Coccidiosis and Anticoccidial programme
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The document discusses coccidiosis, a parasitic disease of poultry caused by Eimeria species. It affects the intestinal system and can cause poor performance and death. Anticoccidial drugs are used to control the parasites and prevent disease. The life cycle of Eimeria involves sporulated oocysts being shed in feces and undergoing sporulation to become infective. Upon ingestion by a host, sporozoites are released and invade intestinal cells. Anticoccidials work by disrupting parasite development through various mechanisms like inhibiting folate synthesis, acting as thiamine antagonists, and affecting mitochondrial function or cell membranes. Common drugs include ionophores, synthetic compounds, and phyt
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Coccidiosis and Anticoccidial programme
- 1. Coccidiosis & Anticoccidials Life cycle of coccidian Host range Tissue tropism Anticoccidial drugs The most common poultry disease Caused by a parasitic organism (Eimeria Spp.) It damages the host’s intestinal system Cases loss due to less performace & death Anticoccidials are the molecule that used to counteract the causal agents of coccidian parasites
- 2. Life cycle; How it grow on? OCYST Infected Chicken shed with faeces. SPORULATION Heat, Humidity, O2 SPORULATED OCYST The Infective form , it can take as little as 1 week, or as long as 1 year. Each Sporulated Ocyst contains 04 SPOROCYST, Each Sporocyst contains 2 SPOROZOITES
- 3. Disruption of Ocyst by the action of Gizzard & HCL Release of Sporozoites & invade into Gut cell Reproduce asexually & produce Merozoites. 1st generation of Merozoites are released & invade new cell. Production of 2nd generation of Merozoites & further Gametes Ocyst formation & it sheds in droppings Sprulated Ocyst Life cycle How it grow on?
- 5. Eimeria tenella Eimeria maxima Eimeria acervulina Coccidiosis; Tissue tropism?
- 6. Anticoccidials Drugs Mode of Action Resistances Cross resistance
- 7. Anticoccidial drugs categories Polyether antibiotics or ionophores Produced by fermentation process Supress parasite by ions imbalance 1 Synthetic/Chemical compounds Produced by chemical synthesis Have a specific mode of action 2 Phytogenic molecule Natural products from plant extract. 3
- 8. 1. Affecting cofactor synthesis Pteridine + PABA Pteroic acids + Glutamic acid Trihydrofolate (THF) Dihydrofolate (DHF) Thymidine Purines Amino Acids Dihydropteoate synthase Dihydrofolate synthesis Dihydrofolate reductase Ethopabate Folate antagonist Blocks synthesis PABA Most active against E. maxima & E. brunetti. © Rogers et al. 1964 Sulphonamides synthetase reaction Block the conjugationInterfere with the dihydropteroate of pteridine & PABA. Effective against E. brunetti, E. maxima & E. acervulina. Less effective against E. tenella & E. necatrix © Ryley and Betts 1973 Pyrimethamine Inhibiting the enzyme dihydrofolate reductase. Have synergistic effect with sulphonamides © Kendall and Joyner 1956 Ethopabate, sulphonamides and pyrimethamine affect the second generation of schizonts
- 9. 2. Thiamine antagonist Glucose Glucose-6-P Glyceraldehyde-3-P Pyruvate dehydrogenase (PDH) Pyruvate Acetyl-CoA Lactate TCA Cycle a-Ketoglutarate Succinyl-CoA Nucleic Acid Pentose Phosphate Pathway © Frank LL, JPEN 2015 Activate membrane transport of nerve cell TPP Transeketolase Pyruvate dehydrogenase TPP TPP THIAMIN (Vit-B1) Pyruvate dehydrogenase
- 10. THIAMIN (Vit-B1) 2. Thiamine antagonist © Frank LL, JPEN 2015 Activate membrane transport of nerve cell TPP Transeketolase Pyruvate dehydrogenase TPP TPP Amprolium Taken by the receptor instead of Thiamine Pyruvate dehydrogenase Glucose Glucose-6-P Glyceraldehyde-3-P Pyruvate dehydrogenase (PDH) Pyruvate Acetyl-CoA Lactate TCA Cycle a-Ketoglutarate Succinyl-CoA Nucleic Acid Pentose Phosphate Pathway
- 11. 3. Affecting mitochondrial function Quinolone & Pyridine group Block electron transport & inhihit the respiration of Coccidia. Quinolone Buquinolate Decoquinate Nequinate (methyl benzoquate) Pyridine group Meticlorpindol Quinolone & Pyridine are synergistic. © Challey and Jeffers 1973 Nicarbazin (4,4′-dinitrocarbanilide) Inhibit succinate-linked NAD reduction in mitochondria Inhibit energy dependent transhydrogenase and accumulation of Ca2+ ions in mitochondria ©Dougherty 1974 Robenidine Inhibits the oxidative phosphorylation of mitochondria ©Wong et al. 1972
- 12. 4. Affecting cell membrane function Polyether antibiotics/Ionophores Influence the transport of mono- or divalent cations (Na+, K+ and Ca++) across cell membranes inducing osmotic damage. These drugs are accumulated by extracellular stages (like sporozoites and merozoites) of the parasite in the lumen of the intestine. © Berger 1951; Shumard and Callender 1967,Long and Jeffers 1982 The chemical structure of an ionophore is doughnut-shaped
- 13. Cross resistance among ionophores Narasin Salinomycin Monensin Monovalent Ionophore Lasalocid Divalent Ionophore Maduramycin Semduramicin Monovalent glycoside
- 14. Efficacy of ionophores to common coccidian 6 5 4 3 2 1 Salinomycin Monensin Narasin Semduramicin Lasalocid Maduramycin Semduramicin Lasalocid Salinomycin Monensin Narasin Maduramicin Maduramicin Semduramicin Lasalocid Monensin Salinomycin Narasin E. acervulina E. maxima E. tenella 6+4+2=12 5+3+3=11 4+2+1=07 6+5+3=14 5+4+2=11 1+1+6=08 Efficacy point to common coccidian Cumulative Efficacy 1 2 3 3 4 5 @ Adapted from McKenzie et al., 1991, 1993, Ricketts et al., 1992, Logan et al., 1993
- 15. Efficacy of chemical to common coccidian @ Adopted from different source CHEMICAL E. acervulina E. maxima E. tenella Resistance Issues Diclasuril 5 2 5 Use one flock/year to void resistance Decoquinate 4 2 4 Robenidine 5 3 5 Use one flock/year to void resistance Clopidol 3 2 3 Use one flock/year to void resistance Clopidol + ethilbenzocuate 5 2 5 Use one cycle/year to void resistance Nicarbazin 3 5 5 Do not use 125 ppm over 28°C. No resistance Nicarbazin + Salinomycin 5 5 3 Nicarbazin+ Narasin 4 4 3 No resistance problems. Can be used for years Nicarbazin + Semduramicin 4 5 5 No resistance problems. Can be used for years
- 16. Coccidiosis Strategies of Anticoccidial program in Poultry
- 17. Anticoccidial Program Shuttle Program Straight Program Rotations
- 18. Shuttle(Sh) Straight (St) ATCP Step Down Step Up Grower Starter 1 1 1 1 1 1 1 1 Program 02 Program 03 Program 01 Rotation Rotation: Resting helps to recover efficacy
- 19. Rotation: Resting helps to recover efficacy @ Chapman et al, 2013 Efficacy Parameters 0 6 12 18 24 Month of Use Divalent Ionophores Monovalent Ionophores Use Resting Use Use Use Resting Resting
- 20. History of ATC use & Infestation Load Factors should be considered on designing programme Thus, in planning shuttle programs we can use drugs that are particularly effective against the species expected to cycle at that stage of a grow-out. E. acervulina (18-28 days) E. maxima (25-35 days) E. tenella (7-42 days) 15 10 20 25 30 35 40 45 Days of Broiler life cycle Starter Feed Grower Feed Finisher Feed
Editor's Notes
- such as Ageratum conyzoides extract (Billy goat weed), green tea, maslinic acid (found in leaves and fruit of olive tree), extract of Musa paradisiacal root, coumestans from Eclipta alba, extract of a wild mushroom (Ganoderma lucidum), extract of Artemisia sieberi, extract of Neem (Azadirachta indica)Synthetic + Synthetic Synthetic + Ionophore
- Affecting cofactor synthesis Several anticoccidial products influence essential biochemical pathways of the parasitic cell by affecting an important cofactor (Greif et al. 2001). Ethopabate- folate antagonist and blocks a step in the synthesis of para-aminobenzoic acid (PABA) and prevents the formation of nucleic acids of vitamins (Rogers et al. 1964). It is most active against Eimeria maxima and Eimeria brunetti. Sulphonamides- prevent the synthesis of dihydrofolate by interfering with the dihydropteroate synthetase reaction, blocking the conjugation of pteridine and PABA. Dihydropteroate synthetase is only present in the parasite. They are very effective against E. brunetti, E. maxima and Eimeria acervulina and to a much lower degree against Eimeria tenella and Eimeria necatrix (Ryley and Betts 1973). Pyrimethamine. It prevents the reduction of dihydrofolate to tetrahydrofolate by inhibiting the enzyme dihydrofolate reductase. Pyrimethamine has a clear synergistic effect with sulphonamides (Kendall and Joyner 1956). Ethopabate, sulphonamides and pyrimethamine affect the second generation of schizonts (Reid 1973, 1975). Thiamine analogues, like amprolium, block the absorption of thiamine completely and have probably an antagonistic effect on the vitamin B1 supply. Amprolium seems especially efficacious during schizogony as then the demand of thiamine is at its highest (James 1980. It affects the first generation of schizonts and to a lesser extent the gametogony (Reid 1973) allowing immune response to develop.
- Thiamine analogues, like amprolium, block the absorption of thiamine completely and have probably an antagonistic effect on the vitamin B1 supply. Amprolium seems especially efficacious during schizogony as then the demand of thiamine is at its highest (James 1980. It affects the first generation of schizonts and to a lesser extent the gametogony (Reid 1973) allowing immune response to develop. Thiamine Analogues sinterferes with thiamine metabolism. It is a thiamine antagonist, blocking the thiamine receptors, thus preventing carbohydrate synthesis. It has a coccidiostatic effect at lower doses and coccidiocidal at higher doses. It is used to prevent and treat intestinal coccidiosis by blocking the thiamine transporter of Eimeria spp. meronts, which results in disruption of cell metabolism. It inhibits the development of merozoites and formation of second-generation meronts. It also has some activity against the sexual stages and oocyst sporulation (and possibly inhibits development of sporozoites) (Mehlhorn and Aspӧck, 2008; Clarke et al., 2014).
- Products affecting mitochondrial function Quinolone drugs, amongst which buquinolate, decoquinate and nequinate (methyl benzoquate) are listed, show anticoccidial activity at very low concentrations. These products inhibit the respiration of coccidia by blocking the electron transport in their mitochondria (Wang 1975). Quinolones arrest the development of sporozoites (Yvoré 1968; Reid 1973). Meticlorpindol is the most important compound of the pyridone group. Similar to the quinolones, it inhibits electron transport in mitochondria, but possibly at another level as cross-resistance with quinolones does not occur. A synergistic effect between meticlorpindol and 4-hydroxiquinolones has been described (Challey and Jeffers 1973). A widely used pyridone–quinolone combination drug is Lerbek®, consisting of meticlorpindol and methyl benzoquate. The true mode of action of nicarbazin (4,4′-dinitrocarbanilide) is unknown. The product has been shown to inhibit both the succinate-linked NAD reduction in mitochondria of beef hearts and the energy dependent transhydrogenase and accumulation of Ca2+ ions by rat liver mitochondria (Dougherty 1974). The exact anticoccidial mechanism of robenidine (a guanidine derivative) is still unknown. However, from studies in mammals, it is assumed that it inhibits the oxidative phosphorylation of mitochondria (Wong et al. 1972). Another anticoccidial drug possibly affecting mitochondrial function is the triazinetrione compound toltrazuril, which is applied in drinking water for preventive and therapeutic treatment. Harder and Haberkorn (1989) showed that activities of some enzymes of the respiratory chain, such as succinate-cytochrome C reductase, nicotinamide adenine dinucleotide (NADH) oxidase and succinate oxidase from mouse liver, were reduced in the presence of toltrazuril. They also showed an inhibitory effect on the dihydroorotate-cytochrome C reductase from mouse liver. More recently, it has been suggested that toltrazuril might affect plastid-like organelles (Hackstein et al. 1995). Toltrazuril is efficacious against all intracellular stages (schizogony and gametogony) of all important Eimeria spp. in the chicken (Mehlhorn et al. 1984, 1988). It induces cidal changes in the organelles of the parasite at multiple levels and does not seem to impair the development of natural immunity (Greif and Haberkorn 1997; Greif 2000).
- Generally an orderly sequence is observed for infestation. 18 - 28 days - upper gut E.acervulina 25 - 35 days - mid-gut E.maxima 32 - 42 days - caecal - E.tenella (although can occur much earlier) Thus in planning shuttle programs we can use drugs that are particularly effective against the species expected to cycle at that stage of a grow-out.
- Generally an orderly sequence is observed for infestation. 18 - 28 days - upper gut E.acervulina 25 - 35 days - mid-gut E.maxima 32 - 42 days - caecal - E.tenella (although can occur much earlier) Thus in planning shuttle programs we can use drugs that are particularly effective against the species expected to cycle at that stage of a grow-out.