EuroTier 2008
Coccidiosis
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Occurrence: Worldwide Age affected: Piglets pre-weaning, weaners (growers / finishers, sows, boars) | |
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Photo: Ananmnŏse – LDA22 |
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Effects: Paste-like or watery diarrhoea, stunting, death in piglets.
Pig health & diseases main page
Coccidia are single cell protozoan parasites which multiply in the cells lining the intestine. Isopora suis is the main pathogen of piglets and is responsible for the most coccidial diarrhoea. Cryptosporidium parvum may also affect piglets but occurs commonly in weaned pigs and Eimeria species occur in weaned pigs, finishers and gilts but not in piglets. The resistant oocysts of I. suis are eaten and reach the upper small intestine where small sporozoites hatch and invade cells of the intestinal lining within 24 hours. The multiply asexually, damaging their host cell, to give rise to first stage merozoites and then to a further two stages within cells of the small intestinal lining. Each fourth stage cell reaches the lower part of the small intestine at about 4-5 days after infection and invades an epithelial (lining) cell to produce the sexual stage. Some become groups of microgametes and some remain single to become macrogametes. Mating in the gut produces oocysts which appear in the faeces as oocysts within 5 days of infection. Eimeria species multiply in the same way as I. suis, but Cryptosporidium remains in the absorptive, apical part of the cell and appears to prevent absorption of nutrients and cause cell death.
Coccidiosis causes malabsorption, diarrhoea, loss of condition and some deaths. The faeces of piglets may be whitish and firm, there may be transient pasty diarrhoea or profuse yellowish, watery diarrhoea between 5-15 days of age and most commonly from 7-10 days of age. Affected piglets may be thinner than unaffected litter mates and remain gaunt and hairy for some weeks thereafter. Severely affected piglets may die. Mortality rates may reach 20%. The diarrhoea responds poorly to antimicrobial therapy and growth depression occurs in recovered animals. I. suis diarrhoea rarely continues beyond weaning. Wasting and diarrhoea have been recorded in gilts, finishing pigs and wild boar infected with Eimeria spp. In experimental E. neodebliecki infection, frothy, mucoid diarrhoea occurred 9-12 days post infection. Most infections with C. parvum are asymptomatic (90% in one study). Clinical signs rarely appear before 3 days of age and are most commonly reported in piglets at 10-21 days of age. Affected piglets are depressed and pass a watery, sometimes brownish diarrhoea which may persist for 3-5 days. The organism can be demonstrated in the faeces of diarrhoeic weaners. Affected weaned pigs are often depressed and anorexic, in poor condition with a rough dirty coat and pasty faeces.
The occurrence of whitish malabsorptive diarrhoea in piglets ages 5-15 days and its failure to respond to antimicrobial therapy suggest coccidiosis due to I. suis. Oocyts can be seen in faeces by light microscopy. Carcases of affected piglets are in poor condition and dehydrated. Obvious lesions are restricted to the jejunum and ileum which appear thickened with a necrotic lining. The intestinal contents may be creamy or watery with flecks of milk and the villi are stunted when viewed using a dissecting microscope. The presence of coccidia in histological sections and in stained impression smears of jejunal and ileal mucosa confirms the diagnosis. Oocyts are sporulated in potassium dichromate to confirm the species involved. The clinical signs and the failure of diarrhoea in older pigs to respond to antimicrobial therapy may suggest coccidiosis caused by Eimeria species. The diagnosis can be confirmed in the same way as for I. suis coccidiosis in piglets. C. parvum is diagnosed by laboratory means only and can be seen in stained faecal smears as 3-4 micron orange-red ovals or circles and fluoresce with auramine. They are clearly visible by microscopy on the brush borders of infected epithelial cells. Antigen ELISAs and DNA probes can also be used.
Coccidiosis in piglets can be treated with trimethoprim sulphonamide and they should be supported with electrolyte. Toltrazuril given as an oral suspension by stomach tube on day 3 prevents diarrhoea, prevents oocyst shedding and can maintain piglet growth. Scrupulous attention should be given to hygiene in control, as the high levels of oocysts passed by piglets and their ability to survive for months make environmental contamination important. Sows should be cleaned on entry to the farrowing houses which should be disinfected or fumigated with methyl bromide or ammonia (final concentration 2%). Steam cleaning at 65˚C for 15 minutes, flame guns, and proprietary disinfectants can also be used to destroy oocysts. Less disease and oocyst shedding ahs been demonstrated on fully slatted cleaned floors. Trimethoprim sulphonamide may be given b y injection or orally to older pigs with Eimeria species and the inclusion of an anticoccidial such as amprolium at 1 kg permix per tonne in sow feed for 7-10 days prior to farrowing and for 2 weeks afterwards will reduce the shedding of oocysts by sows and other pigs. No treatment has yet been shown to affect C. parvum. The oocysts can be destroyed by the same disinfectants as those of the other coccidia.
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