Necrotic enteritis

Necrotic
Enteritis
SUBMITTED BY
ASHIK AHMED DURBER(18VMICROJD 15M)
MS IN MICROBIOLOGY
DEPT. OF MICROBIOLOGY AND HYGIENE

Outline
Introduction
Etiology
Pathogenesis
Predisposing factors
Clinical signs
Post mortem lesions
Diagnosis
Treatment

Introduction
Necrotic enteritis (NE) is an enteric bacterial disease of chickens,
turkeys, and a few other avian species caused by Clostridium
perfringens.
Necrotic enteritis in poultry is caused by Clostridium perfringens
type A.
The disease is characterized by damage to the intestinal mucosa by
toxins produced by Clostridium perfringens.
NE is associated with:
1. Increased mortality.
2. Increased feed conversion ratio.
3. Decreased weight gain.

Etiology
Clostridium perfringens
Gram-positive
Obligatory anaerobe
Non-motile
Rod-shaped
Spore-forming bacterium

Natural Hosts
Necrotic enteritis is most common in broiler chickens and
young broiler breeder pullets.
In commercially reared broiler
chickens, clinical disease usually
occurs between 2 - 5 weeks of
age.
The disease is also seen in
turkeys (young meat-type) and
table-egg layers.

Pathogenesis
NE occurs when C. perfringens;
1. Proliferates in the intestinal tract.
2. Produces potent toxins that severely damage the
intestinal mucosa.
3. Toxins absorbed from the intestinal tract resulting in toxemia,
which is responsible for death of the bird. Thus, NE is a type of
“enterotoxemia”.
Clostridium perfringens is divided into five toxinotypes (A, B, C, D,
and E) based on four major toxins (alpha, beta, epsilon, and iota).The
majority of isolates from NE cases are type A, with a few cases caused
by type C.
Alpha toxin produced by types A and C
Beta toxin produced by type C

Pathogenesis
Toxins/Virulence Factors:
Alpha toxin, produced by C. perfringens toxinotype type A, as
well as 4 other toxinotypes, are considered to be important
virulence factors in the pathogenicity of the organism.
Alpha toxin is a zinc metalloenzyme with phospholipase activities;
It hydrolyzes phospholipids in membranes of red and white
blood cells, thrombocytes, endothelial cells and muscle
cells.
Thus, the toxin is hemolytic, cytotoxic, necrotizing and potentially
lethal.

Clinical Signs
Typical clinical signs of NE in chickens include:
Depression
Reluctance to move
Diarrhoea
Ruffled feathers
Somnolence
Decreased appetite/anorexia
Dehydration
Huddling

Clinical Signs
NE has a short clinical course.
Birds in the flock are found dead without premonitory clinical
signs. Some birds may appear listless and lethargic for a few
hours before death. Mortality in broiler flocks due to NE 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 feed conversion ratios.

Predisposing Factors
1. Small intestinal coccidiosis
NE cases are commonly associated with varying degrees of Eimeria
maxima infection. Protein-rich exudate leaking from the damaged
mucosa may provide necessary nutrients for the growth of C.
perfringens.
2. Diets high in cereal grains
Such as rye, wheat and barley.
They contain high levels of non-digestible, water soluble, non-starch
polysaccharides.
Higher viscosity of wheat and barley ingesta may contribute to
greater bacterial numbers in the intestines, probably because of a
slower intestinal transit time associated with these diets.

Predisposing Factors
3. High amounts of animal protein
Fish meal and bone meal, in the diet, increase the risk of NE compared to
feeds formulated with plant sources of protein.
The increased risk associated with high glycine and methionine levels in
animal protein; both of which enhance C. perfringens growth in vitro.
4. Animal fat
It increases the numbers of C. perfringens in the ileum, compared with soy
oil.
5. Infection of chickens with immunosuppressive viruses
Infection with infectious bursal disease IBD
Chicken anemia virus CAV
Marek's disease virus MDV

Diagnosis
Post mortem lesions
NE lesions tend to become less obvious or even unrecognizable in
birds in an advanced state of autolysis, so
freshly dead birds or euthanized birds are preferable for
postmortem examination.
Gross lesions of NE are usually characteristic and allow
preliminary diagnosis of the disease.

Sample collection:
Clostridium perfringens can be isolated from:
1. Intestinal contents
2. mucosal scrapings
3. Hemorrhagic lymphoid nodules,
4. Swabs of pseudomembraneous lesion.
Specimens should be fresh and processed as soon as possible to
avoid overgrowth by other organism.
If transportation is necessary, anaerobic transport tubes (port-a-
cul) are recommended.

Culturing:
Clostridium perfringens can be isolated in reducing
medium[blood agar plate] or in anaerobic jars which is
incubated at 37 degree C.
Clostridium perfringens colonies on blood agar are smooth,
circular.

Cultural
characteristics:
Clostridium perfringens:
Grows at a temperature 15-50°C.
Optimum growth at 45°C for most strains.
Generation time for most strains;
Less than 20 minutes at 33°C to 49°C. Generation time of 8
minutes has been reported.
Spores can withstand 100°C for two hours.

BIOCHEMICAL REACTIONS:
Glucose, lactose and maltose are fermented with acid and gas
production
1. Methyl Red positive
2. Indole positive
3. VP positive
4. H2S production positive
5. Nitrate reduction test positive

Laboratory
diagnosis:
Nagler’s Reaction
Rapid detection of C.perfringens from clinical sample done to
detect the lecithinase activity of alpha toxin.
Characteristics opalescence is produced around colonies in
positive test due to breakdown of lipoprotein complex in the
medium.

Gross Lesions
Lesions in the intestinal tract is usually confined to the jejunum and
ileum.
It varies in appearance from bird to bird depending on:
1. Severity of infection.
2. Stage of development.
3. Presence or absence of coccidiosis.
4. Freshness of the carcass.

Gross Lesions
When birds have NE it is best to examine euthanized or fresh
dead birds for lesions;
1. Once the intestine starts to decompose after death, NE
lesions tend to be less obvious and, in some cases, difficult to
recognize.
2. Carcasses of birds with necrotic enteritis undergo postmortem
autolysis quickly, probably because of toxemia.
3. Jejunum and ileum may appear dilated, have a thin friable
wall, and be filled with gas.
4. Wall of the affected segment of the small intestine is firm
giving the gut the feel of a piece of hose.

Prevention
Preventing NE can be accomplished through;
1. In feed antibiotics
2. Ionophorous coccidiostats
3. Competitive exclusion products
4. Preventing coccidiosis
In Feed Antibiotics
C. perfringens is sensitive to several in-feed antibiotic growth
promoters.
Use of these antibiotics as feed additives suppresses the
number of C. perfringens in the intestinal tract and reduces the
incidence of NE.

Prevention
Ionophorous Coccidiostats
C. perfringens is sensitive to the ionophorous coccidiostats
monensin, salinomycin and narasin.
Incorporating these coccidiostats into the feed is effective in
reducing the number of C. perfringens in the intestine and
protecting against experimental NE.

Prevention
Competitive Exclusion Products
The intestinal tract of birds contains several bacteria that
compete with each other. NE occurs when C. perfringens
overgrows other bacteria in the intestinal tract.
Keeping a healthy balance of intestinal microflora is a key
element in NE prevention.
Giving certain beneficial bacteria to birds is effective in reducing,
the severity of NE “Competitive exclusion”.
Competitive exclusion products need to be given to the birds
after hatching.
Beneficial bacteria in these products may reduce colonization of
C. perfringens in
young chicks.

Prevention
Preventing Coccidiosis
Preventing coccidiosis, whether by coccidiostats or
vaccination, is probably the most important measure to
prevent NE.

Necrotic enteritis

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