Pathology in Practice

Benjamin Adu-Addai Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48910.

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Rebecca C. Smedley Diagnostic Center for Population and Animal Health, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48910.

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Thomas P. Mullaney Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48910.
Diagnostic Center for Population and Animal Health, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48910.

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History

A male foal had difficulty nursing during the first 24 hours after birth and was bottle fed. It also had difficulty passing meconium. The foal's condition seemed to improve during the next day. On the morning of the third day, the foal was observed nursing; however, in the afternoon of that day, the foal became weak, could not rise, began flailing, and was mentally dull. Late that evening, the referring veterinarian administered fluids and dextrose solution IV but the foal did not respond. It died a few hours later at 4 days of age.

Clinical and Gross Findings

Postmortem examination was performed (Figure 1). The foal weighed 48.2 kg (106 lb), and its nutritional and hydration states were considered adequate. The conjunctivae were yellow. Multiple ulcers were present on the tongue, and one was located on the rostral portion of the gingiva of the mandible. The subcutaneous tissue surrounding the umbilicus was yellow and gelatinous. Internally, the serosal surface of the urinary bladder, where the urachus attached, was hemorrhagic; the mucosa had multifocal areas of hemorrhage, up to 7 mm in diameter, and mild diffuse emphysema. The pericardial sac was yellow and contained approximately 100 mL of clear yellow fluid. The cranioventral regions of the lungs were congested with mottled pink to dark red areas and were firm on palpation. Also, multifocal, pale tan, slightly raised foci (1 to 4 mm in diameter) were visible; these extended into the underlying parenchyma on cut section. Pale tan foci ranging between pinpoint to 5 mm in diameter were diffusely scattered on the serosal surface and within the parenchyma of the liver on cut section. There were multifocal petechiae on the serosal surfaces of the spleen and ileum; the mucosal surface of the ileum was slightly thickened and corrugated. Multifocal, slightly raised, pale tan foci were evident on the mucosal surfaces of the duodenum, ileum, and colon. There were no remarkable gross findings in the kidneys.

Figure 1—
Figure 1—

Photographs of the cranial and caudal lobes of the left lung (A), liver (B), and luminal aspect of the colon (C) of a foal that failed to thrive from birth and died at 4 days of age. A—Notice the dark red to pink mottling of the cranioventral aspect of the left lung and the icterus of the pericardial sac and other connective tissue. B—Along the serosal surface of the liver, there are diffusely scattered pale tan foci that range from pinpoint to 5 mm in diameter. C—Multifocal, slightly raised, pale tan foci (arrows) are present on the mucosal surface of the colon.

Citation: Journal of the American Veterinary Medical Association 245, 12; 10.2460/javma.245.12.1339

Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →

Histopathologic Findings

Within sections of the lungs, multifocal to coalescing areas of necrosis and inflammatory cells replaced the normal alveolar parenchyma (Figure 2). These foci were composed of amorphous eosinophilic necrotic cellular debris admixed with degenerate and viable neutrophils, fewer macrophages, lymphocytes, and plasma cells. Multifocally, there were areas of hemorrhage and many colonies of coccobacilli. Approximately 70% of the alveolar spaces contained edema and fibrin. Many bronchioles and occasional bronchi also contained fluid, fibrin, degenerate inflammatory cells, sloughed epithelial cells, and coccobacilli. One bronchus contained a few sloughed squamous epithelial cells. Occasionally, fibrin thrombi were seen within pulmonary vessels.

Figure 2—
Figure 2—

Photomicrographs of sections of lung tissue from the foal in Figure 1. A—Notice the multifocal to coalescing areas of necrosis (asterisk) and inflammatory cells (arrow) that have replaced the normal alveolar parenchyma. H&E stain; bar = 500 μm. B—Within necrotic foci, there are numerous colonies of coccobacilli (asterisks) and degenerate neutrophils. H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 245, 12; 10.2460/javma.245.12.1339

Examination of sections of liver tissue revealed randomly distributed areas of necrosis and inflammatory changes that effaced the normal hepatic cord architecture. These areas were characterized by cellular debris, degenerate neutrophils, and numerous coccobacilli. Multiple vessels contained fibrin, degenerate neutrophils, bacterial colonies, and occasionally fibrin thrombi.

Histopathologic findings in sections of the spleen included multifocal central follicular lymphoid depletion in the white pulp and patchy areas of remaining resident macrophages. The red pulp had evidence of marked congestion and extramedullary hematopoiesis mixed with degenerate and viable neutrophils. In sections of mesenteric lymph nodes, there was also marked central depletion of the lymphoid follicles along with multifocal areas of hemorrhage and fibrinoid material within markedly dilated lymphatic vessels and subcapsular sinuses. Occasional bacterial colonies were present.

Tissues sections of the ileum and the colon contained multifocal erosions and ulcers with necrotic cellular debris, fibrin, inflammatory cells, and multifocal bacterial colonies. In addition, the duodenum, ileum, and colon had multifocal, superficial to deep mucosal necrosis with cell debris, neutrophils, and colonies of coccobacilli. The Peyer's patches were moderately depleted of lymphocytes. Occasionally, ileal crypts were dilated and contained degenerate and necrotic cellular debris and inflammatory cells.

The umbilical cord was edematous with multiple vascular thrombi and multifocal hemorrhage, necrosis, degenerate neutrophils, and occasional colonies of bacterial coccobacilli. Within sections of the urinary bladder, marked multifocal subepithelial hemorrhage, edema, and emphysema were evident. There were also multifocal areas of necrosis throughout the wall of the bladder, and many vessels contained fibrin. Within 1 section of the right kidney, there was a focally extensive area of hemorrhage within the pelvis.

Laboratory Findings

Bacterial culture of liver tissue samples yielded numerous Actinobacillus equuli and few Escherichia coli, but there was no growth of Salmonella organisms. The serum concentration of IgG was 804 mg/dL. With the assay used, the ideal serum IgG concentration for a foal > 18 hours old but < 2 weeks old is > 725 mg/dL; an adequate value for healthy foals of this age range is > 440 mg/dL.

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: bacterial fibrinosuppurative and necrotizing bronchopneumonia and hepatitis, suppurative splenitis and funisitis, fibrinous and hemorrhagic lymphadenitis, erosive to ulcerative enterocolitis, and necrotizing cystitis with multifocal hemorrhage, edema, and emphysema; multiple fibrin thrombi; and marked lymphoid depletion of the spleen, mesenteric lymph nodes, and Peyer's patches.

Case summary: A equuli septicemia in a neonatal foal.

Comments

The findings for the foal of the present report were consistent with septicemia attributable to A equuli infection. Actinobacillus equuli is a gram-negative coccobacillus that naturally resides as a commensal organism on the mucosal membranes of adult horses but is commonly a cause of fatal septicemia in newborn foals (sleepy foal disease).1,2 This bacterium has 2 subtypes: one that is hemolytic (Actinobacillus equuli subsp haemolyticus) and another that is nonhemolytic (Actinobacillus equuli subsp equuli). Hemolysis is induced by the A equuli RTX toxin (Aqx gene), which is absent in the nonhemolytic strains.3–6 Both bacterial subtypes have been associated with disease. Actinobacillus equuli subsp haemolyticus is an opportunistic pathogen that causes various disease conditions in foals and older horses, including stillbirth, metritis, mastitis, septicemia, arthritis, endocarditis and pericarditis, meningitis, respiratory tract infections, enteritis, peritonitis, periorchitis, and wound inflammation.1,7,8 Actinobacillus equuli subsp equuli is also an opportunistic pathogen of horses and pigs but is most prominently associated with acute, highly fatal septicemia of newborn foals.1,3,9 Sleepy foal disease usually occurs sporadically; however, owing to the commensal nature of the organism in mares, it can affect several foals in a stabled population for a long period.1

Infection of foals is typically through the mouth, respiratory tract, or umbilicus during or immediately following birth.1 In a study9 of 30 foals and adult horses, 28 were found to have equine strains of A equuli in the oral cavity. In another study,10 the prevalence of isolation of A equuli from the oral cavities of 174 adult horses and foals across 10 farms ranged from 12% to 88%. In horses, transplacental invasion by Strongylus vulgaris larvae has been suggested as a cause of in utero A equuli infection.1 Presumably, this would occur by the larvae carrying the bacteria into the uterus of the mare, although this theory has not yet been substantiated. Actinobacillus spp have also been cultured in cases of mare reproductive loss syndrome, which is characterized by early fetal loss, late fetal loss, fibrinous pericarditis, and unilateral uveitis.11 Multiple epidemics of this syndrome have occurred; the primary ones were in 2001 and 2002 in Kentucky, Ohio, West Virginia, and Tennessee. An association between mare reproductive loss syndrome and the presence of eastern tent caterpillars in the pastures of affected horses has been identified. Suppurative funisitis is described as a characteristic lesion of late fetal loss; fetal bronchopneumonia is also described.11

In the foal of the present report, the findings at necropsy were consistent with widespread bacterial septicemia. The foal also had evidence of widespread hemolysis (icterus), which was likely a result of disseminated intravascular coagulation associated with sepsis or perhaps bacterial toxin–induced RBC destruction. Although A equuli was cultured from liver tissue samples obtained from the foal, the subtype was not identified. According to Rycroft et al,1 purulent nephritis is the most common lesion in neonates with sleepy foal disease. The absence of kidney lesions in the foal of this report was an unusual finding that may be attributable to strain variability. The A equuli strain detected on individual farms and within individual horses may vary over time.10 Sternberg et al12 found that the isolates from healthy and clinically ill horses could not be differentiated on the basis of results of ribotyping and biochemical fingerprinting. To effectively resist A equuli infection, foals require high serum concentrations of maternal antibodies against the bacterium.13 In cases of fatal sleepy foal disease, Rycroft et al14 identified that, when sera from the dams and offspring were compared by immunoblotting, concentrations of specific antibodies against A equuli were high in mares and significantly lower in affected foals. Foals with sepsis deplete circulating IgG at a rapid rate. The foal described in the present report had a serum IgG concentration of 804 mg/dL, which is indicative of an ideal level of passive transfer of maternal antibodies on the basis of the assay used at the laboratory; nonetheless, this foal died of actinobacillosis. During the year in which this foal was born, 4 other foals had been born on the same farm, with no reported illness. Adult horses on the farm also were reported to be healthy. Further epidemiological investigation of infections with this bacterium is required.

References

  • 1. Rycroft AN, Garside LH. Actinobacillus species and their role in animal disease. Vet J 2000; 159: 1836.

  • 2. Berthoud H, Frey J, Kuhnert P. Characterization of Aqx and its operon: the hemolytic RTX determinant of Actinobacillus equuli. Vet Microbiol 2002; 87: 159174.

    • Crossref
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  • 3. Christensen H, Bisgaard M, Olsen JE. Reclassification of equine isolates previously reported as Actinobacillus equuli, variants of A. equuli, Actinobacillus suis or Bisgaard taxon 11 and proposal of A. equuli subsp. equuli subsp. nov. and A. equuli subsp. haemolyticus subsp. nov. Int J Syst Evol Microbiol 2002; 52: 15691576.

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    • Export Citation
  • 4. Kuhnert P, Berthoud H, Straub R, et al. Host cell specific activity of RTX toxins from haemolytic Actinobacillus equuli and Actinobacillus suis. Vet Microbiol 2003; 92: 161167.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Pusterla N, Jones ME, Mohr FC, et al. Fatal pulmonary hemorrhage associated with RTX toxin producing Actinobacillus equuli subspecies haemolyticus infection in an adult horse. J Vet Diagn Invest 2008; 20: 118121.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6. Christensen H, Bisgaard M. Revised definition of Actinobacillus sensu stricto isolated from animals. A review with special emphasis on diagnosis. Vet Microbiol 2004; 99: 1330.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Dill SG, Simoncini DC, Bolton GR, et al. Fibrinous pericarditis in the horse. J Am Vet Med Assoc 1982; 180: 266271.

  • 8. Al-Mashat RR, Taylor DJ. Bacteria in enteric lesions of horses. Vet Rec 1986; 118: 453458.

  • 9. Bisgaard M, Piechulla K, Ying YT, et al. Prevalence of organisms described as Actinobacillus suis or haemolytic Actinobacillus equuli in the oral cavity of horses. Comparative investigations of strains obtained and porcine strains of A. suis sensu stricto. Acta Pathol Microbiol Immunol Scand [B] 1984; 92: 291298.

    • Search Google Scholar
    • Export Citation
  • 10. Sternberg S. Isolation of Actinobacillus equuli from the oral cavity of healthy horses and comparison of isolates by restriction enzyme digestion and pulsed-field gel electrophoresis. Vet Microbiol 1998; 59: 147156.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Sebastian MM, Bernard WV, Riddle TW, et al. Review paper: mare reproductive loss syndrome. Vet Pathol 2008; 45: 710722.

  • 12. Sternberg S, Brandstrom B. Biochemical fingerprinting and ribotyping of isolates of Actinobacillus equuli from healthy and diseased horses. Vet Microbiol 1999; 66: 5365.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Stewart GM, Mason RJ, Thomson MA, et al. Noncytotoxic antibodies to paternal antigens in maternal sera and placental eluates. Transplantation 1984; 38: 111115.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14. Rycroft AN, Woldeselassie A, Gordon PJ, et al. Serum antibody in equine neonatal septicaemia due to Actinobacillus equuli. Vet Rec 1998; 143: 254255.

    • Crossref
    • Search Google Scholar
    • Export Citation
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