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European Coccidiosis Discussion Group

February 14th 2001 - Central Veterinary Laboratory, Weybridge, UK

Notes by Paul McMullin of a selection of the presentations:

Remus, J. Practical benefits of Betaine usage in coccidia-damaged broilers.
Keywords : coccidiosis; Betaine; lesion scores; coccidiostats; control; vaccines;
Notes : The coccidial parasite damages gut epithelium causing effects such as diarrhoea, poor nutrient utilisation and poor performance. Betaine is widely distributed in nature. It is a methyl group donor allowing the methylation of homocysteine in the liver to methionine, thus reducing demand for dietary methionine. It is the active form of choline for methylation. In coccidial challenge S.methylmetionine production in the liver is increased 3-fold. However the main effect of betaine may be as an osomlyte. These maintain water balance in cells preventing cellular dehyration. Electrolytes have similar effects but they are charged particles which have other effects. Osmolytes are quickly transported into cells, are charge neutral and help protect enzymatic activity (especially the energy systems of the mitochondria). Water is very important - 85% of the hatchling, 60% of the adult carcase (muscle is 72-75%) Coccidiosis disturbs water and ion balance. Work done on birds at 21-35 days using betaine in water showed that heat and cocci stress are synergistic in reducing water retention (83%, 87% and 63%) - betaine supplementation substantially ameliorated this effect. Even unchallenged birds have changes in the E.M. appearance of enterocytes. Betaine has also been shown to be synergistic with Salinomycin at 44 and 66 ppm in reducing lesion scores and FCR. Similar improvements were demonstrated with tests of tensile strength of the gut. When interactions with various coccidiostats are examined the effects are largest when the coccidiostat is exerting less control. 0.15% betaine supplementation has also been shown to improve digestibility in coccidiosis-challenged birds. Previous work has demonstrated that betaine does not directly harm coccidia - its effects are mediated by its effects on the host. Villus height is maintained in E.acervulina birds supplemented with 0.1% betaine. Separate work shows that the ratio of villus height to crypt depth , though slightly increased in unchallenged birds is markedly increased in challenged birds. Work with a coccidiosis vaccine (Coccivac) has shown reduction of lesion scores, and improved FCR and breast weight in vaccinated birds treated with betaine. Work on the immune system in Germany and the University of California suggests that macrophages and liver Kuppfer cells are betaine accumulating. Betaine increases the number of leucocytes in villi significantly in coccidios-vaccinated birds. The improvement in villi height seen in challenged birds supplemented with betaine help explain improvements in tensile strength, lesion scores, nutrient absorption and FCR. Practical feed addition levels range from 750-1500g/tonne

Bedford, M. Microflora changes in the caeca in response to E.maxima challenge.
Keywords : coccidiosis; administration; Eimeria maxima; caecum; CC ratios; nutrition; enzymes; Betaine; necrotic enteritis; Clostridium perfringens;
Notes : Evidence for environmental and dietary factors: Germ free chicks differ in their response to indigestible diet - they are much more tolerant. The intestinal flora varies with major cereal in the ration. Enteric disease often shows an association with particular cereals - e.g. wheat is a high risk source for necrotic enteritis (even for migrating geese in Canada). Small differences in digestibility dramatically alter avilability of nutrients in the distal small intestine and caecum. Small intestine bacterial populations are dramatically reduced by antimicrobial growth promoters such as avoparcin. Enzymes also do this to some extent but also produce xylose from partially digested fibres which serves as substrate for some bacterial populations. The work on microbial populations here is based on GC:AT ratios of microbial populations. Each species has a similar DNA sequence and, hence GC:AT ratio. This technique relies on dying purified DNA with a heavy dye with affinity to GC then separating density gradient centrifugation - can be profiled, fractionated and sequenced. Broilact-treated Finnish chickens produces a characteristic tri-peak profile in the caecum but a different 2-peak profile in the ileum. Low profiles are mycoplasmas, clostridium perfringens, Campylobacter - Bifidobacterium is in the 60+ area. Bird-to-bird variation is minor except where flock uniformity (weight gain) is poor. Finnfeeds interest in coccidiosis relates to coccidial stress on GI tract mnicroflora. There are stress factors on all commercial farms. Challenge with E.maxima results in a signature of poor digestion - tripling of short chain fatty acids. Pancreatic enzyme production is, incidentally, reduced by about 50% . Challenge converts a single-peak caecal GC profile to a triple-peak one at 8 days p.i. the right-hand peak is a bifidobacterium which causes growth depression but not necrotic enteritis on inoculation. This organism is commonly raised in NE. Challenge with E.maxima results in C.perfringens in the ileum, challenge with C.p. does not result in persistence. Combined administration of enzyme and betaine reduces presence of CP in ileum after E.max challenge (a LR lactobacillus did not). Conclusions: Diet and environment significantly influences bacterial species and numbers in the intestinal tract. Most of the changes are not seen with traditional methods.

Pearson, D. Coccidiosis in Broilers.
Keywords : coccidiosis; lesion scores; diagnosis; control; coccidiostats; vaccines; necrotic enteritis;
Notes : This paper reviews the history of coccidiosis in broilers in the UK, current problems, diagnosis and control. In the 1970's there was widespread use of chemical coccidiostats which tended to last for relatively short periods. In the late 70's the first ionophore came along. In the early 80's ionophore mono-programmes were normal and problems were minor until acute Gumboro disease becae widespread. In the 90's chemical shuttle and rotation programmes returned, in particular with nicarbazin. Control was generally reasonable but some breakdowns occur. In the latter half of the 90's the loss of antimicrobial growth promoters has had an impact on product choice. Currently we have a limited portfolio of products and need to manage them. Clinical disease is there but not very common, intestinal coccidiosis is mainly maxima and acervulina, but the commonest problem is E.tenella. Intestinal coccidiosis is generally related to the breakdown in chemical efficacy. Diagnosis is based on gross pathology, detection of oocysts, faecal oocyst counts, and occasionally histology. It can be misdiagnosed and confused with necrotic enteritis. Clinical caecal coccidiosis is the most common and is associated with lack of sensitivity to ionophores. It is easily diagnosed by clinical signs and confirmed with PM findings (schizonts in caecal wall smear) - occasionally confused with severe E.maxima infections and haemorrhagic enteritis. Sub-clinical coccidiosis is much more difficult to evaluate. It is mainly intestinal coccidiosis and may be mixed with necrotic and other types of enteritis, "dysbacteriosis" and sub-optimal performance. Lesion scoring is the tool used most commonly - has the advantage of simplicity, difficulties relate to timing of sample, consistency of operator etc. It is helpful to plot the scores by species over time - generally most birds examined have 0 scores. There is no clear annual cycle. Interpretation of intestinal smears usually involves rough evaluation of numbers of coccidial oocysts and other stages. Control: More specific anti-coccidial disinfectant (Oocide) is now in use which appears to have some beneficial effects. Use of shuttles and rotation have also been used, though of late there has been some reduction in rotation. Vaccines are the other possibility. Shuttles - a winter programme usually involves nicarbazin up to 16 days (possibly up to 28 days). nFront end chemicals run the risk of Clostridium perfringens proliferation. Vaccine - would cost for the authors company 3m/year. It appears that there would be some loss of performance as well. The other issue is that there is a lack of an effective treatment for coccidiosis - we have only a single, not very effective product (perhaps by the substitution of the pyrimethamine in older products with trimethoprim).

Kaldhusdal, M. Clostridium perfringens into the limelight.
Keywords : coccidiosis; enzymes; necrotic enteritis; Clostridium perfringens; ionophore anticoccidials; disinfection;
Notes : This paper covers the importance of C.p., the disease forms and their epidemiology, prevention and experimental model work. C.perfringens is anaerobic, spore-forming but extremely rapid in proliferating (generation inteval as short - about 8-10 minutes). It requires 13 amino acids for growth but will grow well between 20 and 50 C and produce numerous toxins. The first reference to necrotic enteritis was in the Australian Veterinary Journal in the 30's. Work was done by Parrish at the CVL in 1961 (J.Comp.path). There are 3 forms:
Clinical (acute) necrotic enteritis (the classical form)
Increased mortality with diffuse necrosis of the intestinal mucosa, and diarrhoea is not a consistent finding. When the affected musa is sloughed off the remaining gut wall is very thin.
CP-associated hepatic change (cholangio-hepatitis). These changes are usually detected at slaughter - originally described by Randall et al in the UK. There is multifocal necrosis, and hepatitis, cholecystitis, inflammation of the bile ducts and bile duct proliferation as well as periacinar cell infiltration. Occasionally there may be massive hepatic necrosis though its association with CP is not as well established.
Sub-clinical necrotic enteritis. In this case there are not very distinct clinical symptoms, and, as for coccidiosis, this is probably the main problem. This requires lesion scoring with examination for a range of subtle lesions. Economic evaluation of flocks with high and low liver condemnations - difference of -2% weight, +.82% mortality, condemnations +1.02%, overall profit was reduced by 33% (to NOK0.7).
Epidemiology : Feed antibiotics, anticoccidials and feed ingredients are all important, as is feeding regimen and the presence of C.perfringens spores in feed (however this has not been determined in detail). Immunity plays a part - maternal immunity can have an effect. There are large differences between farms, most likely related to cleaning and disinfection of house and equipment. Coccidiosis is the most likely interacting infection. Prevention: "Now that growth promoters are probably coming to an end" problems are likely. Non-antibiotic feed additives, acids, prebiotics, enzymes, Broilact appears to reduce the frequency of NE. So far the most practical approach is to vaccinate the parents - the problems are that maternal immunity wanes quickly. Experimental Model. This is a multi-factorial disease, the agent is ubiquitous but CP strains are not well characterised. The author is beginning work on a challenge model.