Gizzard Erosion Research Articles

Prevalence of gizzard erosion among commercial layer chicks in the mining area of Karnataka

An epidemiological study was conducted to determine the prevalence of various disease conditions among commercial layer flocks in the mining area of northern Karnataka. Flocks — 3 younger and 9 adult— showing poor performance were chosen from 6 different multiage commercial layer farms in the mining area for the study. Flock details including, breed, age, clinical history, mortality pattern, body weights and egg production were systematically recorded. In addition, ND-HI titers, IBD and IBV ELISA antibody titers and trace elements (iron, manganese, lead and cadmium) concentrations in feed, water and tissue samples, gross and microscopic lesions were studied. The study revealed gizzard erosion with cumulative mortality of 8.72, 8.3 and 16.83% in 3 flocks aged 2, 4 and 5 weeks, respectively. Anorexia, uneven growth, dullness, 26.83–48.19% lower body weights, droopy wings, ruffled feathers, pasty vents and penguin posture were the predominant clinical signs observed. Feed samples revealed Fe, Mn, Pb and Cd at 1,100–1,200, 240–340, 4.8–5.2 and 0.0–0.16 ppm, respectively; however water samples did not reveal any abnormality. The liver, kidney and gizzard tissues had higher levels of Fe, Mn, Pb and Cd. The study indicated that exposure to higher levels of Fe and Pb trace elements induced oxyradical cell injury leading to immunosuppression and gizzard erosion.

Infection with an apathogenic fowl adenovirus serotype-1 strain (CELO) prevents adenoviral gizzard erosion in broilers

Gizzard erosion in broilers due to an infection with virulent fowl adenovirus serotype 1 (FAdV-1) is an emerging disease. Although experimental studies were performed, a possible prevention strategy was not reported so far. The present study was set up to determine (i) a possible influence of birds’ age at time of inoculation on the pathogenicity of a European FAdV-1 field strain (PA7127), (ii) the virulence of a apathogenic FAdV-1 strain (CELO), and (iii) its capability to protect SPF broilers from adenoviral gizzard erosion caused by the field virus.Oral infection of birds with PA7127 at 1-, 10- and 21-days of life, resulted in reduced weight gain compared to non-infected birds, with significance for birds infected at day-old. Independent of the birds’ age at time of inoculation, clinical signs appearing approximately one week after challenge coincided with gizzard lesions.Birds infected exclusively with CELO at the first day of life did not show any clinical signs or pathological changes in the gizzard, confirming the apathogenicity of this European FAdV-1. A similar result was obtained for birds orally infected at the first day of life with CELO and challenged three weeks later with the pathogenic PA7127 strain. Therefore, complete protection of adenoviral gizzard erosion in broilers by vaccination of day-old birds could be demonstrated for the first time, although virus excretion was detected post challenge. Establishment of an amplification refractory mutation system quantitative PCR (ARMS-qPCR) facilitated the identification of the FAdV-1 strain and presence of challenges virus was confirmed in one sample.

Effect of Moringa oleifera leaf meal on growth performance, apparent digestibility, digestive organ size and carcass yield in broiler chickens

The effects of dietary supplementation of Moringa oleifera leaf meal (MOLM) as a growth promoter on the growth performance, apparent digestibility, digestive organ size, and carcass yield of broiler chickens were investigated. A total of 2400 one-day-old Cobb-500 broiler chicks of mixed sex were randomly allocated to five dietary treatments in six replications of 80 birds per pen. Fresh, green and undamaged mature M. oleifera leaves were collected from a number of trees from the same village to avoid variations in soil micronutrient content; and were grinded to produce MOLM. Dietary treatments were as follows: positive control (+C) with 668g salinomycin and 500g zinc bacitracin per kg of feed; MOLMlow (ML; 1, 3 and 5); MOLMmedium (MM; 3, 9 and 15g); MOLMhigh (MH; 5, 15 and 25g)] per kg of feed; and a negative control (−C; without supplementation). Diets were fed for 35d in starter, grower and finisher phases; and birds were provided feed and water ad libitum. At 35d of age, 12 birds per treatment, two from each replicate pen, were randomly selected, electrically stunned at 70V and killed by cervical dislocation for determination of carcass and organ weights. Bird weight at 7 and 21d of age, birds fed MH had the highest BW, while +C had the lowest (P<0.05). No significant differences were observed in FI between treatments during periods from 0 to 21d and 0 to 35d; FCR was the highest (P<0.05) in birds supplemented with MOLM, except for MM; and was the lowest in those on the +C. Birds in ML had the highest thigh weights, and MH had the lowest (P<0.05). Gizzard erosion score was the lowest in MH and the highest in MM (P<0.001). Mortality rate was the highest (P<0.05) in MH from day 22 to 28 and was the lowest in ML and MM (1.3% vs. 0.21%); and was mainly due to sudden death. There were no significant differences in apparent digestibility for ash, ether extract (EE), crude fiber (CF), crude protein (CP), acid detergent fiber (ADF) and neutral detergent fiber (NDF) among treatments. It was concluded that supplementation of M. oleifera leaf meal up to 25g per kg of feed did not impair nutrient utilization efficiency, but enhanced the bird's genetic potential for growth performance.

Phylogenetic analysis of fowl adenoviruses isolated from chickens with gizzard erosion in Japan.

ABSTRACTThirty-four fowl adenoviruses (FAdVs) isolated from chickens with gizzard erosion (GE) from 1999 to 2010 were characterized phylogenetically together with foreign isolates. The phylogenetic analysis based on part of the hexon gene classified these 34 FAdV isolates into 3 groups: FAdV-1, −8a and 8b, thereby suggesting that FAdVs associated with GEs in chickens are diverse. All 30 FAdV-1 isolates were genetically identical, and they were also identical with FAdV-1 isolates from GEs in chickens in European countries (Germany, Poland, Austria, Hungary and Italy). Thus, the same type of FAdV-1 has been associated with outbreaks of GE in Japanese chickens for the past 10 years, which may have spread from a common ancestor, although the epidemiological relationship is unknown.

Molecular typing of fowl adenoviruses, isolated in Hungary recently, reveals high diversity

Molecular typing of 26 recent fowl adenovirus (FAdV) isolates obtained in Eastern Hungary between 2006 and 2011 was performed. The viruses were isolated on primary chicken embryo liver cell cultures from carcasses of chickens, sent for diagnostic investigation. The isolates were subjected to a PCR to amplify a fragment from the hexon gene. Sequence analysis of the amplicons revealed the presence of all the five FAdV species in the country, among them FAdV-B, which has been barely found in Hungary before. The three strains classified as FAdV-B might represent a novel type within this species, as their nucleotide sequence identity to strain 340 (type FAdV-5) is below the commonly accepted intratype limit. Most of the strains (63%) were classified into species FAdV-E (12 strains) and FAdV-D (7 strains) in the study. Four of the isolates proved to be the mixture of two adenovirus strains belonging to two different FAdV types, in three from these four cases, these two types even belonged to two different species. Analysing the pathological findings bolsters certain established connections between some FAdV types and disease conditions. Gizzard erosion was found in connection with FAdV-1 strains only, and inclusion body hepatitis with FAdV-D and -E strains.

Quantity of virulent fowl adenovirus serotype 1 correlates with clinical signs, macroscopical and pathohistological lesions in gizzards following experimental induction of gizzard erosion in broilers

In the present study day-old specific-pathogen-free (SPF) and commercial broilers with maternally derived fowl adenovirus serotype 1 (FAdV-1) antibodies were orally infected with a European “pathogenic” FAdV-1, isolated from broilers showing signs of gizzard erosion. During the experiment, broilers were observed and weighed daily up to 17 days post infection (dpi). Clinically, both infected groups showed significant decrease of weight compared to respective negative control groups. Birds were examined by necropsy at 3, 7, 10, 14 and 17 dpi. Pathological changes in the gizzards were noticed in both experimentally infected groups from 7 dpi onwards. Macroscopically, erosion of the koilin layer and inflammation or ulceration of the gizzard mucosa were observed. Histologically, presence of FAdV-1 in intranuclear inclusion bodies of degenerated glandular epithelial cells was demonstrated by in-situ hybridization and inflammatory cell infiltration of the lamina propria, submucosa and muscle layer was detected. Tissue samples were investigated by a recently developed real-time PCR and the viral DNA load was calculated from gizzard, liver, spleen and cloacal swabs with the highest amounts of FAdV-1 DNA found in the gizzard. For the first time, successful reproduction of clinical signs in broilers as well as pathological lesions in the gizzard were achieved with a European FAdV-1 isolate displaying some genetic differences to so far reported virulent FAdV-1 from Japan. Furthermore, highest viral load in gizzards could be linked with macroscopical and histological lesions. Therefore, the conducted analyses provide important insights into the pathogenesis of adenoviral gizzard erosion.

Adenoviral Gizzard Erosion in Broiler Chickens in Germany

Avian adenovirus infections cause important disease complexes in chickens, but many of the viruses also infect chickens without resulting in overt disease. Previously several outbreaks of gizzard erosions caused by a fowl adenovirus A serotype-1 (FAdV-1) were reported from Japan. Here we report an outbreak of gizzard erosions in 12 broiler flocks in Germany in 2011. Chickens had a reduced daily weight gain and a higher total mortality rate of up to 8%. The birds showed a severe detachment of the koilin layer and ulcerative to necrotizing lesions of the underlying mucosa. Histopathologically, necrotizing ventriculitis with basophilic, intranuclear inclusion bodies in epithelial cells was diagnosed. Immunohistochemistry, egg culture, and electron microscopic examination revealed adenovirus-like particles in the samples. No concurrent infectious agent could be identified. The virus was genotyped as FAdV-1 by PCR and subsequent sequencing. Phylogenetic analysis of the hexon loop L1 gene yielded 100% sequence identity to the chicken embryo lethal orphan strain. These findings suggest that outbreaks of adenoviral gizzard erosion can lead to significant economic losses in Germany and may be caused by an unusual virulent FAdV-1 strain.

Vertical transmission and clinical signs in broiler breeders and broilers experiencing adenoviral gizzard erosion

The present report documents an outbreak of adenoviral gizzard erosion in 22 broiler flocks in Germany. The clinical picture was characterized by uneven growth of affected broilers that resulted in considerably lower than average weight at slaughtering. Fowl adenovirus serotype 1 (FAdV-1) was isolated from gizzard lesions and histological examinations demonstrated FAdV-1-positive intranuclear inclusion bodies in gizzard epithelial cells of affected broilers by in-situ hybridization. Birds from all affected flocks originated from one broiler breeder farm. During production of affected birds, broiler breeders were between 27 and 32 weeks old. Enzyme-linked immunosorbent assay and specific virus neutralization assay of sera from parent birds demonstrated an acute FAdV-1 infection within the first 5 weeks of the production cycle. Clinically, broiler breeders exhibited a moderate fall in the hatchability of their chicks, while egg production remained normal. No further clinical signs could be observed. Genetically identical FAdV-1 strains were isolated from gizzards of embryos at the lowest point of hatchability and from affected broiler flocks raised on independent farms. For the first time, direct detection of viable FAdV-1 from gizzards of embryos and progenies of one FAdV-1-seropositive broiler breeder farm in the course of an outbreak of adenoviral gizzard erosion could be demonstrated, highlighting the importance of vertical transmission of this disease. Additionally, growth retardation and subsequent reduced average weight at the time of slaughter of broiler chickens underline the economic impact of adenoviral gizzard erosion for poultry production.

Biology of fowl adenovirus type 1 infection of heterologous cells

The JM1/1 strain of fowl adenovirus (FAV) serotype 1 isolated from gizzard erosion was used to investigate the biology of FAV in homologous (susceptible) and heterologous cells. The FAV JM1/1 strain is capable of efficient multiplication in primary chicken kidney (CK) cells, but not in Crandell-Rees feline kidney (CRFK) cells or Vero cells. FAV adsorption in heterologous cells was slightly higher than in CK cells. An early gene encoding a DNA-binding protein and a late gene encoding the hexon protein were expressed in CK cells. Only the early gene was expressed in Vero cells. Neither of these genes was expressed in CRFK cells. These results suggest that the virus was unable to multiply effectively due to suppression of viral gene expression in the heterologous cells used in this study.

First Report of Coccidiosis and Gizzard Erosion in a Zebra Finch (Taeniopygia guttata) of Iran

Coccidiosis and gizzard erosion are rare conditions in cage bird. A male zebra finch was presented with a history of watery diarrhea, anorexia, ruffled feathers, weight loss, and lethargy and died finally. Gross necropsy revealed small areas of erosions and hemorrhages on the gizzard wall. The intestine was oedematous. The spleen appeared pale and small. The testes were asymmetric.Histologically, necrosis of mucosal layer with infiltration of inflammatory cells observed in cecum. Eimeria stages were detected in the enterocytes. In Gizzard, hemorrhage and ulceration of mucosal layer with infiltration of polymorphonuclear cells in to the underlying mucosa were seen. In hepatic tissue, mild focal necrosis with mononuclear cells infiltration was seen. The disease was diagnosed as coccidiosis and gizzard erosion.

Outbreak of gizzard erosion associated with fowl adenovirus infection in Korea

The pathogenicity of a fowl adenovirus serotype-1 (FAdV-1, K181 strain) isolated from a case of gizzard erosion in layer chickens was investigated in specific-pathogen-free (SPF) chicks. One-week-old SPF chicks were inoculated orally or intramuscularly with the isolate of FAdV-1 and euthanized for necropsy at 7, 14, and 21 d postinoculation. Although there were no clinical signs after inoculation, gizzard erosions were observed grossly and the virus was recovered from the gizzards in the inoculated chickens. Histologically, in the chickens that were infected orally, the lesions found in the gizzard consisted of severe degeneration and necrosis of glandular epitheliums and eosinophilic inclusion bodies. These results indicate that the Korean FAdV-1 isolate could induce gizzard lesions in chickens. Moreover, the present investigation reproduced an outbreak of gizzard erosion caused by FAdV-1 infection and, for the first time, described the isolation of FAdV-1 from chickens in Korea. These findings provide important information on the epidemiology and pathogenesis of FAdV-1 infection in chickens.

Non-soluble fibres and narasin reduce spontaneous gizzard erosion and ulceration in broiler chickens

The prevalence and severity of gizzard erosion and ulceration syndrome (GEU) in broilers is affected by a number of predisposing and preventive factors. Two broiler experiments with almost identical basal diets were conducted to investigate the effect of dietary oat hulls, access to litter and the antimicrobial compound narasin on GEU. The effects on particle size of duodenal digesta, ileal starch concentration, caecal Clostridium perfringens counts, necrotic enteritis and production performance were also examined. Oat hulls reduced GEU severity and starch levels in the ileum in both experiments. Access to litter reduced GEU scores when oat hulls were included in the feed. Access to litter also improved feed efficiency and reduced C. perfringens counts. Narasin reduced GEU severity when the feed was supplemented with oat hulls. Oat hulls were associated with improved feed efficiency in Experiment 1 and impaired feed efficiency in Experiment 2. The inconsistent effect of oat hulls on production performance appeared to be related to an association between oat hulls and high C. perfringens counts in Experiment 2; an association that was absent in Experiment 1. In general, oat hulls interacted with litter access and narasin in exerting a positive effect on gizzard health. However, the association between oat hulls and necrotic enteritis detected in Experiment 2 suggests that the positive effect of oat hulls on GEU occasionally may be outweighed by a negative effect on gut health. In conclusion, our findings demonstrate that the severity of GEU in broilers was influenced by non-soluble fibres and narasin.

Effect of direct-fed microbials on performance and Clostridium perfringens colonization of turkey poults

Clostridium perfringens is recognized as an enteric pathogen in humans, domestic animals, and livestock. This organism is associated with necrotic enteritis, gangrenous dermatitis, clostridial dermatitis (turkeys), and gizzard erosions in poultry. This study was conducted to evaluate the effectiveness of a direct-fed microbial (DFM), Primalac (Star Labs, Clarksdale, MO), in preventing intestinal colonization of turkey poults with C. perfringens. One-day-old turkey poults (n = 128) were randomly divided into 4 treatments with 4 replicates (8 birds/pen). Treatments were as follows: 1) basal diet without DFM (C); 2) basal diet supplemented with Primalac (1.5 kg/ton; PM); 3) basal diet with poults gavaged with C. perfringens (CCP); and 4) basal diet supplemented with Primalac and poults gavaged with C. perfringens (PMCP). Feed and water were provided ad libitum throughout the trials, and birds were inoculated with C. perfringens (10(8)cfu/mL) on d 3 and 7. On d 21, 2 birds/pen were killed, spleen and bursa of Fabricius were collected and weighed, and cecal contents were used for C. perfringens enumeration. Feed consumption, BW, and feed conversion were calculated throughout the trial (weekly and cumulatively). Data were analyzed using GLM of SAS (SAS Institute, Cary, NC; P < 0.05). Among the inoculated groups, birds fed the DFM-supplemented diet had significantly lower cecal C. perfringens counts than the birds fed the diet without the DFM. The C. perfringens (log(10) cfu/g) in ceca were as follows: C, 5.88; CCP, 7.26; PM, 5.35; PMCP, 6.19 ± 0.36. No differences were observed for BW (814 ± 11 g), feed conversion (1.33 ± 0.03), organ weights, or relative organ weights. Further studies are needed to fully ascertain the potential of using DFM to reduce the numbers of C. perfringens in the gastrointestinal tract of turkey poults.

Molecular characterization of fowl adenoviruses isolated from chickens with gizzard erosions

Broiler chickens with clinical signs of uneven growth, depression, and dull feathers were submitted to our laboratory and, at necropsy, lesions in proventriculus, gizzard, and intestines were detected. Fowl adenovirus serotype 1 (FAdV-1) was isolated from digestive tissues. The virus, assigned as FAdV-PL/G068/08, showed 99.5% nucleotide homology and 99.2% amino acid homology in hexon gene with chicken embryo lethal orphan (CELO) strain classified as the European reference of FAdV-1. One-day-old and 21-d-old SPF chickens were inoculated with FAdV-PL/068/08 by both nasal and ocular routes and then observed daily and examined by necropsy at 6, 10, and 14 d postinoculation. Experimental infection with isolated virus was fatal for younger chickens and major lesions occurred in the gizzards. No clinical or pathological changes were observed in chickens infected at 21 d of age, but the presence of intranuclear inclusion bodies in gizzard epithelial cells was detected. Molecular characterization was based on the long and short fibers genes sequencing and comparison of obtained sequences with other FAdV-1 strains. The homology between FAdV-PL/G068/08 and other sequences available in GenBank was between 98.9 and 99.8% (short fiber region) and 99.0 and 99.7% (long fiber region) at nucleotide level and between 98.4 and 100% (short fiber region) and 99.3 and 99.9% (long fiber region) at amino acid level. No correlation between identified amino acid changes in short and long fiber proteins and pathogenicity of studied FAdV-1 strains was observed. Although short and long proteins were indicated as factors influencing virus pathogenicity, the role of identified sequence differences in infectivity determination remain unclear.

Comparison of the Fibers of Fowl Adenovirus A Serotype 1 Isolates from Chickens with Gizzard Erosions in Europe and Apathogenic Reference Strains

A total of 18 samples from 4 outbreaks of gizzard erosions in broiler chickens in Europe were used in the current study. Fowl adenoviruses were found in samples from all 4 outbreaks, and isolates were identified as Fowl adenovirus A (FAdV-A) serotype 1. As described earlier, polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis of the long fiber gene was conducted. However, all 18 samples showed the same pattern as apathogenic FAdV-1 strains: Ote and chicken embryo lethal orphan (CELO) viruses. Nucleotide and amino acid sequences of the long and short fiber of several isolates from broiler chickens with gizzard erosions were analyzed, and 100% identity between the field isolates on the protein level was revealed. Only 1 nonsynonymous mutation (T→A) was present in the long fiber of studied isolates compared to the CELO strain. The same mutation was also present in the Ote strain. Four nonsynonymous mutations were present in the long fiber of studied isolates compared to Ote strain. In the short fiber, 6 nonsynonymous mutations were found in the studied isolates compared to the CELO strain. However, the short fiber of pathogenic isolates was 100% identical to apathogenic Ote strain. In conclusion, the usefulness of PCR-RFLP analysis of the long fiber gene of FAdV-1 isolates in distinguishing between those that induce gizzard erosions and those that do not remains questionable for the isolates obtained from European poultry flocks. The role of certain FAdV-1 strains with their long and short fiber in pathogenicity regarding gizzard erosions is still not clear.

VITAMIN B12 and gizzard erosions in chicks.

VITAMIN B12 and gizzard erosions in chicks.

Synthesis of (S)‐Gizzerosine (I), a Potent Inducer of Gizzard Erosion in Chicks.

AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.

若齢肉用鶏群における鶏アデノウイルス感染による筋胃びらんの発生および再現試験

Gizzard erosion of broiler chicks accompanied by severe hemorrhage and sudden death at two to three weeks of age was investigated virologically and serologically. Fowl adenovirus serotype 1 (FAV1) was isolated from the affected gizzard, and an antibody to FAV1 was detected with higher positive rates in this and nearby farms, but not in remote farms, suggesting FAV1 had already invaded some farms around this farm. The pathogenicity of the present FAV1 isolated to broiler chicks with maternal antibody was shown to be almost same as FAV1 isolated from a slaughtered bird previously. The factors influencing the occurrence of gizzard erosion in young broiler chicks have not been cleared, but could involve subclinical gizzard erosions due to FAV1 infection at early ages of broiler.

Reproduction of Adenoviral Gizzard Erosion by the Horizontal Transmission of Fowl Adenovirus Serotype 1

The horizontal transmission ability of fowl adenovirus (FAV) serotype 1 99ZH strain, isolated from chickens exhibiting gizzard erosion, was investigated. Twelve 13-day-old specific pathogen-free chickens were inoculated orally with 10(6) TCID(50)/0.05 ml of the strain. An in-pen contact group (chickens in the same pen with inoculated chickens), hedge contact group (chickens in a pen connected with pens housing inoculated chickens), non-contact group (chickens in a separate pen placed at a distance of 70 cm from the connected pens), human exposure group (chickens in the next room and attended last every day) and negative control group were examined. Each group consisted of 11 or 12 uninoculated chickens. Gizzard lesions were grossly or histologically observed from 10 days after exposure (DAE) in the in-pen contact group, and from 15 DAE in the hedge contact and non-contact groups. The FAV gene was detected by polymerase chain reaction performed on cloacal swabs taken on 5 and 13 DAE from chickens in both contact groups, and on 20 and 26 DAE from those in the non-contact group. Serum neutralizing antibodies against FAV serotype 1 were detected in chickens from 13 and 26 DAE in both contact groups and in the non-contact group, respectively. In the human exposure and negative control groups, no infection was observed. We conclude that FAV-99ZH strain spreads rapidly through direct contact with inoculated chickens, and slowly through non-contact transmission, and that adenoviral gizzard erosion is reproduced by this horizontal transmission.

Characterization of Monoclonal Antibodies Against Fowl Adenovirus Serotype 1 (FAV1) Isolated from Gizzard Erosion

Six clones of monoclonal antibodies (Mabs) to fowl adenovirus (FAV) serotype 1 were produced. All Mabs reacted positively by enzyme-linked immunosorbent assay. Three Mabs recognized the putative 100-kD hexon protein and reacted to serotype 1 specifically by western blot analysis but did not react to other FAV serotypes (2, 3, 4, 5, 6, 7, and 8a). These Mabs will be useful for immunodiagnosis of FAV serotype 1 infection in chickens with gizzard erosion and in further research studies involving the genomes and proteins of FAV serotype 1.