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Biomedical subjects

V Sivanandan

Publications and source records attributed to V Sivanandan.

At least 37 records · Page 2Linked to original sources

Immunocompetent cells of the turkey: age and organ distribution patterns of T and B lymphoid cells.

The percentage of lymphoid cells from the bursa of Fabricius, thymus, spleen, peripheral blood, and cecal tonsils reactin with chicken antisera to turkey bursa and thymus were evaluated, using 1-day-old to 5-week-old turkeys. For this, rabbit anti-chicken globulin fluorescein isothiocyanate conjugate was used. The percentage of lymphoid cells showing immunoglobulin surface determinants from these organs also was examined, using a direct immunofluorescence test with a rabbit anti-turkey globulin fluorescein isothiocyanate conjugate. This study suggests that the bursa-specific antigen and immunoglobulin surface determinants could be used as markers for bursa-derived cells in the turkey. It also was found that thymus-specific antigen could be used as a marker for thymus-derived cells.

Age Factors↗

Immunocompetent cells of the turkey: antigenic surface determinants of turkey lymphoid cells.

The serologic properties of chicken antiserums to turkey bursa and thymus were assayed by the cytotoxicity tests and indirect immunofluorescence. The following antigenic surface determinants were detected, using proper absorptions on thymic and bursal lymphoic cells: (a) common lymphocyte antigens present on both kinds of cells, (b) thymus-specific antigens, (c) bursa-specific antigens, and (d) immunoglobulin surface determinants in bursa cells, as revealed by direct immunofluorescence.

Animals↗

Novel infectious bronchitis virus S1 genotypes in Mexico 1998-1999.

Seventeen infectious bronchitis virus (IBV) field isolates recovered from commercial broiler flocks in Mexico were identified by reverse transcription-polymerase chain reaction cycle sequencing of the S1 gene. The isolates were obtained from broilers on farms from the neighboring states of Queretaro and San Luis Potosi in 1998 and 1999. Flocks had an ongoing history of bacterial-complicated respiratory disease with mortality rates as high as 28% in spite of receiving live vaccinations for Massachusetts and Connecticut strains of IBV. Sequence analysis of the S1 gene identified two unique genotypes that have been described, as of this time, only in Mexico and thus appear to represent strains indigenous to the country. The Mex/1765/99 genotype was isolated from 64% (11/17) of the respiratory disease outbreaks. Three isolates (18%) were similar to the BL-56 genotype, a unique Mexican IBV strain observed initially in 1996. In addition to the two indigenous strains, three isolates (18%) were found to be the Connecticut genotype.

Animals↗

Influenza in commercial broiler breeders.

Influenza was detected in a flock of broiler breeders during routine serological monitoring. Although there were no clinical signs, egg production may have been affected in hens on one story of a two-story breeder house. Intensive measures were taken to avoid transmission to other farms. Two months after the flock was found to be serologically positive, sentinel hens were placed in the flock, and they became serologically positive 1 month later. In spite of this evidence for virus being present in the flock, no detectable transmission to any other farm occurred.

Animals↗

Serological response in broiler chicks to different commercial Newcastle disease and infectious bronchitis vaccines.

Broiler chicks were administered vaccines against Newcastle disease and infectious bronchitis (both Arkansas and Massachusetts strains) at 2 weeks of age as either primary or secondary vaccinations. The vaccine was administered as a spray at 2 weeks of age to chicks that had received Newcastle disease vaccine alone, bronchitis vaccine alone, both vaccines in combination, or no vaccine at day 1 in the hatchery. The Newcastle disease hemagglutination-inhibition response was significantly lower in chicks receiving Newcastle disease vaccine as a secondary vaccine at 2 weeks than in those receiving the vaccine as a primary vaccination at that age. In contrast, the bronchitis hemagglutination-inhibition response was significantly higher in chicks receiving bronchitis vaccine as a secondary vaccination at 2 weeks than in those receiving the vaccine as a primary vaccination at that age.

Administration, Inhalation↗

Endotoxin lipopolysaccharide from Escherichia coli and its effects on the phagocytic function of systemic and pulmonary macrophages in turkeys.

The effect of Escherichia coli lipopolysaccharide (LPS) on the competence of pulmonary macrophages and phagocytic cells from the systemic circulation of turkeys was examined using luminol-enhanced zymosan-stimulated chemiluminescence. The results showed a rapid and accelerated oxidative burst in both systemic and pulmonary macrophages in LPS-treated turkeys that was significantly greater than in untreated controls. However, this increased oxidative metabolism induced by LPS was not associated with enhanced intracellular bacterial killing by pulmonary macrophages. Turkeys treated with LPS showed a highly significant decrease in pulmonary bactericidal activity against Staphylococcus aureus challenge, indicating a defect in pulmonary macrophage function induced by LPS.

Animals↗

Isolation of H13N2 influenza A virus from turkeys and surface water.

This is the first report of the isolation of H13N2 avian influenza virus (AIV) subtype from domestic turkeys. This subtype was also isolated from nearby surface water. The observation of large numbers of gulls in close association with turkeys on range before the virus isolations suggests that this virus subtype was transmitted from gulls to range turkeys. Turkey flocks infected by this virus subtype did not show any clinical signs of the disease, although seroconversion did occur. The H13N2 isolates were found to be non-pathogenic in chickens.

Animals↗

A broad-spectrum avian influenza subtype antigen for indirect enzyme-linked immunosorbent assay.

A broad-spectrum viral antigen for the detection of avian-influenza-virus-specific antibodies, using the indirect enzyme-linked immunosorbent assay (ELISA), was identified. Purified and disrupted antigens were used, which helped to increase the sensitivity of the assay. All of the antigens tested were able to detect antibodies to homologous and heterologous viruses to varying degrees. The H9N2 antigen was the best single antigen to use in the ELISA to screen for avian influenza virus antibodies. It detected antibodies against six viruses as early as day 4 postinfection.

Animals↗

Effects of avian infectious bronchitis virus (Arkansas strain) on vaccinated laying chickens.

Twenty-four-week-old white leghorn layers were inoculated subcutaneously with a killed Newcastle-infectious bronchitis (Massachusetts type) virus (MIBV) vaccine. The birds were challenged 194 days later intraocularly with Arkansas strain of infectious bronchitis virus (AIBV). The challenged hens laid significantly (P less than 0.005) fewer eggs than the unchallenged layers, and the eggs laid by the challenged groups weighed significantly less (P less than 0.001) than those laid by the unchallenged groups. Further, the internal quality (Haugh units) and shell quality of eggs laid by the challenged hens were significantly (P less than 0.005) inferior to the quality of eggs from unchallenged hens, and the challenged hens laid more soft-shelled, misshapen, and small-sized eggs than the unchallenged hens. The Arkansas serum hemagglutination-inhibition (AIBV-HI) titers of challenged birds increased continuously through 29 days post-challenge. The MIBV hemagglutination-inhibition (MIBV-HI) titers of killed-MIBV-vaccinated birds decreased during the same period. The study indicates that killed MIBV vaccine offered no protection to birds exposed to AIBV. The same vaccine was quite effective against a homologous (MIBV) virus challenge.

Animals↗

A dot-immunobinding assay for infectious bronchitis virus.

Common Whatman filter paper grade 1 and nitrocellulose membrane were compared for their sensitivity in a dot-immunobinding assay for detection of serum antibody titers to Arkansas avian infectious bronchitis virus (AIBV). For a blue to purple color detection, serum antibodies were bound to AIBV antigen adsorbed on the filter-paper discs or nitrocellulose membrane. Rabbit anti-chicken IgG horseradish-peroxidase (HRP) conjugate and hydrogen peroxide with 4-chloro-1-naphthol (HRP-color development reagent) were applied. The study indicates that very small amounts of antigen/antisera are needed for the dot-immunobinding assay. The test is sensitive, economical, and easy to run and can be completed within 6-8 hours.

Animals↗

Effects of infectious bronchitis virus (Arkansas strain) on laying chickens.

Seventy-seven-week-old white leghorn layers were inoculated intraocularly with the Arkansas strain of infectious bronchitis virus (AIBV) to study the effects of the virus on egg production and on antibody response of the birds. Infected hens laid fewer eggs than the controls, and those eggs weighed less than eggs laid by controls. Further, the shell quality and internal quality of eggs laid by infected birds were inferior. The serum hemagglutination-inhibition (HI) titers of infected birds increased continuously through 4 weeks postinfection; serum HI titers of the controls were negligible.

Animals↗

Histopathologic changes induced by serotype II infectious bursal disease virus in specific-pathogen-free chickens.

Specific-pathogen-free (SPF) chickens were infected with infectious bursal disease virus (IBDV) serotype II (turkey, Missouri isolate) at 1 day or 4 weeks of age. Chickens infected at 1 day had small bursas 3 weeks postinfection (PI). Bursas were necrotic and inflamed through 1 week PI. Post-necrotic atrophy of the bursas was marked at 3 weeks PI, and plasma cells in the Harderian gland were depleted. Chickens infected at 4 weeks had slightly enlarged spleens with small gray foci on the surface at 1 week PI. The bursas had massive necrosis and hemorrhages on the mucosal surface and had gelatinous yellowish transudate covering the serosal surface; some bursas were gray. Bursas were smaller than normal through the end of the experiment (4 1/2 weeks PI). At 1 week PI, histologic lesions were multifocal lymphoid necrosis of spleens and necrotic inflammation of the bursas. Post-necrotic atrophy of the bursas was found 2 weeks PI through the end of the experiment. Compared with uninfected controls, infected chickens had significantly more pyroninophilic blast cells in the spleen at 1 week PI and the bursas at 4 1/2 weeks PI. Plasma cells in the Harderian glands of this infected group were depleted as well.

Animals↗

Comparative serological evaluation of avian influenza vaccine in turkeys.

Four- and six-week-old turkeys were vaccinated subcutaneously using avian influenza virus (AIV) A/Duck/613/MN/79 (H4N2) killed oil-emulsion vaccine. Sequential serological tests using agar gel precipitin (AGP), hemagglutination inhibition (HI), and enzyme-linked immunosorbent assay (ELISA) for measuring antibodies to AIV were performed up to 4 weeks postvaccination, when birds were challenged intranasally using A/Turkey/MN/80 (H4N2) live AIV. The ELISA was 25 to 1600 times more sensitive than the HI test and was able to detect antibody production earlier than the HI test. All turkeys with an ELISA titer of greater than or equal to 800 were protected against homologous challenge, as measured by virus recovery 3 days postchallenge. Four turkeys out of 20 serologically negative by AGP and HI tests but ELISA-positive were protected.

Animals↗

Pathogenicity of avian influenza viruses isolated from wild mallard ducks and domestic turkeys.

Groups of turkeys were exposed to different isolates of avian influenza virus from wild mallard ducks and domestic turkeys by the intracerebral, intravenous, intratracheal, and intra-airsac routes, and pathogenicity indices were calculated. For the intracerebral pathogenicity study, body weight was also measured. For intravenous, intratracheal, and intra-airsac pathogenicity studies, necropsy lesions were scored and serological responses were recorded. Only the intracerebral pathogenicity index and body weight gain post intracerebral infection demonstrated any differences between isolates. The other procedures failed to demonstrate any pathogenicity whatsoever. There was a correlation (R = 0.73) between intracerebral pathogenicity index and reduced weight gain postinfection. These studies suggest that growth suppression may be an objective measure of pathogenic potential of influenza viruses found to be nonpathogenic by other methods.

Animals↗

Protection and immunity in commercial chicken layers administered Mycoplasma gallisepticum liposomal bacterins.

Six liposomal Mycoplasma gallisepticum (MG) bacterins, differing in charge and size, and two oil-emulsion vaccines (sonicated and non-sonicated) were given to white leghorns in two doses, at 13 weeks and again 1 month later. At 21 weeks of age, all chickens were challenged with a viable 20-hour culture of MG cells (17,800 colony-forming units) intratracheally and with nonviable MG organisms (0.09 mg protein) injected subcutaneously in the wattle center. The three chicken groups that had the lowest tracheal MG-infection rates postchallenge were those given adjuvants of small multilamellar positively charged liposomes (16.67%), large multilamellar negatively charged liposomes (16.67%), and non-sonicated oil-emulsion bacterin (37.5%). These three groups also had significant levels of antibody in sera 4 weeks after the second dose of vaccine. The group given the small multilamellar positively charged liposome also showed significant delayed-type hypersensitivity (wattle swelling) (P less than or equal to 0.05). The group given the large multilamellar negatively charged liposomes had the highest local antibody response (P less than or equal to 0.01) and was the only group that had no microscopic lesions in the trachea.

Animals↗

The in vitro response of turkey lymphocytes to steroid hormones.

The in vitro mitogen response of whole blood turkey lymphocytes to various concentrations of steroid hormones was evaluated. Corticosterone (COS) at concentrations between 1 and 80 ng/ml significantly suppressed the proliferative response (3H-thymidine incorporation) to phytohemagglutinin (PHA) and concanavalin A (ConA). Non-mitogen-stimulated (NMS) cells were suppressed at concentrations of COS above 5 ng/ml. Progesterone significantly suppressed NMS cells at concentrations of 80 ng/ml, PHA-stimulated cells at concentrations of 500 ng/ml, and ConA-stimulated cells at concentrations of 1000 ng/ml. beta-Estradiol enhanced the response of NMS cells at concentrations of 500 ng/ml, had no effect on PHA-stimulated cells, and suppressed the response of ConA-stimulated cells at concentrations greater than 500 ng/ml. Testosterone affected only the ConA response, causing suppression at concentrations above 2000 ng/ml. Corticosterone and progesterone caused 80 and 95% suppression, respectively, of the proliferative response to ConA when compared with non-hormone-treated cells. The possible implications of steroid hormone-induced immunosuppression in the pathogenesis of aspergillosis is discussed.

Animals↗

Serologic evidence of infectious bursal disease virus serotype II infection in Minnesota turkeys.

Serum samples from seven randomly selected Minnesota turkey flocks were tested for antibodies to infectious bursal disease virus serotype I (Lukert strain, isolated from chickens, and North Carolina strain, isolated from turkeys) using a virus-neutralization (VN) test. All flocks were found to have low antibody titers to both Lukert and North Carolina strains. Five out of the seven flocks had high VN titers to the Missouri strain, a serotype II virus isolated from turkeys.

Animals↗