Observations on the persistence and vertical transmission of Salmonella enterica serovars Pullorum and Gallinarum in chickens: Effect of bacterial and host genetic background

Commercial laying hens inoculated with a strain of Salmonella enterica ser. Pullorum when they were 4 days old showed no morbidity, but harboured infection until they came into lay, and then produced S. Pullorum-contaminated eggs and infected progeny. There was limited evidence of transmission of maternal immunity to the progeny. Attempts were made to set up similar infections in hens with Salmonella Gallinarum, but without success. Infection either resulted in clinical disease or elimination of the pathogen. Infection of birds when in lay produced a similar result. The possibility of eggs becoming contaminated with S. Gallinarum after they were laid in the nest box was evaluated but there was no evidence for this. In-bred chicken lines with a SalI-susceptible phenotype showed greater localization of S. Pullorum in the reproductive tract than did a SalI-resistant line. In addition, in-bred birds, which were SalI resistant but showed greater susceptibility to intestinal colonization by Salmonella, infected with S. Gallinarum when they were 1 week old, showed longer term persistence in the liver and spleen than did a resistant line.     

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.     

Egg transmission of a respiratory isolate of Mycoplasma synoviae and infection of the chicken embryo

Egg transmission of Mycoplasma synoviae (Ms) was demonstrated in broiler breeder birds of over 40 weeks of age from a commercial flock that had been infected during rearing and in birds experimentally inoculated before onset of lay. Infection of growing birds with Ms did not prevent egg transmission in adult life. The embryonated eggs of experimentally infected hens were less susceptible to infection by inoculation than those of specific pathogen-free birds. Some chicks with maternal antibody were found to be infected at hatching and in these maternal antibody was not mycoplasmacidal. Indeed by protecting the embryo maternal antibody may have promoted hatching of infected chicks.     

Pathogenesis of Gallibacterium anatis in a natural infection model fulfils Koch's postulates: 1. Folliculitis and drop in egg production are the predominant effects in specific pathogen free layers

Pathogenicity of Gallibacterium anatis was studied in specific pathogen free layers in a controlled environment, applying the intranasal route for experimental infection. At 30 weeks, 37 hens were infected with 0.4 ml of 1.53 × 10⁸ colony-forming units/ml suspension of G. anatis strain 07990 whereas equal numbers of hens were left uninfected for control. Following experimental infection, clinical signs and the number and weight of the eggs were recorded daily until 5 weeks post infection. Three birds from each group were killed at 3, 7, 10, 28 and 38 days post infection (d.p.i.) for necropsy and sampling for bacteriological and histopathological examinations. Additionally, necropsy examination was performed on all remaining birds at 38 d.p.i. G. anatis infection was found to have an immediate and severe effect on egg production, showing early and persistent colonization in respiratory and reproductive organs as well as in the gut of infected layers. In birds killed at various time points, G. anatis infection caused focal necrosis in the liver (1/37), folliculitis (2/37), pericarditis (3/37), haemorrhagic follicles (2/37), ruptured follicles (20/37), yolk in the body cavity (2/37) and egg peritonitis (1/37). The inflammation of the ovaries could be further confirmed by histopathological examination. Recovery of G. anatis from yolk at 10 d.p.i. indicates the potential of vertical transmission. Altogether, lesions reflect typical findings of G. anatis infection reported in natural cases. Thus, for the first time, lesions and the consecutive disease caused by G. anatis infection have been reproduced experimentally in a natural infection model.     

A comparative study on the pathogenesis of egg contamination by different serotypes of Salmonella

Salmonella enterica serotype Enteritidis is the predominant serotype associated with egg-borne salmonellosis in humans. Apparently this serotype possesses particular characteristics that increase its chance to contaminate eggs. To identify these characteristics, two Salmonella serotype Enteritidis strains as well as one strain of each of the serotypes Salmonella Typhimurium, Salmonella Heidelberg, Salmonella Virchow and Salmonella Hadar strain were used to examine different aspects related to egg contamination. After an intravenous infection of laying hens, it was observed that the ability of the serotype Enteritidis strains to colonize the reproductive organs was significantly higher compared with the Salmonella Heidelberg, Salmonella Virchow and Salmonella Hadar strains but not with the Salmonella Typhimurium strain. Inoculating low numbers of the different Salmonella serotypes in egg albumen at 42°C demonstrated that the growth of the strains belonging to the Salmonella serotypes Virchow and Hadar was seriously repressed. The other serotypes, however, survived in albumen for 24 h. Furthermore, using two different specifically designed egg infection models, it was shown that all strains used in this study were able to penetrate into and multiply inside the yolk at 25°C. These findings indicate that the ability to grow in eggs post lay is not specific for the serotype Enteritidis. In conclusion, comparing strains belonging to different Salmonella serotypes has revealed that most probably a preferential colonization of the reproductive organs and an enhanced survival at 42°C allows the serotype Enteritidis to contaminate eggs.     

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 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.     

A critical review of Salmonella Typhimurium infection in laying hens

Salmonella Typhimurium has been reported to contaminate egg production across the world, but where Salmonella Enteritidis is endemic it is this latter serovar that dominates egg-borne salmonellosis. However, Salmonella Typhimurium is a major food-borne pathogen so it is important to understand how it can impact the microbiological safety of eggs and what serovar-specific control strategies may be appropriate in the future as control over Salmonella Enteritidis continues to improve. To that end, the present review examines the published literature on Salmonella Typhimurium in laying hens and eggs, with particular reference to comparative studies examining different serovars. Experimentally Salmonella Enteritidis is more often isolated from egg contents and seems to adhere better to reproductive tract mucosa, whilst Salmonella Typhimurium appears to provoke a more intense tissue pathology and immune response, and flock infections are more transient. However, it is observed in many cases that the present body of evidence does not identify clear differences between specific behaviours of the serovars Typhimurium and Enteritidis, whether in laying hens, in their eggs, or in the laying environment. It is concluded that further long-term experimental and natural infection studies are needed in order to generate a clearer picture.     

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 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.     

Further studies on vertical transmission of reticuloendotheliosis virus in turkeys

Turkey hens were inseminated with infected semen from REV tolerant turkey stags at weekly intervals for 6 weeks, and subsequently with semen from uninfected control stags for a further 6 weeks. Cell cultures prepared from eggs produced during the experimental period were assayed for REV by an indirect fluorescent antibody test. Poults hatched from such eggs were also assayed for REV at 1 day of age or maintained to 28 weeks of age to study lateral spread of virus to uninfected hatch mates. REV was detected in 27.5% of embryos from hens inseminated with REV infected semen and 8.7% of 1-day-old poults hatched were found to be viraemic. Following the change to insemination with uninfected semen, REV was detected in 0.7% of embryos examined. REV was isolated from the lower oviduct of two of 18 hens, 12 weeks after first insemination with infected semen. REV spread readily to uninfected poults maintained in contact with progeny of hens inseminated with REV-infected semen, in that 50% had neutralising antibody by 8 weeks of age. At 28 weeks of age the leukosis mortality in such poults was 16%.     

The detection of maternal antibodies to mycoplasma gallisepticum in chicks by the rapid serum agglutination and haemagglutination inhibition tests

Eggs from hens infected with Mycoplasma gallisepticum and hens free from M. gallisepticum and M. synoviae were hatched and samples of blood were taken between 1 to 21 days after hatching. Antibodies (M. gallisepticum) responsible for both rapid serum agglutination (RSA) and haemagglutination inhibition were detected in the sera of progeny of infected hens, but these declined until they were undetectable by 18 days of age. By 4 days after hatching only approximately 65% of the birds were positive to the RSA test. This work re-emphasises the need to sample chicks early in life when attempting to detect maternally derived antibody.     

Experimental infection of laying hens with Serpulina intermedia causes reduced egg production and increased faecal water content

Serpulina intermedia strain HB60, isolated from an Australian hen with diarrhoea, was used to infect 10 individually caged 14-week-old laying hens. Another 10 birds were sham inoculated with sterile broth. Birds were kept for 16 weeks, and faecal water content, egg production and body weights recorded. Strain HB60 was isolated from the faeces of nine of the infected birds at irregular intervals throughout the experiment, and from their caeca at slaughter. Infected birds tended to be lighter and their faeces, on average, were significantly wetter (by 2.85%; P < 0.002) than those of the controls. Significant reductions in mean number of eggs laid (1.4/week; P < 0.002) and mean egg weights (1.16 g; P < 0.05) were recorded in infected birds. Colonization did not induce any characteristic pathological changes. S. intermedia is potentially an economically significant cause of reduced egg production, and wet faeces in layer and broiler breeder flocks.     

Characterization of the invasiveness of monophasic and aphasic Salmonella Typhimurium strains in 1-day-old and point-of-lay chickens

Egg-related outbreaks of salmonellosis are a significant health concern. Although Salmonella Enteritidis (SE) is the major egg-associated serotype, Salmonella Typhimurium (ST) can also infect the hen's reproductive tract and contaminate eggs. Recently, monophasic and aphasic variants of ST have been reported with increased frequency in Europe, and the isolation of these variants from laying flocks triggers the same legislative restrictions associated with biphasic ST strains. However, little is known about the colonization, invasiveness and persistence of monophasic and aphasic ST strains in laying hens. In this study, seven groups of 1-day-old and point-of-lay commercial Hy-line chicken layers were separately challenged with four different strains of monophasic ST, one aphasic ST, one biphasic ST and one egg-invasive SE strain. Tissue samples and cloacal swabs (point-of-lay chickens only) were collected at regular intervals post challenge in order to recover the Salmonella challenge strains. In 1-day-old chicks, only the aphasic ST strain and the SE strain were recovered after direct plating, suggesting that the number of salmonellas colonizing the tissues of the chicks infected with the other strains was likely to be low. Interestingly, all of the strains colonized well in the point-of-lay chickens, and there was no statistical difference in the overall number of positive samples or Salmonella counts between the seven strains. Salmonella was recovered from the point-of-lay birds to the end of the study (20 days after challenge). Monophasic and aphasic ST strains colonized point-of-lay birds as efficiently as biphasic ST and SE strains. Further studies are necessary to estimate the invasiveness of these strains in naturally-infected vaccinated laying hens, and to assess the impact of natural infection on egg contamination.     

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.     

Experimental infections with the protozoan parasite Histomonas meleagridis: a review

In recent years, a number of studies about Histomonas meleagridis, and more specifically about experiments in vivo involving H. meleagridis to investigate the pathogenicity and efficacy of drugs or vaccines, have been published. Together with older publications, a considerable amount of information about experimental infections with H. meleagridis exist, which is helpful for planning future animal studies and can reduce the number of birds used in such studies toward better animal welfare. One hundred sixty-seven publications describing experimental infections with H. meleagridis were published in scientific journals between 1920 and 2012. One hundred forty-two of these publications describe infections of turkeys (Meleagris gallopavo) and 52 infections of chickens (Gallus gallus). In 18 studies, experiments involving other species were done. The most popular routes of infection were the intracloacal application of histomonal trophozoites from culture material, from lesions or from feces of infected birds, or using larvae of the cecal worm Heterakis gallinarum (83 studies) and the oral application of eggs or other stages of the cecal worm containing histomonal stages (83 studies). During the last 10 years, intracloacal application of trophozoites has become the most popular way to experimentally infect birds with H. meleagridis due to its high reproducibility and reliability. In most studies, infection doses of several 10,000 or 100,000 histomonal trophozoites were used for infection, and the resulting mortality in turkeys was more than 70 %. First mortality can occur as early as 6 days p.i.; peak mortality usually is 13–15 days p.i. Lower infection doses may delay mortality about 2 days. In chickens infected by the intracloacal route, mortality and clinical signs are rare, but infection rates are similar. Cecal lesions can be observed from 3 to 4 days p.i., lesions up to 3 weeks p.i.; liver lesions may be lacking completely or be present only in a small number of birds. In most studies infecting birds with Heterakis eggs containing histomonal stages, several 100 to 1,000 Heterakis eggs were used. However, lower doses might be sufficient, as infection with as few as 58 eggs per bird caused a mortality up to 90 % in turkeys. Clinical symptoms start 9 days p.i., and first mortality occurs after 12 days, while most of the infected birds die between 19 and 21 days p.i. The infectivity of Heterakis eggs containing histomonal stages for chickens is similar as for turkeys, but mortality and clinical signs are rare. Further infection was done by oral application of histomonal trophozoites either grown in culture or using lesions or feces of infected birds (26 studies). These yielded very mixed results, with infection rates between 0 and more than 80 % in turkeys and chickens. After successful oral infection of turkeys, mortality occurs at roughly the same time as after intracloacal infection. Further 18 studies employed seeder birds to infect in-contact birds. Other means of infection were exposure to contaminated soil or litter (22 studies), feeding contaminated earthworms (7 studies), intracecal inoculation (4 studies), or parenteral injection (4 studies). Main methods to assess the course of the infection were mortality, observation of clinical signs and pathological lesions, monitoring of the weight of the infected birds, and detection of the parasite by various methods.     

The efficacy of Salenvac,a Salmonella enterica subsp. Enterica serotype Enteritidis iron-restricted bacterin vaccine,in laying chickens

The protective effect of two vaccination regimes using Salenvac, a commercially available iron-restricted Salmonella enterica subsp. Enterica serotype Enteritidis PT4 bacterin vaccine, was verified in laying birds. Immunization was intramuscular at 1 day old and again at 4 weeks of age (V2), or at 1 day and 4 weeks with a third dose at 18 weeks of age (V3). Challenge S . Enteritidis (5 to 7.5) × 10 7 colony forming units) was given intravenously at 8, 17, 23, 30 and 59 weeks of age. For all age groups, both vaccination regimes reduced significantly the number of tissues and faecal samples that were culture positive for the challenge strain. For laying birds, fewer eggs ( P < 0.001) were culture positive for S . Enteritidis after challenge from vaccinated laying birds (56/439 batches of eggs) than unvaccinated birds (99/252 batches). The data give compelling evidence that the vaccine is efficacious and may contribute to the reduction of layer infection and egg contamination.     

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.     

Susceptibility of different turkey lines to <Emphasis Type="Italic">Histomonas meleagridis</Emphasis> after experimental infection

In the present investigation, three turkey lines, namely wild Canadian turkeys (WCT), British United turkey (BUT-Big6) and Kelly–Bronze turkeys (KBT) were compared for their susceptibility to infection with Histomonas meleagridis. All birds were kept on wood shaving as litter from day 1 on during the entire observation period. On day 28, 18–20 birds per turkey line were infected with H. meleagridis intracloacally. All birds were observed for 4 weeks after infection. The mortality rate was 95% in WCT, 78% in BUT-Big6 and 75% in KBT. In WCT, the first deaths occurred at day 6 and ended at day 13 post-infection, whilst for BUT-Big6 and KBT, birds died from days 10 to day 20. In KBT group, the mortality started at day 10 and lasted until day 17 after infection. At necropsy, all birds that died showed lesions typical for histomoniasis in the caeca and liver. The obtained results demonstrate that all tested turkey lines are susceptible to infection; however, the mortality rate for the wild Canadian turkey is statistically significantly higher compared to the other tested two lines.     

Passive immunisation of turkey poults against turkey coryza (bordetellosis) by vaccination of parent breeders

Seventy turkey parent breeders were vaccinated subcutaneously at 24 and 28 weeks of age with a bacterin consisting of equal parts of a heat-inactivated suspension of the coryza producing Bordetella-like strain IPDH 591-77 and Freund's complete adjuvant. One group of 70 breeder hens served as un-vaccinated controls. Two and 3.5 months after the second vaccination eggs were collected and incubated. After hatching, 3-day-old poults from vaccinated and unvaccinated hens were challenged by direct-contact exposure to artificially infected poults. The results of clinical, cultural and histopathological examinations indicated that the majority of the progeny of vaccinated turkey breeder hens was protected against infection with the bacterial turkey coryza agent within the first 10 to 17 days after hatching. Agglutinating antibodies against the turkey coryza agent could be detected in vaccinated hens as well as in their progeny.