Avian coccidiosis.dr mahmoud sedeek

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Avian coccidiosis

By:

Dr :Mahmoud Sedeek

Some important notes:

Coccidiosis :–  Infection by sufficient numbers of Eimeria.– Produce clinical manifestations, macroscopic lesions,

economic losses.– It has self-limiting nature.

 Coccidiasis:– Light infection, does not produce clinical signs or

macroscopic lesions. Sub-clinical Coccidiosis:

– Infection that reduce body weight, cause poor F.C.

Coccidia characterized by

Host specific

Tissue specific

Immune specific

Why Coccidia is worldwide disease

Direct life cycle.

Short incubation period (4-7 days).

Resist environmental conditions and disinfectant.

introduction

Coccidia are almost universally found wherever chickens are raised.

Coccidiosis remains one of the most expensive and common diseases of poultry production in spite of advances in chemotherapy

Economic Importance:

Broiler growth and weight are reduced. feed conversion rate is reduced by 5-10%. increase in condemnation rate at processing. increase in mortality rates. increase the susceptibility to other disease agents. Costs of treatment and prevention($ 300 Million/ year

(1991) Subclinical Coccidiosis cost 4.7Cents/broiler. A survey in Russia ( 1990 ) revealed that :

Mortality of 15%, loss of 100-270 Grams/broiler

Etiology:

Eimeria species (intracellular parasite) , host-specific protozoa

Nine species of Eimeria been identified in chickens:

Seven of these species are frequently encountered in broiler E.acervulina, E. brunette , E. maxima , E. mitis, E. necatrix, E. praecox and E. tenella.

Oocyst survive for years. Dryness and direct sun are lethal.

Mode of infection

Ingestion of sporulated oocyst.

Mode of transmission

Mechanical transmission through persons and equipements.

Life Cycle of Eimeria:

Infection occurs when susceptible chicks ingest a sporulated oocyst(contain four sporocysts each contain two sporozoites) .

Liberation of sporozoites in digestive tract by mechanical and biochemical actions .

The liberated sporozoites invade epithelial cells, transformed into Trophozoite ( 12-48 hours ).

Trophozoites enlarge,divides transforme to Schizont which contain merozoites .

Trophozoites mature, rupture ( day 3 ) releasing merozoites which invade other epithelial cells to repeat development of Trophozoites and Schizonts .

Merozoites of second generation Schizont either invade other epithelial cells ( 3 rd. generation ), or transforme into Gametocytes.

• Male gametocyt mature, rupture release large numbers of minute biflagellate microgametocyte.

• Microgametocyte unite with Macrogametocyte to form Zygot ( immature oocyst ) .

• Immature oocyst rupture, pass out with feces .

• Sporulation of Oocyst occurs after 24 hours in presence of moisture, oxygen, sutible temperature .

Clinical signs

Signs include watery and/or bloody droppings. Depression. Mortality (0-50%), and morbidity (0-100%). Culls appear as pale birds with anaemia, depression. Poor weight gain and feed conversion. Drop in egg production

Emaciation ,pale legs and peak

Pm lesions

diagnosis

Case history.

Clinical signs.

Pm lesions.

Microscopic examination.

Prevention & control

Why Coccidia prevention is better than treatment????

Prevention based mainly on:

Anticoccidial feed additives.

Vaccination.

Managemental points

1-Anti coccidial feed additives

A-Chemicals

B-Ionophores

A-Avialable chemicals

Amprolium 125 p.p.m. Arpinocid 60 p.p.m. Clopidol 125 p.p.m. Decoquinate 30 p.p.m. Dinitolmide 125 p.p.m. Halofuginone 3 p.p.m. Nicarbazine 125 p.p.m. Robendine 33 p.p.m. S.Q+ Ormthoprim 125 p.p.m. S.Quinoxalline 150 p.p.m. Diclazuril 1 p.p.m.

B-Avialable Ionophore

Lasalocid 75-125 p.p.m. Maduramicin 5 P.p.m. Monensin 80-120 p.p.m. Salinomycin 45- 66 p.p.m. Narasin 70 p.p.m. Semduramycin 25 p.p.m.

Characters of Ideal anticoccidials :

1-Efficacy : Broad spectrum activity.

2-Safety : Wide margin of safety , at least three-fold difference between registered and toxic level.

3-Cost effectiveness : least effective cost.

4-Residues : Should be metabolized, excreted, without toxic residues.

5-Carcass and meat quality : should not affect organoleptic criteria.

Characters of Ideal Coccidiostat :

6-Compatibility with feed : electrostatic properties of compound should permit accurate addition, proportioning and distribution, and should be compatible with feed ingredients ( vitamins, minerals and growth enhancers ).

7-Assay techniques : rapid, reliable and inexpensive.

Programmes of coccidiostate feed additives

• Medication to Market Age( continous program)

• Shuttle Programs

• Rotation program

Medication to market age( continuous program)

we put broilers on medication until slaughter time, or until laying birds are put into cages. Some governments have regulatory restriction ( Do not feed medicated drugs for 3 – 5 days prior to slaughter ( broilers ) or past 16 wks ( layers ).

This is to allow drug residues to be excreted prior to human consumption of meat or eggs.

Some drugs are considered safe and can be used continuously ( amprolium ).

Rotation program

Use one Anticoccidial drug every 2 cycles

Shuttle program

We use anti coccidial drugs till 21 days of age in broiler then change it

Anticoccidial toxicity

A- Ionophores toxicity:

1- Monensin 200 p.p.m. to turkeys cause 30% mortality( dose 150-170 p.p.m.).

2-Salinomycin 50 p.p.m. cause paresis to turkeys( dose 60 p.p.m ).

3-Maduramycin 10 p.p.m. for broilers reduce weight by 15%( dose 5p.p.m.).

B-Chemicals toxicity :

 1-Nicarbazine ( dose 125 p.p.m.)– Higher level in broilers : suppress weight– Broilers under heat stress cause 90%

mortality– Breeders fed 100p.p.m. lead to : low egg, weak

shell– Breeders fed 150p.p.m. for 5-7 days lead to

drop of hatchability by 10%.

B-Chemicals toxicity :

2-Amprolium ( dose 125 p.p.m. )

–  Three times recommended dose : cause growth depression

– Adding 300p.p.m. in hot climate lead to Thiamine deficiency.

C-Anticoccidial Interaction :

Tiamulin x Ionophores Sulfa.

Chloramphenicol x ( Monensin )

Causes of Coccidiostat failure :

Not effective against all species of Eimeria

More than average exposure oocysts Low inclusion level of Coccidiostat Faulty management ( wet litter ) Intercurrent disease Drug resistance after prolonged uses.

2- vaccination

immunization

Planned immunity ____(vaccination)

Accidental immunity____ (trickle infection)

Avialable vaccines

Live virulent vaccine (wild).(coccivac B,D_Immunocox)

Live attenuated vaccine.( livacox , paracox)

Recombinent vaccine.

• Two- three cycles of infection are usually sufficient to protect chickens.

• more pathogenic ___ less immunogenic

• Keep in mind to make littre moisture from 5 th day after vaccination by sprinkling water to make sporulation easy.

3-Managemental points.

Keep litter dry.

Prevent fecal contamination of food and water.

Keeping layers in cages.

Slat floor.

4- disinfection

Ammonia ( for 500 s .meter)– Spread 50 kg. Lime-powder– Add 100 kg. Sulphoric -ammonia– Add 500 liters water– Lit it work for 20 minutes– Left to dry

Results : – Ammonia gas kill oocysts.– Calcium- sulphate close cracks.

treatment

Amprolium : 30mg./kg./daily/ for 6 days. Ethopabate increase efficacy against

intestinal Coccidiosis.  Sulphadimidine : 200mg./daily/ 2-3 days.  Sulphaquinoxalline : 40mg./kg./daily/ 2-3

days.  Toltrazuril: 25p.p.m., or 7.5mg./kg./daily/

2days.

treatment

Slpha + diaveridine.

Sulpha + pyrimethamine.

Thank u very much