Consequences of Concurrent Infections with Ascaridia Galli and Eimeria in Broiler Chickens

Abstract

Ascaridia galli and Eimeria species constitute the aetiology of ascaridosis and coccidiosis respectively in chickens, and the two diseases are the most important internal parasitic infections that militate against the development of the poultry industry.  Natural infections of both parasites are known to occur in chickens but it is not yet fully known how conjoint infections with both parasites can influence the pathology they inflict cause to the chickens.  A. galli has been reported to enhance the pathogenicity/pathology of Pasteurella multocida and Escherichia coli when the organisms occurred concurrently with the nematode.  This study was therefore conducted to investigate the influence of A. galli to the response of two-week old broiler chickens to single and concurrent infections with the parasites either given at the same time or at different times with the hope that the results would greatly inform decisions to be taken in mitigating the infections.

Forty two broiler chickens were used for the study.  The birds were allocated into six groups of 7 birds each and placed in separate pens.  Five of the groups were either infected with A. galli only, caecal Eimeria isolate only,  A. galli  and caecal Eimeria isolate at the same time, A. galli and later caecal Eimeria isolate or caecal Eimeria isolate and later A. galli while the sixth group remained as uninfected controls.  The dose levels used were 1000 embryonated A. galli eggs and 12,000 sporulated Eimeria oocysts per chicken by oral administration.  Packed cell volume (PCV), body weight (BW), feed consumption (FC), faecal egg counts (EPG), faecal oocyst counts (OPG), caecal gross lesion score (GLS) for Eimeria infected birds, clinical signs and worm burdens (WB).  The infections had a negative impact on the birds evident by low PCV, low BW gain, reduced feed consumption, listlessness, bloody diarrhoea and mortalities when compared with the uninfected controls that did not exhibit such effects. 

A drop in the PCV from day 8 to day 12 of the birds infected with A. galli and later Eimeria group occurred following the administration of the protozoan infection.  The A. galli and later Eimeria group also had the least weight gain from day 12 to day 42.  Similarly their feed intake was also least from day 10 to day 26 in the A. galli and later Eimeria group in comparison with all the other infected and the uninfected control birds.  The greatest mortalities (5 birds) also occurred in the A. galli and later Eimeria group.

It was concluded that the infections lead to poor performance of the chickens, however, the effect of the infection was severest in the chickens that were infected with A. galli and later with Eimeria.  It was suggested that A. galli caused immunedownregulation of the chickens allowing the Eimeria to exert maximally its pathogenic effects on the birds.  It was also suggested that the initial A. galli infection possibly attracted influx of large numbers of macrophages into the lamina propria where they in turn greatly enhanced the transportation of sporozoites from the lamina propria into the glands of Lieberkuhn.  EPG, OPG and worm counts were not so high suggesting that both A. galli and Eimeria somewhat inhibit each other to an extent.  It is therefore strongly recommended that the infections should be diagnosed regularly and controlled promptly when present particularly if they are concurrent as the effects can be disastrous in situations where A. galli infections precede Eimeria infections as in the semi intensive and free range systems of poultry production.