Coccidiosis: Introduction - The Merck Veterinary Manual

Coccidiosis: Introduction

Etiology

Clinical Findings

Coccidiosis is caused by protozoa of the phylum Apicomplexa, family Eimeriidae. In poultry, most species belong to the genus Eimeria and infect various sites in the intestine. The infectious process is rapid (4-7 days) and is characterized by parasite replication in host cells with extensive damage to the intestinal mucosa. Poultry coccidia are strictly host-specific, and the different species parasitize specific parts of the intestine. Coccidia are distributed worldwide in poultry and wild birds. (See also cryptosporidiosis, Cryptosporidiosis.)

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. Both clinically infected and recovered birds shed oocysts in their droppings, which contaminate feed, dust, water, litter, and soil. Oocysts may be transmitted by mechanical carriers (eg, equipment, clothing, insects, and other animals). 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. (See also coccidiosis in mammals, Coccidiosis: Introduction.)

Pathogenicity is influenced by host genetics, nutritional factors, concurrent diseases, 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. Most species develop in epithelial cells lining the villi. Protective immunity usually develops in response to moderate and continuing infection. True age-immunity does not occur, but older birds are usually more resistant than young birds because of earlier exposure to infection.

Clinical Findings:

Signs range from decreased growth rate to a high percentage of visibly sick birds, severe diarrhea, and high mortality. Feed and water consumption are depressed. Weight loss, development of culls, decreased egg production, and increased mortality may accompany outbreaks. Mild infections of intestinal species, which would otherwise be classed as subclinical, may cause depigmentation. Survivors of severe infections recover in 10-14 days but may never recover lost performance.

Chickens:

E tenella infections are found only in the ceca and can be recognized by accumulation of blood in the ceca and by bloody droppings. Cecal cores, which are accumulations of clotted blood, tissue debris, and oocysts, may be found in birds surviving the acute stage.

Coccidiosis (site parasitized by Eimeria tenella), poultry

Eimeria tenella, gross lesions, broiler chicken

E necatrix produces major lesions in the anterior and middle portions of the small intestine. Small white spots, usually intermingled with rounded, bright- or dull-red spots of various sizes, can be seen on the serosal surface. The white spots are diagnostic for E necatrix if clumps of large schizonts can be demonstrated microscopically. In severe cases, the intestinal wall is thickened, and the infected area dilated to 2-2.5 times the normal diameter. The lumen may be filled with blood, mucus, and fluid. Fluid loss may result in marked dehydration. Although the damage is in the small intestine, the sexual phase of the life cycle is completed in the ceca. Oocysts of E necatrix are found only in the ceca. Due to concurrent infections, oocysts of other species may be found in the area of major lesions, misleading the diagnostician.

Coccidiosis (site parasitized by Eimeria necatrix), poultry

Eimeria necatrix, gross lesions, chicken

Eimeria necatrix, developmental stages

E acervulina , the most common infection, is characterized by numerous, whitish, oval or transverse patches in the upper half of the small intestine and may be easily distinguished on gross examination. The clinical course in a flock is usually protracted and results in poor growth, an increase in culls, and slightly increased mortality.

Coccidiosis (site parasitized by Eimeria acervulina), poultry

Eimeria acervulina, gross lesions, chicken

Eimeria acervulina, developmental stages

E brunetti is found in the lower small intestine, rectum, ceca, and cloaca. In moderate infections, the mucosa is pale and disrupted but lacking in discrete foci, and may be thickened. In severe infections, extensive coagulative necrosis and sloughing of the mucosa occurs throughout most of the small intestine.

Coccidiosis (site parasitized by Eimeria brunetti), poultry

Eimeria brunetti, gross lesions, chicken

Eimeria brunetti, oocysts

E maxima develops in the small intestine, where it causes dilatation and thickening of the wall; petechial hemorrhage; and a reddish, orange, or pink viscous mucous exudate and fluid. The oocysts and gametocytes (particularly macrogametocytes), which are present in the lesions, are distinctly large.

Coccidiosis (site parasitized by Eimeria maxima), poultry

Eimeria maxima, oocysts

E mitis is recognized as pathogenic in the lower small intestine. Lesions resemble moderate infections of E brunetti but can be distinguished by finding small, round oocysts associated with the lesion.

Coccidiosis (site parasitized by Eimeria mitis), poultry

Coccidiosis (proposed site parasitized by Eimeria mivata), poultry

E praecox , which infects the upper small intestine, does not cause distinct lesions but may decrease rate of growth. It is considered to be of less economic importance than the other species.

Coccidiosis (site parasitized by Eimeria praecox), poultry

E hagani and E mivati are of dubious status but are thought to develop in the anterior part of the small intestine.

Coccidiosis (proposed site parasitized by Eimeria hagani), poultry

Turkeys:

Only 4 of the 7 species of coccidia in turkeys are considered pathogenic— Eimeria adenoeides , E dispersa , E gallopavonis , and E meleagrimitis . E innocua , E meleagridis , and E subrotunda are considered nonpathogenic. Oocysts sporulate within 1-2 days after expulsion from the host; the prepatent period is 4-6 days.

E adenoeides and E gallopavonis infect the lower ileum, ceca, and rectum. The developmental stages are found in the epithelial cells of the villi and crypts. The affected portion of the intestine may be dilated and have a thickened wall. Thick, creamy material or caseous casts in the gut or excreta may contain enormous numbers of oocysts. E meleagrimitis chiefly infects the upper and mid small intestine. The lamina propria or deeper tissues may be parasitized, which may result in necrotic enteritis ( Necrotic Enteritis: Introduction). E dispersa infects the upper small intestine and causes a creamy, mucoid enteritis that involves the entire intestine, including the ceca. Large numbers of gametocytes and oocysts are associated with the lesions.

Common signs in infected flocks include reduced feed consumption, rapid weight loss, droopiness, ruffled feathers, and severe diarrhea. Wet droppings with mucus are common. Clinical infections are seldom seen in poults >8 wk old. Morbidity and mortality may be high.

Ducks:

A large number of specific coccidia have been reported in both wild and domestic ducks, but validity of some of the descriptions is questionable. Presence of Eimeria , Wenyonella , and Tyzzeria spp has been confirmed. T perniciosa is a known pathogen that balloons the entire small intestine with mucohemorrhagic or caseous material. Eimeria spp also have been described as pathogenic. Some species of coccidia of domestic ducks are considered relatively nonpathogenic. In wild ducks, infrequent but dramatic outbreaks of coccidiosis occur in ducklings 2-4 wk old; morbidity and mortality may be high.

Geese:

The most striking coccidial infection of geese is that produced by Eimeria truncata , in which the kidneys are enlarged and studded with poorly circumscribed, yellowish white streaks and spots. The tubules are dilated with masses of oocysts and urates. Mortality may be high. At least 5 other Eimeria spp have been reported to parasitize the intestine.

Diagnosis:

The location in the host, appearance of lesions, and the size of oocysts are used in determining the species present. 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, mortality, feed intake, growth rate, and rate of lay are important for diagnosis. Necropsy of several fresh specimens is advisable. Classical lesions of E tenella and E necatrix are pathognomonic, but infections of other species are more difficult to diagnose. Comparison of lesions and other signs with diagnostic charts allows a reasonably accurate differentiation of the coccidial species. Mixed coccidial infections are common.

Release of merozoite from mature schizont

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

Control:

Practical methods of management cannot prevent infection. Poultry that are maintained at all times on wire floors to separate birds from droppings 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 degree of which largely depends on the extent of infection and the number of reinfections. Protective immunity is primarily a T-cell response.

Commercial vaccines consist of low doses of live, sporulated oocysts of the various coccidial species administered at low doses to day-old chicks. Because the vaccine serves only to introduce infection, chickens are reinfected by progeny of the vaccine strain on the farm. The vaccine strains of coccidia may or may not be attenuated. The self-limiting nature of coccidiosis is used as a form of attenuation for some vaccines, rather than biological attenuation.

Layers and breeders that are maintained on floor litter must have protective immunity. Often, they are given a suboptimal dosage of an anticoccidial drug during early growth, with the expectation that immunity will continue to develop from repeated exposure to wild types of coccidia. This method has never been particularly successful because of the difficulty in controlling all of these factors. Immunity is not necessary in broiler chickens or cage layers. Prevention of infection by anticoccidial drugs is preferred.

Anticoccidial Drugs:

Many products are available for prevention or treatment of coccidiosis in chickens and turkeys (see Table: Drugs for Prevention of Coccidiosis in Poultry and Table: Drugs for Treatment of Coccidiosis in Chickens). Detailed instructions for use are provided by all manufacturers to help users comply with regulatory approvals and management considerations. High dosages may sometimes be used over short periods for treatment or if a high level of exposure is anticipated.

Anticoccidials are given in the feed to prevent disease and the economic loss often associated with subacute infection. Prophylactic use is preferred because most of the damage occurs before signs become apparent, and because drugs cannot completely stop an outbreak. Water medication is generally preferred over feed medication for therapeutic treatment. Antibiotics and increased levels of vitamins A and K are sometimes used in the ration to improve rate of recovery and prevent secondary infections.

Continuous use of anticoccidial drugs promotes the emergence of drug-resistant strains of coccidia. Various programs are used in attempts to slow or stop selection of resistance. For instance, producers may use one anticoccidial continuously through succeeding flocks, rotate anticoccidials every 4-6 mo, or change anticoccidials during a single growout (ie, a shuttle program). While there is little cross-resistance to anticoccidials with different modes of action, there is widespread resistance to most drugs. Change of drug may be beneficial when resistance has been established. “Shuttle programs,” in which 1 group of chickens is treated sequentially with different drugs (usually a change between the starter and grower rations), are common practice in many countries, and offer some benefit in reducing emergence of resistance. In the USA, the FDA considers shuttle programs as extra-label usage, but producers may use such programs on the recommendation of a veterinarian.

The effects of anticoccidial drugs may be coccidiostatic, in which growth of intracellular coccidia is arrested but development may continue after drug withdrawal, or coccidiocidal, in which coccidia are killed during their development. Some anticoccidial drugs may be coccidiostatic when given short-term but coccidiocidal when given longterm. Most anticoccidials currently used in poultry production are coccidiocidal.

The natural development of immunity to coccidiosis can be slowed by use of some highly effective anticoccidials. In the production of broilers during a short growout of 37-44 days, this may be of little consequence. However, natural immunity is important in replacement layers because they are likely to be exposed to coccidial infections for extended periods after terminating anticoccidial drugs. Anticoccidial programs for layer and breeder flocks are aimed at allowing immunizing infection while guarding against acute outbreaks.

Anticoccidials are commonly withdrawn from broilers 3-7 days before slaughter to meet regulatory requirements and to reduce production costs. Because broilers have varying susceptibility to infection at this point, the risk of coccidiosis outbreaks is increased with longer withdrawal.

Turkeys are given a preventive anticoccidial for confinement-reared birds up to 8-10 wk of age. Older birds are considered less susceptible to outbreaks.

The modes of action of anticoccidial drugs are poorly understood. Some that are better known are described below. Knowledge of mode of action is important in understanding toxicity and side effects.

Amprolium is structurally similar to and is a competitive antagonist of thiamine (vitamin B₁). Because rapidly dividing coccidia have a relatively high requirement for thiamine, amprolium has a safety margin of ~8:1 when used at the highest recommended level in feed. Maximal effect occurs about day 3 of the life cycle of coccidia. Because amprolium has poor activity against some Eimeria spp , its spectrum has been extended by using it in mixtures with the folic acid antagonists, ethopabate and sulfaquinoxaline.

Clopidol and quinolines (eg, decoquinate, methylbenzoquate) halt development of the sporozoites or trophozoites of Eimeria spp by inhibiting the electron transport system within parasite mitochondria. This action is coccidiostatic. Clopidol and quinolines have a broad species spectrum, but resistance may develop rapidly.

Folic acid antagonists include the sulfonamides, 2,4-diaminopyrimidines and ethopabate. These compounds are structural antagonists of folic acid or of para-aminobenzoic acid (PABA), which is a precursor of folic acid. (The host does not synthesize folic acid and has no requirement for PABA.) Coccidia rapidly synthesize nucleic acids, especially during schizogony, which accounts for activity against these stages. Although resistance to antifolate compounds is widespread, they are commonly used for water treatment when clinical signs are already evident. Diaveridine, ormetoprim, and pyrimethamine are active against the protozoan enzyme dihydrofolate reductase. They have synergistic activity with sulfonamides and often are used in mixtures with these compounds.

Halofuginone hydrobromide is related to the antimalarial drug febrifuginone and is effective against asexual stages of most species of Eimeria . It has both coccidiostatic and coccidiocidal effects.

The ionophores (monensin, salinomycin, lasalocid, narasin, maduramicin, and semduramicin) form complexes with various ions, principally sodium, potassium, and calcium, and transport these into and through biological membranes. The ionophores affect both extra- and intracellular stages of the parasite, especially during the early, asexual stages of parasite development. Drug tolerance was initially slow to emerge, probably because of the biochemically nonspecific way these fermentation products act on the parasite. Recent surveys suggest that drug tolerance is now widespread, but these products remain the most important class of anticoccidials.

Some ionophores depress weight gain when given at or slightly above the recommended levels. Primarily, this is the result of reduced feed consumption, but the reduced growth may be offset by improved feed conversion.

Nicarbazin was the first product to have truly broad-spectrum activity that is still in common use. While not completely understood, the mode of action is thought to be via inhibition of succinate-linked nicotinamide adenine dinucleotide reduction and the energy-dependent transhydrogenase, and the accumulation of calcium in the presence of ATP. Nicarbazin is toxic for layers, and a 4-day withdrawal period is required in broilers. Medicated birds are at increased risk of heat stress in hot weather.

Nitrobenzamides (eg, dinitolmide) exert their greatest coccidiostatic activity against the asexual stages. Efficacy is limited to E tenella and E necatrix unless combined with other products.

Robenidine, a guanidine compound, allows initial intracellular development of coccidia but prevents formation of mature schizonts. It is both coccidiostatic when given short term and coccidiocidal long term. Drug resistance may develop during use. A 5-day withdrawal period is needed to eliminate untoward flavor caused by residues in poultry meat.