Co-expulsion of Ascaridia galli and Heterakis gallinarum by chickens

Stehr, Manuel; Sciascia, Q.; Metges, C. C.; Gauly, Matthias; Daş, Gürbüz

doi:10.1016/j.ijpara.2018.05.014

Cited by 16 publications

(37 citation statements)

References 81 publications

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“…The presence of H. gallinarum and H. meleagridis was negatively associated, whereas Heterakis-harboring birds were about 2.7 times more likely to harbor A. galli , too. The positive association between co-existence of the two nematodes in the same host might be attributed to the similar cell-mediated host immune responses to both nematodes [ 24 ]. There was no significant interaction between co-existence of A. galli and H. meleagridis .…”

Section: Discussionmentioning

confidence: 99%

“…For this, eggs of A. galli and H. gallinarum were isolated from worms harvested from free-range chickens. The preparation techniques and incubation conditions for the infection material have previously been described by Stehr et al [ 24 ]. On the day of infection, the incubation media of both A. galli and H. gallinarum eggs were separately filtered through a sieve (36 µm mesh size), which was followed by rinsing to collect the washed eggs in saline solution (NaCl, 0.9%).…”

Section: Methodsmentioning

confidence: 99%

“…The quantification of tissue-associated A. galli larvae was restricted to the jejunal section, which is the main preferred site of larval stages [ 27 ]. The procedure for larval recovery using the EDTA-incubation method has been described elsewhere [ 24 ].…”

Section: Methodsmentioning

confidence: 99%

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Excretion of Histomonas meleagridis following experimental co-infection of distinct chicken lines with Heterakis gallinarum and Ascaridia galli

et al. 2021

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Background Histomonosis is a severe re-emerging disease of poultry caused by Histomonas meleagridis, a protozoan parasite which survives in the environment via the cecal worm Heterakis gallinarum. Following infection, the parasites reside in the ceca and are excreted via host feces. In the present work, male birds of conventional broiler (Ross 308, R), layer (Lohmann Brown Plus, LB) and a dual-purpose (Lohmann Dual, LD) chicken line were infected with 250 embryonated eggs of Ascaridia galli and Heterakis gallinarum, respectively, with the latter nematode harboring Histomonas meleagridis, to investigate a co-infection of nematodes with the protozoan parasite in different host lines. Methods In weekly intervals, from 2 to 9 weeks post infection (wpi), individual fecal samples (n = 234) from the chickens were collected to quantify the excretion of H. meleagridis by real-time PCR and to determine the number of nematode eggs per gram (EPG) in order to elucidate excretion dynamics of the flagellate and the nematodes. This was further investigated by indirect detection using plasma samples of the birds to detect antibodies specific for H. meleagridis and worms by ELISA. The infection with H. meleagridis was confirmed by histopathology and immunohistochemistry to detect the flagellate in the cecum of representing birds. Results The excretion of H. meleagridis could already be observed from the 2nd wpi in some birds and increased to 100% in the last week of the experiment in all groups independent of the genetic line. This increase could be confirmed by ELISA, even though the number of excreted H. meleagridis per bird was generally low. Overall, histomonads were detected in 60% to 78% of birds with temporary differences between the different genetic lines, which also showed variations in the EPG and worm burden of both nematodes. Conclusions The infection with H. gallinarum eggs contaminated with H. meleagridis led to a permanent excretion of the flagellate in host feces. Differences in the excretion of H. meleagridis in the feces of genetically different host lines occurred intermittently. The excretion of the protozoan or its vector H. gallinarum was mostly exclusive, showing a negative interaction between the two parasites in the same host. Graphic abstract

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Excretion of Histomonas meleagridis following experimental co-infection of distinct chicken lines with Heterakis gallinarum and Ascaridia galli

et al. 2021

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“…Nematode eggs used as the infection material were collected from worms of naturally infected free-range chickens. Incubation conditions for embryonation of the nematode eggs and the preparation of the final infection inoculum have been described in detail elsewhere ( 25 ). The percentage of incubated, fully embryonated eggs considered infectious was determined ( 26 ).…”

Section: Methodsmentioning

confidence: 99%

“…In brief, the small intestine was opened longitudinally and the intestinal content was washed through a sieve (36 μm) under running water to collect mature and immature stages of A. galli from the intestinal lumen. The tissue-associated A. galli larvae were recovered by using a modified EDTA (10 mM EDTA, 0.9% NaCl)-incubation method for digesting intestinal tissue overnight at 40°C, followed by sieving ( 25 , 27 , 28 ). H. gallinarum was harvested from the caecal lumen contents only as described for A. galli from the small intestine.…”

Section: Methodsmentioning

confidence: 99%

Impact of Nematode Infections on Non-specific and Vaccine-Induced Humoral Immunity in Dual-Purpose or Layer-Type Chicken Genotypes

et al. 2021

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Nematode infections may induce immune-modulatory effects and influence host-immune responses to other pathogens. The aim of the study was to investigate whether a mixed nematode-infection influences non-specific and vaccine-induced humoral immunity against Newcastle Disease Virus (NDV), Infectious Bronchitis Virus (IBV), and Avian Metapneumovirus (AMPV) in already vaccinated hens of a dual-purpose (Lohmann Dual, LD) or a layer genotype (Lohmann Brown Plus; LB). Until 17 weeks-of-age, LD (n = 70) and LB (n = 109) hens were vaccinated against major bacterial and viral diseases and coccidiosis. At 24 weeks-of-age, the hens received either a placebo or an oral inoculation of 1,000 infectious eggs of A. galli and H. gallinarum. Plasma total immunoglobulin (Ig) isotypes (IgY, IgM, IgA) levels and vaccine-induced antibody titers against NDV, IBV, and AMPV were determined from 2 to 18 weeks post-infection (wpi). Infections had no suppressing effect on total Ig isotypes IgY, IgM, and IgA as well as on vaccine-induced antibody titers against NDV, IBV, and AMPV (P > 0.05). Overall, LB hens had higher levels of IgY, IgM, and IgA than those of LD hens (P < 0.05). There were no differences between IBV titers of the two genotypes (P > 0.05). Independent of infection status of the hens, NDV titers were higher in LB hens than in LD hens at wpi 2 (P < 0.05), but not in following weeks (P > 0.05). Uninfected LD hens had lower AMPV titers than their infected counterparts at 6 and 14 wpi (P < 0.05). Regardless of nematode infection, LD hens revealed a higher risk of responding weak to vaccination against NDV (odds ratio = 5.45; P = 0.021) and AMPV (odds ratio = 13.99, P < 0.001) than did LB hens (P > 0.05). We conclude that nematode infections have no adverse effects on non-specific and vaccine-induced humoral immunity in either genotype. LB hens have higher levels of total immunoglobulin isotypes than LD hens. Except for IBV, vaccine-induced humoral immune responses show a dependency on genotype. Dual-purpose hens show lower responsiveness to vaccinations against NDV and AMPV, possibly due to factors associated with increased body fat reserves in this genotype.

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Ascaridia galli infection in chicken: Pathobiology and immunological orchestra

Shohana,

Rony,

Ali

et al. 2023

Immunity Inflam & Disease

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BackgroundAscaridia galli is the largest gut‐dwelling helminth of chickens, which confers adverse effects on meat and egg production; thus, on the animal protein supply and the economy. Both adult and immature parasites affect gut health, but larval stages play a major role in pathology.AimsHere, we present immunology and pathology of A. galli in chickens.Materials and MethodsLiteratures were surveyed through online platforms such as PubMed, Google Scholar and Researchgate.ResultsThe larvae cause excessive mucus production, damage to the intestinal gland, hemorrhage, anemia, diarrhea, and malnutrition. The adult worms can cause death by intestinal obstruction and intussusception. Although both cellular and humoral immunity are involved in fighting against ascariasis, the role of naturally acquired immunity is poorly defined. In cellular immunity, Th‐2 cytokines (IL‐4, IL‐5, IL‐9, and IL‐13), goblet cells (mucin), gut‐associated lymphoid tissues, CD8α+ intraepithelial cells, TCRγδ + T cells, and TGF‐β4 form a protective band. Type 2 immunity provides protection by forming a network of endogenous damage‐associated molecular patterns, chitin, and parasitic antigens. Among antibodies, IgY is the most prominent in chickens and provides temporary humoral protection. During parasitic infection, infiltration of various immune cells is evident, especially in the intestinal epithelium, lamina propria, and crypts of the duodenum and jejunum. In chickens older than 12 weeks, gradual reduction of worm burden is more successful than the younger birds. Female chickens exert a short‐lived but higher level of protection by passing IgY to chicks in the form of egg yolk antibodies. In laying conditions, immunity differs between breeds. This review provides an overview of the silent but inevitable pathological changes induced by A. galli and the interaction of host immunity with the parasite.

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Co-expulsion of Ascaridia galli and Heterakis gallinarum by chickens

Cited by 16 publications

References 81 publications

Excretion of Histomonas meleagridis following experimental co-infection of distinct chicken lines with Heterakis gallinarum and Ascaridia galli

Excretion of Histomonas meleagridis following experimental co-infection of distinct chicken lines with Heterakis gallinarum and Ascaridia galli

Impact of Nematode Infections on Non-specific and Vaccine-Induced Humoral Immunity in Dual-Purpose or Layer-Type Chicken Genotypes

Ascaridia galli infection in chicken: Pathobiology and immunological orchestra

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