Necrotic Enteritis is also known as:
- The Greens
- Mud Fever
- Blue Comb
- Summer Disease
- New Wheat Poisoning
- enteritis, from Greek words enteron (Small Intestine) and suffix -itis (Inflammation), refers to inflammation of the small intestine. It is most commonly caused by the ingestion of substances contaminated with pathogenic microorganisms. Symptoms include abdominal pain, cramping, diarrhea, dehydration and fever.
- necrosis, death of living tissue; specifically : death of a portion of tissue differentially affected by local injury (as loss of blood supply, corrosion, burning, or the local lesion of a disease)
Currently, I have a hen with these symptoms:
- Red skin
- Red feet
- Hot body
- Unfocused and unclear eyes
- Weight loss
- Lost of appetite
- Dark green diarrhea
Right away, I gave her antibiotics with lots of water:
- Pill: Amoxicillin, Erythromycin, Tetracycline at different schedule inside a 24 hour period
- Water Soluble: Tri-Sulfa
I need to give her medication at least every 24 hours. Better every 6-12 hours. If she will digest her feed, I need to hand feed her until she recovers her appetite.
Let us read more about Necrotic Enteritis aka The Greens below from 4 good reference websites.
– Gameness til the End
Necrotic enteritis is an acute enterotoxemia. The clinical illness is usually very short and often the only signs are a sudden increase in mortality. The disease primarily affects broiler chickens (2-5 wk old) and turkeys (7-12 wk old) raised on litter but can also affect commercial layer pullets raised in cages.
Etiology and Pathogenesis:
The causative agent is the gram-positive, obligate, anaerobic bacteria Clostridium perfringens . It is usually isolated on blood agar, incubated anaerobically at 37°C, on which it produces a double zone of hemolysis. There are 2 primary C perfringens types, A and C, associated with necrotic enteritis in poultry. Toxins produced by the bacteria cause damage to the small intestine, liver lesions, and mortality.
C perfringens is a nearly ubiquitous bacteria readily found in soil, dust, feces, feed, and used poultry litter. It is also a normal inhabitant of the intestines of healthy chickens. The enterotoxemia that results in clinical disease most often occurs either following an alteration in the intestinal microflora or from a condition that results in damage to the intestinal mucosa (eg, coccidiosis, mycotoxicosis, salmonellosis, ascarid larvae). High dietary levels of animal byproducts (eg, fishmeal), wheat, barley, oats, or rye predispose birds to the disease. Anything that promotes excessive bacterial growth and toxin production or slows feed passage rate in the small intestine could promote the occurrence of necrotic enteritis.
Clinical Findings and Lesions:
Clostridium spp necrotic enteritis, chicken
Most often the only sign of necrotic enteritis in a flock is a sudden increase in mortality. However, birds with depression, ruffled feathers, and diarrhea may also be seen. The gross lesions are primarily found in the small intestine (jejunum), which may be ballooned, friable, and contain a foul-smelling, brown fluid. The mucosa is usually covered with a tan to yellow pseudomembrane often referred to as a “Turkish towel” in appearance. This pseudomembrane may extend throughout the small intestine or be only in a localized area. The disease persists in a flock for 5-10 days, and mortality is 2-50%.
A presumptive diagnosis is based on gross lesions and a gram-stained smear of a mucosal scraping that exhibits large, gram-positive rods. Histologic findings consist of coagulative necrosis of one-third to one-half the thickness of the intestinal mucosa and masses of short, thick bacterial rods in the fibrinonecrotic debris. Isolation of large numbers of C perfringens , from intestinal contents that produce the double zone of hemolysis as described above, can confirm the diagnosis. Double zone hemolysis should not be used as the sole criteria for identification of C perfringens because some strains do not produce both toxins responsible for the hemolysis characteristics. Differential media specifically designed for isolation of C perfringens is available and may be useful for diagnosis.
Necrotic enteritis must be differentiated from lesions produced by Eimeria brunetti and also from ulcerative enteritis. Uncomplicated coccidiosis rarely produces lesions as acute or severe as those seen with necrotic enteritis. Ulcerative enteritis caused by C colinum usually produces focal lesions from the distal portion of the small intestine (ileum) to the ceca and is almost always accompanied by hepatic necrosis.
Prevention, Control, and Treatment:
Because C perfringens is nearly ubiquitous, it is important to prevent changes in the intestinal microflora that would promote its growth. This can be accomplished by adding antibiotics in the feed such as virginiamycin (20 g/ton feed), bacitracin (50 g/ton feed), and lincomycin (2 g/ton feed). The addition of anticoccidial compounds, especially of the ionophore class, has been extremely helpful in preventing the coccidial damage that leads to necrotic enteritis. Avoiding drastic changes in feed and minimizing the level of fishmeal, wheat, barley, or rye in the diet can also aid in the prevention of necrotic enteritis. Administration of probiotics or competitive exclusion cultures has been used to both prevent and treat clinical necrotic enteritis (presumably by preventing the proliferation of C perfringens ). Treatment for necrotic enteritis is most commonly administered in the drinking water, with bacitracin (200-400 mg/gal. for 5-7 days), penicillin (1,500,000 u/gal. for 5 days), and lincomycin (64 mg/gal. for 7 days) most often used. In each case, the medicated drinking water should be the sole source of water. Moribund birds should be removed promptly, as they can serve as a source of toxicosis or infection due to cannibalism.
An acute or chronic enterotoxemia seen in chickens, turkeys and ducks worldwide, caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis, usually of the mid- small intestine. Mortality may be 5-50%, usually around 10%. Infection occurs by faecal-oral transmission. Spores of the causative organism are highly resistant. Predisposing factors include coccidiosis/coccidiasis, diet (high protein), in ducks possibly heavy strains, high viscosity diets (often associated with high rye and wheat inclusions in the diet), contaminated feed and/or water, other debilitating diseases.
Dark coloured diarrhoea.
Sudden death in good condition (ducks).
Small intestine (usually middle to distal) thickened and distended.
Intestinal mucosa with diptheritic membrane.
Intestinal contents may be dark brown with necrotic material.
Reflux of bile-stained liquid in the crop if upper small intestine affected.
Affected birds tend to be dehydrated and to undergo rapid putrefaction.
A presumptive diagnosis may be made based on flock history and gross lesions Confirmation is on the observation of abundant rods in smears from affected tissues and a good response to specific medication, usually in less than 48 hours.
Penicillins (e.g. phenoxymethyl penicillin, amoxycillin), in drinking water, or Bacitracin in feed (e.g. 100 ppm). Treatment of ducks is not very successful, neomycin and erythromycin are used in the USA. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity.
Penicillin in feed is preventive, high levels of most growth promotors and normal levels of ionophore anticoccidials also help. Probiotics may limit multiplication of bacteria and toxin production. In many countries local regulations or market conditions prevent the routine use of many of these options.
Necrotic enteritis, caused by Clostridium perfringens, is seen as an acute or chronic enterotoxaemia in growing birds and is a cause of wet litter syndrome. It is most prevalent in 2-6 week old broilers, with a peak around 25 days, and is becoming more common in turkeys.
Birds may appear depressed and huddle together; mild enteritis may be evident. Sudden death is possible. Otherwise the birds recover. However, in mild cases growth rate and feed conversion are both adversely affected and this can be economically significant.
Cl. perfringens may:
- Compete with the host for nutrients
- Produce toxins that affect the epithelial cells, which in turn affects absorption of nutrients
- Produce enzymes that deconjugate bile salts, resulting in impaired fat emulsification and lipid absorption.
These factors can have a marked economic effect.
There are major animal health and welfare issues to consider as the wet litter can lead on to hock burns and pododermatitis.
A condition known as cholangiohepatitis can be present at slaughter and is associated with Cl. perfringens. This results in carcass and/or liver condemnation and is obviously economically important. The liver appears pale, enlarged and firm. Often the gall bladder and bile ducts appear enlarged.
Spread of the disease
The organism may be ingested (exogenous disease) or already be present in the intestine and then increase in numbers due to some stimulus (endogenous disease). Some research has indicated that the organism can infect the bird within the first few days of life.
Clostridium perfringens has been detected in the ileum of apparently normal chicks. The organisms establish themselves in the small intestine and multiply profusely. They require anaerobic or low oxygen conditions for growth.
Coccidiosis, a change to a high protein diet, especially one containing fish meal, coarse material in the diet, inadequate decontamination of premises are factors that predispose the bird to clostridial enteritis.
In acute necrotic enteritis, no clinical signs may be apparent until a number of birds start to die. Infection usually occurs in the lower small intestine, although in severe cases this can spread to the whole intestinal tract. Intestines are enlarged (due to gas production) and the serosa may appear discoloured (brown). The contents are brown, liquid and foul-smelling. The lesions are in severe cases described as a towelling effect on the intestinal mucosa. Presence of these intestinal lesions is indicative of Clostridial enteritis.
With sub -acute necrotic enteritis, wet litter may be observed. No obvious lesions may be found. The proximal intestine of normal chickens contains low concentrations of Cl. perfringens but in affected birds higher concentrations are produced. Cl. perfringens is grown using anaerobic conditions and may be identified using an immunofluorescent test or by a specific PCR. Types A and C are common in chickens.
Management and control
Coccidiostats incorporated into the feed may be beneficial.
Antibiotics are used for both the management and prevention of necrotic enteritis.
Timbermont L, Haesebrouck F, Ducatelle R, Van Immerseel F.
Department of Pathology, Bacteriology and Poultry Diseases, Research Group Veterinary Public Health and Zoonoses, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, B-9820, Merelbeke, Belgium. email@example.com
Clostridium perfringens-induced necrotic enteritis and related subclinical disease have become economically significant problems for the broiler industry. Fortunately, scientific interest in this topic has grown: new C. perfringens virulence factors have been discovered and new insight gained about the pathogenesis of necrotic enteritis. It has been shown that alpha toxin, for a long time thought to be the key virulence factor, is not essential for the development of the disease. Moreover, it is now clearly established that only certain C. perfringens strains are capable of inducing necrotic enteritis under specific conditions that predispose to the disease and they constitute only a minority in the intestinal tract of healthy chickens. A novel pore-forming toxin, NetB, has been identified in these virulent avian C. perfringens strains. Using a gene knockout mutant, it has been shown that NetB is a critical virulence factor in the pathogenesis of necrotic enteritis in broilers. In addition to toxin production, other factors have been described that contribute to the ability of certain C. perfringens strains to cause necrotic enteritis in broilers. It has been suggested that proteolytic enzymes play an important role in the initial stages of necrotic enteritis since the villi are first affected at the level of the basement membrane and the lateral domain of the enterocytes. In field outbreaks of necrotic enteritis, a single clone of C. perfringens is dominant in intestines of all affected birds, as opposed to the mixture of different C. perfringens strains that can be isolated from healthy bird intestines. It has been proposed that bacteriocin production is responsible for the dominance of a single strain in necrotic enteritis cases. Furthermore, it has been shown that virulent strains are more able to adhere to extracellular matrix molecules than non-virulent strains. The current knowledge on the pathogenesis of the disease has been summarized in this short review.