Eimeria Explained

Eimeria is a genus of apicomplexan parasites that includes various species capable of causing the disease coccidiosis in animals such as cattle, poultry and smaller ruminants including sheep and goats.[1] Eimeria species are considered to be monoxenous because the life cycle is completed within a single host, and stenoxenous because they tend to be host specific, although a number of exceptions have been identified. Species of this genus infect a wide variety of hosts. Thirty-one species are known to occur in bats (Chiroptera), two in turtles, and 130 named species infect fish. Two species (E. phocae and E. weddelli) infect seals. Five species infect llamas and alpacas: E. alpacae, E. ivitaensis, E. lamae, E. macusaniensis, and E. punonensis. A number of species infect rodents, including E. couesii, E. kinsellai, E. palustris, E. ojastii and E. oryzomysi. Others infect poultry (E. necatrix and E. tenella), rabbits (E. stiedai) and cattle (E. bovis, E. ellipsoidalis, and E. zuernii).[2] For full species list, see below.

The most prevalent species of Eimeria that cause coccidiosis in cattle are E. bovis, E. zuernii, and E. auburnensis. In a young, susceptible calf it is estimated that as few as 50,000 infective oocysts can cause severe disease.[3] Eimeria infections are particularly damaging to the poultry industry and costs the United States more than $1.5 billion in annual losses.[4] The most economically important species among poultry are E. tenella, E. acervulina, and E. maxima.[5] The oocysts of what was later called Eimeria stiedai were first seen by the pioneering Dutch microscopist Antonie van Leeuwenhoek (1632–1723) in the bile of a rabbit in 1674. The genus is named after the German zoologist Theodor Eimer (1843–1898).

Life cycle

The Eimeria life cycle has an exogenous phase, during which the oocysts are excreted into the environment, and an endogenous phase, where parasite development occurs in the host intestine. During the endogenous phase, several rounds of schizogony (asexual reproduction) take place, after which the sexual differentiation of gametes and fertilisation occurs. Parasite transmission occurs via the fecal-oral route. Infections are common in farming environments where many animals are confined in a small space.

right|thumb|450px|Eimeria life cycle

Oocysts

There are two forms of oocyst: sporulated or late oocyst, and unsporulated or early oocyst. An infected host releases oocysts into the environment in their unsporulated form. These contain a multi-layered cell wall making them highly resistant to environmental pressures.[6] Once released, the unsporulated oocysts undergo meiosis upon contact with oxygen and moisture.[7] This process is known as sporulation and the oocysts take approximately 2 to 7 days to become infectious.[8] The sporulated oocyst is said to be tetrasporic meaning it contains four sporocysts, while each sporocyst is dizoic, i.e. it contains two sporozoites.[2]

Once ingested, the oocysts undergo a process called excystation, whereby thousands of sporozoites are released into lumen of the intestine. In the case of E. tenella, this process is thought to occur due to the combination of enzymatic degradation and mechanical abrasion of the oocyst wall in the chicken's gizzard.[9]

Sporozoites

The motile sporozoites invade the enterocytes of small intestine, and migrate to their respective sites of development. Invasion is mediated through specialised membrane-bound structures on the surface of the parasite that release secretions. This results in the recognition of, and attachment to host cell receptors. This process is known as gliding motility, which is conserved across all species of Apicomplexa. Membrane glyconjugates have been proposed as potential host cell receptors for Eimeria species.[10] After invasion, the sporozoites develop into trophozoites, then into schizonts, where they undergo several rounds of asexual reproduction. This results in many nuclei developing within the schizont. Each nucleus develops into a merozoite.[2]

Invasion requires the formation of a moving junction between parasite and host cell membranes. In E. tenella, this involves parasite micronemes and rhoptry proteins including RON2, RON5 and AMA-2.[9] It is unlikely that the host cell is completely passive in the invasion process, although evidence of host physical forces that assist in mediating parasite entry remains controversial.

Merozoites

When schizonts rupture, merozoites are released, which either go on to re-infect more enterocytes or develop into either male or female gametes via the process of gametogenesis. These gametes fuse to form an oocyst, which is then released in its non-infectious, unsporulated form through the faeces of the host.

Merozoite invasion also requires the formation of a moving junction, however the proteins involved in this process differs from those on sporozoites. Rhoptry proteins AMA-1 and RON4 are found exclusively on merozoites. There is also a greater diversity of variant surface antigens found on the surface of merozoites. It is hypothesised that this may be due to the fact that merozoites are short-lived and a greater antigen repertoire would permit faster binding and invasion.[9]

Taxonomy

right|thumb|350px|Evolutionary relationships among Apicomplexa

The Eimeria lie within the family Eimeriidae. Eimeria accounts for close to 75% of the species within this family, and it is the most specious of the genera of the Apicomplexa with 1,700 described species.[11]

Attempts to subdivide this large taxonomic unit into separate genera have been made. The classification of eimeriid coccidian was largely based on morphological and life cycle details.[12] More recently, classification has been done using rDNA and mitochondrial genes, which indicate Eimeria may be paraphyletic to Isospora and Cyclospora [13]

Eimeria: These species are tetrasporocystic with dizoic, nonbivalved sporocysts with or without Stieda bodies. This new genus retains the majority of the species.

Goussia (Labbe 1896): These species are tetrasporocystic, dizoic, lack Stieda bodies, and have sporocyst walls consisting of two valves joined by a longitudinal suture. This genus contains about 20 species.[14]

Crystallospora (Thelohan 1893): The species in this genus is tetrasporocystic and dizoic, and have dodecahedral sporocysts composed of two hexagonal, pyrimidal valves joined at their bases by a suture. This genus contains a single species, Crystallospora cristalloides

Epieimeria

The species in this genus are tetrasporocystic, dizoic, possess Stieda bodies, and undergo merogony and gametogony on the lumenal surface of the intestinal tract. Three species are in this genus.[15]

Species identification

Methods for species identification are varied and among others, include isozyme analysis,[16] the use of rRNA and rDNA probes,[17] DNA assays and recombinant DNA techniques.[18] [19] [20] PCR has proven most useful for outbreak surveillance.[21] Prior to these methods, species identification was based on phenotypic characteristics such as the site of parasite development, the oocyst structure, the host species, cross immunity and the presence of lesions. Out of these, comparing oocyst structures was the most commonly used method.[22] [2]

Genomics

A whole genome sequencing project is in progress with chosen species, Eimeria tenella. The genome is about 60 megabases in size and has a GC-content around 53%. The 14 chromosomes range in size from 1 to > 6 megabases. Since 2013, the sequencing and annotation of a further six avian Eimeria species genomes is in progress.[23]

Pathology and symptoms

See main article: Coccidiosis. Coccidiosis typically results in diarrhoea, weight loss and dehydration. A combination of these factors may result in poor growth and death of the animal, particularly amongst young.[8] Other clinical signs include lethargy, depression, and reduced normal grooming behaviour.[24] Diarrhoea may be bloody due to intestinal epithelium dying off when a large number of oocysts and merozoites burst out of the cells.

The severity of the disease is directly dependent on the number of infective Eimeria oocysts that are ingested.[25] The pathogenesis of infection varies from mild to severe, and is largely dependent on the magnitude of infection.[26] In light infections, the damage to the gut might only be minimal and be rapidly repaired as cells are rapidly replaced by the body. However, in heavy infections, it may only take two weeks for many intestinal epithelial cells to be infected with either Eimeria meronts or gametocytes. These cause the epithelial cells to burst, which causes significant damage to the intestine epithelial layer, resulting in the release of blood, fluid, and electrolytes into the intestine.[27]

Prevention and treatment

Good animal husbandry practices and prophylactic application of anticoccidial drugs that target different stages of the parasite lifecycle, such as sulfonamides, ionophores and toltrazuril, are the preferred methods of disease prevention, particularly in the poultry industry.[28]

The following drugs can be used for treatment of coccidiosis in cattle: amprolium, sulfaquinoxaline, and sulfamethazine. However, it is often more effective to prevent this disease in cattle, which can be aided by the products lasalocid, decoquinate, and monensin.

There is a growing problem of drug resistance, as well as possible drug residues in the meat once the animal is butchered. As a result, other avenues of control are being explored, particularly vaccine development, although several live attenuated vaccines have been in use since the 1950s.[29] [30] So far, the best practice is to vaccinate the chicks once they hatch from the egg so they are immune for life.

Infection with Eimeria results in life-long immunity to that particular parasite species, but does not give cross protection against other species. For these reasons, vaccines for control seem promising, of which live attenuated vaccines are most effective. However, the search for highly immunogenic antigens and overcoming antigenic variation of the parasites remains a challenge. Immunity to the parasite varies depending on parasite and host species, as well as the site of invasion. CD4+ T cells and interferon gamma (γ) are crucial components of natural immunity to infection.[31] Humoral immunity is thought to play little role in protection, and is most likely mediated through secretory IgA antibodies.[10]

Host-parasite relations

Fish

Reptiles

Birds

Mammals

List of species

External links

Notes and References

  1. Chartier, Paraud . Coccidiosis due to Eimeria in sheep and goats, a review . Small Ruminant Research . 103 . 1 . 84–92 . 2012 . 10.1016/j.smallrumres.2011.10.022.
  2. Fayner R . Epidemiology of protozoan infections: the coccidia. Veterinary Parasitology. 6 . 75–103. 1980. 1–3. 10.1016/0304-4017(80)90039-4.
  3. Daugschies A, Najdrowski M. Eimeriosis in Cattle: Current Understanding . Veterinary Medicine. 52 . 10 . 417–427 . 2005 . 10.1111/j.1439-0450.2005.00894.x. 16364016 .
  4. Yun CH, Lillehoj HS, Lillehoj EP . Intestinal immune responses to coccidiosis . Developmental & Comparative Immunology . 24 . 2–3 . 303–324 . 2002 . 10.1016/S0145-305X(99)00080-4. 10717295 .
  5. Shirley MW, Ivens A, Gruber A. etal. The Eimeria genome projects: a sequence of events . Trends in Parasitology . 20 . 5. 199–201 . 2004 . 10.1016/j.pt.2004.02.005. 15105014 .
  6. Belli SI, Smith NC, Ferguson DJ . The coccidian oocyst: a tough nut to crack!. Trends in Parasitology . 22 . 9. 416–423 . 2006. 10.1016/j.pt.2004.02.005. 15105014.
  7. Ryan R, Shirley M, Tomley F . Mapping and expression of micronemes genes in Eimeria tenella. International Journal for Parasitology . 30 . 14. 1493–1499 . 2000. 10.1016/s0020-7519(00)00116-8. 11428341.
  8. Foreyt WJ. Coccidiosis and Cryptosporidiosis in Sheep and Goats . . 6 . 3 . 1990 . 655–670 . 10.1016/S0749-0720(15)30838-0. 2245367 .
  9. Lal K. etal. Proteomic comparison of four Eimeria tenella life-cycle stages: Unsporulated oocyst, sporulated oocyst, sporozoite and second-generation merozoite . . 9. 19 . 2009 . 4566–4576 . 10.1002/pmic.200900305. 19795439 . 2947549.
  10. Augustine PC. Cellular invasion by avian Eimeria species . . 11 . 2000 . 1 . 113–122 . 10.1016/S0020-7519(00)00150-8. 11286188 .
  11. Ogedengbe JD, Ogedengbe ME, Hafeez MA, Barta JR. Molecular phylogenetics of eimeriid coccidia (Eimeriidae, Eimeriorina, Apicomplexa, Alveolata): A preliminary multi-gene and multi-genome approach . International Journal for Parasitology. 41 . 8. 843–850. 2015. 10.1016/j.ijpara.2011.03.007. 21515277 .
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  13. Morrison DA, Bornstein S, Thebo P, Wernery U, Kinne J, Mattsson JG. The current status of the small subunit rRNA phylogeny of the coccidia (Sporozoa) . International Journal for Parasitology. 34 . 4. 501–514. 2004. 10.1016/j.ijpara.2003.11.006. 15013740 .
  14. Jirku M, Jirku M, Obornik M, Lukes J, Modry D. Goussia Labbé, 1896 (Apicomplexa, Eimeriorina) in Amphibia: Diversity, Biology, Molecular Phylogeny and Comments on the Status of the Genus . Protist. 160 . 1. 123–136. 2009. 10.1016/j.protis.2008.08.003. 19038578 .
  15. Lom J, Dykova I. Pathogenicity of some protozoan parasites of cyprinid fishes . Symposia Biologica Hungarica. 23 . 99–118. 1981.
  16. Shirley MW . Enzyme variation in Eimeria species of the chicken. Parasitology . 71 . 3. 369–376. 1975 . 10.1017/s0031182000047144. 1202411. 41849277.
  17. Ellis J, Bumstead J . Eimeria species: studies using rRNA and rDNA probes. Parasitology . 101 . 1. 1–6. 1990 . 10.1017/s0031182000079671. 2235066. 30056695.
  18. Shirley MW . Eimeria necatrix: Selection and characteristics of a precocious (and attenuated) line. Avian Pathology. 13 . 4. 657–668. 1984. 10.1080/03079458408418564. 18766877. free.
  19. Shirley MW . Eimeria tenella: genetic recombination of markers for precocious development and arprinocid resistance. Applied Parasitology. 37 . 4. 293–299. 1996. 9060177.
  20. Procunier JD, Fernando MA, Barta JR . Species and strain differentiation of Eimeria spp. of the domestic fowl using DNA polymorphisms amplified by arbitrary primers. Parasitology Research. 79 . 2. 98–102. 1993. 8475039 . 10.1007/bf00932253. 20235745.
  21. Allen PC, Fetterer RH. Recent advances in biology and immunobiology of Eimeria species and in diagnosis and control of infection with these coccidian parasites of poultry. Clinical Microbiology Reviews . 15 . 1. 58–65. 2002 . 10.1128/cmr.15.1.58-65.2002. 11781266. 118059.
  22. Joyner LP, Norton CC . The activity of methyl benzoquate and clopidol against Eimeria maxima: synergy and drug resistance . Parasitology. 76 . 3. 369–377. 1978. 275786 . 10.1017/s003118200004823x. 23567308 .
  23. Shirley MD. etal. The Eimeria genome projects: a sequence of events. Trends in Parasitology . 20 . 5. 199–201 . 2004. 10.1016/j.pt.2004.02.005. 15105014.
  24. Lillehoj HS, Trout JM . Avian gut-associated lymphoid tissues and intestinal immune responses to Eimeria parasites. Clinical Microbiology Reviews . 9 . 3. 349–360 . 1996 . 8809465 . 10.1128/CMR.9.3.349-360.1996 . 172898 .
  25. Lindsay DS. etal. Specificity and cross-reactivity of hybridoma antibodies generated against Eimeria bovis sporozoites. Veterinary Parasitology . 32 . 2–3. 145–151 . 1989 . 10.1016/0304-4017(89)90115-5. 2672546 .
  26. Chapman HD. etal. Absorption and deposition of xanthophylls in broilers challenged with three dosages of Eimeria acervulina oocysts. British Poultry Science . 55 . 2. 167–173 . 2014. 10.1080/00071668.2013.879095. 24720798. 26935206 .
  27. Web site: Maas. J.. Coccidiosis in Cattle. California Cattlemen's Magazine. 24 April 2014.
  28. McDonald V, Shirley MW . Past and future: vaccination against Eimeria. Parasitology . 136 . 12. 1477–1489. 2009. 10.1017/S0031182009006349. 19523251. 43277313.
  29. Chapman HD. etal. Sustainable coccidiosis control in poultry production: the role of live vaccines. International Journal for Parasitology . 32 . 5. 617–629 . 2002. 10.1016/S0020-7519(01)00362-9. 11943233 .
  30. Ahmad. TA. El-Sayed. BM. El-Sayed. LH. 2016. Development of immunization trials against Eimeria spp.. Trials in Vaccinology. en. 5. 38–47. 10.1016/j.trivac.2016.02.001. 1879-4378. free.
  31. Smith AL, Hayday AC . Genetic analysis of the essential components of the immunoprotective response to infection with Eimeria vermiformis. International Journal for Parasitology . 28 . 7. 1061–1069 . 1998. 10.1016/S0020-7519(98)00081-2. 9724877.
  32. Skirnisson . K. . Thorarinsdottir . S. Th. . Two new Eimeria species (Protozoa: Eimeriidae) from wild rock ptarmigans, Lagopus muta islandorum, in Iceland. Parasitology Research . May 2007 . 101 . 4 . 1077–81 . 10.1007/s00436-007-0589-5. 17557155 . 21559619 .
  33. Yang . Rongchang . Brice . Belinda . Ryan . Una . Morphological and molecular characterization of Eimeria purpureicephali n. sp. (Apicomplexa:Eimeriidae) in a red-capped parrot (Purpureicephalus spurius, Kuhl, 1820) in Western Australia . International Journal for Parasitology: Parasites and Wildlife . April 2016 . 5 . 1 . 34–39 . 26977403 . 10.1016/j.ijppaw.2016.01.003. 4781968 .

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