coccidiosis

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Identity

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Preferred Scientific Name

• coccidiosis

International Common Names

• English: avian coccidiosis, eimeria, atoxoplasma, caryospora in birds; coccidiosis in piglets and older swine; coccidiosis, eimeria infection, in ruminants; Eimeria infections in livestock; Eimeria infections in poultry; eimeriosis; nervous coccidiosis in young cattle

Pathogen/s

Top of page Eimeria
Eimeria abramovi
Eimeria acervulina
Eimeria adenoeides
Eimeria ahsata
Eimeria alabamensis
Eimeria albemarlensis
Eimeria albigulae
Eimeria alijevi
Eimeria amphorae
Eimeria anatis
Eimeria anseris
Eimeria antrozoi
Eimeria apionodes
Eimeria arizonensis
Eimeria arloingi
Eimeria auburnensis
Eimeria bakuensis
Eimeria bateri
Eimeria battakhi
Eimeria beecheyi
Eimeria bemricki
Eimeria bentoniensis
Eimeria bilamellata
Eimeria bohemii
Eimeria boveroi
Eimeria bovis
Eimeria brasiliensis
Eimeria brunetti
Eimeria caesicia
Eimeria cahirinensis
Eimeria californicensis
Eimeria callospermophili
Eimeria cameli
Eimeria cameronensis
Eimeria caprina
Eimeria caprovina
Eimeria catronensis
Eimeria caviae
Eimeria cernae
Eimeria chamaeleolidisbarbati
Eimeria chaparralensis
Eimeria chiropteri
Eimeria christenseni
Eimeria chrysemydis
Eimeria cochabambensis
Eimeria coecicola
Eimeria colchici
Eimeria columbae
Eimeria columbarum
Eimeria cottunculusi
Eimeria coturnicis
Eimeria crandallis
Eimeria credintsi
Eimeria cylindrica
Eimeria cylindrospora
Eimeria danailovi
Eimeria debliecki
Eimeria delicata
Eimeria dicotylensis
Eimeria dispersa
Eimeria dorneyi
Eimeria dromedarii
Eimeria duodenalis
Eimeria egregia
Eimeria ellipsoidalis
Eimeria evoti
Eimeria exigua
Eimeria falciformis
Eimeria faurei
Eimeria flavescens
Eimeria gallopavonis
Eimeria geochelona
Eimeria giganteos
Eimeria gilruthi
Eimeria gnui
Eimeria godmani
Eimeria granulosa
Eimeria graptemydos
Eimeria greniere
Eimeria gruis
Eimeria gulruthi
Eimeria gymnopthalmi
Eimeria hagani
Eimeria hirci
Eimeria humboldtensis
Eimeria hungaryensis
Eimeria ictidea
Eimeria innocua
Eimeria inornata
Eimeria intestinalis
Eimeria intricata
Eimeria irresidua
Eimeria jacksonensis
Eimeria jeddahensis
Eimeria kharjensis
Eimeria kofoidi
Eimeria kotlani
Eimeria labbeana
Eimeria langebarteli
Eimeria lateralis
Eimeria lepidophymae
Eimeria leporilli
Eimeria leuckarti
Eimeria limifronsi
Eimeria liolaemi
Eimeria macusaniensis
Eimeria magna
Eimeria magnarabbits
Eimeria marginata
Eimeria marmorata
Eimeria marmosopos
Eimeria marsica
Eimeria maxima
Eimeria media
Eimeria megalostomata
Eimeria meleagridis
Eimeria meleagrimitis
Eimeria melis
Eimeria micouri
Eimeria minasensis
Eimeria mitis
Eimeria mivati
Eimeria molossi
Eimeria morainensis
Eimeria mulardi
Eimeria mustelae
Eimeria mutica
Eimeria necatrix
Eimeria neodebliecki
Eimeria ninakohlyakimovae
Eimeria nocens
Eimeria numidae
Eimeria onychomysis
Eimeria ovina
Eimeria ovinoidalis
Eimeria pacifica
Eimeria pallida
Eimeria panguii
Eimeria papillata
Eimeria parva
Eimeria patagonensis
Eimeria pavonis
Eimeria pecari
Eimeria pellita
Eimeria peltocephali
Eimeria perforans
Eimeria perminuta
Eimeria petrogale
Eimeria phasiani
Eimeria pilarensis
Eimeria pipistrellus
Eimeria piriformis
Eimeria pleistocenensis
Eimeria polita
Eimeria porci
Eimeria praecox
Eimeria pragensis
Eimeria procera
Eimeria pseudemydis
Eimeria pseudogeographica
Eimeria punctata
Eimeria quadricornis
Eimeria raillieti
Eimeria rajasthani
Eimeria randolphi
Eimeria redukeri
Eimeria reichenowi
Eimeria rioarribaensis
Eimeria roperi
Eimeria sanctaluciae
Eimeria scabra
Eimeria schmidti
Eimeria scincellae
Eimeria sevilletensis
Eimeria sharmani
Eimeria sigmodontis
Eimeria simonkingi
Eimeria somateriae
Eimeria southwelli
Eimeria spari
Eimeria sparis
Eimeria spermophili
Eimeria spinosa
Eimeria stiedai
Eimeria stigmosa
Eimeria subrotunda
Eimeria subspherica
Eimeria suis
Eimeria tenella
Eimeria tilburyi
Eimeria tokayae
Eimeria trachemydis
Eimeria truncata
Eimeria tsunodai
Eimeria tuskegeensis
Eimeria uptoni
Eimeria uzura
Eimeria vejdovskyi
Eimeria vermiformis
Eimeria vilasi
Eimeria vison
Eimeria vittati
Eimeria waeli
Eimeria webbae
Eimeria weybridgensis
Eimeria wyomingensis
Eimeria yemenensae
Eimeria zuernii
Isospora
Isospora abdallahi
Isospora acanthodactyli
Isospora achiotensis
Isospora aegyptia
Isospora ashmoonensis
Isospora atrata
Isospora automoli
Isospora belli
Isospora bigemina
Isospora caerulei
Isospora canis
Isospora certhiae
Isospora chalchidis
Isospora clethrionomydis
Isospora concentrica
Isospora dilatata
Isospora diplometoponi
Isospora felis
Isospora gardneri
Isospora gonatodi
Isospora gonocephali
Isospora gryphoni
Isospora hominis
Isospora jaracimrmani
Isospora lacertae
Isospora ladiguensis
Isospora laidlawi
Isospora limifronsi
Isospora magna
Isospora melis
Isospora muriyu
Isospora ocellati
Isospora ohioensis
Isospora pari
Isospora ptyodactyli
Isospora rivolta
Isospora schoenobaeni
Isospora serini
Isospora seychellensis
Isospora striata
Isospora suis
Isospora thibetana
Isospora tiaris
Isospora tigris
Isospora ubique
Isospora vulpina
Tyzzeria
Tyzzeria parvula
Tyzzeria perniciosa
Wenyonella anatis
Wenyonella bahli
Wenyonella gallinae
Wenyonella philipevinei

Overview

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Coccidiosis is a disease that is caused by microscopically visible parasites named ‘coccidia’ [mainly Eimeria spp and Isospora spp]. These parasites invade animal intestines and, in some species, other organs. Coccidiosis is spread all over the world.

Almost all types of animal are able to accommodate this agent, but not all of them fall ill. Coccidiosis represents a serious sickness for only a few animal species.

The disease is mostly important in young animals.

In large commercial stocks of farmed animals the disease reaches a significant economic importance. Great financial losses are possible, due to inadequate productivity of animals plus the costs for prophylaxis and therapy.

History

Antoni van Leeuwenhoek (1674) observed and described for the first time a parasite in the bile of rabbits which is now known as Eimeria stiedai. Hake (1839) concluded from his studies that they represented a new form of "pus globule". Lindemann (1885) placed them under the name Monocystis stiedae among the group of Gregarines. Levine in Long (1982) established the biology of the coccidia which proposed the taxonomy of this group of agents.

Pathogens

Chickens

E. tenella (Raillet and Lucet, 1881; Fantham, 1909)
E. necatrix (Johnson, 1930)
E. acervulina (Tyzzer, 1929)
E. maxima (Tyzzer, 1929)
E. mitis (Tyzzer, 1929)
E. mivati (Edgar and Siebold, 1964)
E. brunetti (Levine, 1942)
E. praecox (Johnson, 1930)
E. hagani (Levine, 1938)
E. sporadica (Plaan, 1951)
Wenyonella gallinae (Ray, 1945)
 

Turkeys

E. adenoeides (Moore and Brown, 1951)
E. dispersa (Tyzzer, 1929)
E. gallopavonis (Hawkins, 1952)
E. innocua (Moore and Brown, 1952)
E. meleagridis (Tyzzer, 1929)
E. meleagrimitis (Tyzzer, 1929)
E. subrotunda (Moore, Brown and Carter, 1954)
 

Quail

Japanese Quail (Coturnix coturnix japonica)
E. bateri (Bhatia, Panday and Pande, 1965)
E. uzura (Tsunoda and Muraki, 1971)
E. tsunodai

Common Quail
E. bateri
E. coturnicis
Wenyonella bahli

Pheasants

E. colchici (Norton, 1967)
E. dispersa (Tyzzer, 1929)
E. duodenalis (Norton, 1967)
E. langeroni (Yakimoff and Matschoulsky, 1937)
E. pacifica (Ormsbee, 1939)
E. phasiani (Tyzzer, 1929)
E. megalostomata
E. picta
 

Guinea fowl

E. numidae (Pellerdy, 1962)
E. greniere (Yvore and Aycardi, 1967)
 

Goose

E. anseris (Kotlán, 1932)
E. nocens (Kotlán, 1933)
Tyzzeria parvula (Kotlán, 1933; Klimes, 1963)
E. stigmosa (Klimes, 1963)
E. kotlani (Gräfner and Graupmann, 1964)
E. truncata (kidney) (Railliet and Lucet, 1891)
 

Duck

E. abramovi (Svanbaer and Rakhmatullina, 1967)
E. anatis (Scholtyseck, 1955)
E. battakhi (Dubey and Pande, 1963)
E. boschadis (Walden, 1961)
E. danailovi (Gräfner, Graubmann and Betke, 1965)
E. saitamae (Inoue, 1967)
Tyzzeria perniciosa (Allen, 1936)
Wenyonella anatis (Pande, Bhatia and Srivastava, 1965)
Wenyonella philiplevinei (Leibowitz, 1968)
E. baschadis (renal epithelium)

 

Pigeon

E. labbeana (Labbé, 1896; Pinto, 1928)
E. columbarum (Nieschulz, 1935)
 

Cattle

worldwide 21 Eimeria species
E. bovis (Züblin, 1908 and Fiebiger, 1912)
E. zuernii (Rivolta, 1878 and Martin, 1909)
E. ellipsoidalis (Becker and Frye, 1929)
E. auburnensis (Christensen and Porter, 1939)
E. wyomingensis (Huizinga and Winger, 1942)
E. pellita (Supperer, 1952)
E. cylindrica (Wilson, 1931)
E. brasiliensis (Torres and Ramos, 1939)
E. alabamensis (Christensen, 1941)
E. subspherica (Christensen, 1941)
 

Sheep

worldwide 15 Eimeria species
E. bakuensis (Musaev, 1970)
E. ovinoidalis (McDougald, 1978)
E. parva (Kotlán, Moscy and Vajda, 1929)
E. crandallis (Honess, 1942)
E. ahsata (Honess, 1942)
E. weybridgensis (Norton, Joyner and Catchpole, 1974)
E. faurei
E. intricata (Spiegl, 1925)
E. granulosa (Christensen, 1938
E. pallida (Christensen, 1938)
E. marsica (Restani, 1971)
 

Goat

worldwide 13 Eimeria species
E. arloingi (Marotel, 1905)
E. ninakohlyakimovae (Yakimoff and Rastegaieff, 1930)
E. alijevi (Musaev, 1970)
E. christenseni (Levine, 1962)
E. hirci (Chavalier, 1966)
E. caprina (Lima, 1979)
E. caprovina (Lima, 1980)
Note: the coccidia of domestic sheep and goats are very host specific, but they are also found in the ibex and mouflon.
 

Porcine / pig

13 Eimeria species
E. debliecki (Douwes, 1921)
E. suis (Nöller, 1921)
E. scabra (Henry, 1931)
E. perminuta (Henry, 1931)
E. spinosa (Henry, 1931)
E. polita (Pellérdy, 1949)
E. porci (Vetterling, 1965)
E. neodebliecki (Vetterling, 1965)
Isospora suis (Biester, 1934)
 

Horse

3 Eimeria species
E. leuckarti (Flesch, 1883)
 

Rabbit

Intestine (9 species):
E. coecicola (Cheissin, 1947)
E. exigua (Yakimoff, 1934)
E. flavescens (Marotel and Guilhon, 1941)
E. intestinalis (Cheissin, 1948)
E. irresidua (Kessel and Jankiewicz, 1931)
E. magna (Pérard, 1925)
E. media (Kessel, 1929)
E. perforans (Leuckart, 1879)
E. piriformis (Kotlán and Pospesch, 1934)
Bile duct:
E. stiedai (Lindemann, 1865)

Host Animals

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Hosts/Species Affected

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All species of vertebrates are able to accommodate coccidia, but not all of them become sick. Those who do develop different levels of clinical signs ranging from subclinical to serious illnesses.

Here, we will only consider the coccidiosis of farm animals, and especially poultry.

Poultry that are co-infected with immunosuppressive viruses (infectious bursitis disease virus, chicken infectious anaemia virus, Marek’s disease virus, and avian leukosis virus) are more likely to develop coccidiosis. Also, vitamin A deficiency accelerates the development, duration, and severity of coccidiosis.

Eimeria species in pigs are not very significant. The only effect is the reduction of productivity. Most of the infections do not result in any clinical signs. However, sometimes watery diarrhoea is seen. The most pathogenic Eimeria species are: E. debliecki, E. scabra, E. polita and E. spinosa.

Eimeria species which are found in sheep and goats cause great problems during lamb fattening. Symptoms are seen especially in animals that are 4-7 weeks old. There is diarrhoea, which is green and sometimes bloody. Anorexia, reduced weight gain, weight loss and dehydration follow. Mortality is often high. The pathogen Eimeria species in sheep are: E. bakuensis, E. ahsata and E. ovinoidalis. The most important Eimeria species in goats are: E. arloingi, E. ninakohlyakimovae, E. alijevi and E. christenseni.

Outbreaks of coccidiosis in calves can be recognized after a change of housing. Serious courses of disease are possible. As a rule, coccidiosis in adult cattle is mostly subclinical. The Eimeria species with the highest pathogenicity in cattle is E. zuernii.

Coccidiosis in horses is not very important. A direct relationship between infection with oocysts and diarrhoea cannot be demonstrated. The most common Eimeria species in horses is E. leuckarti.

Systems Affected

Top of page digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of poultry
digestive diseases of small ruminants
multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of poultry
multisystemic diseases of small ruminants
nervous system diseases of large ruminants

Distribution

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Coccidia are disseminated among all species of domestic and free-living animals all over the world. Outbreaks are especially likely under moist and warm climatic conditions, and in intensive husbandry systems.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Pathology

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Different species induce different clinical signs and different post-mortem findings.

Almost every species has specific sites in which the development takes place. The results are characteristic lesions which are quite indicative for the causal agent.

Caecal coccidiosis

The pouch of the caeca is enlarged and filled with bloody masses and pieces of mucosa. Later the intestinal content becomes caseous. The caecal wall and the mucosa are thickened, and haemorrhagically inflamed.

Microscopically small areas of haemorrhage and necrosis of the tunica muscularis are found.

The typical caecal cocccidiosis is caused by *E. tenella in chickens.

In other species of poultry, coccidiosis is caused by the following Eimeria species:

Turkeys: E. adenoides, E. meleagrimits, E. gallopavonis, E. meleagridis, E. dispersa

Pheasants: E. colchici, E. phasiani

Guinea fowls: E. grenieri

Geese: Tyzzeria parvula

Intestinal coccidiosis

The different Eimeria species are localized at diverse places in the intestine. The localizations are typical for each species of Eimeria. Mostly the following lesions are found in the intestine:

The affected part of the mucosa is thickened and haemorrhagic, sometimes oedematous. Petechiae are found. In some cases the mucosa is pale and rough (e.g. E. mivati) or even necrotic (e.g. E. brunetti). The intestine often contains watery fluid, sometimes mixed with blood and pieces of mucosa.

Intestinal coccidiosis is caused by the following Eimeria species:

Chickens:E. necatrix, E. acervulina, E. maxima, E. mitis, E. mivati, E. brunetti, E. praecox, E. hagani, E. sporadica, Wenyonella gallinae

Turkeys: *E. adenoides, *E. dispersa, *E. gallopavonis, E. innocua, E. meleagridis, *E. meleagrimitis, E. subrotunda

Quail:E. bateri, E. uzura, E. tsunodai, E. coturnicis, Wenyonella bahli

Pheasants: E. colchici, E. dispersa, E. duodenalis, E. langeroni, E. pacifica, E. phasiani, E. megalostomata, E. picta

Guineafowl: E. numidae, E. grenieri

Geese: *E. anseris, E. nocens, Tyzzeria parvula, E. stigmosa, E. kotlani

Ducks: E. abramovi, E. anatis, E. battakhi, E. danailovi, E. saitamae, *Tyzzeria perniciosa,Wenyonella anatis, *Wenyonella philiplevinei

Pigeons: *E. labbeana, E. columbarum

(*the asterisked Eimeria species are the most pathogenic)

Renal coccidiosis

Renal coccidiosis is caused by E. truncata in geese and E. baschadis in ducks. The enlarged kidneys are of greyish yellow or greyish red colour. Urates are accumulated and pinhead-sized white foci may be seen. In focal areas eosinophils and signs of necrosis are found.

Hepatic coccidiosis

Hepatic coccidiosis is caused by E. stiedai in rabbits. The liver is enlarged and yellowish nodules are found on the surface.

Diagnosis

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Clinical diagnosis

The most common clinical signs of all cases of coccidiosis are: depression, reduced weight gain and even weight loss, mortality and diarrhoea. The consistency and the colour of faeces may vary: from watery to mucoid fluid and from greyish yellow to black. The droppings might be mixed with blood.

Further on, other general signs of coccidiosis are increased thirst and anorexia. Usually, several animals from one flock are affected, but not all species of coccidia cause the same levels of morbidity and mortality.

Differential diagnosis

It is important to exclude those diseases which cause similar symptoms as well as pathology. Intoxications and infestations with bird mites, but also infectious bursal disease, Marek's disease and intestinal diseases such as salmonellosis and Escherichia coli diarrhoea can show gastrointestinal signs.

If turkeys are ill, coccidiosis can be mistaken for haemorrhagic enteritis. It is necessary to establish the diagnosis with the aid of laboratory methods.

Laboratory diagnosis

The most common approach for the diagnosis of coccidiosis is the necropsy of the animal/s concerned. Coccidia can be seen in smears taken from suspect lesions. For this a small amount of mucosal scraping is taken on a slide and covered with a coverslip. If there are only a few oocysts in the smear it is a sign of a coccidial infection in the intestine, but it is not enough to speak of a clinical coccidiosis. The finding of coccidia together with typical lesions establishes the diagnosis.

If droppings are brought to the laboratory it is advisable to enrich the oocysts with a method called floatation. This procedure is based on the high specific density of the solution. The lighter oocysts are floating on the surface. From there, some drops are taken for microscopic examination.

List of Symptoms/Signs

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Disease Course

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The infection begins with the ingestion of sporulated oocysts from the environment which is frequently contaminated with oocysts that were excreted with faeces. The asexual and sexual developmental stages of coccidia then occur in the intestine. The parasitic stages are responsible for the damage in the mucosa. The lesions depend on the number and virulence of the ingested oocysts. The increase is self-limited.

In long-term disease, permanent re-infections take place. However, it is not a chronic disease, because the infection rests subclinically without clinical signs.

Epidemiology

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The life cycles of all coccidia species are similar. Some species vary in the number of asexual generations and in the time required for each developmental stage. The life cycle of Eimeria tenella is typical for all Eimeria.

Life cycle of E. tenella

The life cycle of replication of all Eimeria species, including Eimeria tenella, is divided into an internal and an external phase. The external phase begins with the excretion of non-sporulated oocysts with the faeces. The sporulation of the oocysts follows in the environment. The duration of this phase depends on ambient temperature and moisture. It is normally completed within 2 days.

Under oxygen supply the diploid sporont goes through meiosis, at the end of which it is haploid. This sporont is divided into four sporoblasts, which develop into four sporocysts with two sporozoites each.

The endogenous phase begins with the ingestion of sporulated oocysts. During 1-2 days after a host ingests these sporulated oocysts, their cell wall has been crushed in the gizzard and the sporozoites are released. The motile sporozoites penetrate the intestinal mucosa and enter epithelial cells of the lamina propria. From here they are transported to the intestinal crypts of Lieberkühn in the caeca. Here the sporozoites develop the first generation of schizonts. One schizogony (asexual reproduction cycle) results in about 900 merozoites which are released in the intestinal lumen after 60–72 hours. Then they penetrate new epithelial cells. Here the second generation of schizonts develops with 200–300 merozoites each.

Either a third generation of schizonts develops in new cells or the gametogony follows. This also occurs in new epithelial cells, and the merozoites are rounded up to female macrogametes and male microgametes. The latter develop into microgametocytes with two flagella. The result of the following fertilization between the macrogametes and the microgametocytes are so-called zygotes. A very resistant wall is built up around them. The resulting oocysts will be excreted in the faeces.

The lateral spread of all coccidial oocysts starts from the faeces. Often they are spread by personnel who do not disinfect their clothes and shoes and work under bad hygiene conditions. The mode of transmission is horizontal from animal to animal. The medium is always the faeces.

Impact: Economic

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The economic importance of coccidiosis results from different causes. On the one side there are mortality, reduced meat yields, suboptimal egg production, and insufficient feed utilization. On the other side there are the costs for diagnosis, treatment, prophylaxis, disinfection, and disposal of dead animals.

Coccidiosis is still one of the most common diseases of poultry production. In 1991 in the USA the expenditure for preventive medication was US$90 million, and over US$300 million worldwide.

Coccidia are frequently found in chickens brought to diagnostic laboratories. Surveys in North and South America demonstrate that coccidia are detected in nearly all broiler farms. A similar situation prevails in Europe and elsewhere.

Turkeys have coccidiosis but the lesions are not as severe as in chickens. The parasites often remain unrecognised and the animals recover quickly. Only five species are economically important (see Pathology section).

There are great losses in geese when the renal epithelial cells are infected with E. truncata. Young goslings often die when they are infected with this species. E. anseris is found in the intestine of geese; however, the mortality is not so high. Coccidiosis is sporadic in geese.

Outbreaks are known from domestic duck farms in New York, New Jersey (USA), Hungary and Japan.

The worldwide costs of coccidiosis in cattle are about US$700 million per year.

Zoonoses and Food Safety

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Isospora (I.) belli and I. hominis cause intestinal coccidiosis in humans. There is no clue for any intermediate host. Transmission tests in laboratory animals were not successful. Only I. belli is contagious for gibbons.

Disease Treatment

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Drug treatment

It is important to treat birds immediately after the onset of coccidiosis. If the diagnosis is fixed, all the animals which were in contact should be treated. Birds which have not developed signs should also be treated. By the time the clinical signs are obvious, the second generation of schizonts was already formed. That means the drugs do not influence the lesions of the schizonts. For the healthy birds this is only a prophylaxis. This is the reason for the importance of immediate treatment after the first symptoms are seen, even if it is only a suspicion.

As a rule in Germany, sulfachlorpyracin (Esb3®) is used. It is given for 3 days, then there is a pause of 2 days and then it is given once again for 3 days.

There are fowls which do not tolerate the sulfonamids. For these cases the veterinarians can apply Amprolvet® or Amprolvet Super® into the drinking water. However, in Germany there is no license for food-producing birds.

A very effective remedy for all kinds of fowls is toltrazuril (Baycoc®) which does not interfere with the formation of immunity. It is given in the drinking water. Several additional anticoccidials are available. A great problem is the rapid development of drug-resistance of some strains of coccidia. There are three methods to avoid this resistance: ‘shuttle’, ‘switch’ and ‘rotation’ programmes.

Shuttle or dual programme

Switch the anticoccidial drugs in the middle of the bird’s growing period. This programme is called ‘shuttle’ in the USA and a ‘dual’ programme in other countries. The purpose of shuttle programmes is to reduce the development of drug resistance.

Switch programme

Change the anticoccidial drugs from one crop to the other. The same product is used from day of hatching out to slaughter.

Rotation programme

Switch the anticoccidial drugs over longer intervals. Most of the producers make switches in the spring and in the autumn. Producers often notice a boost in productivity for a few months after change of anticoccidial drugs.

These three programmes are successful in many countries.

This method of prophylaxis does not solve the whole problem, but is a delay of the beginning of resistance.

Anticoccidial drugs are remedies which can be added into the food to protect the animals from coccidiosis.

It is forbidden to apply anticoccidial drugs to laying hens.

Medicinal plants and herbal preparations

There is a herbal drug under the name Ropapharm®. It is an extract of thyme and Oreganum. This remedy reduces bacterial multiplication and enhances immunity development.

Drug resistance

Drug resistance means the tolerance of a drug by coccidia after it is given to the animals. Drug resistance is known in Europe, in the USA and in South America. Even when coccidia develop less resistance to drugs, other long-term exposure to any drug might produce resistance eventually. Genetic changes of Eimeria species cause this type of resistance. It takes a long time before the coccidia will become tolerant. Once established in a strain of coccidia, it will remain there for many years. Reversion to drug susceptibility is possible.

Prevention and Control

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Prophylaxis

Prevention of coccidiosis is very important. Once diarrhoea has developed, most of the damage to the intestine has already occurred.

There are several ways to prevent chickens from getting coccidiosis:

• 
  
  The control of coccidiosis is achieved primarily by the use of anticoccidial drugs which can be added into the feed. But, because of the risk of increased drug resistance, other methods become important.
  
  
• The use of feed additives: for example Betaine, a product from sugar beets.
  
• The chick’s feed and water should be placed separately from droppings.
  
• It is better to let the birds sit and defecate over wire netting.
  
• Water vessels should stand on wire mesh to eliminate a concentration of wet droppings.
  
• Improvement of climate in the stables, to avoid moist litter. Litter should be changed often and should be dry.
  
• It is necessary to prevent overcrowding.
  
• If an outbreak occurs, the treatment must begin immediately.
  
• Keeping flies away from the animals.
  
• Vaccination with live coccidia: seven species are the most common and important (E. tenella, E. maxima, E. acervulina, E. brunetti, E. necatrix, E. praecox and E. mitis).
  
• Hygienic conditions must be optimal: regular and thorough disinfection of the stables and permanent cleaning of the feeding and watering vessels.
  
• Coccidiostats are substances which do not prevent infection but development of coccidia.
  
• Visitors should wear one-way boots and protective clothes or new coveralls.

Immunization and vaccines

Immunity is defined as the body’s power to resist the deleterious effects of an infectious agent, usually by preventing the multiplication of the causative parasite or micro-organism.

The permanent use of special anticoccidia in the food leads to the development of coccidia which are resistant against these remedies.

There are two modes of resistances. Firstly, the relative resistance; in this case, higher doses are still effective. Secondly, complete resistance occurs when even the highest possible doses are not able to prevent disease.

The use of attenuated Eimeria strains for vaccination results in good protection against the disease, but does not completely prevent replication of virulent Eimeria.

Continuous passages of Eimeria in chicken embryos are one possibility for attenuation. A strain of E. tenella was attenuated in more than 62 passages in embryos. The initial pathogenicity disappeared during these passages.

Another way of 'attenuation' is the selection and the subsequent multiplication of oocysts in vivo. These strains are named 'precocious strains'. They have a defect in the second generation of schizonts and are therefore less pathogenic than the originals but immunogenic.

The inoculation of virulent strains is also possible, but it is necessary to control the number of oocysts in the dose.

In Germany, the concept of preventive medication is widely used because most of the damage occurs when clinical signs are obviously seen.

The live vaccine Paracox8®, which is used in Germany, is judged as successful. It contains eight attenuated species of Eimeria. The vaccine is given once into the drinking water for animals that are 5-9 days old. The result is an infection with a small number of oocysts which develop and induce immunity. This type of immunization is thus only possible in floor-maintained chickens where they are in contact with their own faeces.

However, this method of vaccination has met with a limited success. It could be possible that the young animals are already infected with pathogenic coccidia. In such situations vaccination with attenuated strains is not able to prevent a strong outbreak. If birds, especially chickens, live in cages the 'trickle-immunization' can be successful: a small quantity of oocysts is given into the food in the first 3 weeks of life.

Coccidiocidal drugs destroy all parasites whereas coccidiostatic drugs arrest only the development. A relapse of coccidiosis is possible with coccidiostatic drugs.

Most Eimeria species are able to produce immunity after natural exposure if they live in immunocompetent hosts. Immunity is the result of permanent oocyst-assimilation and asexual reproduction.

The first generation of schizonts from E. tenella is less able to produce immunity. In comparison, the second generation of schizonts from E. tenella and E. maxima leave high immunity.

The immunity is specific to each species. This attribute is important for the identification of special species of coccidia. There are variants from E. acervulina and from E. maxima. This is important for the immunizations. There is probably a specific immunity against different strains of the same species. At this time antibodies against the extracellular invasive stages were produced.

There are differences with regard to the immunogenicity of the coccidia.

For example, E. tenella and E. necatrix are located deep in the tissue but they are not the most immunogenic species. It is E. maxima and E. brunetti which have the highest immunogenicity. The other coccidia that are parasites on the surface of intestinal tissue are intermediate in immunogenicity.

In summary: all species can produce immunity. They can live in the presence of sporulated oocysts in the straw and it guarantees good protection.

Local Control

Humans are one of the greatest transmitters of coccidial oocysts. That does not mean that they are infected but they use (for example) contaminated equipment. Parasites and diseases can be carried on equipment. Equipment should thus never leave a farm. Infectious material can be transported on crates, footwear and utensils to other places. Poultry-hauling equipment can disseminate the parasites through feathers, faeces, blood, exudates and skin encrustations left in the cages. All hauling equipment should be washed and disinfected after use. Footwear and gloves, even hands, can also transmit the protozoans to other fowls.

Visitors are often a source of infection. They should change their clothes before visiting a farm and change them again at the end, when leaving the farm.

Carrier birds, for example sparrows, are a great problem for chickens that live on the ground during the day. They can be mechanical vectors of coccidia.

Fowls of multiple ages which are in contact or proximity can be the carriers and shedders and serve as a source of infection on breeding farms. As a solution, it is best to isolate the younger ones from the older animals until they have been vaccinated or have obtained another prophylaxis.

Husbandry Methods and Good Practice

It is necessary to observe precautionary measures at the start of keeping poultry.

The younger fowls should live in complete separation from the older ones until they are vaccinated or have received another prevention.

In addition to sanitary practices, environmental factors (temperature, humidity) play an important role. Coccidia survive for months under warm and moist conditions outside the host.

Farms are not always limited to a single age of poultry. The farm should be divided into separate quarantinable units for different age groups of birds: rearing area, pedigree unit, production groups. Each area must be periodically depopulated, cleaned and sanitized. If coccidiosis breaks out in one area it must be under control so that it will not infect the other units. Provide special equipment for each unit.

It is necessary to pay attention to any free-flying wild birds that can expose poultry to coccidia. Therefore bird-proof houses are built with controlled light intensity, temperature and ventilation. The equipment storage areas should also be bird-proofed.

An apron of concrete at the entrance to a poultry house prevents people bringing in the protozoans. Rain and sunshine may help to keep the apron clean. Further on, a water faucet, boot brush and a place to disinfect shoes are also desirable.

Improper ventilation can lead to wet litter. The litter must be kept dry so that the coccidial oocysts are inhibited in their development.

Inside the building, the surface should be of impervious material (for example concrete), so that it is easier to wash and disinfect.

Outbreaks of coccidiosis occur often if chickens or other poultry reared in cages are brought to litter floors. An effective vaccination is thus necessary. Roost areas over screened dropping pits are often seen in breeder hen houses and in rearing houses for layers and breeders. They separate the chickens from their faeces. However, it is necessary to clean them periodically.

In spite of all prevention methods, poultry may receive coccidiosis. It is important to consider possible means of treatment before it is needed.

References

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Greuel E, 1992. Kokzidiosen. In: Heider G, Monreal G, Mészáros J, eds. Krankheiten des Wirtschaftsgeflügels, Band II, Spezieller Teil 2. Jena, Germany: Gustav Fischer Verlag, 365-395

Gylstorff I, Grimm F, 1987. Vogelkrankheiten. Stuttgart, Germany: Ulmer, 345-362

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McDougald LR, 1997. Protozoa - Introduction. In: Calnek BW, Barnes HJ, Beard CW, McDougald LR, Saif YM, eds. Diseases of Poultry. Ames, Iowa, USA: Mosby-Wolfe

McDougald LR, Reid W, 1997. Coccidiosis. In: Calnek BW, ed. Disease of Poultry 10th edition. London, UK: Mosby Wolfe, 865-883

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OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties

Pellérdy LP, 1974. Coccidia and Coccidiosis. Berlin, Hamburg, Germany: Parey

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Rommel M, 1992. Parasitosen der Wiederkäuer - Protozoen. In: Eckert J, Kutzer E, Rommel M, Bürger HJ, Körting W, eds. Veterinärmedizinische Parasitologie. Berlin, Hamburg, Germany: Parey, 109-174

Rommel M, 1992. Parasitosen des Kaninchens - Protozoen. In: Eckert J, Kutzer E, Rommel M, Bürger HJ, Körting W, eds. Veterinärmedizinische Parasitologie. Berlin, Hamburg, Germany: Parey, 646-652

Rommel M, 1992. Parasitosen des Nutzgeflügels - Protozoen. In: Eckert J, Kutzer E, Rommel M, Bürger HJ, Körting W, eds. Veterinärmedizinische Parasitologie. Berlin, Hamburg, Germany: Parey, 664-694

Rommel M, 1992. Parasitosen des Schweines - Protozoen. In: Eckert J, Kutzer E, Rommel M, Bürger HJ, Körting W, eds. Veterinärmedizinische Parasitologie. Berlin, Hamburg, Germany: Parey, 444-458

Rommel M, 1992. Protozoologische Methoden. In: Eckert J, Kutzer E, Rommel M, Bürger HJ, Körting W, eds. Veterinärmedizinische Parasitologie. Berlin, Hamburg, Germany: Parey, 46-51

Siegmann O, 1993. Endoparasiten - Protozoen - Apicomplexa. In: Siegmann O, ed., Hinz, K-H, Kaleta EF, Kösters JM, Lüders H, Monreal G. Kompendium der Geflügelkrankheiten. Berlin, Hamburg, Germany: Parey, 261-265

Zander DV, Bermudez AJ, Mallison ET, 1997. Principles of Disease Prevention: Diagnosis and control. In: Calnek BW, Barnes HJ, Beard CW, McDougald LR, Saif YM, eds. Diseases of Poultry. Ames, Iowa, USA: Mosby-Wolfe, 3-45

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