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