Sudden death in a three-month-old male intact Boer goat

Abigail English Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA

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Chloe C. Goodwin Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA
Southeastern Cooperative Wildlife Disease Study, Department of Population Health, College of Veterinary Medicine, University of Georgia, Athens, GA

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Nicole L. Gottdenker Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA

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History

A 3-month-old 20.7-kg male intact Boer goat presented to necropsy with a history of sudden death. The goat was apparently healthy up until the time of death. It had received 2 doses of Clostridium perfringens types C and D and Clostridium tetani toxoids. The owner reportedly lost 3 other goat kids over the previous 10 days.

Clinical and Gross Findings

Body condition score was 3/5 with marked postmortem abdominal bloat, and there were numerous chewing lice dispersed in the hair coat. The liver contained multifocal to coalescing, firm, round, white, encapsulated nodules ranging from pinpoint to 3.5 X 2.5 X 2.0 cm. Nodules were filled with lamellated, firm, white caseous material (Figure 1). The hepatic and pancreatic lymph nodes were enlarged, up to 4.0 X 2.5 X 2.0 cm.

Figure 1
Figure 1

Gross photographs of the liver from a 3-month-old goat at necropsy. A—Gross photograph of the entire liver; multifocal, firm, white nodules were present throughout all liver lobes. B—Gross photograph of a hepatic cross-section after formalin fixation; on cut section, nodules contained lamellated, firm, white caseous material.

Citation: Journal of the American Veterinary Medical Association 261, 8; 10.2460/javma.23.02.0106

Histopathologic Findings

Inflammatory infiltrates associated with portal triads were dominated by epithelioid macrophages and multinucleated giant cells surrounded by lamellated fibroblasts and lymphoplasmacytic aggregates (granulomas; Figure 2). Larger granulomas had central areas of acellular eosinophilic material and cellular debris, which were occasionally mineralized (caseous necrosis). Macrophages frequently contained numerous, gram-positive, Ziehl-Neelsen acid-fast–negative coccobacilli. In less-affected areas, portal triads were frequently surrounded and expanded by layered collagen.

Figure 2
Figure 2

Photomicrographs of histology from the liver of a 3-month-old goat at necropsy. Granulomas contain numerous epithelioid macrophages (white arrowhead) and frequent multinucleated giant cells (black arrow), with moderate numbers of neutrophils (black arrowhead). Lesions are well encapsulated by concentric layers of fibroblasts. H&E stain; bar = 50 μm. Inset—Macrophages within the granulomas contain numerous short, gram-positive bacilli (white arrow). Gram stain; bar = 10 μm.

Citation: Journal of the American Veterinary Medical Association 261, 8; 10.2460/javma.23.02.0106

Hepatic and pancreatic lymph nodes had variably enlarged, coalescing cortical follicles with germinal centers and thickened medullary cords. Follicles sometimes compressed subcapsular and medullary sinuses. Bacteria were not observed with H&E, gram, or Ziehl-Neelsen acid-fast stains.

Laboratory Findings

Aerobic culture of the liver showed heavy growth of organisms consistent with Nocardia spp or Rhodococcus spp. PCR testing of formalin-fixed paraffin embedded tissue scrolls (3 to 10 µm) were positive for Rhodococcus equi; the specimen was negative for the erythromycin resistance genes erm(46) and erm(51).

Morphologic Diagnosis

Liver: severe, multifocal, chronic, caseating, granulomatous hepatitis with intrahistiocytic gram-positive coccobacilli consistent with R equi.

Comments

R equi is a gram-positive, acid-fast–negative bacterium in the order Actinomycetales, along with Cornyebacterium, Mycobacterium, and Nocardia.1 R equi is a common pathogen in horses, most classically causing a pyogranulomatous pneumonia in foals. Some foals may also have significant systemic disease with R equi infection that can manifest as granulomatous enterocolitis and typhlitis, mesenteric lymph node abscessation, or less commonly as arthritis or osteomyelitis. Although the organism is common in the soil and is shed in the feces of horses and other grazing animals, it rarely causes disease outside of its preferred host species. However, R equi has rarely been documented as a cause of lymphadenopathy or disseminated infection in ruminants.1 Sporadic cases in goats occur worldwide, primarily through isolated cases with very few farms showing multiple case occurrences.2,3 Affected goats are commonly young and have chronic weight loss, variable pyrexia, and multifocal hepatic and occasionally splenic or pulmonary abscesses or osteomyelitis at necropsy. As the liver is frequently the primary affected organ involved in R equi disease in goats, the primary proposed pathogenesis involves an ascending infection from the intestines through the portal vein.3 The abscesses in this case were primarily periportal, supporting this proposed pathogenesis. There is speculation that immunosuppression due to caprine arthritis-encephalitis virus, severe helminthic infection, or Eimeria infection could predispose individual goats to infection with R equi, but this connection is theoretical, and several cases have been serologically negative for caprine arthritis-encephalitis virus.2 No parasites were observed on McMaster fecal egg count in this goat.

R equi is commonly classified as virulent, intermediately virulent, or avirulent on the basis of the presence or absence of the plasmid encoded virulence-associated protein genes vapA or vapB. Strains that are vapA+ are considered virulent, while strains which are vapA–/vapB+ are intermediately virulent, with vapA–/vapB+ strains considered avirulent. Strains contributing to infection in ruminants was initially thought to be primarily avirulent, but a third virulence-associated protein gene, vapN, has been sequenced from strains in cattle and goats, suggesting that it could contribute to virulence and infection in these species.4 Identification of virulence gene phenotype in this case was not pursued.

Another important differential for lesions seen in this case is Cornyebacterium pseudotuberculosis. This related actinomycete causes caseous lymphadenitis in goats and sheep, causing significant losses due to carcass condemnation and decreased production.5 Characteristic lesions are similar to R equi infection, consisting of caseous lesions in lymph nodes, which can also affect internal organs. The disease is difficult to treat with antibiotics because the organism is protected within the caseous lesions, and affected animals may be culled rather than treated at risk of clinical remission while maintaining a carrier state. Because lymphadenitis and abscessation due to corynebacteria is well-known in small ruminants, the clinical diagnosis is often presumptive rather than based on culture or PCR of the organism. The lack of testing in presumed C pseudotuberculosis cases in small ruminants could suggest a higher R equi prevalence than reported.4,5 Moreover, identification of the bacterial isolate using routine matrix-assisted laser desorption/ionization–time-of-flight (MALDI-TOF) mass spectrometry yielded Nocardia spp or Rhodococcus spp but could not differentiate between the two. Nocardia spp and Rhodococcus spp are closely related species within the family Nocardiaceae, which likely explains the limitation of MALDI-TOF in this case. Thus, pathologic changes, aerobic bacterial culture, bacteria morphology, bacteria staining properties, and PCR assays were all essential to a definitive diagnosis.

In conclusion, this case highlighted an uncommon pathogen associated with caseous hepatic abscessation in goats and emphasized the importance of culture and molecular diagnostics for organism identification in this disease process.

Acknowledgments

No external funding was used in this case. The authors declare that there were no conflicts of interest.

References

  • 1.

    Muscatello G, Leadon DP, Klayt M, et al. Rhodococcus equi infection in foals: the science of ‘rattles.’ Equine Vet J. 2007;39(5):470478. doi:10.2746/042516407x209217

    • Search Google Scholar
    • Export Citation
  • 2.

    Tkachuk-Saad O, Lusis P, Welsh RD, Prescott JF. Rhodococcus equi infections in goats. Vet Rec. 1998;143(11):311312. doi:10.1136/vr.143.11.311

    • Search Google Scholar
    • Export Citation
  • 3.

    Jeckel S, Holmes P, King S, Whatmore AM, Kirkwood I. Disseminated Rhodococcus equi infection in goats in the UK. Vet Rec. 2011;169(2):56. doi:10.1136/vr.d4267

    • Search Google Scholar
    • Export Citation
  • 4.

    Stranahan LW, Plumlee QD, Lawhon SD, Cohen ND, Bryan LK. Rhodococcus equi infections in goats: characterization of virulence plasmids. Vet Pathol. 2018;55(2):273276. doi:10.1177/0300985817747327

    • Search Google Scholar
    • Export Citation
  • 5.

    Dorella FA, Pacheco LG, Oliveira SC, Miyoshi A, Azevedo V. Corynebacterium pseudotuberculosis: microbiology, biochemical properties, pathogenesis and molecular studies of virulence. Vet Res. 2006;37(2):201218. doi:10.1051/vetres:2005056

    • Search Google Scholar
    • Export Citation
  • Figure 1

    Gross photographs of the liver from a 3-month-old goat at necropsy. A—Gross photograph of the entire liver; multifocal, firm, white nodules were present throughout all liver lobes. B—Gross photograph of a hepatic cross-section after formalin fixation; on cut section, nodules contained lamellated, firm, white caseous material.

  • Figure 2

    Photomicrographs of histology from the liver of a 3-month-old goat at necropsy. Granulomas contain numerous epithelioid macrophages (white arrowhead) and frequent multinucleated giant cells (black arrow), with moderate numbers of neutrophils (black arrowhead). Lesions are well encapsulated by concentric layers of fibroblasts. H&E stain; bar = 50 μm. Inset—Macrophages within the granulomas contain numerous short, gram-positive bacilli (white arrow). Gram stain; bar = 10 μm.

  • 1.

    Muscatello G, Leadon DP, Klayt M, et al. Rhodococcus equi infection in foals: the science of ‘rattles.’ Equine Vet J. 2007;39(5):470478. doi:10.2746/042516407x209217

    • Search Google Scholar
    • Export Citation
  • 2.

    Tkachuk-Saad O, Lusis P, Welsh RD, Prescott JF. Rhodococcus equi infections in goats. Vet Rec. 1998;143(11):311312. doi:10.1136/vr.143.11.311

    • Search Google Scholar
    • Export Citation
  • 3.

    Jeckel S, Holmes P, King S, Whatmore AM, Kirkwood I. Disseminated Rhodococcus equi infection in goats in the UK. Vet Rec. 2011;169(2):56. doi:10.1136/vr.d4267

    • Search Google Scholar
    • Export Citation
  • 4.

    Stranahan LW, Plumlee QD, Lawhon SD, Cohen ND, Bryan LK. Rhodococcus equi infections in goats: characterization of virulence plasmids. Vet Pathol. 2018;55(2):273276. doi:10.1177/0300985817747327

    • Search Google Scholar
    • Export Citation
  • 5.

    Dorella FA, Pacheco LG, Oliveira SC, Miyoshi A, Azevedo V. Corynebacterium pseudotuberculosis: microbiology, biochemical properties, pathogenesis and molecular studies of virulence. Vet Res. 2006;37(2):201218. doi:10.1051/vetres:2005056

    • Search Google Scholar
    • Export Citation

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