The term "enterotoxemia" refers to disease caused by the production of exotoxins of Clostridium perfringens in the intestines of animals. It affects sheep, goats, cattle, foals, and piglets. Clinical signs vary according to the toxinotype involved and the host species.
Enterotoxemia Caused by Clostridium perfringens Type A
Type A strains of Clostridium perfringens all have the genes capable of encoding alpha toxin (CPA), and some strains encode other minor toxins too. C perfringens type A is commonly part of the normal intestinal microbiota of animals and is associated with enteric disease in many species; however, evidence to support the role of this organism in enteric disease exists in only a few specific instances.
Yellow Lamb Disease
Yellow lamb disease (also known as type A enterotoxemia or enterotoxemic jaundice) is a clinical manifestation of enterotoxemia in sheep. Historically, hemolysis and subsequent signs of icterus in cases of yellow lamb disease were described in association with C perfringens type A; however, an outbreak in lambs has also been reported involving C perfringens type D (1). Both types of the disease manifest in anemia, icterus, and hemoglobinuria. The type D disease also includes signs of abdominal pain, and both forms of the disease are highly fatal.
Gross lesions in cases of yellow lamb disease are likely to include, in addition to icterus and hematuria, an enlarged, pale, friable spleen. The liver is often enlarged and orange, and the kidneys can appear dark and swollen. Serosanguineous fluid can be present in multiple body cavities with the type D–associated form of the disease. Microscopic changes associated with intravascular hemolysis and anemia might be present; therefore, necropsy findings alone are not specific enough to make a diagnosis of yellow lamb disease.
When necropsy findings are taken in conjunction with clinical findings and diagnostic testing to rule out other causes of intravascular hemolysis, a presumptive diagnosis of yellow lamb disease can be made. The detection of C perfringens type A or CPA in the intestinal tract does not provide enough evidence to make the diagnosis, because of the high prevalence of both in the intestinal tract of healthy sheep.
No vaccines are labeled for the prevention of yellow lamb disease; however, those containing CPA toxoid might offer some protection. In addition, management factors aimed at preventing C perfringens type D enterotoxemia might also help to prevent yellow lamb disease.
Enteric Disease Caused by Clostridium perfringens Type A in Pigs
C perfringens type A is implicated as a cause of watery, mucoid, nonhemorrhagic diarrhea in suckling and feeder pigs, but supporting evidence is limited (2). Most of the C perfringens type A strains found in pigs also produce C perfringens beta2 toxin (CPB2), which has been proposed as a cause of enteritis in pigs; however, reports demonstrate mixed results related to this virulence factor (3, 4).
A causative relationship between C perfringens type A enteric infection and enteric disease in pigs has not been conclusively established. Diagnosis is challenging because this organism is a normal inhabitant of the GI tract of pigs, and isolation of C perfringens or CPA detection with a commercial ELISA alone cannot confirm the diagnosis.
To date, no commercial ELISAs exist for CPB2 detection. The testing strategy should be comprehensive because combined infections are possible and C perfringens is part of the normal microbiota.
There are no specific guidelines for treatment or prevention of C perfringens type A–induced enteric disease in pigs.
Other Diseases Caused by Clostridium perfringens Type A
Hemorrhagic to necrotizing enteritis of veal calves, called bovine necrohemorrhagic disease, has been associated with C perfringens type A. However, that association is based only on experimental infections, and it is possible that unidentified virulence factors play a role.
CPB2-toxigenic C perfringens has also been suggested to play a role in typhlocolitis in horses (5), but more studies are needed. C perfringens type A might also play a role in enteric disease in some avian species; however, this association has not been fully determined or reproduced experimentally.
Enterotoxemia Caused by Clostridium perfringens Type B
Disease associated with Clostridium perfringens type B, which carries the genes encoding alpha (CPA), beta (CPB), and epsilon (ETX) toxins, has been reported in lambs, calves, and, rarely, foals. Ingestion of the organism from feces or soil is the main source of transmission.
CPB and ETX are the main causes of disease. CPB acts locally and creates intestinal wall damage but is quickly broken down by intestinal proteases. ETX acts systemically and creates widespread vasculopathy but requires activation by intestinal proteases. For these reasons, disease cases tend to show marked evidence of either toxin but not both.
Animals < 3 days old have low activity of intestinal proteases, and colostrum contains protease inhibitors, so neonates are more likely to experience disease caused by CPB. In contrast, older animals with higher protease activity are more at risk of disease caused by ETX.
Clinical Findings of Enterotoxemia Caused by Clostridium perfringens Type B
Lamb dysentery is an acute disease of neonatal lambs, with clinical signs of acute abdominal pain and distention, as well as hemorrhagic diarrhea. Older lambs, which are more prone to ETX-associated disease, are more likely to show neurological signs secondary to vasculopathy. These signs can include opisthotonus, blindness, incoordination, and respiratory difficulty—similar to the signs associated with disease caused by C perfringens type D. Death is more common in younger neonates and can occur within hours after clinical onset.
Calves < 10 days old show clinical signs of C perfringens type B–associated disease similar to those described in lambs (6).
In rare instances, hemorrhagic diarrhea has been associated with C perfringens type B in foals during the first few days of life.
Lesions of Enterotoxemia Caused by Clostridium perfringens Type B
The major lesion associated with CPB in young lambs is necrohemorrhagic enteritis with mucosal ulceration, along with gas distention in intestinal loops, which can also appear dark red to purple. Intestinal contents might be indistinguishable from frank blood. Older lambs affected by ETX might have fibrin in the pericardial sac, along with possible pulmonary edema, a congested or pale and friable liver, splenomegaly, and renal edema. Individuals that survive for several days might have symmetrical encephalomalacia.
Grossly and histologically, C perfringens type B infections in older lambs affected by ETX alone can appear indistinguishable from those affected by C perfringens type D. The intestinal lesions in calves and foals are similar to those described for lambs, and gross changes in the nervous system have not been described in these species.
Diagnosis of Enterotoxemia Caused by Clostridium perfringens Type B
Clinical signs
Bacterial isolation or PCR assay
Toxin identification
A presumptive diagnosis of enterotoxemia caused by C perfringens type B is based on clinical signs and gross and microscopic findings. Further diagnostic support can include isolating the organism from affected intestine and typing it using PCR assay. CPB can be detected as well; however, failure to do so should not exclude infection by this pathogen as a possible diagnosis, given that it is rapidly broken down by intestinal proteases.
Pearls & Pitfalls
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PCR assay to detect toxin genes in the intestinal content or feces can also aid in diagnosing C perfringens type B enterotoxemia. Detection of the genes encoding CPA, CPB, and ETX indicates either a type B infection or a combination of types C and D, which can also occur. C perfringens type B can also be present in some healthy animals, so all findings must be taken into account when making the diagnosis.
Treatment and Control of Enterotoxemia Caused by Clostridium perfringens Type B
Treatment generally ineffective
Vaccination
Treatment of infection with C perfringens type B is usually ineffective because of the severity of the disease.
The disease is best controlled by vaccination of the pregnant dam a few weeks before parturition with a vaccine containing CPB and ETX toxoids. This vaccination protocol results in colostral antibodies that should be effective in the neonate for the first 4–6 weeks of life. It is recommended that, at the end of that initial protected period, neonates receive two vaccines, 4–6 weeks apart, followed by annual boosters.
Enterotoxemia Caused by Clostridium perfringens Type C
Clostridium perfringens type C causes necrotizing enteritis or enterocolitis in a variety of species. Neonates are the most susceptible to disease, but adults can also be affected. Lambs experience hemorrhagic enteritis; adult sheep experience a disease called "struck," characterized by sudden death, which is common. Affected goats, cattle, pigs, and horses typically show necrotic enteritis.
Humans can also be infected; the associated disease is called "enteritis necroticans" or "pigbel." Rabbits, mice, and guinea pigs have been used as experimental models for disease caused by C perfringens type C.
The toxins produced by all strains of C perfringens type C include CPA, perfringolysin O (PFO), and CPB toxins; however, other strains can produce additional toxins, such as enterotoxin (CPE), CPB2, and others. CPB is considered the most important contributor to the disease associated with C perfringens type C infection; therefore, trypsin inhibitors, which are especially present in sow colostrum, likely play a role in disease because CPB is normally quickly degraded by trypsin.
The case fatality rate in cases of C perfringens type C–associated enterotoxemia across species is usually very high. C perfringens can persist in the environment and is also capable of colonizing the intestinal tract of older animals; however, it's not considered a common commensal. Transmission can occur via carrier animals or the contaminated environment.
Clinical Findings of Enterotoxemia Caused by Clostridium perfringens Type C
Peracute and acute forms of C perfringens type C–associated disease in young animals predominate, typified by animals being found dead or with signs of colic, lethargy, depression, and usually bloody diarrhea. Subacute or chronic forms of the disease can occur, and they often result in intermittent or persistent diarrhea and weight loss.
"Struck" in sheep is characterized by adult animals found dead or showing acute signs of abdominal pain or neurological signs just before death; diarrhea is not typical in these cases. Although not well documented, likely because of its rare occurrence, this form of disease can also occur in adult goats and cattle.
Lesions of Enterotoxemia Caused by Clostridium perfringens Type C
Lesions due to C perfringens type C infection are common in the small intestine; they can also be present in the cecum and colon. Typically, lesions involve serosal congestion and/or hemorrhage, along with mucosal and submucosal hemorrhage, sometimes with emphysema. Additional systemic lesions, such as petechiae and ecchymoses, can be present throughout, along with serous or hemorrhagic fluid in body cavities—all secondary to toxemia and/or septicemia.
Microscopic evidence of necrotizing and hemorrhagic enteritis or colitis is also typical in cases of C perfringens type C enterotoxemia. Large, thick gram-positive bacilli can be apparent in the lumen or associated with denuded intestinal mucosa.
Diagnosis of Enterotoxemia Caused by Clostridium perfringens Type C
Clinical signs
Histological evaluation
Bacterial culture
PCR assay or immunohistochemistry
Diagnosis of infection by C perfringens type C relies on the presence of compatible clinical, gross, and histological findings, as well as identification of the organism through culture, followed by typing via PCR assay or immunohistochemistry, and/or detection of associated toxins.
Treatment and Control of Enterotoxemia Caused by Clostridium perfringens Type C
Supportive care
Vaccination
Optimal feeding practices
Treatment of enterotoxemia caused by C perfringens type C is typically of limited value because of the rapid progression of disease once it has become clinically apparent. However, supportive measures to correct fluid and electrolyte imbalances while also relieving pain and inflammation, controlling sepsis, and reestablishing a normal GI microbiome are important. Hyperimmune plasma and oral or parenteral type C antitoxin can be useful.
Dams can provide colostral immunity to their offspring if given a C perfringensvaccine during their pregnancy. Sows should receive this vaccine at service or midgestation and again 2–3 weeks before farrowing, and then again 3 weeks before each subsequent farrowing. In primiparous sows, it It is likely best to administer three vaccines before farrowing.
Sheep and goats are typically vaccinated for both type C and type D at the same time; the recommendation is two doses 2–6 weeks apart for sheep, followed by annual boosters. Lambs can receive their first dose of vaccine at the age of 4–6 weeks. Goats require a similar initial series but need boosters every 3–4 months because of a shorter duration of immunity.
To confer colostral immunity, one of the boosters for both sheep and goats should be administered approximately 2–4 weeks before parturition. Dry cows and heifers should be in two doses, administered 2–4 weeks apart, followed by annual boosters a month before parturition. Calves can receive their first vaccine at the age of 8–12 weeks. Although type C toxoid is not labeled for use in horses, mares may receive it initially twice, 4–6 weeks apart, with annual boosters 2–3 weeks before parturition.
Where C perfringens type C is endemic, type C antitoxin may be administered orally to foals approximately 6 hours after birth to induce passive immunity. Carbohydrate and protein overload is a risk factor for C perfringens type C. Calves fed improperly mixed milk replacers, or milk or replacers that are not at body temperature, might be at higher risk of disease.
Enterotoxemia Caused by Clostridium perfringens Type D
Enterotoxemia caused by Clostridium perfringens type D (also called pulpy kidney disease or overeating disease) affects sheep and goats but rarely occurs in cattle. It has a worldwide distribution and results in focal symmetrical encephalomalacia (FSE) in affected sheep secondary to pure enterotoxemia. Affected goats experience pure enterotoxemia or localized enteric disease, or a combination of both.
Etiology of Enterotoxemia Caused by Clostridium perfringens Type D
Enterotoxemia caused by C perfringens type D requires an alteration of the microenvironmental conditions in the intestinal tract and is therefore not contagious; however, it can and often does arise in the form of an outbreak. CPA and ETX toxins are produced by C perfringens type D, but ETX seems to be the main virulence factor in sheep and goats.
Lambs and goats > 2 weeks old are the most likely to be affected by C perfringens type D–associated disease; however, adults and occasionally lambs and kids < 2 weeks old can be affected. In cattle, the disease, although rare, affects primarily animals < 6 months old.
C perfringens spores are ingested from feed or water that has been contaminated by soil where they are ubiquitous. The spores germinate in the animal's intestinal tract and, when the microenvironmental conditions are favorable, they proliferate and produce toxins. Predisposing factors that result in favorable microenvironments include feeding large amounts of grains, concentrates, or lush pasture.
A sudden abundance of starch in the rumen results in some undigested starch reaching the intestine, where it provides an ideal substrate for C perfringens type D to replicate and produce ETX. ETX increases mucosal permeability and results in circulating toxin in the bloodstream and subsequent distribution to organs.
Clinical Findings of Enterotoxemia Caused by Clostridium perfringens Type D
Lambs with enterotoxemia caused by C perfringens type D often die after a short course of neurological and respiratory signs such as tachypnea, bruxism, staggering, hyperesthesia, opisthotonos, and seizures. Neurological signs such as aimless wandering, blindness, opisthotonus and head pressing secondary to brain edema, and sometimes symmetrical encephalomalacia can also occur. Some affected lambs die without showing any clinical signs beforehand.
Subacute or chronic forms of C perfringens type D–associated disease might occur more commonly in vaccinated lambs. Hyperglycemia and glycosuria are inconsistent findings with all forms of this disease in lambs; however, these signs can also be present with other disorders and therefore cannot be relied upon for a diagnosis of type D enterotoxemia.
In goats, the course of disease caused by C perfringens type D also ranges from peracute to chronic, and the acute form is similar to the form observed in lambs, which occurs mostly in young, unvaccinated animals. Older goats can experience a subacute form of this disease that often includes diarrhea, which can be hemorrhagic, and they might have neurological or respiratory signs, with death typically occurring within 2–4 days.
Vaccinated adult goats might experience a chronic form of type D enterotoxemia over the course of days to weeks, generally characterized by watery diarrhea that might be hemorrhagic, as well as weakness, weight loss, and agalactia. Similar to sheep, affected goats might experience hyperglycemia and glycosuria, but these are not consistent findings.
In the rare cattle cases of infection with C perfringens type D, affected cows might be found dead, or they might display recumbency, dyspnea, tachypnea, obtundation, dullness, blindness, opisthotonos, and hindlimb paddling before death.
Lesions of Enterotoxemia Caused by Clostridium perfringens Type D
Necropsy findings in cases of C perfringens type D–associated enterotoxemia might reveal only a few hyperemic areas on the intestine and hydropericardium, hydrothorax, and ascites with or without fibrin. Rapid postmortem autolysis of the kidneys has led to the popular term pulpy kidney disease (see ); however, pulpy kidneys are not always found in affected young lambs and are seldom found in affected goats or cattle.
Necropsy photograph of kidneys from sheep. The kidney in the middle is from an unaffected adult sheep; the other two kidneys are from adult sheep with enhanced autolytic changes due to Clostridium perfringens type D infection. They are slightly enlarged and appear pale and pulpy. They were also soft and friable upon palpation.
Courtesy of Cornell University College of Veterinary Medicine.
Cerebellar herniation or FSE can occur in lambs or adult sheep with the subacute or chronic form of C perfringens type D–associated disease (see ). Although FSE does not occur commonly, it is considered pathognomonic for this disease.
Necropsy photograph showing multiple cross-sections of the brain of a lamb with Clostridium perfringens type D infection that resulted in focal symmetrical encephalomalacia. Note the multiple areas of hemorrhage present in each section ventrally and bilaterally.
Courtesy of Cornell University College of Veterinary Medicine.
Lesions in goats infected by C perfringens type D are similar to those described for sheep, except that FSE is rare. In goats with the subacute or chronic form of disease, necrotic enterocolitis can be present.
Edema and malacia can be detected microscopically in the basal ganglia and cerebellum of lambs with C perfringens type D infection. Goats tend to have suppurative and fibrinonecrotizing enteritis, colitis, or enterocolitis. Because of the rare occurrence of type D disease in cattle, lesions are not well described; however, FSE was thought to be caused by ETX in some calves, and pulmonary congestion and edema have been described in affected cattle (7, 8).
Diagnosis of Enterotoxemia Caused by Clostridium perfringens Type D
Sudden death in overfed sheep
Demonstration of epsilon toxin in small intestinal fluid
In sheep, a presumptive diagnosis of enterotoxemia due to C perfringens type D can be based on compatible history and clinical signs. Hyperglycemia and glycosuria can be useful to support a diagnosis, but they are inconsistently present. Gross and microscopic lesions suggestive of disease, along with isolation of C perfringens type D from small or large intestinal contents, supports a diagnosis. However, these findings are not confirmatory, because this organism is also present in some healthy sheep.
The presence of FSE or microvascular damage in vulnerable brain regions, along with perivascular edema, is diagnostic for C perfringens type D–associated disease. In addition, detection of ETX in small intestinal contents from animals with these clinical findings and lesions confirms the diagnosis.
In goats with acute or subacute disease, diagnostic strategies similar to those used for sheep are relevant; however, perivascular edema in the brain is much less common. In subacute or chronic cases in goats, the detection of ETX, along with necrotizing colitis or enteritis, is diagnostic of C perfringens type D enterotoxemia.
In the rare cattle cases of type D disease, similar diagnostic strategies have been described (observation of perivascular edema in the brain, detection of ETX in the small intestine).
Control of Enterotoxemia Caused by Clostridium perfringens Type D
Vaccination
Dietary changes in feedlot lambs
Vaccination using an ETX toxoid is an important prevention strategy for C perfringens type D–caused enterotoxemia in sheep and goats. The vaccination protocol depends on the age of the animals, the frequency with which the disease appears on a particular property, and the method of husbandry.
In general, sheep require two doses of vaccine 2–6 weeks apart, followed by annual boosters. Goats tend to have lower titers for shorter periods of time after vaccination and therefore require the same two-dose initial series but need boosters every 3–4 months thereafter.
If very young animals are affected, it is best to provide colostral immunity by immunizing pregnant ewes and does. Again, these animals must receive a two-dose series initially, and the timing should allow for administration of a booster approximately 2–4 weeks before parturition.
Although type D enterotoxemia is not common in cattle, at least some protection can be afforded by common clostridial disease vaccines already in use, because many of them contain ETX, among other toxoids.
Nutritional management is also key to controlling type D enterotoxemia in sheep and goats and possibly other ruminant species. Avoiding sudden large exposure to starch-rich feeds is important.
No treatment strategies are widely available; ETX antitoxin has been used in experimental situations, but it is expensive and impractical.
Enterotoxemia Caused by Clostridium perfringens Type E
Until genotyping PCR assays to identify this organism in feces and intestinal contents became more readily used, Clostridium perfringens type E was rarely reported as the cause of disease in domestic and wild animals. The true role of C perfringens type E in enteric disease is still not well defined.
C perfringens type E produces alpha (CPA) and iota (ITX) toxins. The enteric disease associated with this organism is likely due to the effects of ITX. Clostridium spiroforme produces a toxin similar to ITX, and these two toxins are difficult to differentiate using standard immunological tests. Because of this similarity, enterotoxemia in rabbits was once thought to be associated with C perfringens type E. Instead, enterotoxemia in rabbits is due mainly to C spiroforme, and the misdiagnosis was due to similarities shared by CPA and ITX.
C perfringens type E is associated with diarrhea, abomasitis, hemorrhagic enteritis, and sudden death in calves up to approximately 2 months of age. It has also been associated with high mortality rates in ostrich chicks, as a result of enteritis. In addition, this organism has been implicated in disease in goat kids and lambs, but reports are limited.
Diagnosis of C perfringens type E infection is challenging because the methods used to detect ITX can cross-react with the toxin of C spiroforme, and no commercially available assays detect either toxin. Postmortem lesions associated with this pathogen are not well described.
Currently, diagnosis of C perfringens type E infection relies on isolation of the organism from anaerobic culture of the intestine in animals with compatible disease. As with other strains of C perfringens, however, this organism can be present in the intestinal tract of some healthy animals, so the interpretation of results is challenging.
Enterotoxemia Caused by Clostridium perfringens Type F
Clostridium perfringens type F carries the genes that encode the CPA and CPE toxins, but it does not have the genes that encode for beta, epsilon, iota, or necrotic enteritis beta-like toxins. CPE has been implicated in enteric disease of dogs, horses, and possibly pigs; however, the true involvement of type F in disease is not well understood.
NetF is a pore-forming toxin that is produced by some C perfringens type F isolates and is associated with necrotizing enterocolitis in foals and with acute hemorrhagic diarrhea syndrome (AHDS) in dogs. C perfringens type F is also associated with food poisoning and antimicrobial-associated diarrhea in humans.
Dogs of any age or breed can be affected by AHDS, but small breeds 2–4 years old are overrepresented. Affected dogs typically present with acute-onset vomiting and hemorrhagic diarrhea. Some exhibit depression and a painful abdomen. Overall, AHDS cases can vary from mild to severe, and death is not common.
It is important to remember that there are other causes of hemorrhagic gastroenteritis in dogs, and the gene for NetF production has been found in only 10% of C perfringens isolates from dogs with diarrhea (9). Lesions typically include bloody small intestinal content, with congestion and watery contents in both the small and large intestines.
The disease associated with NetF in foals was described in 2015 (9). Most affected foals are < 6 days old, and some can begin experiencing clinical signs as early as 12 hours after birth. Mortality rates are high, and affected foals can die within a day after the onset of clinical signs, which usually include diarrhea, depression, signs of abdominal pain, and dehydration.
The trypsin-inhibitory action of colostrum likely plays a role in the pathogenesis of NetF-associated disease in foals. Lesions consistent with fibrinonecrotic enteritis, intestinal hemorrhage, and intestinal mucosal thickening are typical. In some cases, emphysema is present in the intestinal wall and the contents of the intestine are usually hemorrhagic. This intestinal lesion can be segmental or more diffuse. There can also be evidence of sepsis secondary to these findings.
Diagnosis of NetF-associated disease in foals and dogs involves demonstrating the presence of the netF gene in C perfringens isolates or the presence of the gene via PCR assay on intestinal contents or feces of animals with compatible clinical signs and lesions. Some healthy dogs have NetF-producing C perfringens strains, so the interpretation of test results requires caution. Testing should be performed in the first 7 days of clinical disease to avoid false-negative results due to declining NetF later in the course of disease.
Treatment of NetF-associated enterotoxemia in dogs centers around supportive care; antimicrobials often are not necessary, because of the typically fast recovery. An autogenous bacterin toxoid vaccine is available to prevent disease in foals. In addition, hyperimmune plasma from horses immunized against C perfringens types A, C, and D and against NetF toxin is available for both prevention and treatment in foals.
C perfringens type F–associated disease in pigs is less well understood. The CPE enterotoxin has been detected in feces from piglets with diarrhea and not from healthy controls (10). Challenging piglets with enterotoxigenic C perfringens (not definitively characterized) resulted in a range of disease from mild diarrhea to profuse bloody diarrhea (2). More work needs to be done to better characterize this organism in pigs.
Enterotoxemia Caused by Clostridium perfringens Type G
Necrotic enteritis is a clostridial disease of poultry and other avian species that occurs worldwide. An acute form of the disease is characterized by either hemorrhagic or nonhemorrhagic enteritis. In addition, a subclinical or chronic form is characterized by poor weight gain and poor feed efficiency.
Clostridium perfringens type G produces CPA and necrotic enteritis–like B toxin (NetB). The hemorrhagic form of necrotic enteritis seems to be associated with C perfringens type A; the subacute form is associated with C perfringens type G.
Further complicating this disease, Paraclostridium sordellii appears to be associated with outbreaks of necrotic enteritis in broiler chickens. Altogether, multiple clostridial species and types of C perfringens are most likely involved in necrotic enteritis; however, C perfringens type G appears to be the type most commonly associated with the disease.
Acute necrotic enteritis in chickens typically results in depression, reluctance to move, diarrhea, ruffled feathers, decreased appetite, and huddling. Progression is rapid, with death often occurring within hours and mortality rates of approximately 50% (11). Necrotic enteritis in other avian species typically presents similarly but is rarely well described. Subclinical necrotic enteritis in poultry, when detected, is usually characterized by a drop in production, without any other signs.
Lesions associated with acute necrotic enteritis are more likely to occur in the small intestine and include gas distention with foul-smelling contents, fibrin, and sloughed mucosal cells. Intestinal ulcerations might be evident, with or without a pseudomembrane. Subclinical necrotic enteritis usually results in similar lesions; however, it can also result in severe edema of the intestinal wall.
Unlike chickens with necrotic enteritis, affected turkeys tend to have lesions extending into the colon, and the duodenum is also more likely to be affected. In ostriches, diffuse small intestinal enteritis with fibrinohemorrhagic fluid is typical of necrotic enteritis outbreaks.
After damage to the intestine, C perfringens can induce multifocal necrotic hepatic lesions and congestion, as well as distention of the gallbladder and bile duct.
Diagnosis of necrotic enteritis relies on identifying the characteristic lesions and ruling out other common pathogens that might produce similar clinical signs. Anaerobic culture to detect C perfringens can also assist in the diagnosis; however, the culture must be performed specifically on a swab of a lesion in the intestine to identify intralesional C perfringensrather than normal microbiota. Additional rapid commercial assays are needed.
Prevention of necrotic enteritis includes decreasing the amount of trypsin inhibitors in feed, because trypsin inactivates C perfringens toxins. Some feed components that are high in trypsin inhibitor activity include fish meal and potato protein. Other diets (eg, those high in wheat, rye, or barley) can slow intestinal movement and predispose animals to necrotic enteritis.
Antimicrobial growth promoters were once a mainstay of necrotic enteritis control; however, many countries have decreased or eliminated their use. To date, no vaccine is commercially available, and many producers rely on probiotics to help decrease lesions and mortality rates due to this disease.
Key Points
Clostridium perfringens is classified into seven different types (A–G) according to the genes present for the production of various toxins.
The alpha, beta, epsilon, and iota toxins, as well as enterotoxin and necrotic enteritis beta-like toxin, are used in the C perfringens classification system.
Together, the actions of these toxins produce the various enteric and sometimes systemic disease states characteristic of C perfringens infections in animals.
For More Information
Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.
Uzal FA, Giannitti F, Asin, J. Yellow lamb disease (Clostridium perfringens type A enterotoxemia of sheep): a review. Animals. 2022;12(12):1590.
Also see pet owner content regarding enterotoxemia in dogs and horses.
References
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