Egg transmission of avian reoviruses in chickens: Comparison of a trypsin-sensitive and a trypsin-resistant strain

Two groups of commercial Light Sussex hens with no cultural evidence of reovirus infection and very low titres of neutralising antibodies were mated with cockerels from 17 weeks of age. At 27 weeks of age the birds were separated into three groups, and were inoculated intranasally and intravenously with avian reovirus strain R2 which is resistant to trypsin, with strain TR1 which is sensitive to the enzyme or sham-inoculated. Of the eggs laid by the hens infected with strain R2, 13/29 infertile eggs and embryos which fails to hatch were positive for virus, as were 6/70 hatched chicks. Despite this, virus was never isolated from cloacal swabs from the hens. Virus-infected eggs were laid between days 5 to 17 post inoculation (p.i.). Virus was isolated from the liver of all six R2 virus-positive chicks, from the hock joint of four and from the intestine of three. In contrast, for the group infected with the trypsin-sensitive virus TR1, of 120 eggs laid in the 5-week period, virus was isolated once only, from a chick hatched from an egg laid 7 days p.i. This infected chick was one of 83 which hatched and virus was found only in the joint. In a further experiment, two groups of mature SPF hens were inoculated with the reoviruses as above. Cloacal swabs and tissue examination showed greater virus excretion and tissue distribution of R2 than TR1. These results helped to explain the much higher egg transmission rate of R2 than TR1. However, the rate of vertical transmission of chicken reoviruses in nature, where the infectious dose would normally be lower than given here, is likely to be low.     

Further studies on the eradication and epizootiology of lymphoid leukosis virus infection in a commercial strain of chickens

The feasibility of eradicating exogenous lymphoid leukosis virus (LLV) from a commercial egg-layer grandparent strain of chickens was examined by selecting replacement chicks from hens expected to have a reduced likelihood of transmitting LLV, followed by testing of progeny chicks and removal of those showing evidence of infection, together with their early contacts. Chicks from unselected hens were hatched and reared separately for comparison. The selected chicks came from hens negative for LLV in vaginal swabs and for LLV and/or group-specific antigen (gsa) in egg albumen, but at hatching 2.5% were infected by LLV in cloacal swab tests compared with 4.1% of unselected chicks, an insignificant difference. The infected chicks from the selected group, and their cage mates, were culled, leaving 85 hens of which seven were identified at different times as being infected and were removed. At 70 weeks 75 hens remained free of LLV infection. Of 369 eggs laid by the selected hens, 0.3% contained LLV in the albumen, and none contained gsa in albumen or LLV in corresponding embryos. Chicks hatched from the selected group were free of LLV infection. LLV infection was allowed to spread naturally in the unselected hens and 85.4% were infected at 70 weeks. Of these hens, 60.0% produced eggs with LLV in albumen, 41.2% with gsa in albumen, and 32.9% with LLV-infected embryos. Of 509 eggs from these hens, 25.1% had LLV in albumen, 30.5% had gsa in albumen, and 10.4% had LLV-infected embryos. In confirmation of other studies, shedding of LLV to embryos was associated with presence of LLV in vaginal swabs and serum. Analysis of associations within eggs between LLV and gsa in the albumen, and LLV in the embryo, provided strong evidence that virus in the oviduct was the cause of embryo infection; no firm evidence was obtained for the occurrence of embryo infection by a non-oviduct route. Infection of cocks in the selected and unselected groups was similar to that in hens in the respective groups. Some cocks used to inseminate unselected hens had infected semen, but this did not influence the frequency of embryo infection. In a comparison of eight tests on hens or eggs from the unselected group for selection of embryos with decreased probability of being infected with LLV, the procedures most likely to be used under practical conditions, namely classification of hens according to LLV in vaginal swabs or gs-antigens in egg albumen, ranked third and fifth respectively, and did not differ from the highest ranking procedure. Age at first egg was significantly earlier, and hen-housed egg production tended to be better, in selected hens compared with unselected hens, but environmental differences other than infective status may have been responsible. In comparisons within the unselected group, hen-housed and hen-day egg production were significantly poorer in viraemic tolerant hens than in immune hens or uninfected hens.     

Effect of lymphoid Leukosis virus on performance of layer hens and the identification of infected chickens by tests on Meconia

The effect of subclinical infection with lymphoid leukosis virus (LLV) on the productivity traits of layer hens was investigated. In hens that shed gs-antigen of LLV to albumen, onset of sexual maturity was delayed by a mean of 11 days and the number of eggs laid was reduced -by 68 per hen up to 75 weeks of age. Shedding hens laid on average 2 g lighter eggs and of lesser specific gravity. Thirty-four % less chickens were obtained in the reproduction programmes from LLV-shedders in comparison with non-shedders. LLV had no significant effect on fertility and hatchability. Reduced egg-related performance was only directly related to LLV-shedding and dams' shedding status had no effect on the egg-related performance of their LLV-free progeny. Dams' shedding status, however, correlated with higher mortality (10% higher) among their progeny. The percentage of non-layers was also higher in progeny of LLV-shedders. Meconia were highly suitable samples for identifying both transmitting dams and infected chickens but only if the test for infectious virus was performed. ELISA on meconia was less reliable than the test for virus and therefore is not recommended for the detection of residual of infected chickens in the flocks selected for reduced gs-antigen shedding.     

Lateral transmission of egg drop syndrome-76 virus by the egg

Experiments were carried out to determine if eggs produced by infected hens could be involved in the lateral spread of EDS virus. It was demonstrated that birds which ate the abnormally shelled eggs produced 8 to 17 days after experimental infection with EDS virus, or normally shelled eggs produced 8 to 15 days after infection, became infected with the virus. Laying hens which ate abnormally shelled eggs from a naturally occurring case of EDS subsequently developed the disease. Whilst it is probable that surface contamination of the egg was important, it was demonstrated that virus was present in the contents of eggs laid 11 to 20 days after infection. It is concluded that the infected egg may be important in the lateral spread of EDS virus, and that attention should be given to the risk from re-used egg trays.     

Induction of eggshell apex abnormalities in broiler breeder hens

Recently, the causal relationship between eggshell apex abnormalities (EAA) and Mycoplasma synoviae was described. This eggshell pathology has only been documented in table egg layers both spontaneously and experimentally infected with M. synoviae, suggesting that meat-type layers are less prone to this condition. In this study the susceptibility of specified pathogen free (SPF) broiler breeder hens to produce eggs with EAA after M. synoviae infection was assessed. Five groups of 12 hens each were made: a negative control group, a group inoculated intratracheally (i.t.) with a M. synoviae EAA strain at 19 weeks of age, a group inoculated i.t. with this strain at 19 and 26 weeks of age, a group inoculated with M. synoviae i.t. at 19 weeks of age and infected 5 days earlier with infectious bronchitis virus D1466 (IBV), and a fifth group similar to the former but inoculated i.t. twice with an M. synoviae EAA strain at 19 and 26 weeks of age. Eggs with EAA were only produced after a single i.t. inoculation with the M. synoviae EAA strain if preceded by an infection with IBV. The production of eggs with EAA started 6 weeks after M. synoviae EAA inoculation and the proportion of eggs with EAA during the experiment was 9/449 (2%), which was much lower than that in SPF layer hens (14–22%). The present results suggest that broiler breeder hens are less susceptible to producing eggs with EAA after an infection with a M. synoviae EAA strain preceded by an IBV infection, compared with table egg layers. Similar to SPF egg layers, the mean daily egg production per hen was significantly reduced by the M. synoviae EAA strain and there was a general negative effect on eggshell strength by this strain, suggesting it could also have a detrimental effect on hatching egg quality.     

Effect of vaccination of hens with an avirulent strain of Salmonella typhimurium on immunity of progeny challenged with wild-Type Salmonella strains.

The avirulent Salmonella typhimurium chi3985 was used to vaccinate white leghorn chickens at 16 and 18 weeks of age, and the effect of maternal antibody on Salmonella colonization of progeny of vaccinated hens was assessed with S. typhimurium F98 or chi3985. Progeny of hens that had been vaccinated at 1 and 3 or 2 and 4 weeks of age with chi3985 were used to determine the effect of maternal immunity on vaccine efficacy. Vaccination of hens induced long-lasting Salmonella-specific antibodies which were transferred into eggs and were detected as immunoglobulin G (IgG) in the egg yolk. Maternal antibody was detected in the progeny of vaccinated birds as IgG and IgA in serum and intestinal fluid, respectively. The titer of maternally transmitted IgG or IgA was highest in the first week of life of the progeny and declined with age. Maternal antibodies prevented colonization of the chicks by S. typhimurium chi3985 and reduced colonization by S. typhimurium F98. Overall, chicks from vaccinated hens had significantly higher antibody responses than did the progeny of nonvaccinated hens after oral infection with Salmonella strains. Maternal antibody reduced the efficacy of vaccination of progeny with chi3985 at 1 and 3 weeks of age. But vaccination at 2 and 4 weeks of age induced excellent protection against challenge with S. typhimurium F98 or S. enteritidis 27A PT 8 in birds from vaccinated hens and in specific-pathogen-free chickens. Vaccination of chickens at 2 and 4 weeks of age has been shown to protect the birds against challenge with homologous and heterologous Salmonella serotypes. A combination of vaccination of adult animals and use of the progeny of vaccinated birds will enhance effective control of Salmonella infections in the poultry industry. This will complement the present control of Salmonella-associated food poisoning caused by Salmonella enteritidis in eggs because the avirulent S. typhimurium vaccine strain chi3985 induced excellent protection against S. enteritidis in chickens.     

Avian pneumovirus infection of laying hens: Experimental studies

Administration of a virulent strain of avian pneumovirus (APV) to specific pathogen free laying hens by the oculonasal route failed to induce a drop in egg production or any adverse effects on eggshell quality. However, intravenous (i.v.) inoculation of the same strain caused a substantial drop in egg production and a high incidence of soft and thin-shelled eggs. Some respiratory signs were also observed and the hens appeared sick, with diarrhoea being observed in approximately one-half of the hens between 4 and 11 days post-inoculation (p.i.). APV antigen was detected in the oviduct epithelium up to 9 days p.i. This challenge model was then used to investigate the efficacy of live attenuated turkey rhinotracheitis (TRT) vaccine administered alone at 1 day old, or an inactivated TRT vaccine (at 16 weeks), or a combined programme using both vaccines, in protecting against this challenge. Neither the live nor the inactivated vaccine alone protected against clinical signs (respiratory infection or diarrhoea). However, the inactivated, but not the live, vaccine did protect against the effect of the i.v. challenge on laying performance. In contrast, the combined vaccination programme protected completely against both clinical signs and poor egg-laying performance. This protection lasted until at least 60 weeks of age. On the basis of the results with this experimental model, it is concluded that the use of live priming followed by administration of inactivated TRT vaccine is necessary to provide complete protection of laying chickens against APV challenge.     

Analysis of avian leukosis virus infections with an enzyme immunoassay.

An enzyme-linked immunosorbent assay (ELISA) for avian leukosis virus group-specific antigen was used to study infections with and shedding of avian leukosis virus in a commercial flock of chickens with a known high incidence of infection. Avian leukosis virus group-specific antigen was detected in serum or cloacal washings from 76% of a group of 100 61-week-old hens. With eggs collected during the next 3 weeks, antigen was detected in the albumen of 88% of the eggs from ELISA-positive hens and 2% of the eggs from ELISA-negative hens. Results of assays for infectivity correlated closely with the ELISA results. Serum and cloacal specimens were almost equally sensitive in detecting infection; however, a higher proportion of cloaca-positive hens (97%) than serum-positive hens (91%) shed virus in their eggs. Similar results were obtained from a second sampling of eggs taken when the hens were 84 weeks old, after an intervening molt. Avian leukosis virus infection was correlated with reduced egg production and increased mortality. Eggs were produced by 100% of the ELISA-negative birds during both sampling periods, whereas only 69% of the ELISA-positive birds produced eggs at 61 weeks and 76% produced eggs at 84 weeks. All birds that were ELISA negative at 61 weeks survived the experiment. Of 14 ELISA-positive birds that died and were examined postmortem between 61 and 84 weeks, 8 had malignancies, and the remainder died of a variety of nonmalignant diseases.     

Effect of type 1 fimbriae of Salmonella enterica serotype Enteritidis on bacteraemia and reproductive tract infection in laying hens.

Research on the role of type 1 fimbriae of Salmonella enterica serotype Enteritidis in poultry to date has been focused on the intestinal phase of the infection. This study aimed to investigate the role of type 1 fimbriae in a systemic infection by intravenously inoculating chickens with a fimD mutant or its parent strain. The fimD mutant was present in the blood for 3 weeks after infection, while the wild type parent strain was cleared within the first 3 days. The fimD mutant was isolated at least as much as the parent strain from the liver and spleen for up to 3 weeks after inoculation. The wild type strain was cleared from the caeca in the second week, while the fimD mutant was isolated from the caeca for up to 3 weeks after infection. The ovaries were more heavily infected by the fimD mutant than by the wild-type strain. In the first and second week after inoculation, the oviducts were more frequently infected by the mutant strain. The eggs of birds infected with the fimD mutant were less frequently contaminated with Salmonella. The shells of the eggs were more frequently contaminated by the wild type strain than with the mutant strain. Thus, the absence of type 1 fimbriae prolongs bacteraemia, modifies reproductive tract infection and reduces egg shell contamination by Salmonella enterica serovar Enteritidis.     

Natural infection of ducks with Mycoplasma synoviae and Mycoplasma gallisepticum and Mycoplasma egg transmission

Mycoplasma gallisepticum (MG), M. synoviae (MS), M. cloacale (MC) and M. anatis were isolated from ducks kept in a yard in close contact with chickens that were infected with MG, MS and some other avian Mycoplasma species. MG, MS and MC were isolated also from embryonated duck eggs and from infertile duck eggs laid during the first four weeks of egg production. Infected ducks did not show clinical signs of MG or MS infection in chicken. Detectable MG and MS agglutinating antibodies were not present in duck sera. However, they were found in two yolks of 10 tested from embryonated eggs. In the haemagglutination - inhibition (HI) tests yolks from embryonated eggs yielded significantly higher (P<0.01) titres of MS antibodies than duck sera. Geometric mean value of MS HI titres in tested duck sera was 20, while those of yolks from embryonated eggs was 333. It is probably the first report concerning isolation of MS from the naturally infected ducks and furthermore, concerning isolation of MG, MS and MC from naturally infected embryonated eggs.     

Vertical transmission of reticuloendotheliosis virus in chickens

In this study, the vertical transmission of reticuloendotheliosis virus (REV) in chickens was examined using 6-month-old birds with viraemia which had persisted since birth. Eggs collected from such hens were incubated within 24 hours of lay and it was found that 18 of 35 of the progeny were infected with REV. Seventeen of the 18 died before they were 28 days of age, due to a nervous syndrome. Some of the eggs laid by viraemic hens were stored at room temperature between 1 and 10 days and were then incubated. Hatched progeny from the eggs stored up to 4 days were infected. Hens free of REV, but inseminated by roosters with persistent viraemia seroconverted to REV. A small proportion of chickens which hatched (2/24) were infected with REV. Embryos were a better source for virus isolation than albumen samples.     

Vaccination of chickens decreased Newcastle disease virus contamination in eggs

Newcastle disease is an important health issue of poultry causing major economic losses and inhibits trade worldwide. Vaccination is used as a control measure, but it is unknown whether vaccination will prevent virus contamination of eggs. In this study, hens were sham-vaccinated or received one or two doses of inactivated LaSota vaccine, followed three weeks later by virulent Newcastle disease virus (NDV) challenge. Eggs were collected daily and shell, albumen and yolk were subjected to virus isolation, as were oral and cloacal swabs at 2 and 4 days post-challenge (dpc). A second experiment evaluated the distribution of the virus in the reproductive tract of non-vaccinates. All vaccinated chickens survived challenge, and the levels of virus shed from cloacal swabs were decreased significantly when compared to shams. In non-vaccinated hens, virus was detected in the ovary and all segments of the oviduct. Yolk, albumen and eggshell surface from eggs laid at day 4 and 5 post-infection by sham-vaccinated hens were positive for NDV, but eggs from LaSota vaccinated hens lacked virus in internal egg components (i.e. yolk and albumen) and had reduction in the number of positive eggshell surfaces. These results indicate virulent NDV can replicate in the reproductive tract of hens and contaminate internal components of eggs and eggshell surface, but vaccination was able to prevent internal egg contamination, reducing eggshell surface contamination, and reducing shedding from digestive and respiratory tracts in virulent NDV challenged hens.     

Maternal transmission of immunity to Eimeria maxima: enzyme-linked immunosorbent assay analysis of protective antibodies induced by infection.

Vaccination of broiler chickens against Eimeria infection is problematic because of the need to ensure that birds are protected from the time of hatching. We have therefore investigated the feasibility of protecting hatchling broilers via maternal transfer of protective antibodies from hens to their offspring. Oral infection of broiler breeder hens with 20,000 sporulated Eimeria maxima oocysts caused production of antibodies which were passed into the egg yolk and subsequently to hatchlings. The level of specific antibodies in the yolks to unsporulated oocysts, sporulated oocysts, merozoites, and gametocytes was assessed by enzyme-linked immunosorbent assays. The levels in yolks of antibodies to all developmental stages peaked 3 to 4 weeks after infection of the hens. Groups of 10 hatchlings were challenged at 3 days of age by oral infection with 100 sporulated E. maxima oocysts. In the first experiment, the mean 4-day (days 6 to 9 post-infection) total number of oocysts excreted in the feces of chicks from eggs collected 3 weeks after infection of the hens was (0.6 +/- 0.4) x 10(6) (mean +/- standard error) compared with (9.9 +/- 1.4) x 10(6) for the progeny of uninfected hens, which represents a greater than 90% reduction. However, oocyst excretion by chicks from eggs collected 7 or 8 weeks after infection of the hens was only 47 or 68% lower than control values, reflecting declining levels of protective antibodies. In a second experiment, in which the hens were somewhat older and pretreated by intramuscular injection of saline in the emulsifying agent, Arlacel A, the period for which protective antibodies were transferred to hatchlings was prolonged. Thus, oocyst excretion by challenged hatchlings from eggs collected for an 8-week period after infection of the hens was more than 90% lower than oocyst excretion by control chicks, and even hatchlings of eggs collected 19 weeks after infection of the hens showed a 60% reduction in oocyst output. In both experiments, the levels of immunoglobulin G (IgG) antibodies to all developmental stages in yolks or hatchling sera were very strongly correlated with maternally derived immunity to E. maxima. In contrast, parasite-specific IgM or IgA was not detectable, either in egg yolk or egg white. These results demonstrate the ability of IgG antibodies to protect against E. maxima in poultry, thus raising the possibility of using protective maternally derived IgG antibodies to identify potentially protective parasite antigens and indicating the feasibility of using maternal immunization as a means for parasite control.     

Protective effect of antibodies to two viral envelope glycoproteins on lethal infection with Newcastle disease virus

Summary The protective effect of humoral immunity against lethal infection of chickens with Newcastle disease virus was studied.Chickens hatched from eggs laid by hens vaccinated with live attenuated Newcastle disease virus vaccine possessed antibody to various components of the virus, and were resistant to a challenge with a virulent strain of Newcastle disease virus which was 100 per cent fatal for the offspring of nonvaccinated hens.Passive administration of antiserum raised against whole virions provided susceptible chickens protection comparable to that seen in the birds with maternal antibody.When administered passively, both anti-HN serum with virus neutralizing activity, and anti-F serum with only marginal virus neutralizing activity significantly prolonged the survival of infected birds but failed to achieve the level of protection as afforded by the anti-whole NDV serum.The protection provided by the simultaneous presence of anti-HN and anti-F serum was significantly greater than that afforded by either alone and comparable to that of anti-whole NDV serum, indicating the complementary effect of anti-HN and anti-F antibodies not only in cell cultures as reported previously (19), but also in a natural host.With 3 Figures     

Oral ingestion of egg yolk immunoglobulin from hens immunized with an enterotoxigenic Escherichia coli strain prevents diarrhea in rabbits challenged with the same strain.

White Leghorn hens were immunized with enterotoxigenic Escherichia coli B16-4 with heat-labile enterotoxin and colonization factor antigen I in Freund's adjuvant. Specific antibodies were detected by an enzyme-linked immunosorbent assay in the serum after 8 days and in eggs after 10 days, with levels reaching peaks at 15 and 20 days after the first immunization, respectively. The protective effects of the egg yolk antibodies were tested in the rabbit reversible ileal tie model of diarrhea. Five control rabbits developed severe diarrhea within 72 h after inoculation with enterotoxigenic E. coli B16-4. Oral ingestion of egg yolks from immunized hens for 4 days prior to inoculation protected five rabbits from diarrhea after challenge with the same strain of E. coli. The rabbits showed no adverse effects from the ingestion of the egg yolks. Four rabbits fed control eggs were also afforded some protection in that three rabbits developed mild diarrhea and one rabbit remained entirely well. In vitro experiments showed that immunoglobulin from egg yolks interfered with the binding of E. coli to purified small bowel mucins; immunoglobulin from immunized hens reduced binding more than immunoglobulin from nonimmunized hens. These findings indicate that eggs from hens immunized with appropriate antigens have potential as a useful source of passive immunity.     

Further studies on vertical transmission and persistence of Salmonella enterica serovar Enteritidis phage type 4 in chickens

One-week-old commercial layers were infected orally with 10⁸ colony forming units of Salmonella enterica serovar Enteritidis phage type 4. No mortality was observed. The inoculated organism was isolated in decreasing viable numbers from a number of tissues, particularly the spleen, liver and caeca. Organisms present in the spleen were primarily localized within macrophages. No Salmonella Enteritidis organisms were isolated between 10 and 24 weeks of age, when the experiment was terminated after several weeks of lay. When two groups of adult hens, housed with males, were infected, contaminated eggs were found within 2 weeks of infection in one of the experiments only. Progeny hatched from these eggs showed no mortality unless they were infected artificially with the S. Enteritidis strain. In this case, the percentage mortality fell as the hatches progressed, indicating increasing immunity to infection. The faecal excretion of the inoculated phage type 4 strain by infected but healthy progeny was followed. Although most birds ceased to excrete by 11 to 12 weeks of age, a small number of the birds continued to excrete until they themselves came into lay. The small numbers of birds in which this occurred indicates that tolerance to infection does not occur readily following infection of hens laying fertile eggs or in progeny birds infected before or within hours of hatching. Birds infected when they were less than 24 h old remained persistently infected until they were well into lay. However, control birds infected when 1 week old, on this occasion, showed a high level of excretion until the birds began to lay at 18 weeks. Inbred lines of chickens showing differences in their susceptibility to systemic salmonellosis did not show significant differences in the extent to which S. Enteritidis localized in the organs of the reproductive tract or in the number of infected eggs produced.     

Experimental evaluation of an inactivated vaccine against chicken anaemia virus.

An assessment of the performance of an inactivated chicken anaemia virus (CAV) vaccine following administration to specific-pathogen-free (SPF) breeder hens before the egg production period is reported. Antibodies to CAV in adult hens and maternally-derived antibodies to CAV in the progeny chicks were assayed by ELISA. Progeny of vaccinated chickens showed sufficient levels of maternally-derived antibody to CAV for up to 3 to 4 weeks of age. Following challenge at 1, 10, 20 and 30 days of age of chicks from CAV-vaccinated and non-vaccinated hens with virulent CAV, haematocrit levels and weights of thymus in vaccinates remained within normal ranges. Chicks derived from non-vaccinated hens developed anaemia and thymus atrophy following challenge. These results support the view that vaccination of breeder flocks with an inactivated vaccine to CAV could be an effective means of control of CAV-induced clinical disease.     

Enzyme immunoassay for detection of antibodies against eastern equine encephalomyelitis virus in sentinel chickens

We developed an enzyme immunoassay (EIA) for the detection of immunoglobulin M (IgM) and IgG subclass antibodies directed against eastern equine encephalomyelitis (EEE) virus in chickens. The assays were compared with the serum plaque reduction neutralization test (PRNT) and the hemagglutination inhibition (HI) test for ability to detect antibodies against EEE virus in laboratory-infected birds. No cross-reactivity was detected in serum from chickens inoculated with St. Louis encephalitis or Highlands J virus. The interval after infection when EEE virus-specific antibodies were first detected by IgM and IgG EIAs was found to be similar to that determined by the PRNT and HI tests: 2 to 4 days. The IgG EIA, PRNT, and HI test detected antibodies to EEE virus for at least 27 to 30 days after inoculation. In contrast, serum from five of seven chickens did not contain detectable IgM 30 days after infection. Similarly, in all three naturally infected sentinel chickens from Maryland, IgM class antibody was undetectable 1 to 5 weeks after IgM was initially detected. EIAs provide simple and rapid alternatives to traditional tests for monitoring EEE virus infections in sentinel chicken flocks. Moreover, the IgM EIA provides a means to separate recently infected chickens from those infected greater than or equal to 1 month earlier.     

Vaccination of chickens against Newcastle disease with a food pellet vaccine.

The Australian, heat-resistant, a virulent V4 strain of Newcastle disease (ND) virus was selected for further heat resistance to give a variant designated V4-UPM. V4-UPM was sprayed on to food pellets which were fed to chickens in amounts calculated to give about 10(6) EID50 per chicken. Chickens vaccinated only once by feeding developed no haemagglutination-inhibition (HI) antibodies and were not protected against challenge with a viscerotropic velogenic strain of ND virus. Chickens given food pellet vaccine at 3 and 6 weeks of age developed HI antibodies and were substantially protected against parenteral and contact challenge with virulent ND virus. Similar protection was achieved when the V4-UPM vaccine was given intranasally on two occasions or when the vaccine virus was allowed to spread by contact from intranasally vaccinated chickens to nonvaccinated chickens. Heat resistant ND vaccine incorporated in food pellets may provide a method for protecting village chickens against ND in tropical countries.     

Performance of meat-type chickens test-positive and -negative for lymphoid leukosis virus infection

Four "sire-line" and seven "dam-line" breeding stocks of meat-type chickens were purchased as 1-day-old chicks from commercial breeders. One egg from each of 61 to 81 hens per stock was tested at 245-280 days of age for presence of group specific antigen of the lymphoid leukosis virus (LLV). Subsequently, cloacal swabs collected at 42 days of age from 93 male and 188 female progeny of particular "dam-line" stocks were tested for LLV. The percentage of LLV shedders in the individual stocks varied from 0 to 15%. Egg production to 385 days was lower in shedders than in non-shedders by 10 eggs per hen housed and by eight eggs per surviving hen. In the crossbred progeny of the "dam-line" stocks tested for LLV at broiler age, males had a significantly lower percentage of positives (2%) than females (11%). The broiler-age body weight of the test-positive females was 5% lower and, to 315 days of age, their mortality was 29% higher and egg production per hen housed 28 eggs lower than in the negative birds.