Economic effects of clinical chicken anemia agent infection on profitable broiler production.

An outbreak of anemia dermatitis syndrome caused by chicken anemia agent (CAA) occurred in 15 broiler flocks. An average of 29% of chickens in these flocks were derived from a common breeder flock. The breeder flock had no antibody to CAA at 20 weeks of age but had seroconverted by 31 weeks. Diseased broiler flocks were derived from eggs laid by the breeder flock between 25 and 30 weeks of age. CAA infection in the breeder flock was subclinical, with no apparent effects on mortality or performance. A strategic program of therapeutic and/or prophylactic antibiotic therapy was begun in affected broiler flocks as soon as the disease was diagnosed. Nevertheless, when the cost of therapy was taken into account, affected broiler flocks had a net income 17.3% to 19.6% lower than normal flocks. Average bird weights were 3.3% to 3.5% lower in affected flocks than in unaffected flocks, and affected flocks had a significantly greater proportion of lighter birds. Average mortality in affected flocks was 2.0% to 2.3% higher than in normal flocks, with peak mortality occurring in the third week of life. There was no apparent effect on feed-conversion ratio.     

Vertical transmission of a fluoroquinolone-resistant Escherichia coli within an integrated broiler operation

The epidemiology of an enrofloxacin-resistant Escherichia coli clone was investigated during two separate outbreaks of colibacillosis in the Danish broiler production. In total five flocks were reported affected by the outbreaks. Recorded first-week mortalities were in the range of 1.7-12.7%. The clone was first isolated from dead broilers and subsequently demonstrated in samples from associated hatchers and the parent flock with its embryonated eggs, suggesting a vertical transmission from the parents. The second outbreak involved two broiler flocks unrelated to the affected flocks from the first outbreak. However, the clone could not be demonstrated in the associated parent flock. Furthermore, samplings from grand-parent flocks were negative for the outbreak clone. The clonality was evaluated by plasmid profiling and pulsed-field gel electrophoresis. None of the recognized virulence factors were demonstrated in the outbreak clone by microarray and PCR assay. The molecular background for the fluoroquinolone-resistance was investigated and point mutations in gyrA and parC leading to amino-acid substitutions in quinolone-resistance determining regions of GyrA and ParC were demonstrated. Vertical transmission of enrofloxacin-resistant E. coli from healthy parents resulting in high first-week mortality in the offspring illustrates the potential of the emergence and spreading of fluoroquinolone-resistant bacteria in animal husbandry, even though the use of fluoroquinolones is restricted.     

Egg production drops in breeder turkeys associated with western equine encephalitis virus infection

Egg production drops associated with western equine encephalitis (WEE) virus infection occurred in three turkey breeder flocks in California during summer 1993 and again in one flock the following year. Egg production losses totaled 8.76%, 9.57%, 9.71%, and 10.12% and were accompanied by an increase in small white-shelled and shell-less eggs. The outbreaks coincided with peak WEE virus activity in the state on the basis of statistics compiled by the California Department of Health Services on seroconversion rates in sentinel chicken flocks. Paired serum samples taken 2-3 wk apart showed increased titers to WEE between acute and convalescent sera in turkeys from three affected flocks. Convalescent sera were not available for testing from the fourth flock. WEE virus was isolated from one breeder hen submitted to the diagnostic laboratory during the early stages of the outbreak.     

Immune responses of breeding chickens to trivalent oil emulsion vaccines: responses to infectious bronchitis

Three similar flocks of broiler breeder parent chickens that had been given live infections bronchitis (IB) vaccines during rearing were injected at 20 weeks of age with three different oil emulsion vaccines: a commercial monovalent Newcastle disease (ND) vaccine (flock A); an experimental bivalent vaccine containing ND and infectious bursal disease (IBD) components (flock B); and an experimental trivalent vaccine containing ND, IBD and IB components (flock C). One week after vaccination 40 hens from flock A and 40 from flock C were taken to the laboratory and their egg yields individually recorded. At 37 weeks of age they were challenged by aerosol exposure to virulent IB virus. The egg production dropped significantly in the hens from flock A but not in the hens from flock C. On the farm, flock C showed a higher mean IB virus antibody titre four weeks after vaccination but titres rose in all three flocks indicating the presence of active IB virus infection. No differences in egg yields were found between the three farm flocks.     

Influence of feed on the course of tenosynovitis caused by REO virus infection in broilers

The first outbreak of tenosynovitis caused by infection with REO virus in the Netherlands, involving 15 broiler flocks, is described. The disease could be reproduced easily by subcutaneous, oral and contact infection of susceptible broilers with the isolated virus. The 15 affected flocks all came from one broiler parent flock and were fed with feed from one mill (A). Twenty other flocks, also coming from this parent flock and reared in the same period on feed from another feed mill (B) did not suffer from tenosynovitis. The parent flock showed no disease symptoms but seroconversion to REO virus occurred after the onset of the problems in the offspring. The influences of the different feeds on the course of the synovitis could be reproduced experimentally, but with less extreme differences than observed in the field. The possible ways in which feeds may influence tenosynovitis causing REO virus infection are discussed.     

Phenotypic and genotypic characterization of Salmonella arizonae from an integrated turkey operation

Fifty cases submitted between 2000 and 2002 were selected for retrospective analysis to evaluate possible relationships between Salmonella arizonae isolated from breeder flocks, hatching eggs, and meat bird flocks belonging to a single turkey integrator. In all the meat bird cases selected for this study, arizonosis was the primary diagnosis. In birds under 1 month of age, clinical signs and pathologic changes were observed in older birds. The Salmonella arizonae isolates were analyzed by antibiotic resistance pattern and serotype and genotyped by pulsed-field gel electrophoresis (PFGE). Serotyping and PFGE yielded similar results, but the antibiotic resistance patterns did not correspond to either serotyping or PFGE typing. The presence of common pulsed-field patterns in breeder flocks, eggs, and meat bird flocks suggested that S. arizonae was being transmitted vertically from the breeder flock.     

Clinical outbreak of Bordetella avium infection in two turkey breeder flocks

An acute upper respiratory disease was observed in two broad-breasted white (BBW) turkey primary breeder flocks. Associated clinical signs included sneezing, depression, and a deep dry cough originating from large conducting airways. Morbidity reached approximately 15-20% of the hens in an affected house. None of the turkeys died, and total feed consumption was not affected. A minimal effect upon egg production was noticed. Sera from an acutely affected flock exhibited a marked rise in titer to Bordetella avium compared with preinfection sera samples. In Case 1, B. avium was isolated in pure culture from affected birds. In Case 2, B. avium was diagnosed by serological results and clinical signs; bacteriological examination was not attempted. The findings presented here are consistent with an acute clinical outbreak of B. avium-induced turkey rhinotracheitis (turkey coryza) in BBW turkey breeder hens.     

Breeder age affects small intestine development of broiler chicks with immediate or delayed access to feed

1. The relationship between breeder age and chick gastrointestinal tract development to 21 days of age, as influenced by immediate or delayed access to feed, was examined in three consecutive trials.

2. Ross 708 chicks, derived from breeder flocks at 31 (young), 40 (middle) and 63 (old) weeks of age were placed randomly into either a control group with immediate access to feed and water, or a 48?h feed delayed (FD) group with free access to water.

3. FD negatively affected body weight (BW) of chicks derived from young and old flocks through the first and second weeks of age, respectively. Chicks from the older flock absorbed more yolk in the first 48?h with no FD effect. When feed was made available, chicks from the FD group showed a large increase in small intestine weight relative to BW, surpassing (P? 4. Morphological measurements in all intestinal sections had higher values in chicks derived from the middle age breeder flock. FD to newly hatched chicks from the young breeder flock shortened villi (P?P? 5. Crypt depths were maximised between 7 and 14?d post-hatch in chicks from young and old breeder flocks, but crypt depths in chicks from the middle aged flocks continued to deepen.

6. The increased crypt depth may augment the number of enterocytes available for villus growth, and facilitate longer villi and greater villus surface area, in chicks from the middle age flocks. Intestinal morphological variation was associated with breeder flock age, which accounted for differential growth in chicks derived from young, middle, and old aged breeder flocks.     

Characterization of Enterococcus hirae outbreaks in broiler flocks demonstrating increased mortality because of septicemia and endocarditis and/or altered production parameters

In Denmark, increased problems associated with streptococci and enterococci have been observed in broilers and broiler parent flocks, resulting in increased mortalities, uneven flocks, and subsequent downgrading and increased condemnations. Postmortem lesions associated with recent outbreaks due to Enterococcus hirae have been accompanied or dominated by septicemia and endocarditis. As a result of infection at an early age and relatively low mortality rates, outbreaks are not always clearly defined and may go unnoticed or may be attributed to poor chick quality. For the same reasons, the pathogenesis and epidemiology of observed outbreaks has only remained speculative. Four separate outbreaks associated with E. hirae infections in broiler flocks occurring between 1998 and 2002 have been investigated. Two of the outbreaks indicated evidence of two separate clones, with 89% and 79% of isolates involved in the individual outbreaks belonging to a single pulsed-field gel electrophoresis (PFGE) profile, respectively. Another outbreak (outbreak 4) demonstrated clear clonality, with all isolates demonstrating affinity to one of two PFGE profiles that differed by only two bands. However, all three outbreaks demonstrated a different clone. The remaining outbreak was nondonal, with isolates distributed between six separate PFGE profiles. One of the outbreaks (outbreak 4) was descended from a parent broiler flock previously associated with an outbreak of Streptococcus gallinaceus; the flock also exhibited septicemia and endocarditis. Initial indications suggested the possibility of vertical transmission of S. gallinaceus to the current broiler flock, causing infection. By extended phenotypic characterization and subsequent genetic characterization, including 16S rRNA sequencing, all strains from the four outbreaks were confirmed as E. hirae. This investigation highlights the problems associated with characterizing enterococci infections in broiler flocks.     

The occurrence of a reovirus variant in a German broiler flock

Broilers deriving from a parent flock, which had been effected in the 6th. month of hatching egg production, show arthritis beginning with the 12th day of life. The tarso-metatarsal joint has been affected. Birds show stunting. Body weights at slaughter and feed conversion of the affected flocks were reduced. The percentage of condemned birds before slaughter was highly increase and came up to 3-5%. Chickens of other breeder flocks, which were reared with the diseased birds, showed viral arthritis at an age of 18-20th day of life. The boilers derived from parent flocks which had been vaccinated twice during the with a 1133 reo live vaccine and before laying with an oil based vaccine of the antigen type WVU. A reovirus has been isolated (isolate K 171/87), which caused viral arthritis in 1133-immune day old chicks after parenteral and oral application. Infection of these chickens with the pathogenic reovirus of the antigen type 1133 didn't cause a disease. Also by serological examinations it was shown, that the reo-isolate K 171/87 possesses a different antigenicity. The kind of occurrence indicates, that this reovirus infection has been transmitted vertically from one parent flock and it spread laterally to chickens of other parent flocks in broiler farms.     

Neoplasms in the oviducts of turkeys

The reproductive tracts of turkey breeder hens from five flocks were examined grossly and histologically. Hens from one flock had a normal reproductive history, but hens from the four other flocks had poor records in both egg production and hatchability. Nodular growths occurred in the oviducts of birds in all five flocks. The incidence of lesions varied from flock to flock and from bird to bird. In four flocks, lesions were small and consisted of areas of dysplasia with adenomatous change. Histologically, the lesions in some birds in the fifth flock were adenocarcinomas. No metastases were observed.     

Molecular epidemiology of Pasteurella multocida in turkeys.

Pasteurella multocida isolated from turkeys during an outbreak of fowl cholera was characterized by serotype and heterogeneity of genes encoding rRNA (ribotype) to investigate the epidemiology of the organism. Isolates were collected between October 1985 and July 1986. The M9 or Clemson University fowl cholera vaccine-like strain was detected in 17% of the flocks with fowl cholera. One particular strain, isolated only from breeder flocks, was recovered from 7 of the 10 breeder flocks examined in this study. Intracompany transmission appeared to be common, implying a failure in biosecurity. Circumstantial evidence indicated that in the field; the incubation period of P multocida in a turkey flock may be between 2 to 7 weeks. Wildlife did not appear to be an important reservoir of P multocida for turkeys during this study period. Ribotyping results tended to discount several of the possible interflock transmissions, as suggested by examination of serotyping results alone; however, serotyping in combination with ribotyping proved helpful in understanding the epidemiology of P multocida in turkeys.     

Field experiments with viral arthritis/tenosynovitis vaccination of breeder chickens

Vaccination of three commercial broiler-breeder flocks at 15 weeks old with viral arthritis/tenosynovitis via the drinking water resulted in serologic conversion of two flocks to agar-gel-precipitin (AGP)-positive, while the third flock was still AGP-negative at 24 weeks, but was AGP-positive at 30 weeks old, presumably as a result of natural exposure. Progeny from the two successfully vaccinated breeder flocks remained free of clinical viral arthritis/tenosynovitis and had average condemnation rates of 0.99%. In contrast, six hatches of progeny from the third breeder flock experienced clinical viral arthritis/tenosynovitis and average condemnation rates of 3.64%.     

Disease prevalence in Georgia turkey flocks in 1986

Disease prevalence in turkeys was estimated by totaling the flock size of necropsy cases submitted to the University of Georgia in 1986 for each disease reported and comparing it with the population at risk. Fowl cholera was the most prevalent disease in both commercial tom flocks (18.0%) and breeder hen flocks (14.7%). Prevalence of colibacillosis was 15.9% in commercial tom flocks, and prevalence of aspergillosis was 8.5% in commercial tom and 4.9% in breeder hen flocks.     

Pasteurella multocida recovered from live turkeys: prevalence and virulence in turkeys

Swabs of the oropharynges of 801 live turkeys (621 meat birds and 180 breeders), collected from 15 flocks that had experienced an outbreak of fowl cholera and from 12 non-outbreak flocks, were screened for the presence of Pasteurella multocida. Turkeys from outbreak flocks were sampled within 2 to 9 weeks of the outbreak. Forty-nine isolates of P. multocida were recovered from turkeys in 11 of the outbreak flocks, and none were recovered from turkeys in non-outbreak flocks. Isolation rates varied from 0 to 72% of turkeys sampled in a flock. Nineteen isolates were tested for virulence by injecting them intravenously into turkeys, and 14 were lethal. Results demonstrated that for purposes of disease control, meat birds in fowl-cholera-outbreak flocks should be considered carriers of potentially virulent P. multocida for the life of the flock.     

Salmonella typhimurium outbreak in broiler chicken flocks in Mexico

A Salmonella typhimurium outbreak in 1-to-2-week-old broiler flocks in Mexico is reported. Clinical signs were growth retardation, blindness, twisted necks, and lameness. Gross lesions consisted of hypopyon, panophthalmitis, hepatomegaly with necrotic foci, enlarged spleen, pericarditis, coagulated and unabsorbed yolks, and purulent arthritis. Mortality and cull rates in different flocks ranged from 1.7% to 10.6% during the first two weeks of age. All internal organs, eyes, and hock joints of diseased chickens that were cultured were Salmonella-positive. The bacteria were also isolated from the breeder source flock. Disease was thought to be transmitted through eggs at hatch.     

Investigation of H7N2 avian influenza outbreaks in two broiler breeder flocks in Pennsylvania, 2001-02

An avian influenza (AI) outbreak occurred in meat-type chickens in central Pennsylvania from December 2001 to January 2002. Two broiler breeder flocks were initially infected almost simultaneously in early December. Avian influenza virus (AIV), H7N2 subtype, was isolated from the two premises in our laboratory. The H7N2 isolates were characterized as a low pathogenic strain at the National Veterinary Services Laboratories based on molecular sequencing of the virus hemagglutinin cleavage site and virus challenge studies in specific-pathogen-free leghorn chickens. However, clinical observations and pathologic findings indicated that this H7N2 virus appeared to be significantly pathogenic in meat-type chickens under field conditions. Follow-up investigation indicated that this H7N2 virus spread rapidly within each flock. Within 7 days of the recognized start of the outbreak, over 90% seroconversion was observed in the birds by the hemagglutination inhibition test. A diagnosis of AI was made within 24 hr of bird submission during this outbreak using a combination of virus detection by a same-day dot-enzyme-linked immunosorbent assay and virus isolation in embryonating chicken eggs. Follow-up investigation revealed that heavy virus shedding (90%-100% of birds shedding AIV) occurred between 4 and 7 days after disease onset, and a few birds (15%) continued to shed virus at 13 days post-disease onset, as detected by virus isolation on tracheal and cloacal swabs. AIV was not detected in or on eggs laid by the breeders during the testing phase of the outbreak. The two flocks were depopulated at 14 days after disease onset, and AIV was not detected on the two premises 23 days after depopulation.     

Epidemiology and financial impact of fowl cholera in turkeys: a retrospective analysis

A retrospective study of the epidemiology and financial impact of fowl cholera (FC) in California meat turkeys during 1984 was performed. Data were collected from 64 flocks--23 FC-outbreak flocks and 41 controls (non-outbreak)--raised in the Central Valley of the state. Mean flock age at the time of the FC outbreak was 11.3 weeks. Flocks that reported a colibacillosis outbreak had increased odds (P = 0.11) of also having an FC outbreak. (This association may or may not indicate a cause-effect relationship.) There was no significant difference between FC-outbreak and control flocks in number of diseases reported, age at onset, or duration of diseases or syndromes except age at onset of roundheart disease. The relative mortality rates were 52% higher in FC-outbreak toms and 26% higher in FC-outbreak hens than in their controls. Medication costs were nearly tripled, and the relative condemnation rate was 60% higher in FC-outbreak flocks than in control flocks. The average costs of FC were nearly $0.40 per bird, or $18,750 per flock, in an outbreak flock of 50,000 birds, and $0.12 per bird, or $6000 per flock, in non-outbreak flocks vaccinated against FC.     

EDS 76 HI antibodies in a flock of free-range layers

An investigation of poor laying performance in a flock of free-range hens revealed high levels of serum antibodies to EDS 76 in the flock initially examined and in another, older flock on the same farm. These flocks had contact with ducks on a farm dam and were supplied with untreated drinking water from the dam. Serological evidence indicated that another flock supplying the same egg packing station had been infected with EDS 76 virus. Little serological evidence of EDS infection was detected from five other flocks supplying the packing station, parent breeders or the ducks resident on the dam. Therefore, the source of the EDS 76 virus remains conjectural.     

Probable infectious stunting syndrome in replacement pullets

Infectious stunting is recorded in detail in three egg-type pullet flocks and one egg-type breeder flock. Three different strains of brown egg birds were involved. The clinical effects were less severe than those usually seen in broilers. Excessive mortality during the first three weeks was a feature of all four flocks. Fibrous atrophy of the pancreas was seen in one flock and could still be found in individual birds at 18 weeks old. Bone disorders were seen in two flocks. Severe anaemia was seen in some birds in one flock. Severe emaciation of the pectoral muscles was an unexplained and prominent feature of all the flocks. As the birds grew the visible and clinical evidence of stunting was much reduced and it appeared that compensatory growth took place so that by 18 weeks old the flocks appeared normal and the culling rate at caging was negligible.