Necrotic enteritis :

• An acute bacterial infection primarily of chickens and turkeys,although other avian species can be affected.
• Characterised by sudden death, friable and distended intestines and severe necrosis of intestinal mucosa.
• The disease primarily affects broiler chicken ( 2-5 w) and turkey(7-12 w old) .
• Infection occurs by faecal-oral route.

Etiology :

            Clostridium perfringens Type ( A or C) and their toxins ( alpha- toxin and sialidase )

• Gram positive
• Obligatory anareobe
• Non- motile
• Rod shaped
• Spore forming bacterium ( spores are highly resistant )
• perfringens are ubiquitous and are a normal inhabitant of the intestinal tract .

Transmission :

• Through contaminated food and water

       Predisposing factors :

• Small intestinal coccidiosis
• Diet high in cereal grains
• High amount of animal protein
• Animal fat
• Infection of chickens with immunosuppressive viruses.

 Pathogenesis :

             Organism enter into body via oral route

                   ⬇

It reaches to the intestine

                   ⬇

Proliferates in intestinal tract

                   ⬇

Produces potent toxins that severely damage the intestinal mucosa

                  ⬇

Toxins absorbed from intestinal tract resulting in toxaemia , which is responsible

      for death of body

Thus, NE is a type of enterotoxemia.

• perfringens divided into 5 toxinotypes ( A,B,C,D,E) based on four major toxins – alpha, beta, epsilon and iota .
• The majority of isolates from NE cases are type A ; few caused by type C.

         Alpha – toxin produced by Type A&C and beta- toxin by Type C 

    Toxin / virulence factor :

• 𝛼- toxin produced by TypeA as well as four other toxinotypes are important virulence factors in the pathogenicity of organism .
• 𝛼- toxin is a zinc metalloenzyme with phospholipase activities.
• It hydrolyses phospholipids in membranes of RBC & WBC , thrombocytes, endothelial cells, and muscle cells.
• Thus, toxin is hemolytic, cytotoxic, necrotizing and potentially lethal.

   Clinical signs :

• NE has a short clinical course :

  Birds are found dead without premonitory clinical signs.Birds appear listless and lethargic for a             

                   a few hours before death.

Mortality in broiler is usually below 10% , but can be as high as 50%. 

• Mild and subclinical NE :

   Birds may not die but show reduced weight gains,higher FCR.

• Typical signs :
• Depression
• Reluctance to move
• Watery diarrhoea
• Ruffled feathers
• Somnolence
• Decreased appetite / anorexia
• Dehydration
• Huddling
• Drooling of saliva

     Postmortem lesions :

• SI ( usually middle to distal ) thickened and distended.
• Intestinal mucosa with diphtheritic membrane ( pseudo membrane ) referred to as a “ Turkish Towel”
• Reflux of bile-stained liquid in crop, if upper SI are affected .
• Affected birds tend to be dehydrated and to undergo rapid putrefaction.
• Gall b;ladder distended.,
• Atrophy of spleen, breast muscles and testes.

Microscopic lesions :

• Necrosis of villi of intestinal muscularis.
• Degeneration and necrosis of hepatocytes , proliferation of CT in spleen and bursa.

Diagnosis :

• Clinical signs and lesions
• Demonstration of gram +ve in necrotic lesions in intestine and liver.

DDx :

• Mycoplasmosis
• Respiratory viruses
• Chronic / localized pasteurellosis
• Vitamin A deficiency