2 year old Thoroughbred colt (Equus caballus)The horse was normal and trained as usual the previous day, but did not consume all of his feed the night prior. The referring veterinarian examined the horse at 11 AM; the temperature was 104.8°F, the heart rate was elevated, and he was reluctant to move. He was treated with Banamine and Bactrim. The horse died spontaneously at 3:30 PM, at which time bloody froth was expelled from both nostrils.

Gross Description:  

The kidneys are bilaterally markedly enlarged. The right kidney weighs 1.85 kg and measures 20 x 19 x 8.5 cm, and the left kidney weighs 1.86 kg and measures 24.5 x 16 x 7 cm (each kidney is approximately 0.42% of body weight; 0.25% is normal). Bilaterally, the perirenal adipose tissue is mildly edematous. There are widespread multifocal, slightly raised, 1 to 10 mm diameter, tan-yellow foci on the subcapsular surface of both kidneys which occasionally bulge from the capsular surface. The discoloration frequently ex-tends into the renal capsule and oc-casionally into the perirenal adipose tissue. The capsules are friable and difficult to peel. Both kidneys moderately bulge on cut surface, and the cortices contain myriad 1mm diameter to 9 x 2 mm yellow-tan foci which occasionally have a cavitated center.

Histopathologic Description:

Predominantly in the cortex, there are multifocal to coalescing, nodular in-flammatory infiltrates predominantly of degenerate neutrophils, fewer macrophages, and cellular debris. This infiltrate is often centered on glomeruli, extending into and sometimes effacing the adjacent interstitium and renal tubules. Renal tubules in inflamed areas are sometimes degenerate or necrotic. Larger blood vessels sometimes contain luminal aggregates of fibrin, degenerate and viable neutrophils, cellular debris and erythrocytes; inflammation often extends into the vessel wall (vasculitis). Many foci of inflammation contain aggregates of gram-negative bacilli.

Morphologic Diagnosis:  

Embolic nephritis, suppurative, acute, multifocal to coalescing, severe, with in-tralesional gram-negative bacilli and vasculitis.

Lab Results:  

Microbiology: Aerobic culture of the kidney yielded heavy growth of Actinobacillus equuli ssp. equuli.


Actinobacillus equuli

Contributor Comment:  

The most frequently isolated agent in equine cases of embolic nephritis is Actinobacillus equuli, most often secondary to septicemia of foals.4 A. equuli is a gram-negative bacillus that can be normal flora of the oral cavity, reproductive tract and intestinal tract of horses.2,5 It is especially known for its tendency to create microabscesses in the kidneys and other organs.4 In foals, A. equuli typically causes septicemia, also known as sleepy foal disease.2 Septicemic lesions typically include embolic lesions in the kidney, lungs and liver, with lesions also reported in the umbilicus, adrenal gland, and joints.2 In adult horses, A. equuli has been reported to cause sepsis, nephritis, en-docarditis, pericarditis, peritonitis, en-teritis, pleuropneumonia, arthritis, pe-riorchitis, and abortion.2,3,5 A. equuli infections in adult horses are thought to be predisposed by stress or other infections, such as respiratory viruses or salmonellosis.2


JPC Diagnosis:  

Kidney: Nephritis, embolic, suppurative, multifocal, marked with necrotizing vasculitis and colonies of bacilli.

Conference Comment:  

Actinobacillosis in adult horses is uncommon and most frequently associated with an underlying disease. There are two subspecies of A. equuli, a hemolytic subspecies termed A. equuli subsp. haemolyticus which is isolated from the normal oral cavity and respiratory tract, and a non-hemolytic form termed A. equuli subsp. equuli, which also resides in the oral cavity as well as the gastrointestinal tract of adult horses and is the agent of septicemia in foals.1 The hemolytic form has been associated with various infections including peritonitis, reproductive failure and respiratory disease. The bacterium possesses an RTX exotoxin known as Aqx that is cytotoxic to equine red blood cells. The non-hemolytic subspecies is more commonly present in cases of septicemia and may also be associated with respiratory disease, embolic nephritis and infection in other organs as well.1 In septicemic cases, Actinobacillus can act as the primary agent or be a secondary infection following other viral or bacterial infections. The presence of endotoxin likely plays a role in the endothelial damage, vasculitis and bacterial emboli which are classically seen in septicemic cases. Although most often associated with foals in conjunction with events such as failure of passive transfer, septicemic lesions such as embolic nephritis, as seen in this case, as well as pneumonia, may be seen in adult horses.1 In cases of embolic nephritis, bacteria become lodged in glomerular capillaries resulting in the presence of suppurative lesions or abscesses and, in some cases, when emboli are large enough, may occlude arteries resulting in septic infarcts. In septicemic foals that survive for a period of time, microabscesses will be seen in multiple organs and polyarthritis will be present. A. equuli may also cause diarrhea and hemorrhagic enteritis in foals. A common agent of embolic nephritis in swine, perhaps the most common, is Erysipelothrix rhusiopathiae; in cattle the common agent is Trueperella pyogenes; and in sheep and goats Corynebacterium pseudotuberculosis may be associated with embolic infections.1 Although uncommon, A. equuli infection can be associated with endocarditis or myocarditis in adult horses6 and has also been associated with reproductive losses. Conference participants described the prolific inflammatory infiltrates as being centered on vessels as well as effacing glomeruli, with adjacent tubules being secondarily affected with varying severity. Tubules are multifocally ectatic and variably contain necrotic, sloughed tubular epithelial cells admixed with fibrin, hemorrhage and proteinaceous fluid. Fibrin thrombi with colonies of coccobacilli are occasionally seen in glomerular tufts. Some conference participants interpreted the most severely affected area of the cortex as coagulative necrosis secondary to infarction due to fibrin thrombi; others attributed the tinctorial change as more consistent with some degree of autolysis. 7The differential diagnosis discussed by participants in the case of this horse included Escherichia coli, Klebsiella sp., Streptococcus sp., Rhodococcus equi and Salmonella species.


1. Cianciolo RE, Mohr FC. Urinary System. In: Maxie MG, ed. Jubb, Kennedy, and Palmer's Pathology of Domestic Animals. 6th ed. Vol 2. St. Louis, MO: Elsevier; 2016:432-433.

2. Layman QD, Rezabeck GB, Ramachandran A, Love BC, Confer AW. A retrospective study of equine actinobacillosis cases: 1999-2011. J Vet Diagn Invest. 2014; 26(3):365-375.

3. Matthews S, Dart AJ, Dowling BA, Hodgson JL and Hodgson DR. Peritonitis associated with Actinobacillus equuli in horses: 51 cases. Aust Vet J. 2001; 79(8): 536-9.

4. Maxie, MG, Newman SJ. Urinary System. In: Maxie MG, ed. Jubb, Kennedy, and Palmer's Pathology of Domestic Animals, 5th ed. Vol 2. Edinburgh: Elsevier Saunders. 2007:479-480. 

5. Patterson-Kane JC, Donahue JM and Harrison LR. Septicemia and peritonitis due to Actinobacillus equuli infection in an adult horse. Vet Pathol. 2001; 38(2): 230-2.

6. Robinson WF, Robinson NA. Cardiovascular system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer's Pathology of Domestic Animals. 6th ed. Vol 3. St. Louis, MO: Elsevier; 2016:31-42.


7. Uzal FA, Plattner BL, Hostetter JM. Alimentary System. In: Maxie MG, ed. Jubb, Kennedy, and Palmer's Pathology of Domestic Animals. 6th ed. Vol 2. St. Louis, MO: Elsevier; 2016:114.

Click the slide to view.

4-1. Kidney, foal.

4-2. Kidney, foal.

4-2b. Kidney, foal.

4-2c. Kidney, foal.

4-3. Kidney, foal.

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