Cloned Histomonas meleagridis passaged in vitro resulted in reduced pathogenicity and is capable of protecting turkeys from histomonosis

Heß, Michael; Liebhart, Dieter; Grabensteiner, Elvira; Singh, Amarjit

doi:10.1016/j.vaccine.2008.05.071

Cited by 46 publications

(52 citation statements)

References 22 publications

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“…Furthermore, the mean lesion scores of the surviving birds were higher in the IM group than in the INC (infected non-immunized control) group, suggesting that immunity induced by dead antigens is not protective against histomonosis. These findings are supported by the results of Hess et al (2008).…”

Section: Discussionsupporting

confidence: 82%

“…Furthermore, a degree of protection against intracloacal challenge with H. meleagridis and against an oral challenge with H. meleagridis-contaminated Heterakis gallinarum eggs was detected after young turkeys were vaccinated with attenuated cultures of H. meleagridis (Tyzzer, 1933(Tyzzer, , 1934(Tyzzer, , 1936Lund et al, 1966). Recently, cloned attenuated H. meleagridis has been shown to induce protection against an intracloacal challenge (Hess et al, 2008). However, examination of the immune response was not included in these studies so it was not possible to link this protection to a systemic or mucosal immune response.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, intramuscular vaccination with inactivated, cloned H. meleagridis was also unable to cause protection (Hess et al, 2008). In contrast, attempts to vaccinate turkeys with in vitro attenuated H. meleagridis have led to partial or even complete protection (Tyzzer, 1933(Tyzzer, , 1934(Tyzzer, , 1936Lund et al, 1966;Hess et al, 2008), although the effector mechanisms of this protective immunity remain unclear. In 1963, Clarkson investigated the protective value of antibodies against this parasite.…”

Section: Introductionmentioning

confidence: 99%

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Passive immunization againstHistomonas meleagridisdoes not protect turkeys from an experimental infection

Bleyen

Ons

Gussem³

et al. 2009

Avian Pathology

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Histomonosis or blackhead is a disease of gallinaceous birds, caused by the protozoan Histomonas meleagridis. As recent regulatory action has removed almost all drugs against this disease from the European market, the development of new prophylactics has become crucial. Identification of the protective immune mechanism would facilitate the choice and development of a vaccination strategy to prevent histomonosis. In this study, turkeys were either actively or passively immunized and were then challenged to assess the role of antibody-mediated immunity in the protection form this disease. Active immunization was performed either by experimental infection and treatment or by intramuscular injection with lysed H. meleagridis. Passive immunization was attempted by intraperitoneal administration of pooled, concentrated, neutralizing antisera from immunized donor animals to naive turkeys. A significantly higher IgG response was observed after infection and treatment than after intramuscular injection, which in turn was higher than the responses of placebo and control birds. While active immunization of turkeys by intramuscular injection of dead H. meleagridis antigens appeared not to be protective against histomonosis, immunization by infection and treatment did induce protection. However, no significant level of protection could be observed in the passively immunized birds. These results suggest that serum antibodies to H. meleagridis may not be a key component in the protection against this parasite. It is, however, possible that the concentration of antibodies at the mucosal site is insufficient. Therefore, further investigation on mucosal immune responses is necessary.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Passive immunization againstHistomonas meleagridisdoes not protect turkeys from an experimental infection

Bleyen

Ons

Gussem³

et al. 2009

Avian Pathology

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“…Clonal cultures were established through micromanipulation (Hess et al, 2006b). The screening was carried out on available low passage numbers of the clonal cultures, since it is well known that pathogenicity declines with increasing passages (Tyzzer, 1936;Hess et al, 2008). All experiments were performed in 2 ml Eppendorf tubes using protozoal cultures propagated for 48 h in Medium 199 supplemented with Earle's salts, L-glutamine, 25 mM HEPES, L-amino acids (M199; Gibco † , Invitrogen TM , Lofer, Austria), 2 mg/ml rice starch (Sigma-Aldrich, Vienna, Austria) and 15% foetal calf serum (Gibco † , Invitrogen TM ) at 408C prior to testing.…”

Section: Methodsmentioning

confidence: 99%

Antihistomonal effects of artemisinin andArtemisia annuaextractsin vitrocould not be confirmed byin vivoexperiments in turkeys and chickens

et al. 2012

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Five different Artemisia annua-derived materials (i.e. dry leaves, pure artemisinin, and hexane, dichloromethane or methanol extracts of leaves) were screened for their in vitro activities against six clonal cultures of Histomonas meleagridis. Except for the methanol extract, all tested materials displayed in vitro activity against all tested protozoal clones. Neither the dry plant material, extracts nor artemisinin showed any antibacterial activity against the xenic bacteria accompanying the six H. meleagridis clones at concentration levels identical to the antihistomonal setting. The dichloromethane extract of dry leaves (Ext-DCM) (minimal lethal concentration01.0 mg/ml) and artemisinin (half-maximal inhibitory concentration 01.295 mg/ml) had the most promising antihistomonal properties and were therefore subsequently tested in a standardized experimental infection model in both turkeys and chickens infected with clonal H. meleagridis. There were no differences between treatment groups, where all infected turkeys showed severe clinical histomonosis and demonstrated severe typhlohepatitis typical for histomonosis. Consistent with the infection model used, the infected chickens did not show any adverse clinical signs but contracted severe lesions in their caeca 7 and 10 days post infection (d.p.i.), liver lesions were absent to mild after 7 d.p.i. and progressed to severe lesions at 10 d.p.i.; thus no differences between treatment groups were observed. In conclusion, neither artemisinin nor Ext-DCM was able to prevent experimental histomonosis in turkeys and chickens at the given concentrations, which is contrary to the antihistomonal effect noticed in vitro even though the same clonal culture was used. The results of this study therefore clearly demonstrate the importance of defined in vivo experimentation in order to assess and verify in vitro results.

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“…Unfortunately, to date, efficacy of these products could not be demonstrated under experimental conditions (van der Heijden & Landman, 2008a, 2008bThofner et al, 2012). In parallel, other scientists have chosen a more conventional approach, that is, vaccinology to solve the "histomonas problem" (Hess et al, 2008;Liebhart et al, 2010;Nguyen Pham et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Quantification of parasite shedding and horizontal transmission parameters inHistomonas meleagridis-infected turkeys determined by real-time quantitative PCR

et al. 2015

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To gain more insight into the within flock transmission of Histomonas meleagridis, the shedding of parasites was quantified by a newly developed real-time quantitative (q)PCR and the basic reproduction number (R 0 ) and the mean number of secondary infections per infectious bird per day in a susceptible population (β) of H. meleagridis in the absence of heterakis were assessed. Forty turkeys were divided into two groups of 10 and 30 birds at 14 days of age. Birds of the first group were inoculated with 200,000 histomonads each, the second group served as a susceptible contact group. Cloacal swabs were taken at −1, 1, 4, 7, 9, 11, 14, 18 and 21 days post inoculation (p.i.) to assess the shedding of the parasite by the qPCR (detection limit 330 histomonads/ml droppings). The experiment ended at 28 days p.i. Mortality was 100% in the inoculated birds and started at day 12 p.i., while in the contacts, it was 83% and started at 16 days p.i. Shedding started 1 day after the inoculation in both groups. The mean shedding levels (and 95% CI) expressed as parasite equivalents per gram cloacal content on a log 10 scale in the inoculated, contact birds that died and contact birds alive were 2.0 (1.6-2.4), 1.6 (1.4-1.9) and 1.2 (0.5-2.0), respectively. Birds that died shed histomonas more often and were infectious for 13.4 days; in contrast, those that recovered were infectious for 5.7 days. R 0 was estimated to be 8.4 and β 0.70. Simulations made with the parameters obtained were in agreement with the experimental results, confirming their validity.

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Cloned Histomonas meleagridis passaged in vitro resulted in reduced pathogenicity and is capable of protecting turkeys from histomonosis

Cited by 46 publications

References 22 publications

Passive immunization againstHistomonas meleagridisdoes not protect turkeys from an experimental infection

Passive immunization againstHistomonas meleagridisdoes not protect turkeys from an experimental infection

Antihistomonal effects of artemisinin andArtemisia annuaextractsin vitrocould not be confirmed byin vivoexperiments in turkeys and chickens

Quantification of parasite shedding and horizontal transmission parameters inHistomonas meleagridis-infected turkeys determined by real-time quantitative PCR

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