Diagnosing Clostridium perfringens-associated necrotic enteritis in broiler flocks by an immunoglobulin G anti-alpha-toxin enzyme-linked immunosorbent assay

2003 ◽  
Vol 32 (5) ◽  
pp. 527-534 ◽  
Author(s):  
Atle Lovland ◽  
Magne Kaldhusdal ◽  
Liv Jorun Reitan
2007 ◽  
Vol 14 (9) ◽  
pp. 1070-1077 ◽  
Author(s):  
R. R. Kulkarni ◽  
V. R. Parreira ◽  
S. Sharif ◽  
J. F. Prescott

ABSTRACT Necrotic enteritis (NE) in broiler chickens is caused by Clostridium perfringens. Currently, no vaccine against NE is available and immunity to NE is not well characterized. Our previous studies showed that immunity to NE followed oral infection by virulent rather than avirulent C. perfringens strains and identified immunogenic secreted proteins apparently uniquely produced by virulent C. perfringens isolates. These proteins were alpha-toxin, glyceraldehyde-3-phosphate dehydrogenase, pyruvate:ferredoxin oxidoreductase (PFOR), fructose 1,6-biphosphate aldolase, and a hypothetical protein (HP). The current study investigated the role of each of these proteins in conferring protection to broiler chickens against oral infection challenges of different severities with virulent C. perfringens. The genes encoding these proteins were cloned and purified as histidine-tagged recombinant proteins from Escherichia coli and were used to immunize broiler chickens intramuscularly. Serum and intestinal antibody responses were assessed by enzyme-linked immunosorbent assay. All proteins significantly protected broiler chickens against a relatively mild challenge. In addition, immunization with alpha-toxin, HP, and PFOR also offered significant protection against a more severe challenge. When the birds were primed with alpha-toxoid and boosted with active toxin, birds immunized with alpha-toxin were provided with the greatest protection against a severe challenge. The serum and intestinal washings from protected birds had high antigen-specific antibody titers. Thus, we conclude that there are certain secreted proteins, in addition to alpha-toxin, that are involved in immunity to NE in broiler chickens.


1999 ◽  
Vol 54 (2) ◽  
pp. 423-427
Author(s):  
Yukiko SAKAITANI ◽  
Norikatsu YUKI ◽  
Yoko TAGAMI ◽  
Masami MOROTOMI

2006 ◽  
Vol 13 (1) ◽  
pp. 150-151 ◽  
Author(s):  
Harry E. Prince

ABSTRACT New assays for antibodies to deamidated gliadin peptides (DGP) expressing celiac disease-specific epitopes were evaluated using 154 sera previously tested for endomysial immunoglobulin A (IgA) (EMA), transglutaminase IgA (TGA), and conventional gliadin antibodies. DGP antibody results showed 97% concordance with EMA and TGA results. Of 56 sera negative for EMA and TGA but positive for conventional gliadin antibodies, 54 (96%) were negative for DGP antibodies.


1998 ◽  
Vol 5 (5) ◽  
pp. 613-616 ◽  
Author(s):  
Felix Grimm ◽  
Friedrich E. Maly ◽  
Jian Lü ◽  
Roberto Llano

ABSTRACT The potential roles of specific antibodies of the different immunoglobulin G (IgG) subclasses in the serological diagnosis of cystic echinococcosis (CE) and alveolar echinococcosis (AE) were investigated by an enzyme-linked immunosorbent assay based on hydatid fluid as antigen. Specific antibodies of subclass 1 were found to be of major importance. In sera collected at the time of diagnosis (i.e., before any therapeutic intervention was initiated) they could be demonstrated in 14 of 15 sera from patients with CE and in all 12 sera from patients with AE. The most discriminatory and the most specific antibodies found in this study belonged to IgG subclass 4. Only one false-positive reaction was observed with 253 sera from healthy volunteers, and no cross-reactions occurred in 80 sera from patients with different parasitic infections. Specific IgG4 antibodies could be demonstrated in 61.0 to 66.7% (CE) or 47.6 to 66.7% (AE) of the cases. Antibody levels of IgG subclass 2 were elevated only moderately, and subclass 3 antibodies were detected in a few cases only. In addition, nonspecific reactions in sera of healthy volunteers or patients with other parasitic infections could partially be attributed to antibodies of subclasses 2 and 3.


1981 ◽  
Vol 68 (2) ◽  
pp. 112-118 ◽  
Author(s):  
J.Andrew Grant ◽  
Randall M. Goldblum ◽  
Richard Rahr ◽  
David O. Thueson ◽  
Jafar Farnam ◽  
...  

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