Avian Coccidiosis

Avian Coccidiosis

Article originally written by Rajesh K. Shah , B.V.Sc & A.H, IAAS

1.   Introduction

  •   Coccidiosis is one of the most important disease of poultry characterized by bloody diarrhoea and high mortality.
  • Coccidia are found in almost all the chicken and are host specific.
  • As soon as there are circumstances which favour their multiplication beyond a certain threshold, the disease is precipitated.
  • It is mostly a disease of young birds because immunity quickly develops after exposure.

It occurs in two forms:

  • Caecal coccidiosis &
  • Intestinal coccidiosis


Coccidiosis is caused by Emeria species of family Eimeridae.

A.Caecal coccidiosis – Eimeria tenella

B.  Intestinal coccidiosis

  • E. necatrix (major)
  • E. maxima
  • E. acervulina
  • E. brunette
  • E. mitis
  • E. hagani
  • E. mivati


  • One of the most important disease of poultry & biggest cause of economic world-wide.
  • 4-8 weeks chicks are affected by E. tenella
  • 6-12 weeks old chicks are affected by E. necatrix .
  • Mortality is around 50%.


Beside age, susceptibility to coccidiosis also depends on several other factors:

  • MD affected birds are more susceptible to coccidiosis.
  • Vit- A deficiency increases susceptibility to coccidiosis.
  • Presence of moisture helps in quick sporulation in coccidial oocyst.
  • Infrequent change and turning of litter increases the concentration of coccidial oocysts beyond the safe limit.
  • Overcrowding
  • Improper management of feeders and waterers.

5.   MOT

  • Ingestion of the infective form of oocysts (sporulated oocyst) is the only method of spread.
  • Oocysts can be spread mechanically by animals, insects, contaminated equipment, wild birds and dust.
  • Spread from one farm to another is facilitated by movement of people and equipment between farms, which may spread the oocysts mechanically.

6.Life cycle & Pathogenesis

  • Life cycle of Eimera doesn’t require any intermediate host, but a part of the life cycle includes development outside the body of the bird.

a.Oocysts with sporozoites within are ingested by birds through feed ,water etc

b.Digestive enzyme dissolves the wall of the oocytes to liberate sporozoits

c.The released sporozoites invade the epithelial cells of the mucosa of the intestine & develop into round bodies ( having a nucleus and are called trophozoites)

d.Tropozoites grow in size & their nucleus divides to form 1st generation schizonts

e.The nuclei of 1st generation schizonts develop into sickle shaped bodies called merozoites.

f.The merozoites break the schizont and the epithelial cells and each one invade other epithelial cells.

g.The merozoites grow as trophozoites & develop again into schizonts, called 2nd Generation schizonts, which liberate merozoites & such generation of schizont and merozoits is repeated 2-3 times.

h.After that merozoites develop in new epithelial cells into sexual phase.

a)Microgametocyte                                                  b)  Macrogametocyte

(male cell, has elongated microgametes inside)                  (egg like,single large body)

i. are liberated, each one penetrates & fuses with macrogamete to form oocyst.

  • The oocyst are liberated by rupture of the cell and are passed out with the faeces.
  • a single ingested oocyst can form about 1.5 lakhs new oocyst in bird.
  • Invasion of host cell is the most important step which has to be repeated several times through rounds of asexual and sexual reproduction in case of Eimeria spp. of chicken.
    • Schizogony occurs in the lamina propria and crypts of lieberkuhn of small intestine and caeca respectively and causes extensive haemorrhage.

7.   Symptoms

  • Symptoms vary with the species of coccidian.
  • E. tenella causes “caecal coccidiosis’
  • Blood droppings
  • High mortality
  • Reduced weight gain
  • Emaciation
  • Mortality occurs between 5 and 6 days following infection.
    • E. necatrix causes “intestinal coccidiosis” associated with
  • Severe weight loss
  • Droppings of affected birds usually contain blood, fluid and mucus.
  • 25% mortality in commercial flock
    • E. brunette is less severe and is associated with
  • Loss of weight gain
  • Poor feed conversion
  • Moderate mortality
    • E. maxima
  • Poor wt. gain
  • Diarrhoea
  • Low mortality
  • extreme emaciation
  • Roughening of the feathers
  • Loss of appetite.

8.   Postmortem Findings

  These vary with the species of coccidia involved.

A. E. tenella:

The caeca may be greatly enlarged and distended with clotted blood.

B. E. necatrix:

a.The middle portion of the small intestine is usually distended to twice its normal size ( ballooning) and the lumen may be filled with blood.

b.Changes may extend throughout the small intestine in severe infection. From the surface, foci of infection appear as small white plagues and tiny red haemorrhage i.e. the infection is seen as white or red foci.

 C. E. brunette:

  • The lining of the small intestine is covered with tiny haemorrhages. The clotted blood and mucosa are seen in droopings. The mucosa may be swollen and thickened.

D. E. maxima:

  • The middle portion of the small intestine may be loose and filled with fluid, containing mucus and blood (ballooning).

E.  E. acervulina:

  • changes can usually be seen from the surface of the duodenum and small intestine.
  • The mucosa may be covered with white plagues, which tend to arrange in transverse fashion and cause a ladder-like appearance because of the striation.

9.   Dignosis

a. By signs and symptoms

  • The presence of faeces with blood, dysentery and diarrhea suggests coccidiosis.

b.  Postmortem examination is necessary to confirm diagnosis.

  • Heamorrhage on intestinal and caeca wall.
  • Enlarged intestine or caeca and distended with clotted blood.
  • Bloody fecal content in caeca.

c.  Examination of feacal content or scraping from affected mucosa of intestine shows oval, thick walled oocysts, large round schizonts, gametocytes etc in significant number.

  • Histopathology:
  • Histopathology of affected part of intestine will show large number of parasitic stages such as trophozoites amnd large schizonts in early stage of disease.

10.   Differential Diagnosis

a. Necrotic enteritis:

  • Postmortem changes are usuallyconfined to the middle part of the small intestine.
  • The intestine is distended with gas and filled with a fowl- smelling brown fluid.
  • The small intestine is greatly thickened due to extensive velvet like necrosis of the mucosal lining.
  • Ulcerative enteritis
  • Deep ulcers throughout intestine, but mainly ieum and caecae, which may be round and lenticular.
  • Blood in intestine.
  • References
    • J.L. Vegad, Poultry Diseases
    • H.V.S. Chauhan & S Roy, Poultry Disease Diagnosis & Treatment
    • The Merck veterinary Manual, 10th Edition

This Post Has 2 Comments

  1. Hey! This is my first visit to your blog! We are a group of volunteers and starting a new initiative in a community in the same niche. Your blog provided us useful information to work on. You have done a marvellous job!

  2. Wow, this piece of writing is pleasant, my sister is analyzing these kinds of things,
    therefore I am going to convey her.

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