THE IMPACT OF COCCIDIAL DRUG-RESISTANCE ON THE COMMERCIAL PERFORMANCE OF BROILERS
R. B. Williams
Coxitec Consulting, Hertfordshire, UK
E-mail address: ray.coxitec@tesco.net
Coccidial
drug-resistance is often said to be a serious problem to the chicken industry,
but broiler performances indicate that resistant parasites are often tolerated
by the host. How can this be? The present retrospective synthesis of laboratory
and field studies of coccidial drug-resistance, population dynamics and
epidemiology is instructive. Some synthetic or ionophorous anticoccidial drugs
may control clinical coccidioses while allowing some oocyst “leakage”. This
phenomenon, when there has been no prior exposure of coccidia to a particular
drug, reflects a fundamental drug-parasite interaction which Ryley (1980) termed
“drug insensitivity”. True drug-resistance involves selection.
Williams (1972) demonstrated pre-existing mutants in coccidial populations,
selectable during a single life cycle in the presence of the synthetic quinolone,
decoquinate. This was termed “inherent resistance”, distinguished from
“acquired resistance”, a gradual physiological adaptation over several
generations facilitating preferential survival of the least sensitive
individuals, not necessarily mutants. Ionophores, which affect ion transport
across cell membranes, are fundamentally different from chemicals active against
cofactor synthesis or electron transport. Selection of physiological variants
during a single passage in monensin-medicated birds results in far less
reduction in sensitivity than selection of decoquinate-resistant mutants
(Williams, 1998). Thus, ionophore-resistance is probably “acquired”, and
quinolone-resistance is “inherent”. Hence, in all cases of drug
insensitivity, inherent resistance or acquired resistance, oocysts are produced
in the presence of drug under commercial conditions. Their effect is crucial.
Oocyst production by chickens first increases, until marked reductions occur
towards the end of each crop, due to development of flock immunity, stimulated
by early exposure to oocysts that have avoided drug action. Adverse litter
conditions further reduce numbers of viable oocysts, but small numbers remain at
the end. The pattern is similar with untreated birds and those receiving live
anticoccidial vaccines. The often innocuous immunization occurs as a result of
the initiation of strongly immunogenic trickle infections by between-crop
carry-over of residual oocysts. The phenomenon is most marked if litter is
replaced between crops.
Other factors moderating the impact of resistant populations include a
physiological compensation that allows infected chicks to attain increased
growth rates during recovery from coccidiosis, and the effect of E. acervulina
in evidently suppressing more pathogenic Eimeria species under certain
conditions (Williams, 1973). Adverse effects of drug-resistant parasites might,
therefore, be ameliorated by such natural events, supported by careful
husbandry.