Coccidiosis in Poultry (Chicken)

Coccidiosis in Poultry (Chicken) is a disease of universal importance in poultry production. It is caused by Eimeria species and clinically characterized by bloody diarrhoea and high mortality in young chicken.

 Etiology

Multiple species of Eimeria causes disease in chicken as follows:

These are intracellular parasites of intestinal epithelium. Both asexual (Schizogony) and sexual (gametogony) occur within the host and sporulation usually takes place outside the host (environment). The time taken for sporulation is 2-4 days. The sporoulated oocyst outer wall enclosing four sporocysts each containing two sporozoites. This is referred to as infective stage. The oocyst commonly found as spherical/ovoid/ellipsoidal shape. It has refractile shell and some species with small pore at one end is called as micropyle covered with prominent polar cap.

Epidemiology

• Distribution: Worldwide.
• The disease is more common in deep litter and intensive system of rearing with dirty environment.
• Overcrowding predispose to infection.
• Sporulation of oocyst can occur within two days of being  passed in faeces.
• Oocysts have a considerable longevity and can persist for several years.

Host affected

• Chicken and broilers are susceptible.
•  Breeder and layer pullets are at greatest risk, Barred Plymouth Rock, Gersey White Giant and Light Sussex are susceptible. White Leghorn, Rhode Island and Newhampsire are resistant.
• The disease is most common at the age of 4-6 weeks.
• Chicks more then 6 weeks are resistant to infection, whereas susceptibility increases with age in E.tenella.
• Transmission depends on housing, management and ingestion of sporulated oocyst in the environment.
• Sparkling beetles, migratory birds and birds recovered from infection act as mechanical carrier.

Immunity

• Previous exposure results in species – specific resistance. Some species induces a solid immunity; other species need several infections and is self – limiting in nature. Both CMI and humoral immunity are elicited.
• Immunity is due to 2^nd generation schizogony only.
• Trickle infection: Continuous  ingestion of  low level of oocysts induces very strong immunity but cause damage the intestine.
• Severity of disease increases with concurrent infections; Marek’s disease increases the severity of coccidiosis.

Life cycle

Pathogenesis

Caecal Coccidiosis

• E. tenella is primarily responsible for caecal coccidiosis although thc gametogonous stages of E necatrix also take place in the  caecum and occasionally some stages of E. Brunetti.
• The E. tenella  infectionprimarily occurs at age of 3-7 weeks.
• The  severity of infection is related to parasitic density and parasites within the mucosa.
• Heavy infection with developing schizont are found deep in the mucosa or submucosa. The mature schizonts are released by destruction of intestinal epithelium leads to severe haemorrhage. Which occur after 72 hrs of infection.
• The prepatent period is 7 days.

Clinical manifestation

•  It occurs due to the ingestion of large number of oocysts over a short period.
• Presence of soft faeces with blood, dullness, listlessness, drooping feathers, anaemia, paralysis and death.
• The  subclinical infection causes impaired absorption results in  poor weight gain and poor feed conversion ratio.

Intestinal coccidiosis

• It is mainly caused by E. acervulina, E. maxima, E.necatrix, E.mitis and E.Praecox.
• The prepatent period vary from 4 to 7 days.
• The subclinical infection is more common.

Clinical signs

• Chronic watery diarrhoea with blood (mucous droppings in E. maxima infection).
•  Stunted growth, reduced egg production, listlessness, anorexia, soiling of vent and feathers.
•  Recovered birds are unthrifty and emaciated for a long time.

Rectal Coccidiosis

• It occur mainly due to infection with  E.brunetti.
• It causes coagulative necrosis with slight haemorrhage.

Clinical signs

• White fluid droppings mixed with blood and mucus.

Necropsy Finding

Diagnosis

• History of the flock.
• Finding various types of lesions and their locations by P.M. examination.
• Faecal examination for the presence of oocysts, but it  is little significance in severe.
• Outbreaks and clinical cases, as the mortality starts before the discharge of oocysts.
• Examination of gut scrapings for the presence of schizonts and unsporulated oocysts.
• Study of sporulated oocysts by allowing sporulation of oocysts after mixing faeces with several volumes of 2.5 % Potassium dichromate solution for 1 day to 2 weeks.

Treatment

• Sulphonamide drugs are the most widely used and it is recommended that these are given for two periods of three days in the drinking water, with an interval of two days between treatments.
• Sulphaquinoxaline sometimes potentiated with diaveridine, or sulphadimidinc are the drugs of choice. Where resistancc has occurred to sulphonamides, mixtures of amprolium and ethopahate have given good results.
• Sulphonamides have the great effect on II stage schizont without inhibiting I stage schizogony and increases their resistance by acquired immunity.
• Fully recommended dose should be given and withdrawn gradually by reducing half of the dose,  otherwise it is lethal.

Prevention

Primary prophylaxis in vaccination in Coccidiosis in Poultry are:

• Coccivac: vaccine with live attenuated oocysts of E. tenella, E. maxima, E. acervulina, E.mivati  of chicken isolates administered to day old healthy chicken through eye spray, cabinet spray or  in feed.
• Coccivac-D: (8 species) for breeders and layers.
• Livacox Q: attenuated quadrivalent vaccine
• Immunocox vaccine

Control

• Trickle infection
  • Initial infection of 100 -700 oocysts/ each species followed by repeated daily doses of 1-5 oocysts for 20 days produces immunity, which is reinforced by reinfection of oocysts in the litter.
• Shuttle programme
  • Use of one product in the starter and another in the grower is called as shuttle programme.
  • This programme is mainly intended to reduce the buildup of drug resistance.
• Step-down programme (Natural infection + anticoccidials)
  • This is followed for control of   coccidiosis in breeders and layers.
  • In this approach the birds are naturally allowed for infection with moderate number of coccidial oocyst for certain period along with administration of broad spectrum anticoccidials drugs at the lowest approval level to provide protection for upto 6-12 wks.  It helps to stimulate  host immune mechanism in birds  to develop protection against the severe outbreak of disease.
• Switch programme: where drugs are switched within life-span of each batch.
• Selective breeding of domestic fowl is to increase the genetic resistance of the host.
• Nutritional supplement/ antagonism- Vitamin- A for recovery of the host; Vitamin-k to reduce the mortality due to haemorrhage and a high protein diet.
• Isolation of sick birds.
• Reduced drug rate to older birds allows limited exposure to developing coccidia so that it leads to acquired immunity.
• Heaping the litter for 24 hours to reach a temperature of 50◦C and forking for destruction of oocysts.
• Avoidance of contamination of feeders and waterers with droppings.
• Continuation of anticoccidials in water for 5 days.
• Burning the infected materials and sprinkling the quick lime @2-3 kg / 10 sq.ft over the litter.
• Avoidance of overcrowding in poultry houses.
• Keep the waterers and feeders at higher level.
• Feeding chicks with coccidiostat in chick mash.
• Thorough disinfection and fumigation (Ammonia + Potassium permanganate) in the premises before the entry of newly hatched chicks.