Coccidiosis in Poultry

Coccidiosis is a protozoal disease causing diarrhea, ,weight loss and decreased production in poultry. It can be fatal. Prevention is key and is achieved with use of anticoccidials or vaccination. Diagnosis is by fecal flotation to detect oocysts, often in combination with characteristic necropsy findings.

Etiology

Coccidia are almost universally present in poultry-raising operations, but clinical disease occurs only after ingestion of relatively large numbers of sporulated oocysts by susceptible birds (eg, those that are immunosuppressed and/or with concurrent disease). Both clinically infected and recovered birds shed oocysts in feces, which contaminate feed, dust, water, litter, and soil. Oocysts may be transmitted via equipment and personnel (eg, shoes) as well as the presence of insects (eg, flies) and rodents. Fresh oocysts are not infective until they sporulate; under optimal conditions (70°–90°F [21°–32°C] with adequate moisture and oxygen), this requires 1–2 days. The prepatent period is 4–7 days. Sporulated oocysts may survive for long periods, depending on environmental factors. Oocysts are resistant to some disinfectants commonly used around livestock but are killed by freezing or high environmental temperatures.

Pathogenicity of coccidiosis is influenced by host genetics, nutritional factors, concurrent diseases, age of the host, and species of the coccidium. Eimeria necatrix and E tenella are the most pathogenic in chickens, because schizogony occurs in the lamina propria and crypts of Lieberkühn of the small intestine and ceca, respectively, and causes extensive hemorrhage. E kofoidi and E legionensis are the most pathogenic in chukars, and E lettyae is most pathogenic in bobwhite quail. Several Eimeria species are pathogenic in pheasants, particularly E phasiani and E colchici. Most species develop in epithelial cells lining the villi.

Protective immunity usually develops in response to moderate and continuing infection. True age-related immunity does not occur, but older birds are usually more resistant than young birds because of earlier exposure to infection.

Clinical Findings and Lesions

Signs of coccidiosis range from decreased growth rate to many sick birds, withsevere diarrheaand high mortality. Decreased feed and water consumption, weight loss, and decreased egg production, may accompany outbreaks. Mild infections which would otherwise be classed as subclinical, may potentially lead to secondary infection, particularly Clostridium spp infection. Birds that survivors severe infections typically recover in 10–14 days but may never recover full growth and production. The lesions are almost entirely in the intestinal tract and often have a distinctive location and appearance that is useful in diagnosis.

Common signs in infected flocks include:

• reduced feed consumption
• rapid weight loss
  lethargy
• ruffled feathers
• severe diarrhea
• watery mucoid feces

Diagnosis

• Fecal flotation
• Histopathologic examination of tissue samples collected at necropsy

Diagnosis is based on the location of lesions in the host and their appearance; the size of oocysts present is used to determine the species. Coccidial infections are readily confirmed by demonstration of oocysts in feces or intestinal scrapings; however, the number of oocysts present has little relationship to the extent of clinical disease. Severity of lesions as well as knowledge of flock appearance, morbidity, daily mortality, feed intake, growth rate, and rate of lay are important for diagnosis. Necropsy of several fresh specimens is advisable. Classic lesions of E tenella and E necatrix are pathognomonic, but infections with other species are more difficult to diagnose. Comparison of lesions and other clinical signs allows a reasonably accurate differentiation of the coccidial species. Mixed coccidial infections are common.

A diagnosis of clinical coccidiosis is warranted if oocysts, merozoites, or schizonts are seen microscopically and if lesions are severe. Subclinical coccidial infections may be unimportant, and poor performance may be caused by other flock disorders.

Control

Use of anticoccidial compounds in feed or water, vaccination, or a combination of both to prevent clinical signs

Once clinical signs appear, use of antibiotics and supportive care is advisable to minimize dehydration and secondary bacterial infection

Practical methods of management cannot prevent coccidial infection. Poultry maintained at all times on wire floors to separate birds from feces have fewer infections; clinical coccidiosis is seen only rarely under such circumstances. Other methods of control are vaccination or prevention with anticoccidial drugs.

Vaccination
A species-specific immunity develops after natural infection, the extent largely depends on the severity of infection and the number of reinfections. Protective immunity is primarily a T-cell response.

Commercial vaccines consist of live, sporulated oocysts of the various coccidial species administered at low doses. Modern anticoccidial vaccines should be given to day-old chicks, either at the hatchery or on the farm. Because the vaccine serves only to introduce infection, chickens are reinfected by progeny of the vaccine strain on the farm. Most commercial vaccines contain live oocysts of coccidia that are not attenuated. The self-limiting nature of coccidiosis is used as a form of attenuation for some vaccines rather than biologic attenuation. Some vaccines sold in Europe and South America include attenuated lines of coccidia. Research has shown promise for vaccination in game birds.

Layers and breeders maintained on floor litter must have protective immunity. Historically, these birds were given a suboptimal dosage of an anticoccidial drug during early growth, with the expectation that immunity would continue to develop from repeated exposure to wild types of coccidia. This method has never been completely successful because of the difficulty in controlling all the factors affecting reproduction of coccidia under practical conditions. Although anticoccidial drugs have been preferred for protection of these birds, vaccination programs are gaining popularity. More effective administration techniques and choice of coccidia strains in the product are improving the feasibility of vaccination in broilers.

Amprolium is an antagonist of thiamine (vitamin B1). Rapidly dividing coccidia have a high requirement for thiamine. Amprolium has a safety margin of ~8:1 when used at the highest recommended level in feed (125–250 ppm). Amprolium spectrum has been extended by using it in mixtures with the folic acid antagonists ethopabate. (RoyalProl Forte)

Diclazuril is highly effective against a broad spectrum of coccidia. (E-Mix)