Pathogenicity of Salmonella enteritidis phage types 4, 8, and 23 in broiler chicks.

Four hundred fifty day-old Hubbard broiler chicks were subdivided into 15 groups of 30 chicks each. Six groups of chicks received 0.5 ml of broth culture containing 5 x 10(6) colony-forming units (CFU) of Salmonella enteritidis (SE) phage types (PTs) 4, 8, and 23 by crop gavage. Similarly, six other groups received 0.5 ml containing 5 x 10(8) CFU of SE. One group was inoculated with 0.5 ml containing 5 x 10(6) CFU of Salmonella pullorum, and another group received 0.5 ml containing 5 x 10(8) CFU of S. pullorum. A group of 30 chicks were kept as uninoculated controls. Chicks were observed daily for clinical signs and mortality. All birds were weighed at 7, 14, and 21 days postinoculation 21 (DPI). Four chicks were randomly selected from each treatment group, euthanatized, and necropsied at 7 and 14 DPI. Gross lesions were recorded and selected tissues were collected for histopathology. The higher rates of illness and mortality were observed in chicks inoculated with 5 x 10(6) and 5 x 10(8) CFU of S. pullorum, followed by SE PT4 of human origin and SE PT4 of chicken origin. Moderate to high mortality was observed in chicks inoculated with the higher dose of SE isolates that belonged to PT8 and one SE of PT23. Variable mortality was evident in groups inoculated with the lower dose of salmonella. The most consistent gross and histopathologic changes, including fibrinous pericarditis and perihepatitis, were seen in the dead birds from various treatment groups. The lower mean body weights were present in all treatment groups compared with uninoculated controls. No illness or mortality was observed in uninoculated control groups.     

Pathogenesis of chicken anemia virus: comparison of the oral and the intramuscular routes of infection

The events during the pathogenesis of chicken anemia virus (CAV) infection following intramuscular (IM) and oral inoculation were further elucidated and compared by sequential clinical, pathologic, and morphometric histopathologic evaluations, and by sequential determination of CAV genome concentrations in different organs. Specific-pathogen-free chickens were inoculated by IM or oral routes with the same dose (2 x 10(6) mean tissue culture infective dose [TCID50]) of CAV isolate 03-4876 at 1 day of age. Weights and hematocrits were obtained at 7, 10, 14, 18, 21, 25, and 28 days postinoculation (DPI). Seven birds from each group were necropsied at 7, 10, 14, and 28 DPI, and samples of thymus, Harderian gland, and cecal tonsils (CT) were obtained for histopathologic examination and CAV genome quantification by real-time polymerase chain reaction. Peak CAV genome concentrations were detected in the thymus at 10 and 14 DPI in the IM and orally infected chickens, respectively. High CAV DNA concentrations were maintained throughout the experimental period until 28 DPI, despite specific seroconversion occurring by 14 DPI in the IM-inoculated chickens. CAV was isolated from both orally and IM-infected chickens 28 DPI. Peak CAV genomes in the thymuses of IM and orally infected chickens coincided with peak lymphocyte depletion in these organs. Lymphocyte repopulation of the thymus occurred by 28 DPI in spite of the presence of the virus in the organs of both infected chicken groups. CAV genomes were detected in the CT, but histopathologic changes were not observed. Compared with the IM route of infection, orally infected chickens did not show apparent signs of illness. Clinical parameters, including reduction of weight gains and hematocrits, and gross and histopathologic changes were delayed and less severe in the orally inoculated chickens. This was concurrent with a delay in accumulation of CAV genomes in the thymus of these chickens.     

Pathogenicity of different serogroups of avian salmonellae in specific-pathogen-free chickens.

The pathogenicity of one isolate of Salmonella typhimurium, four isolates of Salmonella heidelberg, three isolates of Salmonella kentucky, two isolates of Salmonella montevideo, one isolate of Salmonella hadar, and two isolates of Salmonella enteritidis (SE), one belonging to phage type (PT)13a and the other to PT34, was investigated in specific-pathogen-free chicks. Three hundred eighty-four chicks were separated into 16 equal groups of 24 chicks. Thirteen groups were inoculated individually with 0.5 ml of broth culture containing 1 x 10(7) colony-forming units (CFU) of either S. typhimurium (one source), S. heidelberg (four sources), S. montevideo (two sources), S. hadar (one source), S. kentucky (three sources), SE PT 13a (one source) or SE PT 34 (one source) by crop gavage. Two groups of 24 chicks were inoculated in the same way with 1 x 10(7) CFU of SE PT4 (chicken-CA) and Salmonella pullorum. Another group of 24 chicks was kept as an uninoculated control group. The chicks were observed daily for clinical signs and mortality. Isolation of salmonella was done from different organs at 7 and 28 days postinoculation (DPI). All the chicks were weighed individually at 7, 14, 21, and 28 DPI. Two chicks chosen at random from each group were euthanatized and necropsied at 7 and 14 DPI and all the remaining live chickens, at 28 DPI. Selected tissues were taken for histopathology at 7 and 14 DPI. Dead chicks were examined for gross lesions and tissues were collected for histopathology. Chicks inoculated with S. pullorum had the highest mortality (66.66%), followed by S. typhimurium (33.33%). Chicks inoculated with S. heidelberg (00-1105-2) and SE PT4 (chicken-CA) had 12.5% mortality and 8.3% mortality, respectively, with SE PT 13a. Ceca were 100% positive for salmonellae at acute or chronic infection compared with other organs. Mean body weight reduction ranged from 0.67% (inoculated with S. kentucky 00-926-2) to 33.23% (inoculated with S. typhimurium 00-372) in the inoculated groups at different weeks compared with uninoculated controls. Gross and microscopic lesions included peritonitis, perihepatitis, yolk sac infection, typhilitis, pneumonia, and enteritis in some groups, especially those inoculated with S. typhimurium, S. heidelberg (00-1 105-2), SE PT4 (chicken-CA), and S. pullorum.     

Virulence analysis of a Salmonella gallinarum strain by oral inoculation of 20-day-old chickens

In order to know the effect of in vitro passages on the pathogenicity of the Salmonella gallinarum strain INTA 91, a lyophilized culture was compared with the same strain recently isolated from a sick bird. The mean lethal dose (LD50) of the orally administered lyophilized culture was determined as 2.04 x 10(8) colony-forming units (CFU)/chicken. There was no correlation between the LD50 dose and the degree of disease produced; doses 10 or 100 times higher than the calculated LD50 did not produce a more severe disease. In trial 1, chickens were challenged with 1.02 x 10(9) CFU per chicken (5LD50) of the lyophilized strain and reached 52.2% mortality at the end of the assay. In trial 2, three different groups of chickens were infected with a recent isolate of the same strain: 2.04 x 10(8) CFU/chicken, 4.1 x 10(8) CFU/chicken, and 2.1 x 10(9) CFU/chicken (i.e., 1LD50, 2LD50, and 10LD50 of the dose calculated for the lyophilized strain, respectively). These chicken groups presented higher mortality rates (90%, 100%, and 95%, respectively) than previous trials, showing that the S. gallinarum strain used here increased its virulence by in vivo infected chicken passage. In all assays, the disease started after an incubation period of around 5-6 days. To obtain reliable and reproducible results in future challenge experiments, a fixed limited number of in vitro passages of the S. gallinarum strain must be determined.     

Pathogenicity of West Nile virus in chickens

In the fall of 1999, West Nile virus (WNV) was isolated for the first time in the Western Hemisphere during an outbreak of neurologic disease in humans, horses, and wild and zoo birds in the northeastern United States. Chickens are a potential reservoir for WNV, and little is known about the pathogenicity of WNV in domestic chickens. Seven-week-old chickens derived from a specific-pathogen-free flock were inoculated subcutaneously with 1.8 x 10(3) 50% tissue culture infectious dose of a crow isolate of WNV in order to observe clinical signs and evaluate the viremic phase, gross and microscopic lesions, contact transmission, and immunologic response. There were no observable clinical signs in the WNV-inoculated chickens during the 21-day observation period. However, histopathologic examination of tissues revealed myocardial necrosis, nephritis, and pneumonitis at 5 and 10 days postinoculation (DPI); moderate to severe nonsuppurative encephalitis also was observed in brain tissue from one of four inoculated birds examined at 21 DPI. WNV was recovered from blood plasma for up to 8 DPI. Virus titers as high as 10(5)/ml in plasma were observed at 4 DPI. Fecal shedding of virus was detected in cloacal swabs on 4 and 5 DPI only. The WNV also was isolated from myocardium, spleen, kidney, lung, and intestine collected from chickens euthanatized at 3, 5, and 10 DPI. No virus was isolated from inoculated chickens after 10 DPI. Antibodies specific to WNV were detected in inoculated chickens as early as 5 DPI by the plaque reduction neutralization test and 7 DPI by the indirect fluorescent antibody test. Chickens placed in contact with inoculated chickens at 1 DPI lacked WNV-specific antibodies, and no WNV was isolated from their blood plasma or cloacal swabs throughout the 21 days of the experiment.     

Experimental infection of specific pathogen-free pigs with Campylobacter: excretion in faeces and transmission to non-inoculated pigs

Campylobacter species are leading agents of human bacterial gastroenteritis and consumption of food of animal origin is a major source of infection. Although pigs are known to frequently exhibit high counts of Campylobacter in their faeces, more information is needed about the dynamics of this excretion. An experimental trial was conducted to evaluate the faecal excretion of Campylobacter by 7-week-old specific pathogen-free piglets inoculated per os with three Campylobacter strains (one C. coli isolated from a pig, one C. coli and one C. jejuni from chickens) alone or simultaneously (5x10(7)CFU/strain). Non-inoculated pigs were housed in adjacent pens. Pigs were monitored for 80 days for clinical signs and by bacteriological analysis of faeces. Pigs inoculated with porcine C. coli or with a mix of the three strains excreted from 10(3) to 10(6)CFU/g of faeces with a slight decrease at the end of the trial. Animals inoculated with poultry C. coli or C. jejuni strain excreted a lower quantity and some of them stopped excreting. At the end of the trial, only C. coli was detected in the faeces of pigs inoculated simultaneously with the three bacteria. Moreover, the transmission of Campylobacter was noticed between pens for the two C. coli strains and all the neighbouring animals became shedders with a level of excretion similar to the inoculated pigs. Intermittence in the Campylobacter excretion was also observed. Finally, our study highlighted a host preference of Campylobacter, namely C. coli seems to have a higher colonization potential for pigs than C. jejuni.     

The viability of Campylobacter jejuni on refrigerated chicken drumsticks

Radappertized chicken drumsticks were experimentally contaminated with suspensions of Campylobacter jejuni in two trials. Qualitative analysis on drumsticks with an initial level of contamination of 4.8 X 10(3) CFU/cm2 showed that viability was retained for at least 10 days of storage at either 9 degrees or -12 degrees C. In a second quantitative trial, the level of contamination declined from 9.9 X 10(2) CFU/cm2 to 4.5 X 10(1) CFU/cm2 after 7 days at -20 degrees C. Thereafter, C. jejuni persisted at levels ranging from 1.8 X 10(1) to 0.2 X 10(1) CFU/cm2 through the 26th week of storage. Drumsticks held at 4 degrees C showed a significant decline in count from 9.9 X 10(2) CFU/cm2 to 1.8 X 10(2) CFU/cm2 on day 7. It is concluded that the viability of C. jejuni on chicken parts is maintained under both refrigerated and freezing conditions which approximate commercial storage. This is of significance to the meat industry and consumers.     

Campylobacter succession in broiler chickens

The competitive ability of Campylobacter coli OR12 over C. jejuni OR1 has been examined in experimental broiler chickens following the observation that C. coli replaced an established C. jejuni intestinal colonisation within commercial chicken flocks reared outdoors [El-Shibiny, A., Connerton, P.L., Connerton, I.F., 2005. Enumeration and diversity of campylobacters and bacteriophages isolated during the rearing cycles of free-range and organic chickens. Appl. Environ. Microbiol. 71, 1259-1266]. Co-cultures of C. coli OR12 with C. jejuni OR1, revealed that the two species were able to grow together at similar growth rates in exponential growth phase but if the disparity of the inoculum ratios were >log(10)4 in favour of C. coli OR12, C. jejuni OR1 was observed to prematurely enter decline phase. Chickens were pre-colonised with C. jejuni OR1 at 21-days-old to examine succession in vivo. The birds were inoculated between 2 and 12 days later with C. coli OR12, to determine if the second isolate could efficiently colonise and compete with an established C. jejuni strain. C. coli OR12 were able to co-colonise before replacing C. jejuni OR1 as the dominant species when the birds were more than 27 days of age at the time of administration over a 4-day period. If these criteria were met C. coli OR12 became the dominant isolate otherwise co-colonisation occurred until they were met. C. coli OR12 was also found to displace three alternative C. jejuni strains from pre-colonised chickens challenged with C. coli OR12 at 30 days of age and tested at 40 days. These data raise the possibility of manipulating populations of Campylobacter colonising chickens through competition.     

Irrelevance between the induction of anti-Campylobacter humoral response by a bacterin and the lack of protection against homologous challenge in Japanese Jidori chickens

On-farm vaccination of chickens against Campylobacter jejuni is considered a potentially effective countermeasure to decrease campylobacteriosis via consumption of contaminated chicken meat, but is not yet available. In this study, 2 groups of Jidori chicks were immunized subcutaneously with a formalin-killed C. jejuni with 2 different adjuvants. Other chicks served as the unvaccinated control group. Both vaccines induced high levels of anti-Campylobacter IgG but did not decrease bacterial excretion in cecal droppings and bacterial load in the liver and spleen after oral challenge with 10(5) CFU of the homologous strain. Further study is needed to address the observed irrelevance and to develop a novel effective vaccine against C. jejuni.     

Colonization characteristics of Campylobacter jejuni in chick ceca

We report our findings on several parameters influencing cecal colonization of chickens by Campylobacter jejuni. Thirty-five colony-forming units (CFU) of a composite culture of C. jejuni colonized the ceca of one-half of the newly hatched chicks challenged by oral gavage. A challenge dose of 3500 CFU/chick consistently colonized the ceca of all chicks challenged. Challenge doses of approximately 10(5) CFU of C. jejuni per chick resulted in consistent cecal colonization, regardless of whether the birds were challenged 1, 2, or 3 days post-hatch. Four isolates showed consistently strong cecal colonization abilities, whereas two isolates colonized the ceca in only 20 of 122 chicks when given levels of 10(5) CFU per chick. One of these poorly colonizing isolates was repeatedly transferred by fecal-oral passage through chicks; subsequently, this isolate was able to consistently colonize chicks. Competitive exclusion (CE) microflora did not diminish the colonization rates for C. jejuni. Birds treated with five different CE cultures were colonized at a rate of 81 of 84 chicks; control chicks were similarly consistently colonized (45 of 46 chicks).     

Lesions in sheep inoculated with Sarcocystis tenella sporocysts from canine feces

Sarcocystosis was studied in 37 sheep after oral inoculation with 10(4)-5 x 10(7) sporocysts of Sarcocystis tenella from canine feces. Two sheep inoculated with 2.5 x 10(7) and 5 x 10(7) sporocysts became moribund 16 and 19 days post-inoculation (DPI), respectively, due to occlusion of arteries of gut and mesentery by first generation meronts. Sheep inoculated with 10(7) sporocysts remained clinically normal until 21 DPI and those inoculated with 10(5)-10(6) became ill 24-28 DPI due to anemia coincident with maturation of second generation meronts. Inflammation, hepatitis and myocarditis were the main lesions of acute and subacute ovine sarcocystosis. Inflammation began to subside by the time (75 DPI) sarcocysts matured. Sarcocystis-induced encephalitis was distinguished from naturally occurring myelomalacia in sheep caused by an unidentified sporozoan.     

Pathogenicity of Mycobacterium avium complex serovar 9 isolated from painted quail (Excalfactoria chinensis)

Avian tuberculosis accompanied with many tubercular lesions in the liver and spleen was found in a painted quail at a zoological garden in Japan. Mycobacterium avium complex (MAC) serovar 9 without insertion sequence of IS901 was isolated from the liver (1.3 x 10(8) CFU/g), oviduct (9.4 x 10(7) CFU/g), and intestine (1.5 x 10(5) CFU/g). The isolates were inoculated intravenously to chickens. The inoculated chickens showed clinical symptoms of avian tuberculosis. Birds are susceptible to MAC serovar 9 without IS901.     

布鲁菌在豚鼠和奶牛体内诱导的抗体水平和变态反应强度的相关性

为探索布鲁菌在豚鼠和奶牛体内所引起的抗体水平和变态反应强度的相关性,分别用1×104,3×104CFU牛种布鲁菌强毒2308株各感染12只豚鼠,30 d后测定抗体滴度和变态反应强度。感染后35 d,扑杀豚鼠,取脾脏测定每克脾脏含菌量。用布鲁菌A19疫苗,以5×1010CFU皮下注射布病阴性荷斯坦奶牛50头,分别于免疫后15,30,60 d测定抗体滴度,并于免疫后45 d测定变态反应强度。运用SPSS 17.0-Analyze-Correlate-Bivariate Corre-lations程序分析试验数据,结果显示,不同剂量布鲁菌2308感染豚鼠后30 d所诱导的抗体水平、变态反应强度和克脾脏含菌量三者之间均无相关性。A19疫苗免疫奶牛后60 d的抗体水平与免疫45 d的变态反应强度呈正相关,免疫15 d和30 d的抗体水平和变态反应强度无相关性。豚鼠试验结果表明,抗体水平、变态反应强度与个体对布病的抵抗力均无相关性。     

Infectious bursal disease virus-induced immunosuppression exacerbates Campylobacter jejuni colonization and shedding in chickens

Campylobacter jejuni is the leading cause of food-borne bacterial gastroenteritis in humans in the United States. Infectious bursal disease virus (IBDV) causes an immunosuppressive disease in young chickens. To analyze a possible role of IBDV-induced immunosuppression in colonization and shedding of C. jejuni, two experiments were conducted. In both experiments, group 1 consisted of noninoculated control chickens, groups 2 and 3 were inoculated with varying doses of C. jejuni, and groups 4 and 5 were inoculated initially with IBDV followed by doses of C. jejuni similar to groups 2 and 3. Campylobacter jejuni was recovered from the cloaca and cecum, but not the small intestines, from all chickens in groups 2 and 3. In groups 4 and 5, C. jejuni was recovered from the small intestines, cecum, and cloaca from all chickens. The amount (colony-forming units/sample) of C. jejuni recovered from chickens in groups 4 and 5 was significantly greater (P < 0.05) than the amount recovered from chickens in groups 2 and 3; and C. jejuni was also present sooner in these groups than in groups 2 and 3. Bursa samples from chickens in groups 4 and 5 were significantly smaller (P < 0.05) than in the other groups. Additionally, real-time polymerase chain reaction results for IBDV were positive in groups 4 and 5 and negative in all other groups. This study indicated that IBDV infection exacerbated colonization and shedding of C. jejuni, presumably through the immune suppression this virus causes in chickens. It highlights the need for further investigation into the role of immunosuppression in preharvest control strategies for food-borne disease-causing agents.     

Experimental and serologic observations on avian pneumovirus (APV/turkey/Colorado/97) infection in turkeys

An avian pneumovirus (APV) was isolated from commercial turkeys in Colorado (APV/Colorado) showing clinical signs of a respiratory disease. The results of virus neutralization and indirect fluorescent antibody tests showed that the APV/Colorado was partially related to APV subgroup A but was unrelated to APV subgroup B. Turkeys experimentally inoculated with the APV/Colorado were observed for signs, lesions, seroconversion, and virus shedding. Thirty-six 7-wk-old turkeys were distributed into three groups. Eighteen turkeys were inoculated oculonasally with APV/Colorado, six were placed in contact at 1 day postinoculation (DPI), and 12 served as noninoculated controls. Tracheal swabs and blood samples were collected at 3, 5, 7, 10, 14, and 21 DPI. Tissues were collected from three inoculated and two control turkeys on aforementioned days for pathologic examination and APV isolation. Inoculated turkeys developed respiratory disease, yielded APV at 3, 5, and 7 DPI, and seroconverted at 10 DPI. Contact turkeys yielded APV at 7 and 10 DPI. No gross lesions were observed in the turbinates, infraorbital sinuses, and trachea. However, microscopic examination revealed acute rhinitis, sinusitis, and tracheitis manifested by congestion, edema, lymphocytic and heterophilic infiltration, and loss of ciliated epithelia. The inflammatory lesions were seen at 3 DPI and became extensive at 5 and 7 DPI. Active regenerative changes in the epithelia were seen at 10 and 14 DPI. Serologic survey for the presence of antibodies in commercial turkeys (24,504 sera from 18 states) and chickens (3,517 sera from 12 states) to APV/Colorado showed seropositive turkeys in Minnesota, North Dakota, and South Dakota and no seropositive chickens. This report is the first on the isolation of an APV and APV infection in the United States.     

鸡白痢沙门氏菌鸡胚感染模型建立方法的筛选

为筛选出理想的鸡白痢沙门氏菌宿主感染模型的建立方法,本研究通过选择不同接种方式配合不同菌液浓度接种不同胚龄鸡胚建立感染模型,将90枚SPF鸡胚随机分成9组,每组10枚,分别为A、B、C、D、E、F、G、H、I组,A组为空白对照组,其余各组为模型组,模型组分别以气室接种、蛋壳接触接种的方式对不同胚龄（11和14胚龄）SPF鸡胚接种不同浓度（1×10³、3×10³、9×10³、3×10⁵、9×10⁵ CFU/mL）的鸡白痢沙门氏菌C79-3菌株。每天观察情况直至出雏,待雏鸡孵出后按组分笼饲养,每隔12 h观察1次,连续观察7 d,观察各组雏鸡的临床症状、死亡情况,观察期结束对死亡和存活雏鸡进行剖检、组织病理学检查及鸡白痢沙门氏菌的分离鉴定。结果显示,各模型组均有雏鸡出现明显的鸡白痢病症状并死亡,相较于其他模型组,以11胚龄蛋壳接触感染方式接种9×10⁵ CFU/mL的C79-3菌液的F组和14胚龄气室感染方式接种3×10³ CFU/mL C79-3菌液0.1 mL的H组,鸡胚出壳率较高,可分别达到80%和90%,出壳雏鸡呈现明显鸡白痢病特征,剖检可见肝脏出血、盲肠膨大、卵黄囊吸收不良;组织病理切片可观察到肝脏、盲肠、心脏各有不同程度的损伤,发病率分别100%和88.8%,并且鸡白痢沙门氏菌阳性检出率分别达70%和90%。本研究结果表明,以11胚龄蛋壳接触感染方式接种0.1 mL 9×10⁵ CFU/mL的C79-3菌液和14胚龄以气室感染方式接种0.1 mL 3×10³ CFU/mL的C79-3菌液的两种方法均可用于建立稳定的鸡白痢沙门氏菌宿主感染模型。     

Influence of host lineage on cecal colonization by Campylobacter jejuni in chickens

The resistance to cecal colonization by Campylobacter jejuni was assessed by challenging three crossbred stocks of commercially available broiler chickens. These three stocks, designated A, B, and C, were related as follows: Offspring from four pedigreed grandparent flocks were used as progenitors. Stock B was derived by cross-breeding grandparent 1 with grandparent 3. Stocks A and C were crossbreeds from grandparents 1 and 2 and grandparents 3 and 4, respectively. Campylobacter jejuni were gavaged into 48-hour-old chicks, using the same levels of challenge dose for each of the different chicken stocks. Six days post-challenge, the birds were sacrificed, and cecal contents were plated onto Campylobacter-selective media. Results from two replicate trials with three isolates of C. jejuni indicated that chicken stock A was colonized in only two of 60 ceca, stock B in six of 60, and stock C in 19 of 60 chicken ceca. Statistical analysis of these data indicate that resistance to cecal colonization by C. jejuni was significantly (P less than 0.05) influenced through chicken host lineage.     

Experimental infection of chickens, ducks and quails with the highly pathogenic H5N1 avian influenza virus

Highly pathogenic avian influenza viruses (HPAIV) of the H5N1 subtype have spread since 2003 in poultry and wild birds in Asia, Europe and Africa. In Korea, the highly pathogenic H5N1 avian influenza outbreaks took place in 2003/2004, 2006/2007 and 2008. As the 2006/2007 isolates differ phylogenetically from the 2003/2004 isolates, we assessed the clinical responses of chickens, ducks and quails to intranasal inoculation of the 2006/2007 index case virus, A/chicken/Korea/IS/06. All the chickens and quails died on 3 days and 3-6 days post-inoculation (DPI), respectively, whilst the ducks only showed signs of mild depression. The uninoculated chickens and quails placed soon after with the inoculated flock died on 5.3 and 7.5 DPI, respectively. Both oropharyngeal and cloacal swabs were taken for all three species during various time intervals after inoculation. It was found that oropharyngeal swabs showed higher viral titers than in cloacal swabs applicable to all three avian species. The chickens and quails shed the virus until they died (up to 3 to 6 days after inoculation, respectively) whilst the ducks shed the virus on 2-4 DPI. The postmortem tissues collected from the chickens and quails on day 3 and days 4-5 and from clinically normal ducks that were euthanized on day 4 contained the virus. However, the ducks had significantly lower viral titers than the chickens or quails. Thus, the three avian species varied significantly in their clinical signs, mortality, tissue virus titers, and duration of virus shedding. Our observations suggest that duck and quail farms should be monitored particularly closely for the presence of HPAIV so that further virus transmission to other avian or mammalian hosts can be prevented.     

Effect of coated and non-coated fatty acid supplementation on broiler chickens experimentally infected with Campylobacter jejuni

The aim of this study was to examine whether and to what extent the supplementation of feed with a coated or non-coated mixture of fatty acids (caprylic and capric acid) affects broiler chickens experimentally infected with Campylobacter jejuni. The study was carried out using 48 chickens divided into four experimental groups. Throughout the whole rearing period (1-42 days), the chickens were fed a diet supplemented with 0.25% caprylic and capric acid (1:1), coated or non-coated. At the age of 14 and 28 days, chickens were orally challenged with C. jejuni. At regular time intervals post-inoculation, the shedding of C. jejuni was assayed using quantitative real-time PCR. Both supplements significantly decreased faecal C. jejuni counts by 1.2-4.1 log(10) CFU/g 4 days post-inoculation; after this time period, the effect of medium-chain fatty acids (MCFA) was less pronounced or absent. Campylobacter jejuni counts in excreta samples were significantly lower in chickens fed coated MCFA than in those fed non-coated MCFA. No effect of MCFA on feed intake or growth of chickens was observed. In conclusion, (i) MCFA are active against C. jejuni and (ii) the encapsulation enhanced the efficacy of the acids. These results allow the recommendation of using MCFA as feed additives in chickens, preferably 2-3 days before slaughter.