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A prospective cohort study was performed to evaluate the prevalences and loads of Salmonella and Campylobacter spp. in farm and processing plant samples collected from 55 commercial broiler chicken flocks. Environmental samples were collected from broiler houses within 48 h before slaughter, and carcass rinses were performed on birds from the same flocks at 4 different stages of processing. Salmonella was detected in farm samples of 50 (90.9%) flocks and in processing samples of 52 (94.5%) flocks. Campylobacter was detected in farm samples of 35 (63.6%) flocks and in processing samples of 48 (87.3%) flocks. There was a significant positive relationship between environmental farm samples and processing plant carcass rinses with respect to both Salmonella and Campylobacter prevalences and loads. Campylobacter loads were significantly higher than Salmonella loads, and the correlations between samples collected from the same flocks were higher for Campylobacter than they were for Salmonella. Boot socks were the most sensitive sample type for detection of Salmonella on the farm, whereas litter samples had the strongest association with Salmonella loads in pre- and postchill carcass rinses. Boot socks, drag swabs, and fecal samples all had similar sensitivities for detecting Campylobacter on the farm, and all were more strongly associated with Campylobacter loads in carcass rinses than were litter samples. Farm samples explained a greater proportion of the variability in carcass rinse prevalences and loads for Campylobacter than they did for Salmonella. Salmonella and Campylobacter prevalences and loads both decreased significantly as birds progressed through the processing plant.

Campylobacter is an important human pathogen, and consumption of undercooked poultry has been linked to significant human illnesses. To reduce human illness, intervention strategies targeting Campylobacter reduction in poultry are in development. For more than a decade, there has been an ongoing national and international controversy about whether Campylobacter can pass from one generation of poultry to the next via the fertile egg. We recognize that there are numerous sources of Campylobacter entry into flocks of commercial poultry (including egg transmission), yet the environment is often cited as the only source. There has been an abundance of published research globally that refutes this contention, and this article lists and discusses many of them, along with other studies that support environment as the sole or primary source. One must remember that egg passage can mean more than vertical, transovarian transmission. Fecal bacteria, including Campylobacter, can contaminate the shell, shell membranes, and albumen of freshly laid fertile eggs. This contamination is drawn through the shell by temperature differential, aided by the presence of moisture (the "sweating" of the egg); then, when the chick emerges from the egg, it can ingest bacteria such as Campylobacter, become colonized, and spread this contamination to flock mates in the grow house. Improvements in cultural laboratory methods continue to advance our knowledge of the ecology of Campylobacter, and in the not-so-distant future, egg passage will not be a subject continuously debated but will be embraced, thus allowing the development and implementation of more effective intervention strategies.

The objective of this study was to evaluate the effect of vaccination of breeder chickens on Salmonella prevalences and loads in breeder and broiler chicken flocks. Chickens housed on six commercial breeder farms were vaccinated with a killed Salmonella vaccine containing Salmonella Typhimurium, Salmonella Enteritidis, and Salmonella Kentucky. Unvaccinated breeders placed on six additional farms served as controls. Eggs from vaccinated and unvaccinated breeder flocks were kept separately in the hatchery, and the resulting chicks were used to populate 58 commercial broiler flock houses by using a pair-matched design. Vaccinated breeder flocks had significantly higher Salmonella-specific antibody titers than did the unvaccinated breeder flocks, although they did not differ significantly with respect to environmental Salmonella prevalences or loads. Broiler flocks that were the progeny of vaccinated breeders had significantly lower Salmonella prevalences and loads than broiler flocks that were the progeny of unvaccinated breeders. After adjusting for sample type and clustering at the farm level, the odds of detecting Salmonella in samples collected from broiler flocks originating from vaccinated breeders were 62% lower (odds ratio [95% confidence interval] = 0.38 [0.21, 0.68]) than in flocks from unvaccinated breeders. In addition, the mean load of culture-positive samples was lower in broilers from vaccinated breeders by 0.30 log most probable number per sample (95% confidence interval of -0.51, -0.09; P = 0.004), corresponding to a 50% decrease in Salmonella loads. In summary, vaccination of broiler breeder pullets increased humoral immunity in the breeders and reduced Salmonella prevalences and loads in their broiler progeny, but did not significantly decrease Salmonella in the breeder farm environment.

We investigated the feasibility of using Flinders Technology Associates (FTA) filter cards for the storage of allantoic fluid containing an infectious bronchitis virus (IBV), such as Arkansas-DPI, Connecticut, and Massachusetts, and for their identification by reverse transcriptase (RT)-polymerase chain reaction (PCR) and characterization by restriction fragment length polymorphism (RFLP) or nucleotide sequencing. FTA paper is a cotton-based cellulose membrane containing lyophilized chemicals that lyses many types of bacteria and viruses. IBV was inactivated upon contact with the FTA, as shown by the inability of the virus to be propagated in embryonating chicken eggs. RT-PCR of the S1 gene showed that viral RNA in allantoic fluid remained stable after storage on FTA filter cards and that the stability was time and temperature sensitive for the large (1700 base pair [bp]) but not the small (383 bp) PCR products. Analysis of the amplified products showed that molecular characterization is feasible in allantoic fluid stored on FTA under nonfavorable environmental conditions (41 C) for at least 15 days. The use of FTA cards for the collection, transport, and storage of IBV-containing samples is safe, inexpensive, and adequate for molecular diagnosis. We propose that specimens coming from overseas on FTA cards would be first analyzed by RT-PCR with primers yielding a 1700-bp product followed by RFLP of the positive cases. Negative cases would be analyzed with primers yielding a 383-bp product (to exdude detrimental effect of the storage conditions) followed by nucleotide sequencing of the positive cases.

We evaluated the feasibility of using Flinders Technology Associates (FTA) filter paper for the inactivation and storage of mycoplasma DNA templates and their detection by the polymerase chain reaction (PCR). FTA paper is a cotton-based cellulose membrane containing lyophilized chemicals that lyses most types of bacteria and viruses. Mycoplasma gallisepticum (MG) and Mycoplasma synoviae (MS) cultures were spotted at various volumes on the filter paper and stored at different temperatures for various periods of time before performing PCR. MG and MS were readily detected at all time frames (1-60 days) independent of the volume applied (1-100 microl) or storage temperature (4 C-41 C). Sensitivity and specificity of the FTA-PCR were comparable to the standard diagnostic PCR, allowing the detection of MG/MS in field samples without interference by nontargeted mycoplasma. Analysis of 193 field samples by both methods showed nearly 100% agreement with serology and culture results. The long-term DNA stability at a wide range of temperatures makes the FTA cards a good alternative for collecting and simultaneously inactivating mycoplasma. It also offers the convenience of storage and transport of DNA in a cost-effective manner for further molecular analysis, such as restriction enzyme length polymorphism and nucleotide sequencing.

Staphylococcus aureus is an important opportunist that can cause superficial to life-threatening illnesses in a variety of animal species. In poultry, this organism has been implicated in osteomyelitis, synovitis, and cellulitis. Whereas most infections can be treated with antibiotics, because of the organism's propensity to acquire antimicrobial resistance, it is important to continually monitor antibiotic susceptibilities of clinical isolates. We surveyed 77 clinical poultry S. aureus isolates, collected from 1998 to 2000, for susceptibilities to a panel of 18 antimicrobial agents. Thirty-six percent of isolates were susceptible to all antibiotics. Forty-three and 16% of avian S. aureus were resistant to one and two antibiotics respectively. Staphylococcus aureus isolates were commonly resistant to tetracycline (40%; minimal inhibitory concentration [MIC]90 > 32 microg/ml), lincomycin (19%; MIC90 > 32 microg/ml), erythromycin (12%; MIC90 > 8 microg/ml), and kanamycin (8%; MIC90 < 128 microg/ml). All S. aureus isolates were susceptible to chloramphenicol, gentamicin, streptomycin, nitrofurantion, linezolid, quinupristin/dalfopristin, vancomycin, and the production antimicrobials virginiamycin, salinomycin, and flavomycin. A periodic assessment of antimicrobial susceptibilities of important avian pathogens like S. aureus will be important in helping the clinician's choice of antibiotic to control infection.

Eight-wk-old layer cockerels and pullets were presented to the diagnostic lab with a history of increased mortality, ruffled feathers, lameness, and recent vaccination. At necropsy, the birds had large multifocal granulomas in multiple tissues. Only light bacterial growth was seen on culture. On histopathology, a mixed population of fungi was seen within the granulomas including zygomycetes and Aspergillus, with the zygomycetes being the predominant organism. Because of the coinfection with Aspergillus and Penicillium, obtaining the zygomycetes in pure culture was unsuccessful. The source of the zygomycete fungi remains unknown; however, zygomycetes are known to be ubiquitous. Serology was performed to evaluate the flock's immune status. There was no evidence of immunosuppression caused by chicken anemia virus or bursal disease infections. No flock treatment was initiated.

Food poisoning by Staphylococcus aureus affects hundreds of thousands of people each year. Staphylococcus aureus also causes invasive diseases such as arthritis (in poultry) and septicemia (in poultry and humans). Foodborne disease is caused by the ingestion of a staphylococcal enterotoxin (SE). Enterotoxin has also been associated with other S. aureus illnesses in humans and domestic animals. In this study, polymerase chain reaction was used to detect the staphylococcal enterotoxin genes, SEA, SEB, SEC, SED, and SEE, in S. aureus isolates associated with invasive disease in poultry and humans. In the 34 poultry isolates, only one isolate was found to contain a SE gene, sec. In the 41 human isolates, over 51% tested positive for an SE gene with 12.2% positive for the gene for SEA, 2.4% for SEB, 22% for SEC, 24.4% for SED, and 0 for SEE. The disparity between the rates for SE gene(s) in poultry and human isolates suggests a lesser role for the enterotoxins in invasive poultry disease than in human disease.

Control of carcass contamination requires knowledge of the source and dynamics of spread of Salmonella in commercial poultry production. We examined Salmonella contamination at a U.S. commercial quail operation. Pulsed-field gel electrophoresis (PFGE) was used to type isolates in order to trace Salmonella throughout this production environment. During a 6-mo survey, Salmonella serotypes hadar, typhimurium, typhimurium variant Copenhagen, and paratyphi were encountered within this poultry operation. Ninety-four percent of the Salmonella isolated from breeder and production houses and from carcass rinses belonged to Salmonella serotypes typhimurium variant Copenhagen and hadar. There were six distinct S. typhimurium variant Copenhagen genetic types, as identified by PFGE, present within this particular poultry operation. Seventy-nine percent of S. typhimurium variant Copenhagen identified from the environment of the breeder and production houses produced the same PFGE pattern. Thirty-eight percent of S. typhimurium Copenhagen isolated from carcass rinses and the breeder house shared the same PFGE DNA pattern. This study demonstrates the transmission of salmonellae throughout this production environment, from the breeders to their progeny and to the birds ultimately processed for human consumption.

Fluoroquinolone-resistant avian Escherichia coli isolates from northern Georgia were investigated for gyrA and parC mutations. All isolates contained a mutation in GyrA replacing Ser83 with Leu; seven isolates also contained mutations replacing Asp87 with either Gly or Tyr. Random amplified polymorphic DNA analysis revealed that quinolone-resistant E. coli isolates were genetically diverse.

Litter was collected from four turkey farms (eight houses) with a history of fluoroquinolone (FQ) treatment failure, 10 adult broiler breeder chicken farms (43 houses) with one having a history of FQ treatment, and 30 broiler chicken farms (110 houses) with 24 having a history of FQ treatment. In the turkey litter, the percentage of nalidixic acid-resistant (at 100 microg/ml) coliforms/total number of coliforms ranged from 0.6% to 61.9%. Two of the four farms had houses containing coliforms resistant to the two FQs, enrofloxacin (1 microg/ml) and sarafloxacin (1 microg/ml). There was also multiple resistance to other antimicrobials on all four turkey farms (ampicillin, tetracycline, chloramphenicol, kanamycin). The level of total coliforms from the adult broiler breeder litter was low, and there were no nalidixic acid-resistant isolates from any of the 10 farms. In the broiler chickens, 7 of 91 houses with a history of FQ usage contained coliforms resistant to nalidixic acid; however, 2 of the 19 houses on farms with no history of FQ usage had nalidixic acid-resistant coliforms. All of the broiler farms with nalidixic acid-resistant isolates were also resistant to the FQ sarafloxacin, whereas only 3 of the 24 treatment history farms and 1 of the no-treatment history farms exhibited enrofloxacin-resistant coliforms in the litter.

Antibiotic resistance among avian bacterial isolates is common and is of great concern to the poultry industry. Approximately 36% (n = 100) of avian, pathogenic Escherichia coli isolates obtained from diseased poultry exhibited multiple-antibiotic resistance to tetracycline, oxytetracycline, streptomycin, sulfonamides, and gentamicin. Clinical avian E. coli isolates were further screened for the presence of markers for class 1 integrons, the integron recombinase intI1 and the quaternary ammonium resistance gene qacEDelta1, in order to determine the contribution of integrons to the observed multiple-antibiotic resistance phenotypes. Sixty-three percent of the clinical isolates were positive for the class 1 integron markers intI1 and qacEDelta1. PCR analysis with the conserved class 1 integron primers yielded amplicons of approximately 1 kb from E. coli isolates positive for intI1 and qacEDelta1. These PCR amplicons contained the spectinomycin-streptomycin resistance gene aadA1. Further characterization of the identified integrons revealed that many were part of the transposon Tn21, a genetic element that encodes both antibiotic resistance and heavy-metal resistance to mercuric compounds. Fifty percent of the clinical isolates positive for the integron marker gene intI1 as well as for the qacEDelta1 and aadA1 cassettes also contained the mercury reductase gene merA. The correlation between the presence of the merA gene with that of the integrase and antibiotic resistance genes suggests that these integrons are located in Tn21. The presence of these elements among avian E. coli isolates of diverse genetic makeup as well as in Salmonella suggests the mobility of Tn21 among pathogens in humans as well as poultry.

Escherichia coli is a common inhabitant of the gastrointestinal tract of most animals. Like most pathogenic E. coli, avian isolates cannot be distinguished biochemically from the normal commensals inhabiting the gastrointestinal tract of birds. Using a molecular approach, we were able to identify genetic differences among avian E. coli isolates by restriction fragment length polymorphism (RFLP) and random amplification of polymorphic DNA (RAPD) by the polymerase chain reaction (PCR). Several different RFLPs were observed among avian E. coli isolates using DNA probes for 16S ribosomal RNA genes (rrn) and insertion sequence elements (IS2). We were also able to observe differences in DNA banding patterns generated by RAPD analysis. Similarities and differences among avian E. coli were discernible using RFLPs and RAPD analysis, whereas conventional bacteriological methods failed to differentiate these isolates. Based on RAPD patterns, avian E. coli appear to be genetically diverse. Of 16 different RAPD types (RT) encountered, 84% of E. coli fell into seven major RTs. One RT was present in clinical isolates but absent from the commensals isolated in this study. Many of these different E. coli RTs were not geographically restricted to northern Georgia but were also observed in other southern states in the United States. Resistance to various antibiotics was randomly associated with different E. coli RTs. Sarafloxacin resistance was present among different E. coli RTs, suggesting that antibiotic usage is not selecting for a clonal population in avian E. coli. RAPD provides a rapid and powerful tool to study the epidemiology of avian E. coli.

Four hundred thirty-two 1-day-old specific-pathogen-free chicks were randomly divided into 36 groups of 12. All chicks were given 0.2 ml of Newcastle disease antiserum (hemagglutination-inhibition [HI] titer 1:5120) by injection into the yolk sac at hatch. Half of the groups received 0.2 ml of Enterococcus faecalis (4.0 x 10(8) colony-forming units/ml) by injection into the yolk sac at hatch (treatment). The remaining 18 groups received no bacteria (control). Two treatment groups and two control groups were weighed, bled, killed, and yolk sac weighed daily for the first 9 days of life. Feed was weighed at placement and at the end of the trial. Blood was tested for packed cell volume (PCV), total plasma protein, and Newcastle disease HI titer. No significant difference was observed between treatment and control groups for chick body weight, PCV, and feed consumption. Total plasma protein and retained yolk weight were significantly higher for treatment groups over control (P < 0.01 and P < 0.0001, respectively). Also, the geometric mean serum HI titer (log2) for Newcastle disease antibody was significantly higher in the control chicks vs. the treatment chicks (P < 0.01).

Escherichia coli establishes a secondary respiratory tract infection in birds following inhalation of contaminated dust and litter particles. Escherichia coli express adhesins under conditions reflective of the ambient temperatures present in poultry houses. These microbial adhesins allow E. coli to attach to cell types that it initially encounters in the respiratory tract. Ambient temperature-regulated adhesins represent a new class of bacterial hemagglutinins that include pili and the thin, aggregative, flexible filaments known as "curli." This study examines the occurrence of the ambient temperature-regulated adhesins, curli (crl, csgA), and an avian-specific, temperature-sensitive hemagglutinin, tsh, among avian and mammalian E. coli isolates. The avian hemagglutinin gene tsh was present in approximately 46% of clinical avian E. coli isolates. This gene was not detected among commensal E. coli isolated from healthy broiler chickens. Unlike tsh, curli genes were ubiquitous among E. coli. However, curli were observed in only half of the avian E. coli examined by electron microscopy. Curli were not present among several nonavian E. coli positive for crl and csgA. Approximately 25% of avian E. coli isolates agglutinated chicken erythrocytes when bacteria were grown at room temperature. Hemagglutination was not specific to E. coli isolated from poultry. Presence of either tsh or curli genes was not indicative of an isolate's ability to agglutinate chicken red blood cells. No discernible structures were observed mediating attachment of the bacteria to chicken red blood cells. An additional avian-specific hemagglutinin appears to be present among avian E. coli.

Two separate parent broiler flocks originating from the same grandparent flock experienced mortalities of 23% and 40%, respectively, in chicks between 1 and 14 days of age. Chicks affected at 4 days of age had tremors, depression, and hypoglycemia. They had pale yellow, swollen, friable livers. Pancreata were discolored and hemorrhagic. Spleens were swollen and sightly darkened. Microscopic lesions consisted of multifocal areas of acute hepatic and pancreatic necrosis with numerous basophilic intranuclear inclusions with karyomegaly. Splenic sections had severe lymphoid depletion and reticular cell and macrophage hyperplasia. An adenovirus from affected livers was isolated in chicken embryo liver cells. Serologic evidence suggests that the grandparent flock began egg production seronegative to adenovirus antibodies, was exposed during production, and, subsequently, shed adenovirus vertically to its progeny. The clinical syndrome was reproduced by injecting the isolated adenovirus into 1-day-old antibody-negative chicks. Histologic lesions in the experimentally reproduced disease cases were identical to those in the naturally occurring cases.

Infectious laryngotracheitis (ILT), a highly infectious upper respiratory disease of chickens, can cause serious economic loss in areas where the poultry industry is concentrated. To determine the antibody levels associated with vaccine administration, field challenge, and protection, six groups of 20 specific-pathogen-free leghorn chickens were housed in biosecured isolation units. Individual groups served as either negative controls, vaccinated (one full dose per bird of chicken embryo origin [CEO] administered by the eyedrop method) and challenged (intratracheal administration with USDA strain ILT virus at 10(4.1) 50% embryo infective dose [EID50]), or unvaccinated and challenged with USDA strain ILT virus at various dose levels (10(2.1), 10(5.1), or 10(4.1) EID50). Chickens in each group were bled weekly, and their sera were tested for antibody using a commercially available enzyme-linked immunosorbent assay test kit. The antibody response using CEO vaccine resulted in a 400-600 geometric mean titer that appeared to be protective against severe field challenge. Negative controls had no titers, whereas vaccinated and/or challenged chickens had detectable titers within 2 wk of exposure, and these titers remained high for the next 4-7 wk. Mortality in nonvaccinated controls began at 3 days post-challenge and continued for up to 10 days.

Three commercial chicken hatcheries were sampled for environmental bacteria. Isolated bacteria were tested for resistance to commercial preparations of quaternary ammonia, phenolic, and glutaraldehyde liquid disinfectants. Bacterial isolates were exposed to several disinfectant dilutions bracketing the dilutions recommended by the manufacturer for 5-, 10-, and 15-min exposure periods before subculturing to broth medium. Approximately 8% of the isolates from two of three hatcheries were resistant to disinfectant concentrations at and above the manufacturers recommended dilution and time of exposure. Resistant bacteria included Serratia marcescens, Bacillus cereus, Bacillus thuringiensis, Bacillus badius, Enterococcus faecalis, Enterococcus faecium, Pseudomonas stutzeri, and Enterobacter agglomerans.

Eubacterium tortuosum, a gram-positive anaerobic filamentous bacillus, was isolated from splenic and hepatic granulomas of a 56-day-old slaughtered chicken. This isolate was injected intravenously into two groups of 2-week-old broiler chickens, which were necropsied 19 days later. Five of 15 chickens injected with 5 x 10(6) colony-forming units of a 48-hour culture of E. tortuosum developed splenic granulomas typical of those seen in chickens at slaughter. No lesions were observed in chickens given 5 x 10(5) colony-forming units of E. tortuosum or in control chickens receiving phosphate-buffered saline solution. Attempts to reisolate E. tortuosum from experimentally infected chickens were unsuccessful; however, typical filamentous organisms were observed in splenic granulomas of all five affected chickens.

Contamination of poultry carcasses by fecal or ingested material is a major problem in the processing of poultry products. It was determined that the automatic equipment used to process uncontaminated carcasses could be used to clean and reprocess contaminated carcasses and significantly reduce the manual labor required to reprocess these carcasses. The potential for cross-contamination of the automatic viscera removal equipment was tested by microbiological evaluation, and it was determined that cross-contamination by this equipment was not a problem.

Broilers infected with Eimeria brunetti and given dietary zinc were examined for experimental induction of necrotic enteritis. Inoculation with sporulated E. brunetti oocysts at 7 days of age was followed by 5 consecutive days of oral inoculation with cultured Clostridium perfringens. Feed was supplemented with zinc at 1000 ppm. Upon necropsy of broilers 6 days after coccidial inoculation, necrotic enteritis was found in 20% (2/10) of birds given both organisms and dietary zinc. Coccidial lesion scores were also highest in that group. Birds infected with E. brunetti and C. perfringens with no dietary zinc had significantly higher coccidiosis lesion scores (P less than 0.05) than groups inoculated with E. brunetti only, regardless of zinc supplementation. Alpha toxin levels in intestinal contents were low in groups infected with both organisms, regardless of zinc supplementation. Zinc was tested for effects of alpha toxin production in vitro. In the mid-log phase (6 hours incubation), a high level of alpha toxin was produced in zinc-supplemented media, but this was lost quickly in the presence of trypsin. Addition of zinc partly protected the toxin from the action of trypsin.

Inactivated Newcastle disease virus (NDV) and infectious bursal disease virus (IBDV) were incorporated into water-in-oil emulsion vaccines alone or as a bivalent vaccine. Twenty-week-old broiler breeder chickens that had received previous live virus vaccination with NDV and IBDV were injected intramuscularly with the monovalent or bivalent vaccine. The antibody titers to either the monovalent vaccine or bivalent vaccine increased rapidly and then remained at high levels for the duration of the 40-week trial. There were no practical differences in amplitude or duration of the antibody response to either antigen used alone compared to that of the bivalent combination. Progeny hatched from the vaccinated breeders possessed maternal antibody levels at one day of age comparable to those of the hens at the time the eggs were laid. The maternal antibody titers declined at a steady rate until they reached negligibly detectable levels at approximately 3 weeks of age. This trend held true without regard to the initial antibody titer.

Inactivated Newcastle disease (NDV), infectious bursal disease (IBDV), and viral arthritis/tenosynovitis (VA) viruses were incorporated into water-in-oil emulsion vaccines, either alone, in bivalent combinations, or in a trivalent vaccine. Twenty-week-old broiler breeder chickens that had received previous live virus vaccination with NDV, IBDV, and VA were injected intramuscularly with the monovalent, bivalent, or trivalent vaccines. The antibody titers to the antigens contained in the monovalent, bivalent, or trivalent vaccines increased rapidly and peaked 4 to 8 weeks postvaccination. The titers declined during the next 3 months and increased to levels equal to or higher than the initial peak values. The titers remained high through 10 months postvaccination. Progeny hatched at intervals throughout the 40-week trial possessed detectable antibody titers to the appropriate antigens incorporated into the breeder vaccine through 21 days of age.

One-day-old chicks used in this study were from breeder flocks vaccinated with live (B1 and LaSota) or inactivated oil emulsion Newcastle disease (ND) vaccine. Chicks were vaccinated against ND by various procedures. The vaccination response was evaluated by hemagglutination-inhibition antibody titers and by challenge. Chicks from breeder flocks vaccinated with live virus vaccine had a geometric mean hemagglutination-inhibition antibody titer (GMT) for Newcastle of 7 (low maternal antibody titer) at 1 day of age, whereas those chickens derived from breeder flocks vaccinated with inactivated oil emulsion ND vaccine had a GMT of 84 (high maternal antibody titer). One-day-old chicks injected with live B1 vaccine were not immunized against ND regardless of breeder flock source. However, chickens with low maternal antibody titers were effectively immunized against ND when injected at 1 day of age with an inactivated or inactivated plus live ND vaccine. Chicks with high maternal antibody titers were not effectively protected when vaccinated with inactivated vaccine at 1 day of age; however, these chicks were protected when injected with a combined live and inactivated ND vaccine. Chicks from both breeder flocks were effectively immunized against ND when injected at 1 day of age with a live or inactivated ND vaccine and revaccinated by aerosol at 21 days of age with live B1 ND vaccine. Even though they were protected against ND, there appears to have been an interference phenomenon in chicks derived from breeder flocks vaccinated with the live ND vaccine. Beak-O-Vac vaccinated chickens were not effectively protected against ND when compared with chicks vaccinated by aerosol at 1 day of age. Water vaccination at 7, 14, or 21 days of age was as effective as aerosol vaccination when administered to chicks with low maternal antibody titers. However, water vaccination was not as effective as aerosol vaccination when administered to chicks with high maternal antibody titers.

Sera tested for hemagglutination-inhibition (HI) activity against Newcastle disease virus (NDV) and infectious bronchitis virus (IBV) and virus-neutralizing (VN) activity against infectious bursal disease virus (IBDV) and viral arthritis (VA) virus were collected from a wide variety of accessions into the Diagnostic Services Laboratory, Poultry Disease Research Center, University of Georgia. The sera were then segregated according to HI or VN titer to NDV, IBV, IBDV, or VA virus and stored frozen at -20 C until tested by two commercial enzyme-linked immunosorbent assays (ELISAs). There was good correlation of mean Flockchek ELISA titers or EIA Systems sample-to-positive (S/P) ratios with specific HI or VN titers. Flockchek ELISA profile group 3 and EIA Systems mean S/P ratio of 1.12 corresponded to what were considered in our lab to be minimum protective titers for each antigen against virulent challenge in our area.

Inactivated Newcastle disease (NDV), infectious bursal disease (IBDV), and viral arthritis/tenosynovitis (VA) viruses were incorporated into water-in-oil emulsion vaccines either alone, in bivalent combinations, or in a trivalent vaccine. Twenty-week-old broiler breeder chickens with no previous exposure to NDV, IBDV, or VA live virus vaccines were injected intramuscularly with the monovalent, bivalent, or trivalent vaccines. The antibody responses to NDV in all three vaccines were poor, and NDV-hemagglutination-inhibition (HI) geometric mean titers (GMTs) never rose above 20 during the 40-week trial. The antibody response to IBDV showed a strong primary response 4 weeks after vaccination, but IBD-VN geometric mean titers declined steadily to less than 100 by 4 months after vaccination. The antibody GMTs to IBDV continued to decline for the remainder of the trial. The antibody response to VA virus was biphasic, with peak VA-virus neutralization (VN) geometric mean titers occurring at 3 months and 6 months postvaccination. The amplitude of the response to the monovalent, bivalent, and trivalent vaccines was inversely proportional to the number of antigens incorporated into each vaccine. Maternal antibody titers in the progeny against each of the three antigens reflected those of the parents. In no case were maternal antibody titers detectable beyond 14 days of age.

COMBSCORES determined using the ImmunoComb solid-phase immunoassay were compared with hemagglutination-inhibition (HI) titers specific for Newcastle disease virus (NDV) and infectious bronchitis virus (IBV) and with mean enzyme-linked immunosorbent assay (ELISA) titers determined using Agritech Systems, Inc., ELISA. COMBSCORES for NDV and IBV increased proportionately in a stepwise manner as HI titers increased. The ImmunoComb solid-phase immunoassay was ablt to produce endpoint titers on sera with NDV-HI titers of 0 through 320 and IBV-HI titers of 0 through 1024 without reaching the maximum S-value. The ImmunoComb showed good correlation with the HI assay and the Agritech ELISA and should prove to be a useful tool for serological profiling, either alone or in conjunction with the HI test or commercial ELISA.

ImmunoComb scores are highly correlated to hemagglutination-inhibition (HI) titers against infectious bronchitis virus and Newcastle disease virus. Statistical calculations permit using an individual COMBSCORE to predict the corresponding HI titer value. Tables are presented to facilitate the transformation of COMBSCORES into HI titers.

Information was gathered from 64 cases of fowl cholera (FC) in turkey flocks through diagnostic case records, flock records, and telephone and mail surveys. Forty-five cases came from flocks of commercial turkeys, of which 15 were presented twice, and four came from mature breeder flocks. The prevalence of FC was 18.0% of commercial flocks and 14.7% of breeder flocks at risk. The average age at first diagnosis of FC was 90 days in commercial turkey flocks and 32 weeks 5 days in breeder flocks. Acute mortality was the most common presenting complaint, with a 0.37% average mortality in commercial flocks on the day of first presentation, 0.80% in commercial flocks presented a second time, and 0.43% in breeder flocks. Pasteurella multocida was cultured from 69.8% of the 361 tissue samples submitted from these cases. Novobiocin, penicillin, and chlortetracycline (CTC) had the greatest in vitro activity against isolates. Serotype 3-cross-4 was found in all 18 commercial flocks from which isolates were typed. All breeder flocks and 88.6% of commercial flocks were vaccinated before disease onset. Flocks were treated for an average of 14.3 days, most commonly with high levels of sulfadimethoxine and/or CTC. Body weights of affected birds were comparable to those of birds in unaffected flocks, but mortality and feed efficiency were worse.

Chickens vaccinated with a live Newcastle disease (ND) vaccine and subsequently revaccinated with an inactivated oil emulsion ND vaccine had higher and more persistent hemagglutination-inhibition (HI) antibody titers than birds vaccinated with live ND vaccine. The geometric mean HI antibody titers of flocks vaccinated with the inactivated ND vaccine ranged from 121 to 172, whereas the titers of flocks vaccinated every 90 days with a live ND vaccine ranged from 18 to 54. Breeder flocks revaccinated with live LaSota ND vaccine had lower egg production than the flocks vaccinated with inactivated vaccine. The average egg production per hen for the 40-week laying cycle was 174 and 170 eggs per hen for hens in the two houses vaccinated with the inactivated vaccine. Hens vaccinated with the live virus vaccine averaged 167 and 164 eggs per hen. The increase in egg production would more than offset the additional cost of the oil emulsion ND vaccine as well as the cost of injecting each individual bird at 18 weeks of age. Between 8 and 32 weeks after onset of egg production, geometric mean maternal antibody titers in 1-day-old chickens derived from breeders vaccinated with live ND vaccine ranged from 7 to 24, whereas, chicks from breeders vaccinated with the inactivated oil emulsion vaccine had maternal antibody titers that ranged from 64 to 89.

A survey of antibodies against infectious bursal disease virus (IBDV), infectious bronchitis virus (IBV), Newcastle disease virus (NDV), and reovirus (RV) was conducted in broiler-breeder flocks and selected progeny broiler flocks utilizing the enzyme-linked immunosorbent assay. Marked differences in antibody titers between different breeder flocks were related to differences in vaccination programs. Poor performance in some progeny broiler flocks was related to low antibody titers against IBDV in the source breeder flocks. Progeny broiler flocks in which there was a high incidence of condemnations for airsacculitis had elevated antibody titers against IBV. A few progeny broiler flocks that experienced high mortality due to gangrenous dermatitis had no antibody titers against IBDV at processing. Antibody titers against RV were very variable and could not be related to any production problems.