1- Necrotic Enteritis
Definition
Disease of young chickens caused by toxins produced by Clostridium
perfringens type A and type C characterized by sudden onset of high mortality
and necrosis of the mucous membrane of the small intestine, the disease is also
known as clostridial enteritis, enterotoxemia and rot gut.
Etiology
The etiologic agent is a Gram-positive, spore-forming anaerobe; C.
perfringens type A and type C, both of these strains are capable of producing
various toxins and enzymes which are responsible for the associated lesions and
clinical signs. Specifically, alpha-toxin produced by C. perfringens types A and
C and beta-toxin produced by C. perfringens type C.
Hosts
Necrotic enteritis is most common in broiler chickens, young broiler and
young meat turkeys. Broilers aged 2–5 weeks are most frequently affected.
Influencing factors
1- The risk of necrotic enteritis is low when birds are kept on wire floors or other
types of housing that minimizes their contact with feces.
2- Low-level maternal immunity against C. perfringens is associated with an
increased risk of necrotic enteritis in broiler chickens.
3- High levels of glycine may be a predisposing factor for necrotic enteritis.
Pathogenesis
The presence of C. perfringens in intestine alone is not sufficient to induce
necrotic enteritis, but the (1) predisposing factor causing damage to the intestinal
mucosa, and (2) the presence of higher than normal numbers of intestinal C.
perfringens organisms.
Bacterial cells adhere to damaged epithelium where they proliferate and
induce coagulative necrosis. Attraction and lysis of heterophil as well as tissue
necrosis and bacterial proliferation. The alpha toxin (a necrotizing toxin)
produced which destroys cell membranes. Toxins may also enter the blood stream
or bile duct causing systemic effects as in cholangiohepatitis.
Clinical signs
Acute necrotic enteritis is characterized by increased mortality depression,
decreased feed intake, reluctance to move, ruffled feathers and diarrhea.
The mildest form of necrotic enteritis induces no visible illness of the birds but is
associated with temporarily reduced weight gain.
Lesions
Gross lesions: lesions confined to the small intestine, primarily the jejunum,
ileum and cecum. The intestines are friable and distended with gas. The
mucosa is lined by a loosely to tightly adherent yellow too green
pseudomembrane that is often described as having a “Turkish towel”
appearance. Hepatitis characterized by swollen, tan colored livers with necrotic
foci with cholecystitis.
Microscopic lesions: Characterized by severe necrosis of the intestinal mucosa
with an abundance of fibrin admixed with cellular debris adherent to the
necrotic mucosa. Colonization of organisms in necrotic tissues and lamina
propria with fibrin and cellular debris are present in the lumen which
represented the lesions of Turkish towel. in liver bile duct hyperplasia,
fibrinoid necrosis, cholangitis and focal granulomatous inflammation.
Differential Diagnosis
1- Eimeria brunetti or Eimeria maxima infection.
2- Ulcerative enteritis is caused by C. colinum.
Treatment
Necrotic enteritis effectively treated with the administration of lincomycin,
bacitracin, oxytetracycline, penicillin, and tylosin tartrate when used in the water.
Bacitracin, lincomycin, virginiamycin, penicillin, avoparcin, nitrovin and
tylosin have been shown to be effective in preventing and controlling NE when
placed in the feed.
2- Ulcerative Enteritis
Definition
an acute bacterial infection in young chickens, turkeys, and game birds
characterized by sudden onset and rapidly increasing mortality with present of
ulcerative enteritis and yellow to gray necrotic foci in liver and spleen.
Etiology
Clostridium colinum is the etiologic agent, anaerobic, fastidious to culture,
gram-positive, spore-forming, with subterminal, oval spores.
Predisposing Factors
stress, coccidiosis, infectious bursal disease, immunosuppression considered
as predisposing factor to occurrence the infection.
Pathogenesis
Infection can be introduced by feeding on contaminated fecal material by
spores or by recovered carrier birds. Infected birds shed the bacterium in their
droppings. After oral infection, the bacterium adheres to the intestinal villi,
producing enteritis and ulcers in portions of the small intestine and upper large
intestine. Bacilli migrate to the liver via portal circulation, producing necrotic foci
that later coalesce into extensive hepatic necrosis. Infarcts of the spleen are
common.
Clinical signs
Increased mortality without any obvious signs, in other cases signs may
include depression, depressed, listless birds with humped backs, ruffled feathers,
diarrhea, and sometimes bloody or watery white droppings, chickens recover
within 2–3 week, and mortality rarely exceeds 10%.
Lesions
Gross lesions: The most important lesions are found in the intestine, liver and
spleen. There are small, circular to lenticular mucosal ulcers affecting the small
intestine, caeca and upper large intestine, these ulcers may coalesce to form
large ulcer that penetrate as deep as the serosa, which may become perforated
and result in peritonitis. The ulcers may coalesce to form large areas with a
pseudomembrane. In liver there is yellow to gray necrotic foci are the
predominant lesions in the hepatic parenchyma. Splenomegaly with
hemorrhages and necrotic areas may be present.
Microscopic lesions: Intestinal ulcers consist of small haemorrhagic and necrotic
areas, often with clumps of Gram positive bacteria. The ulcers involve villi and
extend into the submucosa. The ulcers sometimes reach as deep as the muscular
layer and serosa. Affected tissue is surrounded by granulocytes and
mononuclear inflammatory cells. Liver lesions consist of multifocal foci of
coagulative necrosis that are often poorly demarcated and with inflammatory
reaction with present of Gram-positive bacteria in these necrotic foci.
Differential Diagnosis
1- Coccidiosis.
2- Necrotic enteritis.
3- Histomoniasis.
Diagnosis
Gross postmortem lesions, isolation of causative agents
Treatment
Streptomycin (0.006%) and furazolidone (0.02%) in the feed are effective
to treat the disease. Bacitracin at 200 g/ton is used for prevention.
3- GANGRENOUS DERMATITIS
Definition
Contagious disease of chickens and turkeys caused by Clostridium
perfringens type A, C. septicum and Staphylococcus aureus. The disease is
characterized by a sudden onset of acute mortality with necrosis of the skin and
subcutaneous tissue, usually involving the breast, abdomen, wing or thigh.
Gangrenous dermatitis has also been referred to as necrotic dermatitis,
gangrenous cellulitis, gangrenous dermatomyositis, avian malignant edema, gas
edema disease, wing rot, and, in some instances, blue wing disease.
Etiology
C. septicum and C. perfringens type A. with Staphylococcus aureus
involved and rarely C. novyi, when S. aureus is present with a clostridial pathogen
the disease is more severe than either alone.
Hosts
Gangrenous dermatitis affects chickens and turkeys and is most commonly
seen in broilers of about 4–7 weeks.
Contributing Factors
In many instances, it is believed to occur as a sequela to other diseases which
produce immunosuppressive effects such as infectious bursal disease (IBD) virus,
chicken infectious anemia virus, reticuloendotheliosis virus, and avian
adenovirus infections, including inclusion body hepatitis virus.
Clinical signs
The clinical signs include increased mortality, marked depression,
incoordination of movement and death within a few hours. The carcasses
decompose rapidly with a foul odor. Mortality varies from low to very high.
Lesions
Gross lesions: consist of dark reddish-purple, weepy areas of the skin, usually
devoid of feathers. Affected areas usually include wings, breast, abdomen, or
legs. Extensive blood-tinged edema, with or without gas (emphysema), is
present beneath the affected skin. Underlying musculature is discolored gray
or tan and may contain edema and gas between muscle bundles. The kidney
and liver are often congested and in some birds the lungs are congested and
oedematous and can resemble a mass of dark-red jelly.
Microscopic changes: are characterized by edema and emphysema with
numerous large, basophilic bacilli or small cocci within subcutaneous tissues.
Severe congestion, hemorrhage and necrosis of underlying skeletal muscle are
often present. Liver, if affected, contains small, randomly scattered, discrete
areas of coagulation necrosis with bacteria.
DIAGNOSIS
Diagnosis is based on the presence of gross lesions and the demonstration
of the pathogens.
CONTROL
Important management measures include a high standard of hygiene,
avoiding overcrowding of stock and the protection of the birds against
immunosuppressive agents.
Treatment
Treatment effectively with the administration of chlortetracycline,
oxytetracycline, erythromycin, penicillin, or copper sulfate in the water.
Chlortetracycline or furoxone in the feed.
4- BOTULISM
Definition
Botulism is an intoxication caused by exotoxins of Clostridium botulinum.
Synonyms are “limberneck” and “Western duck sickness.” can affect a variety of
birds, including broiler chickens, and mammals, including humans.
Etiology
C. botulinum is a gram-positive, spore-forming bacterium capable of
elaborating potent exotoxins under appropriate environmental conditions.
Clinical signs
Clinical signs of botulism in chickens, turkeys, pheasants, and ducks are
similar included flaccid paralysis of legs, wings, neck, and eyelids are
predominant features of the disease. Paralytic signs progress cranially from the
legs to include wings, neck, and eyelids. Initially, affected birds are found sitting
and are reluctant to move. Limberneck, the original and common name for
botulism, precisely describes the paralysis of the neck. Because of eyelid
paralysis, birds appear comatose and may seem dead. Gasping has been reported
when birds are handled. Death results from cardiac and respiratory failure.
Affected chickens have ruffled feathers, which may fall out with handling.
Lesions
There are no specific gross or microscopic lesions.
Diagnosis
Clinical signs and isolation the causative agent and toxins.
Treatment
Antibiotics including bacitracin (100 g/ton in feed), streptomycin (1g/L in
water), or periodic chlortetracycline treatments also reduced mortality. Penicillin
was ineffective in controlling outbreak.