Isolation of chicken anaemia virus from broiler chickens in New Zealand

Chicken anaemia virus was isolated for the first time in New Zealand from the New Zealand domestic chicken population. The virus was recovered from diseased birds in five separate flocks of broiler chickens aged between 14 and 33 days of age. Six isolates were obtained from bone marrow and lymphoid tissues using the MDCC-MSB1 cell line derived from Marek's disease lymphoma. All isolates were resistant to chloroform and survived exposure to 70 degrees C for 5 minutes. The main clinical features consistently associated with the disease outbreaks were increased mortality, yolk sac infections, sub-cutaneous haemorrhages and atrophy of the thymus. Fungal pneumonia occurred in two flocks, and gangrenous dermatitis as a result of bacterial infection in another flock. Microscopic examination showed atrophy of the thymus, reduced medullary haematopoiesis and inflammation resulting from secondary infections.     

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.     

Vaccination against infectious anemia of poultry (CAA)--results of field studies]

Infectious anemia of poultry is a disease of high economical significance. Connatal infection of chicks with the chicken anemia agent (CAA) via the embryonated egg causes anemia along with severe immunosuppression, thus rendering the chicken susceptible for secondary infections. In order to prevent infection of young chicks, it is necessary to induce immunity against CAA in parent flocks, with the aim to prevent connatal spread of the infection and provide maternal protection for baby chicks. In this publication, the efficacy and use of a live CAA vaccine is reported. From autumn 1986 until summer 1990, 3 experimental vaccine charges were applied in 85 broiler parent flocks with totally 3.1 million chickens. In addition, totally 293,000 broiler breeder and 171,000 layer breeder chicken were vaccinated in 1989/90. The vaccine was administered between the 13th and 19th week of life by drinking water without adverse effect to the birds. Chicken anemia symptoms were observed only at the begin of laying period in two parent flocks. These flocks had been vaccinated in the 17th and 19th week, respectively. The offsprings of all other vaccinated parent flocks remained free of chicken anemia. Day-old chicks derived from vaccinated parent flocks were protected against CAA challenge infection. It is emphasized, that vaccination should be performed within the 13th to 15th week of life, because according to our observations, this will lead to an immediate seroconversion.     

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.     

Sources of Salmonellae in broiler chickens in Ontario.

Sources of Salmonellae infecting broiler chicken flocks in Ontario were investigated from July, 1975 to April, 1976. Three broiler flocks were investigated on each of four farms which received chicks from a common hatchery. Samples of feed and new litter were preenriched in nonselective broth subcultured to Salmonella-selective enrichment broth and plated on Salmonella-selective differential agar.Samples of used litter, water, culled chicks, insects, mice, wild birds and environmental swabs were not cultured initially in the nonselective broth. Fecal samples from principal and occasional flock attendants were examined for Samonellae. Salmonella infection, as judged by contaminated flock litter was detected in six flocks on two of the farms while the flocks on the other farms remained negative. Salmonellae were isolated from 23 of 412 feed samples (nine serotypes), six of 35 new wood shaving samples (four serotypes), one of 29 pools of culled chick viscera (one serotype) and 44 of 267 used litter samples (14 serotypes). These results indicate that broiler chicken flocks were infected with diverse Salmonellae introduced in day old chicks, pelleted feeds, wood shavings and residual contamination from the preceding flock.     

A survey of Newcastle disease in Swiss laying-hen flocks using serological testing and simulation modelling

Newcastle disease (ND) is a highly contagious viral disease of birds particularly domestic poultry. Switzerland is currently declared free from ND; since vaccination is prohibited, the detection of antibodies against ND virus (NDV) results in the destruction of the respective flock (stamping-out policy). However, in 1995 and 1996, antibody-positive flocks were detected and sporadic ND outbreaks even occurred in Switzerland. Therefore, a serosurvey was done to look for evidence of NDV infections in Swiss laying-hen flocks. The survey was designed to provide 95% confidence of detecting at least one seropositive flock if the flock prevalence were 1%. Thirty blood samples from each of 260 commercial laying-hen flocks were collected during 1996 in a central poultry slaughterhouse. Sera were screened for NDV antibodies with a commercial blocking enzyme-linked immunosorbent assay (ELISA). Samples with a questionable or positive test result were retested with the same ELISA. A stochastic computer model was applied to define a cut-off number of test-positive samples to help to differentiate between true- and false-positive flocks and to estimate the true flock prevalence of infection. Four flocks were identified as NDV-seropositive and the NDV true seroprevalence among commercial laying-hen flocks in Switzerland was most likely between 1.35 and 1.55%. This indicates that Swiss laying-hen and parental flocks with more than 150 animals have been in contact with strains of NDV that cause subclinical infection in chicken, because no clinical symptoms have been observed. In this context, computer simulation was a useful technique to interpret survey results.     

Epizootiological investigation of an outbreak of pullorum disease in an integrated broiler operation.

An integrated broiler company experienced a major outbreak of pullorum disease during 1990. The outbreak resulted in the distribution of Salmonella pullorum-infected birds to more than 150 roaster flocks in five states. Twenty-two parent (multiplier) breeder flocks became infected. An epizootiological investigation uncovered a grandparent male line breeder flock as the index flock supplying males to the affected parent flocks. Transmission apparently occurred vertically through the egg and horizontally by contact in the hatcheries and by placement of chicks on contaminated litter.     

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.     

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.     

Susceptibility of chicks to infectious bursal disease (IBD) following vaccination of their parents with live IBD vaccine.

Vaccination of parent chickens with a commercial live infectious bursal disease (IBD) vaccine under field conditions at varying ages and by different routes resulted in variable susceptibility to the disease in their chicks. There was little correlation between the methods of vaccination and the levels of immunity in the chicks. There was some evidence that levels of transferred immunity decreased with the age of the parents. Of five flocks examined, the onset of susceptibility to IBD occurred at two days of age in two flocks and about one week of age in the other three. Four flocks were completely susceptible by the 27th day, the other at 31 days. Precipitins were demonstrated at day old in 100 per cent of chicks in three flocks and in 80 per cent in the other two. The precipitins had disappeared in all flocks by 17 days of age.     

Use of inactivated oil emulsion infectious bursal disease vaccines in breeder chickens to prevent immunosuppression in progeny chicks

Two chicken flocks, vaccinated with different inactivated infectious bursal disease vaccines, and one unvaccinated flock provided chicks with high and low levels of and no maternally derived immunity. Following challenge at three ages with a subclinical strain of infectious bursal disease virus the chicks were assessed for bursal damage and suppression of the immune response to Newcastle disease virus. Both high and low levels of maternally derived antibody prevented immunosuppression but the lower level provided only partial protection against bursal damage.     

Early T-maze behaviour and subsequent growth in commercial broiler flocks

Two batches of 2000 mixed-sex broiler chicks were obtained, one in summer and one in winter. Each flock was housed on the floor at a commercial farm. At 2 or 3 d of age, the latencies to escape from a T-maze were measured in 1044 and 1180 chicks in the summer and winter flocks, respectively. Chicks were assigned to high (HP), moderate (MP) or low (LP) performance categories if their escape latencies were below 40 s, between 40 to 90 s, or above 90 s, respectively. Ninety male and 90 female chicks from each of the 3 categories were weighed when they were 3 d old. The birds then remained undisturbed, apart from routine maintenance, until similar numbers were weighed at 49 d of age. Some birds may have been weighed at both ages. Body weights were higher in males than females and higher in the winter than summer flock at 3 d of age. Significant main effects of chick category as well as gender and season were found at 49 d of age. There were no significant interactions. As expected, 49-d body weights were higher in males than females and in the flock reared in winter than in summer. 5. HP chicks (those that showed rapid escape from the T-maze at 3 d) were also significantly heavier at 49 d than their LP counterparts, with MP chicks occupying an intermediate position. This suggests that early performance in a T-maze test is positively associated with subsequent growth. Furthermore, this relationship was apparent in each of the 2 flocks. Given this positive association, we suggest that this simple, rapid and non-invasive behavioural test could be a useful selection criterion for future breeding programmes.     

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.     

Incidence and distribution of "avian adenovirus group II splenomegaly of chickens"

Forty-six percent of 3,585 serum samples from 174 broiler-breeder chicken flocks in 9 states were positive for the precipitating antibody of hemorrhagic enteritis (HE) of turkeys/marble spleen disease (MSD) of pheasants. Seroconversion was detected only in flocks 19 weeks of age and older. The percent of individual serum samples positive within a flock increased with the age of the flock.     

A 1-year epidemiological study of campylobacters in 18 Swedish chicken farms

Broiler chickens are often intestinal carriers of Campylobacter. During processing, Campylobacter may be spread over the carcass. Thus, undercooked chicken meat, or other foods contaminated by raw chicken can act as a source of infection to humans. This study was conducted to identify risk factors for chicken flocks being colonized with Campylobacter. Eighteen chicken farms with altogether 62 chicken compartments were studied for 1 year with visits during each growing period and sampling of chicken caecal contents at slaughter. Four to six subsequent flocks were raised in each compartment during the study. A detailed questionnaire was used to record farm parameters such as building materials, feed and water equipment, hygiene and management routines. Campylobacter prevalence varied between farms, between growing periods within the farms and also during the year, with lowest prevalence during the spring. Campylobacters were isolated from 27% out of 287 flocks. Only two farms were negative at all samplings. Often the flock following a positive flock in a compartment was negative, indicating that normal cleaning and disinfecting routines are sufficient for eliminating the bacteria from the house. Usually only one serotype was found in each positive flock. Campylobacter occurrence increased with the age of the chickens at slaughter, and also with flock size.

Univariable chi-square tests were done of the association between possible risk factors and Campylobacter prevalence. Factors associated with higher Campylobacter prevalence in flocks were lack of or diffuse hygiene barriers, increasing flock size, increasing age at slaughter, short vs. long empty periods, wet litter beds, other poultry nearby or staff handling other poultry, flocks divided before slaughter, staff loading to slaughter at several farms and occurrence of mice. Under Swedish conditions, water does not seem to be a source of infection for chickens. Origin and handling of day-old chickens, feed additives, houses and litter were not associated with higher Campylobacter prevalence.     

A longitudinal study of campylobacter infection of broiler flocks in Great Britain

One hundred flocks associated with five integrated poultry companies were monitored for one production cycle to investigate risk factors for campylobacter infection of poultry broiler flocks. Bacteriological samples were collected from one house of birds on each site at weekly intervals from 3 to 4 weeks of age until the birds were infected with campylobacter or the flock was depopulated (whichever was sooner). Environmental samples were obtained from 20 houses after cleansing and disinfection of the site before chick arrival. Conventional methods were used for the isolation of campylobacter. Questionnaires were used to collect information on potential risk factors for campylobacter infection. Discrete-time survival analysis was used to assess the influence of various exposures on the age at which the flock was infected with campylobacter.More than 40% of flocks were infected with campylobacter by the time the chicks were 4 weeks old and >90% by 7 weeks. Infection spread rapidly to most birds in a flock. Infection was not predictable by campylobacter status of the last flock reared on the site. (However, because most flocks were infected, the power to detect such an association was poor.) There was no evidence of environmental survival of campylobacters in broiler houses after adequate cleansing and disinfection. The most important predictors of protection from campylobacter were related to effective hygiene barriers (such as housing birds in buildings in a good state of repair, appropriate usage of disinfectant boot dips and a high standard of cleansing and disinfection of the drinking-water equipment). There was no evidence that rodents were a source of infection (but most sites operated effective vermin-control programmes).     

Infectious Bursal Disease in New Brunswick

A flock of four week old chickens experienced a disease of sudden onset in which the only symptoms were those of depression shortly before death, and in which the predominant histological lesion was necrosis of lymphocytes in the bursa of Fabricius.

A virus, designated strain Sk-1, was isolated from pooled bursal tissue of affected birds and was serologically identified as a strain of the infectious bursal agent. This virus was chloroform resistant, did not hemagglutinate guinea pig or chicken erythrocytes and did not produce a cytopathic effect in chick embryo tissue cultures. Equivocal results were obtained in filtration studies but the agent was less than 100nm in diameter.

Four week old chicks inoculated with strain Sk-1 developed microscopic lesions in the bursa of Fabricius which were similar to those seen in the original field specimens. Inoculated chick embryos exhibited characteristic macroscopic lesions and necrosis of vascular tissue was a common histological change.

A limited serological survey of local poultry flocks indicated that infection by this agent had occurred in four of the ten flocks examined.

     

A long term observation of antibody status to chicken anaemia virus in individual chickens of breeder flocks

The antibody status to chicken anaemia virus (CAV) in four layer breeder flocks was evaluated. Sera were periodically collected from the same 17 to 20 individual chickens of each flock ranging in age from 10 to 63 weeks old. The neutralising and fluorescence antibody were detectable in individual chickens during the observation periods ranging from 13 to 44 weeks. A high prevalence of both neutralising and fluorescence antibodies was observed; however, the prevalence of fluorescence antibody in older chickens was lower than that of neutralising antibody. The geometric mean (GM) of neutralising antibody titres, after all the chickens examined had seroconverted in flocks 1, 2 and 4, ranged from 373·2 to 2940·6. In flock 1, the GM titre at 63 weeks old was significantly lower than that at 37 and 52 weeks old. In flock 4, the GM titre at 48 weeks old was significantly lower than that at 24 and 35 weeks old. In flock 2, the GM titre at more than 31 weeks old significantly increased compared with that at 25 weeks old; this tendency was not seen in the GM of the fluorescence antibody titres. The results indicate that immunity to CAV can last a long time in naturally infected individual chickens.     

High seroprevalence of Histomonas meleagridis in Dutch layer chickens

Histomona meleagridis is a protozoan parasite that may cause outbreaks of histomonosis with high mortality, especially in turkey flocks. Chickens are less susceptible to the disease than are turkeys, but are considered to act as an important reservoir. To determine the seroprevalence of H. meleagridis in Dutch layer chicken flocks, a large scale seroepidemiologic study (3376 samples) was performed by sampling 12 organic flocks, 24 free-ranging flocks, 40 flocks with floor housing, and 40 flocks with cage housing. At the end of the laying period, approximately 30 blood samples per flock were collected for serology. The seroprevalence found was high. In every flock, at least one of the samples tested positive while in 87% of the flocks, at least one of the samples was strongly positive. There were no significant statistical differences in seropositivity between the housing types. To confirm the enzyme-linked immunosorbent assay (ELISA) results, a small-scale seroepidemiologic study (576 samples) was performed in 29 additional layer chicken flocks kept in different housing systems. Subsequently, a subset of five seropositive flocks was selected. Five birds were obtained from each of these flocks in order to detect the parasite using culture and PCR. In all five flocks, H. meleagridis was either isolated from (culture), detected in (PCR), or both, the birds sampled. Together with the previously performed validation studies, the latter results confirm that the positive ELISA serology found is genuine. We conclude that the seroprevalence of H. meleagridis in layers is, as anticipated, high.     

Subclinical infectious bursal disease in commercial broiler flocks in Saskatchewan.

Five commercial broiler flocks, not vaccinated for infectious bursal disease virus, derived from infectious bursal disease virus-vaccinated breeder flocks were surveyed for evidence of bursal damage and infectious bursal disease virus infection. They were compared with two groups of birds raised in isolation. Serum samples from one day old chicks contained maternal anti-infectious bursal disease virus antibodies which declined to undetectable levels by four weeks of age. Serum antibody levels remained undetectable in both control groups and one commercial flock, whereas four of the five commercial flocks had actively produced anti-infectious bursal disease virus antibodies by slaughter age. The weight of bursae from infectious bursal disease virus-positive flocks declined as compared to controls after four weeks of age. The decline in weight correlated with the appearance of histopathological lesions. Infectious bursal disease virus antigen was demonstrated in selected infected bursae and infectious bursal disease bursae and infectious bursal disease virus was isolated from some of these damaged bursae. Clinical infectious bursal disease was not observed in any of the commercial flocks. The importance of subclinical bursal damage and immunosuppression is discussed.