Eimeria
 

Classification: Taxonomic ranks under review (cf. Illustrated Guide to Protozoa, 2000. Allen Press)

Protista (unicellular eukaryotes)
Apicomplexa (cells with cluster of organelles known as apical complex)
Coccidea (gamonts small and intracellular, form small resistant spores called oocysts)
Eimeriida (gametes develop independently without syzygy; known as coccidian parasites)

Family: Eimeriidae
These protozoa are known as the enteric coccidia; monoxenous (one-host) parasites in the digestive tracts of herbivores or carnivores causing diarrhoeal disease (known as coccidiosis). Parasites form environmentally-resistant oocysts which undergo faecal-oral transmission between hosts. There are three sequential stages in the parasite life-cycle: endogenous multiplication by asexual merogony (variously known as schizogony) followed by sexual gamogony (♂ microgametes fertilize ♀ macrogametes producing oocysts) which are excreted and undergo asexual sporogony (forming sporocysts containing infective sporozoites). Many genera are recognized on the basis of oocyst configuration (the number of sporocysts per oocyst, and the number of sporozoites per sporocyst).

Eimeria spp. [these species cause coccidiosis in vertebrates, especially herbivores]

Parasite morphology: Coccidian parasites form three developmental stages: schizonts, gamonts and oocysts. Schizonts range in size depending on parasite species, location in the host and stage of maturity. They begin as small basophilic rounded cells (mother meronts) located intracellularly within host cells. The meronts form numerous daughter merozoites by endogenous division of the nucleus followed by cytokinesis. Mature schizonts appear as membrane-bound clusters of small basophilic bodies (similar to bunches of grapes). Individual schizonts usually range in diameter from 10-100µm but some species form enormous megaloschizonts (up to 1mm in diameter). Gamonts exhibit sexual differentiation, with microgamonts (♂) apparent as multinucleate basophilic stages ultimately shedding small biflagellated microgametes; and macrogamonts (♀) evident as uninucleate eosinophilic cells with a single ovoid nucleus. Developing oocysts contain numerous eosinophilic wall-forming bodies which give rise to the tough outer oocyst walls. Unsporulated oocysts contain a developing sporoblast which eventually undergoes sporulation forming sporocysts which contain the infective sporozoites. Eimeria oocysts exhibit a characteristic 1:4:2 configuration, that is, each oocyst contains 4 sporocysts each containing 2 sporozoites. Oocysts are generally ovoid to ellipsoid in shape, range from 10-40µm in length by 10-30µm in width, and may contain specialized structures, such as polar caps, micropyles, residual and crystalline bodies.

Host range: Infections have been recorded throughout the world in most vertebrate species, including eutherian and metatherian mammals, birds, reptiles and fish. Most coccidian species are considered to be highly host-specific and only parasitize single host species (oioxenous), although some species in birds and reptiles may parasitize closely-related hosts (stenoxenous) and a few species in fish may parasitize unrelated hosts (euryxenous). Many hosts also harbour multiple species of coccidia which may vary considerably in morphology, developmental cycle, site of infection and pathogenicity. Twelve Eimeria spp. have been described from cattle, 11 species from sheep, 9 from goats, and 7 from chickens. In general, the small rapidly-developing species are generally the most pathogenic.

Site of infection: Most species undergo endogenous development in the intestinal mucosa (small and/or large intestines) whereas some species develop in the liver, gall bladder or kidneys. They generally exhibit rigid tissue tropism, infecting host cells in particular locations. The parasites undergo several cycles of schizogony culminating in the lysis of host cells to release merozoites. Ultimately, gamonts are formed which mature to produce micro- and macro-gametes that undergo fertilization forming a non-motile zygote (oocyst) which is excreted with host faeces.

Pathogenesis: Most species are not significant pathogens and cause little or no disease. Certain species, however, are highly pathogenic and cause catarrhalic or haemorrhagic enteritis by severe erosion of the mucosal membranes through cell lysis resulting in profuse watery-to-bloody diarrhoea. Clinical disease is not usually manifest until cumulative tissue damage associated with second or third generation schizogony. Moderately-affected animals may show progressive signs such as poor weight gain or weight loss, weakness and emaciation, while severely-affected individuals may die soon after the appearance of disease. Pathogenicity depends on many factors; such as parasite species, viability, infectivity, virulence, tropism, host age, nutritional status, immunological competence, as well as prevailing environmental conditions (temperature, moisture) and management practices. Young animals are most susceptible to clinical disease, although survivors develop strong specific protective immunity against subsequent infection and disease.

Mode of transmission: Oocysts excreted with host faeces contaminate the external environment, but they must undergo internal sporulation (sporozoite formation) before they become infective. New hosts are infected when they ingest sporulated oocysts contaminating food or water supplies (faecal-oral transmission). Following ingestion, oocysts and sporocysts excyst in the intestines releasing their contained sporozoites which invade host cells to begin merogony. Excystation stimuli include appropriate post-gastric physico-chemical conditions, such as oxygen levels, pH, bile salts, pancreatic enzymes, etc.

Differential diagnosis: Clinical signs usually coincide with parasite patency (patent period = period during which oocysts are produced). Infections are usually diagnosed by the coprological examination of host faeces for coccidial oocysts (concentrated using various sedimentation-flotation techniques). Unstained oocysts are best observed by light microscopy using suboptimal transmitted illumination (condenser wound down to introduce diffraction), phase-contrast or interference-contrast optics. Fresh faecal samples may only contain unsporulated oocysts so differential specific diagnosis may sometime require short-term storage to facilitate sporulation (2% potassium dichromate is often used to suppress microflora during storage, but not for piscine species, and refrigeration can slow the process down if so required for field samples). Researchers have recently used a range of molecular techniques to characterize genetic variation between and within parasite species, but few techniques are suitable for routine diagnostic use.

Treatment and control: Disease progression is usually so rapid that any therapeutic (curative) treatment may simply be too late. For this reason, continuous in-food or in-water medication is often used for prophylactic (preventative) treatment in many intensive animal industries. A wide range of drugs are available, including those with coccidio-static (reversible suppressive) activity or coccidio-cidal (irreversible lethal) activity. The main drug groups include sulfonamides (sulfanilamide, trimethoprim, ethopabate), pyridinoles (clopidol, decoquinate), nitrobenzamides (zoalene), organic arsenicals (roxarsone), nitrofurans (furazolidone, amprolium), quinazolinones (halofuginone), polyether ionophorous antibiotics (monensin, laslocid, salinomycin, narasin), asymmetric (diclazuril) and symmetric (toltrazuril) triazines. Regrettably, there are mounting problems being encountered with drug resistance amongst many coccidian species, especially that against synthetic drugs which tends to persist within parasite populations. Many industries recommend periodic rotation between different drug groups and the use of combination (cocktail) drugs to minimize the occurrence of resistance. Most coccidial infections stimulate the development of strong protective immune responses, albeit transient unless premunitive (short-lived unless parasites persist). There has been considerable success with control through immunoprophylaxis using attenuated or precocious strains of parasites, particularly in the poultry industry. Researchers are now attempting to develop recombinant subcellular vaccines. Outbreaks can generally be controlled by management practices based around improving hygiene, reducing crowding, removing contaminated litter and isolating infected individuals. Chemical disinfection is usually impractical as the oocysts are resistant to many conventional disinfectants.

Eimeria species

Oocyst size

Host species

Site of infection

Pathogenicity

E. acervulina

18 x 14µm

chickens

anterior small intestine

high

E. brunetti

26 x 22µm

chickens

small and large intestines

high

E. maxima

30 x 20µm

chickens

mid small intestine

moderate

E. mitis

16 x 15µm

chickens

small and large intestines

low

E. necatrix

20 x 17µm

chickens

small intestine, caecum

high

E. praecox

21 x 17µm

chickens

small intestine

low

E. tenella

23 x 19µm

chickens

caecum

high

E. adenoides

25 x 16µm

turkeys

small and large intestines

high

E. dispersa

26 x 21µm

turkeys

anterior small intestine

moderate

E. meleagridis

24 x 18µm

turkeys

caecum

moderate

E. meleagrimitis

19 x 16µm

turkeys

anterior small intestine

high

E. gallopavonis

26 x 21µm

turkeys

small and large intestines

moderate

E. innocua

22 x 21µm

turkeys

small intestine

low

E. subrotunda

22 x 20µm

turkeys

small intestine

low

E. alabamensis

19 x 13µm

cattle

small and large intestines

moderate

E. auburnensis

38 x 23µm

cattle

small intestine

low

E. bovis

28 x 20µm

cattle

small and large intestines

high

E. brasiliensis

37 x 27µm

cattle

unknown

low

E. bukidnonensis

49 x 35µm

cattle

unknown

low

E. canadensis

32 x 23µm

cattle

unknown

low

E. cylindrica

23 x 12µm

cattle

unknown

low

E. ellipsoidalis

23 x 16µm

cattle

small intestine

low

E. pellita

40 x 28µm

cattle

unknown

low

E. subspherica

11 x 10µm

cattle

unknown

low

E. wyomingensis

40 x 28µm

cattle

unknown

low

E. zuernii

18 x 16µm

cattle

small and large intestines

high

E. ahsata

33 x 23µm

sheep

small intestine

low

E. bakuensis

29 x 19µm

sheep

small intestine

low

E. crandallis

22 x 19µm

sheep

small and large intestines

high

E. faurei

32 x 23µm

sheep

small and large intestines

low

E. granulosa

29 x 21µm

sheep

unknown

low

E. intricata

48 x 34µm

sheep

small and large intestines

low

E. marsica

19 x 13µm

sheep

unknown

low

E. ovinoidalis

24 x 20µm

sheep

small and large intestines

moderate

E. pallida

14 x 10µm

sheep

unknown

low

E. parva

17 x 14µm

sheep

small and large intestines

low

E. weybridgensis

24 x 17µm

sheep

small intestine

low

E. alijevi

17 x 15µm

goats

small and large intestines

low

E. aspheronica

31 x 23µm

goats

unknown

low

E. arloingi

28 x 19µm

goats

small and large intestines

high

E. caprina

34 x 23µm

goats

small and large intestines

moderate

E. caprovina

30 x 24µm

goats

unknown

low

E. christenseni

38 x 25µm

goats

small intestine

high

E. hirci

21 x 16µm

goats

unknown

moderate

E. jolchijevi

31 x 22µm

goats

unknown

low

E. ninakohlyakimovae

21 x 15µm

goats

small and large intestines

moderate

E. debliecki

18 x 14µm

pigs

small intestine

moderate

E. polita

26 x 18µm

pigs

small intestine

moderate

E. scabra

32 x 22µm

pigs

small and large intestines

low

E. spinosa

21 x 16µm

pigs

small intestine

low

E. porci

22 x 15µm

pigs

small intestine

low

E. neodebliecki

21 x 16µm

pigs

unknown

low

E. perminuta

13 x 12µm

pigs

unknown

low

E. suis

18 x 14µm

pigs

unknown

low

E. leuckarti

55 x 38µm

horses

intestines

moderate

E. stiedae

35 x 20µm

rabbits

liver

high

E. flavescens

30 x 20µm

rabbits

intestines

moderate

E. intestinalis

26 x 18µm

rabbits

intestines

moderate

E. macropodis

25 x 13µm

kangaroos

intestines

low

 

 

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