Clostridial Diseases of Horses: A Review

Abstract

The clostridial diseases of horses can be divided into three major groups: enteric/enterotoxic, histotoxic, and neurotoxic. The main enteric/enterotoxic diseases include those produced by Clostridium perfringens type C and Clostridioides difficile, both of which are characterized by enterocolitis. The main histotoxic diseases are gas gangrene, Tyzzer disease, and infectious necrotic hepatitis. Gas gangrene is produced by one or more of the following microorganisms: C. perfringens type A, Clostridium septicum, Paeniclostridium sordellii, and Clostridium novyi type A, and it is characterized by necrotizing cellulitis and/or myositis. Tyzzer disease is produced by Clostridium piliforme and is mainly characterized by multifocal necrotizing hepatitis. Infectious necrotic hepatitis is produced by Clostridium novyi type B and is characterized by focal necrotizing hepatitis. The main neurotoxic clostridial diseases are tetanus and botulism, which are produced by Clostridium tetani and Clostridium botulinum, respectively. Tetanus is characterized by spastic paralysis and botulism by flaccid paralysis. Neither disease present with specific gross or microscopic lesions. The pathogenesis of clostridial diseases involves the production of toxins. Confirming a diagnosis of some of the clostridial diseases of horses is sometimes difficult, mainly because some agents can be present in tissues of normal animals. This paper reviews the main clostridial diseases of horses.

Keywords: Tyzzer disease; botulism; clostridial diseases; colitis; enteritis; enterocolitis; gas gangrene; horses; infectious necrotic hepatitis; review; tetanus.

Figure 4

Liver from a foal with Tyzzer disease. (A) A cross section of the liver shows multifocal, random white spots distributed throughout the parenchyma. (B) Multifocal to coalescing areas of coagulative and lytic necrosis with neutrophilic infiltrate; HE. Reprinted with permission from ref. [77]. Copyright 2017 John Wiley & Sons. (C) Focus of necrosis showing faintly stained filamentous basophilic bacilli mostly in the cytoplasm of hepatocytes (arrowhead); HE. (D) Filamentous bacilli in the cytoplasm of several hepatocytes. Steiner stain.

Figure 1

Neonatal foal with enterocolitis produced by Clostridium perfringens type C. (A) The serosal view of a large segment of the small intestine is diffusely congested and emorrhagic and the serosa of the large colon and cecum are dark. (B) The mucosa of the small intestine is necrotic and covered by an orange pseudomembrane. (C) The small intestine shows diffuse mucosal necrosis and multifocal thrombosis (arrowheads); a pseudomembrane (pm) is observed in the lumen; HE. (D) Strong positivity for C. perfringens is observed in the superficial mucosa and lumen of the small intestine; C. perfringens IHC. Reprinted with permission from ref. [10]. Copyright 2012 Vet Pathol.

Figure 2

Horse with enterocolitis produced by Clostridioides difficile. (A) There is diffuse red discoloration in the serosa of most of the small intestine and colon. (B) The mucosa of the colon is congested and hemorrhagic, has thickened folds and it is covered by a fibrinous pseudomembrane. (C) The small intestine shows villus blunting, loss of superficial epithelium, congestion and hemorrhage of the mucosa and severe submucosal congestion and edema. (D) There is diffuse necrosis of the mucosa, which is covered by a pseudomembrane, and congestion and edema of the submucosa. Reprinted with permission from ref. [29]. Copyright 2013 Vet Pathol.

Figure 3

Tissues from a horse with gas gangrene produced by Paeniclostridium sordellii. (A) Severe subcutaneous and interstitial edema. (B) Coagulative necrosis, hemorrhage, edema, and neutrophil infiltration in skeletal muscle; HE. (C) Clusters of Gram-positive rods in necrotic skeletal muscle. Gram stain. (D) Intralesional strong positivity to P. sordellii in affected skeletal muscle. P. sordellii IHC. Reprinted with permission from ref. [40]. Copyright 2019 J Vet Diag Invest.

Figure 5

Liver from a horse with infectious necrotic hepatitis produced by Clostridium novyi type B. (A) A large focus of necrosis involves most of the left hepatic lobe. Photo reproduced from [79]. (B) The area of coagulative necrosis (right) is separated from an area of more viable-looking hepatic parenchyma (left) by a band of inflammatory cells; HE. Reprinted with permission from ref. [79]. Copyright 2018 J Vet Diag Invest. (C) Higher magnification of the band of inflammatory cells, composed mostly of neutrophils, surrounding the focus of necrosis; HE. (D) Strongly positive rods in the periphery of the focus of necrosis; C. novyi IHC.

Figure 6

Tetanus. (A) Foal showing muscle stiffness resulting in a “rocking horse” stance and lock-jaw (photo courtesy of Francisco Lobato). (B) Adult horse; the tail is held out (arrowhead; hoto courtesy of Nicola Pusterla). (C) Smear of Clostridium tetani culture showing Gram-positive rods with terminal spores giving them the typical drumstick appearance; notice that the Gram positivity has been lost in some of these rods. Gram stain.

Figure 7

Botulism. (A) Foal showing muscle weakness, leading to inability to keep its head up and needing help to stand (photo courtesy of Gary Magdesian). (B) Adult horse with decreased muscle tone of the tongue, which is protruding outside the mouth (photo courtesy of Nicola Pusterla). (C) Neck of an adult horse showing gelatinous edema surrounding the nuchal ligament.