid and clinically normal chickens sampled from farms in which flocks experienced botulism. Clostridium botulinum type C could not be cultured from tissues of clinically normal chickens taken from a farm without a flock history of botulism or from caged broilers reared in semi-isolation.

Animal Feed↗

Susceptibility of broiler chickens to Clostridium botulinum type C toxin.

As broiler chickens aged during the first eight weeks of life, they decreased in susceptibility to the lethal effects of Clostridium botulinum type C toxin. Eight-week-old broilers were 2,000 times less susceptible to the lethal effects of the toxin than hatched chicks. Different broiler crosses showed similar susceptibility to the lethal effects of type C toxin at seven weeks of age, but 2.5 times more toxin was required to produce lethality by oral inoculation than was required by subcutaneous inoculation.

Age Factors↗

The immunization of broiler chickens against type C botulism.

Broiler chickens were inoculated with different amounts of a Clostridium botulinum type C toxoid at 1 or 14 or both 1 and 14 days of age. Immunity was assessed following challenge with type C botulism toxin at 3, 6, and 8 weeks of age. Protection induced by toxoid injection was affected more by time and number of inoculations than by the amount of toxoid administered. Single toxoid injections at one day of age furnished poor protection, whereas groups injected at 14 days of age were well protected at 6 and 8 weeks of age but not at 3 weeks of age. Variable results were observed in groups inoculated at both 1 and 14 days of age: immunity was evident in some groups following 3-, 6-, and 8-week toxin challenges.

Animals↗

Isolation and characterization of immunoglobulins G and M of the turkey.

Procedures are described for the isolation and purification of turkey immunoglobulins. Partial characterization of IgM and IgG is presented. Purification was by Sephadex G-200 and DEAE chromatography. IgM and IgG had respective average S values of 16.8-16.9 and 7.4 with 5-20% sucrose density gradients. Selective absorption of turkey sera, containing Mycoplasma meleagridis antibodies, by heavy-chain specific antisera and antibody absorption and elution studies demonstrated IgM and IgG to have activity against M. meleagridis. Information is presented on the distribution of IgM and IgG in body fluids. Evidence for the presence of a 16.1 S molecule believed to be IgA is discussed.

Animals↗