Seven-day old, female, Quarter horse, equine (Equus caballus).Acute onset of diarrhea, colic and death in less than 24 hours from the beginning of the clinical signs.
The carcass was in a very good state of postmortem preservation and the tail and perineal region
were soiled with abundant yellow, dried feces.Â Diffusely, the jejunum and ileum were thickened (~3-4 mm) and had
dark red, edematous mucosa with multifocal pseudomembrane formation, which was more predominant in the ileum
and terminal jejunum.Â The serosa of the jejunum and ileum had multifocal petechiation and a few, focal, larger (up
to 1 cm in diameter) subserosal ecchymoses.
The small intestinal content was composed of scant, red to brown fluid.Â The large colon had a focally extensive area (~50 cm long and involving the left ventral portion, the pelvic flexure and left dorsal portion of the colon) with multifocal to coalescing areas of necrosis and pseudomembrane formation.Â The cecum had a focal, small (~3 cm in diameter) area of dark red mucosa with mural edema adjacent to the ileocecal valve.Â The colonic and cecal content was composed of a moderate amount of light brown fluid.
Jejunum, ileum and colon: There is diffuse, marked, coagulative necrosis of the
mucosa, characterized by severe disruption of the architecture with diffuse mucosal hypereosinophilia, loss of the
mucosal epithelial lining, attenuation or collapse of the intestinal villi and crypts, and occasional multifocal loss of
the mucosa/submucosal boundaries.Â On the mucosal surface, admixed with superficial necrotic debris and within the
pseudomembrane, there are numerous clusters of bacteria, predominantly thick and short rods.Â Within the lamina
propria and in the submucosa, there is moderate to marked hyperemia and hemorrhage, abundant fibrin and cellular
and necrotic debris with very rare neutrophils.Â There is multifocal vascular thrombosis of small to mid-size caliber
blood vessels in the mucosa and submucosa and the submucosal lymphatics are markedly dilated.Â Within the
muscular layer, in one section, there are a few multifocal hemorrhages.Â The serosa is moderately expanded by clear
spaces (edema) and there is mild hemorrhage.
Enterocolitis, necrohemorrhagic, acute, diffuse, severe, with
pseudomembrane formation, mucosal/submucosal vascular thrombosis, edema and massive numbers of Clostridia-like
bacilli attached to the mucosal surface.
The small intestine and colon contents were positive by the ELISA method for Clostridium
perfringens toxins alpha and beta and Clostridium difficile toxins A/B.Â Clostridium perfringens type C (CPE and
beta 2 negative) was isolated from the small intestine and colon and C.Â difficile was isolated only from the colon.
Salmonella PCR and cultures were negative from small intestine.
Equine enteritis and enterocolitis, manifested with diarrhea and colic, are important
causes of morbidity and mortality of foals and adult horses.Â These syndromes have been associated with a variety of
etiologies, including Clostridium spp., Salmonella spp., Ehrlichia risticii, Aeromonas spp, Lawsonia intracellularis,
cantharidin toxicity, and larval cyathostomiasis.(15) Although the first reports associating clostridia with enteritis in
the foal were published in the 1930s,(13) only in the past few decades Clostridium perfringens (C.Â perfringens) and
Clostridium difficile (C.Â difficile) have been increasingly reported as relevant pathogens involved in cases of enteritis
and enterocolitis in horses.(2,3,4,8,12,15,16) C.Â perfringens is classified into five types (A, B, C, D, and E) based on the
production of one or more of four so-called major toxins, namely alpha (CPA), beta (CPB), epsilon (ETX) and iota.
Two other major toxins, namely enterotoxin (CPE) and Beta 2 (CPB2), can also be produced by all types of C.
perfringens, but they are not used in the classification of this microorganism.Â C.Â perfringens type B and C have
been associated with severe necrotizing, hemorrhagic enterocolitis in foals, although type C is considered the most
commonly reported clostridial enteric pathogen in foals in North America.(6)
Clostridium perfringens type C produces two major toxins, CPA and CPB.Â The CPA toxin is a lecithinase, which is considered the main virulence factor in C.Â perfringens type A gas gangrene of humans and animals.Â However, the contribution of CPA to the virulence of type C isolates is negligible.
The CPB toxin, on the other hand, is a necrotizing toxin that forms pores in the membrane of susceptible cells.Â This toxin is considered to be responsible for the intestinal necrosis and systemic alterations seen in type C infections of several animal species, including horses.Â Lethal disease caused by C.Â perfringens type C in many mammalian animal species and humans originates when type C strains proliferate and produce toxins in the intestine.(14) Because CPB is highly susceptible to the action of trypsin, neonatal animals are considered to be particularly susceptible to type C infections due to the low level of intestinal trypsin during the first days of life.Â Although C.Â perfringens type C causes severe intestinal damage, death in affected animals is thought to primarily result from toxemia following absorption of toxins from the intestine into the circulation.(10,11) Therefore, type C infections are considered to be true enterotoxemias, i.e.Â diseases produced by toxins generated in the intestine, but that are absorbed into the general circulation and act on organs distant from the gastrointestinal tract.Â A presumptive diagnosis of C.Â perfringens type C enterotoxemia can be established based on clinical history, i.e.Â acute onset of diarrhea, colic or sudden death, and gross and microscopic lesions.Â This presumptive diagnosis can be reinforced by isolation of large numbers of C. perfringens type C from the small and/or large intestine, because this microorganism is rarely isolated from the gut of normal horses, as opposed to C.Â perfringens type A which is frequently isolated from clinically normal horses (contributors unpublished observations).Â However, failure to isolate C.Â perfringens type C from the gut does not preclude a diagnosis of type C enterotoxemia because confirmation of a diagnosis of type C infection should be based on detection of CPB in intestinal contents.(11) Demonstration of CPB in the gut content can be achieved by in vivo assays in mouse and guinea pig (less common nowadays) or in vitro methods based on enzyme immunoassays, such as ELISA.
To date, the only published reports of enterotoxemia by C.Â perfringens type C in horses confirmed by toxin detection are limited to sporadic cases.Â (3,5,7,8,9) On the other hand, a few reports have been published that describe a larger number of animals in which a diagnosis was based on pathology and isolation of C.Â perfringens type C but without toxin detection.(4,16) To our best knowledge, there is no published information of the pathological findings of C. perfringens type C enterotoxemia based on a large number of cases with a diagnosis confirmed by CPB detection in intestinal contents.
Currently, we are working on a manuscript to be submitted for publication in which the lesions of the intestinal tract in several horses with Clostridium perfringens type C enterotoxemia confirmed by the detection of the beta toxin in the intestinal contents are characterized.Â We believe that the lesions present in the submitted slides are very characteristic of, but not diagnostic for, equine type C enterotoxemia.
Small intestine; and colon (per contributor): Enterocolitis, fibrinonecrotic, diffuse, severe, with
transmural edema, hemorrhage, fibrin thrombi, and myriad surface bacilli.
As mentioned by the contributor, Clostridium perfringens types A-E are distinguished from
one another based on their exotoxin profiles.Â A summary of the toxins produced by each type follows:(1)
- C.Â perfringens type A: Î±
- C.Â perfringens type B: Î±, Î², Îµ
- C.Â perfringens type C: Î±,Î²
- C.Â perfringens type D: Î±, Îµ
- C.Â perfringens type E: Î±, Î¹
Each type produces different syndromes based on the species of animal affected.(1)
|Type A||Type B||Type C||Type D||Type E|
|Piglet||White scours||Hemorrhagic enteritis|
|Cow/calf||Acute intravascular hemolysis (calf); Hemorrhagic bowel syndrome (dairy cattle)||Calf: similar to lamb||Struck-like syndrome in feedlot cattle; Hemorrhagic enteritis (calf)||Enterotoxemia (calf)||Hemorrhagic enteritis (calf)|
|Sheep/lamb||Acute intravascular hemolysis (lamb)||Lamb dysentery||Struck (adults); Hemorrhagic enteritis (lamb)||Enterotoxemia (pulpy kidney, overeating disease)|
|Horse/foal||Necrotizing enteritis (foal)||Hemorrhagic necrotizing enteritis (foal)|
|Dog||Hemorrhagic canine gastroenteritis|
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