Relevance and treatment of coccidiosis in domestic pigeons (Columba livia forma domestica) with particular emphasis on toltrazuril.
Coccidiosis (Drug therapy)
Pigeons (Drug therapy)
|Publication:||Name: Journal of Avian Medicine and Surgery Publisher: Association of Avian Veterinarians Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2009 Association of Avian Veterinarians ISSN: 1082-6742|
|Issue:||Date: March, 2009 Source Volume: 23 Source Issue: 1|
|Geographic:||Geographic Scope: Germany Geographic Code: 4EUGE Germany|
Abstract: Coccidia are common pathogenic parasites in pigeons
(Columba livia). Coccidiosis is most commonly seen in young pigeons and
only rarely in adult birds. Infections in domestic pigeons are typically
mixed and commonly include Eimeria columbarum and Eimeria labbeana. The
reported prevalence of infection is 5.1%-71.9%, and worldwide mortality
in juvenile pigeons varies from 5% to 70%, with most deaths occurring in
the third and fourth month of life. This article summarizes the life
cycle of E columbarum and E labbeana, the route of transmission, and the
common clinical and pathologic signs of coccidiosis. Chemotherapeutic
options discussed include amprolium, sulfonamides, clazuril, and
toltrazuril. Reasons to use toltrazuril include the growing resistance
against other drugs, such as sulfonamides and amprolium, the extended
effectiveness compared with other substances, for example, clazuril, and
the ability of pigeons to develop immunity during treatment.
Key words: coccidiosis, Eimeria labbeana, Eimeria columbarum, immunity, toltrazuril, avian, pigeon, Columba livia forma domestica
Coccidia are protozoal parasites that can affect a wide variety of mammalian and avian species, and they are common pathogens in pigeons. Nine species of Eimeria and one of Isospora have been named in pigeons worldwide; however, only Eimeria labbeana and Eimeria columbarum are relevant for domestic pigeons (Columba livia forma domestica) (Fig 1). (1-4) Eimeria labbeana was first described in 1928 in domestic pigeons and rock doves (Columba livia livia), (5) and E columbarum was first reported in rock doves and domestic pigeons in 1953. (6)
Oocysts of E columbarum are spherical to ovoid and average 20.0 x 18.7 [micro]m in size. Their double-layered wall is smooth and colorless. Mature oocysts contain an oocyst residuum composed of a number of inclusion bodies found partially scattered and partially chained together. (6) Sporulation lasts 34-38 hours, at which point the oocysts contain four 8-11 x 5-6-[micro]m sporocysts, each containing 2 sporozoites. The polar end of the sporocyst contains a Stieda body. The elliptical to spherical oocysts of E labbeana are somewhat smaller than those of E columbarum, which measure 15-18.9 [micro]m x 14-17.5 [micro]m. (7) They have a triple-layered wall that is colorless, light yellow-brown or yellow-green, and covered with plaque-like structures. No micropyle or oocyst residuum is present. (7-9) Sporocysts and sporozoites were 12.5 x 6.5 [micro]m and 7.9-13.5 x 2.2-3.5 [micro]m, respectively. (8)
Most pigeons carry small numbers of coccidia, with no discernible ill effects. The reported prevalence of coccidia in pigeons is 36% in Germany, (10) 50% in Belgium, (11) 15.1% of feral pigeons in Turkey, (12) 50% in Santa Cruz de Tenerife, Spain, (13) 71.9% of feral pigeons in Ljubljana, Slovenia, (14) 35.8% in Chicago, IL, USA, (15) and 11.5% in Chillan City, Chile. (16) Clinical disease is most commonly seen in juvenile pigeons, but a high burden of coccidia can also adversely affect racing performance in adult pigeons.
[FIGURE 1 OMITTED]
Life Cycle and Transmission
Three forms of E labbeana oocysts can be found in pigeon feces? Immature oocysts are small and colorless. Mature oocysts are larger and have a complete triple-layered wall. The outer layer is thin, transparent, and separated distinctly from the middle layer, whereas the inner layer is thinner and darker and borders directly on the sporoblast, which contains strong refractive granules. (8) The third form is a degraded oocyst, which is clark yellow and finely granulated and contains no refractive granules. The wall resembles that of mature oocysts. (8) The duration of 1 exogenous cycle (sporogony) lasts 1-4 days. (7,8,17) Sporogony is hindered or prevented completely by oxygen deficiency, low environmental temperatures, or desiccation. Nothing is known about the endogenous development of E columbarum. Endogenous development of E labbeana is composed of schizogony and gamogony. Endogenous stages occur in epithelial cells of the jejunum and ileum. The various developmental stages of E labbeana inhabit the entire length of the small intestine, primarily the midsection. The organisms migrate approximately 10 cm caudally each day. (18)
Oocysts are spread by aerosol transmission by means of dust from dried feces or debris from nests or footwear. Contaminated water is also a source of infection. After oocysts are ingested, enclosed sporozoites are released into the intestinal lumen. This mobile stage penetrates the epithelial cells lining the small intestinal villi. After 4-8 hours, the sporozoites become rounded and contain a simple, compact, dark nucleus and develop into trophozoites. Schizonts can be detected in the intestinal epithelial cells roughly 24-28 hours after ingestion. (19) Schizogony consists of the development of 3 generations of schizonts. First-generation schizonts develop in 40 to 72 hours, and their lifespan is 5-20 hours. Second-generation schizonts contain 8-30 merozoites that are 4-8 x 1.5-3 [micro]m. (19,20) After 94-102 hours, the merozoites are released from mature second-generation schizonts. Mature third-generation schizonts can be found 140-144 hours after infection; they are 5-12 x 4-8 [micro]m and contain 6-30 merozoites. (18-20) Each schizont releases 5-20 first-generation merozoites, which subsequently penetrate the remaining intact small-intestinal epithelial cells. (20) The merozoites are slightly bent and resemble a sickle with a rounded end and a pointed end. The nucleus is central and fills a third of the cell. (19,21)
Clinical Signs of Coccidiosis
Clinical symptoms of coccidiosis in juvenile pigeons are anorexia, dehydration, and cachexia, and fetid, watery diarrhea. (23) Mortality can be 5%-70% in pigeons 1-4 months of age, with most of the deaths occurring in the third and fourth months. (18) Acute coccidiosis with hemorrhagic diarrhea is only rarely observed in pigeons. (23-25) The pathogenicity of Eimeria species is very low in adult domestic pigeons. (14) However, a severe coccidial infection may substantially reduce a pigeon's flying performance.
Five to six days after pigeons are inoculated with oocysts of E labbeana, a mild catarrhal enteritis, characterized by mild-to-moderate reddening of the intestinal mucosa and increased perfusion, generally involves the cranial two-thirds of the small intestines. (18) On the sixth or seventh day after infection, histopathologic examination reveals pear-shaped protrusions on the tips of the intestinal villi. These distensions are formed by focal and occasionally diffuse cellular infiltration of the lamina propria, sometimes extending into the epithelium. As early as 24-48 hours later, the villi are 2-3 times larger than normal, and a diffuse lymphocytic infiltration is evident. This infiltration is confined solely to the lamina propria, and the subluminal tunica propria is not affected. (18)
Immunity will develop, depending on the number of oocysts ingested. Although immunity will not prevent reinfection, it will lessen the course of the disease. However, oocysts will continue to be produced and shed. In adult animals, a balance is achieved between constant reinfection and the degree of immunity. In pigeons that were experimentally infected and left untreated, an 84% reduction in the number of oocysts shed was observed after reinfection. (26) For this reason, a continuous mild infection of Eimeria species may be desirable in pigeon lofts to prevent clinical coccidiosis. The intraperitoneal application of paramunity inducers can considerably reduce oocyst shedding, but this is not the case with oral application. (27)
The test of choice for detecting coccidian oocysts is flotation. Giemsa-stained intestinal smears or microscopic examinations of intestinal mucosa can also be used to detect Eirneria species. Histologic sections may be stained by using hematoxylin and eosin, Heidenhain, Giemsa, or periodic acid Schiff-aniline blue and orange G methods. (23) In cases of pathologic coccidiosis, clinical signs arise before gamogony; therefore, fecal samples will be negative.
Therapy and Prophylaxis
Treatment of mild cases of coccidiosis is not necessary because this disease is self-limiting, when assuming proper measures are taken to hinder reinfection. A mild coccidial infection in a loft builds immunity; thus, total absence of the organisms is not necessarily desirable. (11) Sanitation is a very important factor in limiting the spread of coccidia. This includes removing all fecal material daily and maintaining a dry loft floor. Eradication of the oocysts is best achieved by dehydration. Oocysts are not infectious until after sporulation has occurred, which is approximately 1-2 days after they are shed. Therefore, daily removal of feces drastically reduces the amount of infectious material. Water and feed dishes should be thoroughly cleaned, and floor feeding should be avoided. In our opinion, because oocysts are resistant to common disinfectants, cresol derivatives are recommended for cleaning.
Amprolium, a pyrimidine derivative, has coccidiostatic properties. It is structurally similar to thiamine and, when ingested by coccidia, competitively inhibits folic acid metabolism. Amprolium is an odorless, water-soluble white powder, and medicated drinking water is generally well accepted. (25) Treatment is not thought to interfere with the development of immunity. (25) Because of amprolium's pharmacologic mechanism, a surplus of thiamine can reduce its efficacy. This is rarely encountered, because significant interference requires a 1 : 2 ratio of thiamine to amprolium. Enteral absorption of amprolium is minimal, and prompt elimination occurs; thus, the drug does not accumulate and is well tolerated. A 0.2% solution of amprolium is given for 5 days. (25) However, over the past few years, breeders have reported a significant loss of efficacy with this medication, which may indicate development of resistance. These claims have not been scientifically verified.
The mode of action of sulfonamides is based on their analogous properties to para-aminobenzoic acid, which is required by schizonts for folic acid synthesis. Sulfonamides competitively inhibit the integration of para-aminobenzoic acid. However, a significant disadvantage of these drugs is the high concentration required, which, in the case of extended treatments, may lead to significant adverse effects, such as reduced activity and feed consumption, growth disturbance, and hemorrhagic syndrome. (28) The suggested daily dose of sulfamethazine is 50-65 mg per pigeon, which is given orally for either 3 days, followed by a 2-3 day break and a subsequent 2-3 day treatment period, or daily for 5 days. However, the declining therapeutic efficacy of sulfamethazine may suggest development of resistance. (25)
Clazuril is poorly water soluble and is available in tablet form solely for use in racing pigeons. This drug belongs to the benzene-acetonitriles and is coccidiocidal. Clazuril works at the endogenous stages of Eimeria species in pigeons. It is rapidly absorbed, with maximum plasma concentrations attained 5-8 hours after dosing. The half-life of clazuril in pigeons is approximately 3 days. When using the recommended monthly dose of 2.5 mg per pigeon, clazuril has a higher efficacy of inhibiting oocyst shedding than toltrazuril. This treatment regimen stopped oocyst shedding faster than did treatment with toltrazuril. (29) However, renewed shedding commences 20 days after treatment, which is earlier than with toltrazuril. (29)
Toltrazuril is also coccidiocidal, and its efficacy is independent of the degree of infection. (30) Toltrazuril interferes with nuclear division and mitochondrial activity, which is responsible for the respiratory metabolism of coccidia. It also damages wall-forming bodies II formed in the macrogamete stage. In addition, toltrazuril causes inflation of the coccidial endoplasmic reticulum and subsequent vacuolization in all intracellular developmental stages. Toltrazuril is reportedly efficient at eliminating third-generation schizonts, gamonts, and perhaps zygotes in pigeons. (26,31)
Toltrazuril is a fine, powdery, white, odorless, crystalline solid that is insoluble in water and stable for 14 days at an environmental temperature of 158[degrees]F. The drug is suspended in drinking water for treatment. Very good results were reported in birds treated with 10 mg toltrazuril on the third day after infection; oocyst shedding was completely suppressed for 22-28 days. Experimentally infected birds treated with toltrazuril during the prepatent period (days 1-5 after infection) shed fewer oocysts after reinfection than untreated birds. (26-31) In the same report, birds treated during the patent period (days 6-7 after infection) exhibited a diminished ability to reduce oocyst shedding after reinfection. (26-31) If toltrazuril was administered on the ninth day after infection, then oocyst shedding was extensively decreased. (32)
The recommended dose of toltrazuril is 20 mg/ kg administered in drinking water for 2 days. At this high a dose, no negative effects on blood parameters or internal organs have been observed. (4) Dosage should be based on the daily water intake of the individual pigeon loft, which may vary considerably because of weather conditions (lower intake in winter), age of the birds (feeding nestlings consume up to 5 times more water than adult pigeons), taste of the medicated water, and flight performance. We recommend that the consumption of drinking water be measured 1 day before treatment. Toltrazuril as Baycox 5% suspension (Bayer, Leverkusen, Germany; approved for swine) has been administered to pigeons directly by a feeding cannula for precise dosing. However, the Baycox 2.5% formulation, which is approved for use in turkeys and chickens, should not be administered directly into the crop by a feeding cannula because of its abrasive alkaline properties (R. Z., unpublished data, 2005). Oral administration by a feeding cannula is time consuming and, therefore, not the method of choice for treating a large number of pigeons. When treating a flock, the Baycox 2.5% solution is recommended. Toltrazuril has been proven ineffective at a daily dose of 20 ppm in drinking water on days 2-4 after infection and when administered in capsule form at a dose of 1 mg per pigeon on the third day after infection. (4) This can be explained by the low antigenic properties of third-generation schizonts and gamonts. (25,31) Because of the significantly increased antigenic properties of destroyed schizonts compared with those of other stages, toltrazuril does not appear to hinder the development of immunity. (30,33-35) Mild-to-severe feather damage has been reported in 8.5-week-old offspring of adult pigeons treated with toltrazuril. (32) In that same report, no impact on the number of eggs, hatch rate, or weight gain of young birds could be assessed. (32) Improvement in flying performance of racing pigeons subsequent to a severe coccidial infection can be achieved by administering a single dose of toltrazuril on day 3 after infection; however, full performance cannot be reestablished. (36)
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Maria-Elisabeth Krautwald-Junghanns, Prof Dr MedVet, Dipl ECAMS, Ralph Zebisch, Dr MedVet, and Volker Schmidt, Dr MedVet, Dipl ECAMS
From the Clinic for Birds and Reptiles, An den Tierkliniken 17, 04103 Leipzig, Germany.
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