Pathology in Practice

Anna K. Blick 1Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Martha Hensel 1Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Aline Rodrigues Hoffmann 1Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Philippa Gibbons 2Department of Large Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Brian F. Porter 1Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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History

A 1-year-old 18.5-kg (40.7-lb) female Boer goat was evaluated because of severe skin lesions of approximately 1 to 2 months' duration. The goat was 1 of 20 affected goats in a herd of 750 goats and sheep from multiple sources.

Clinical and Gross Findings

Multifocal to coalescing scabbed nodular lesions that ranged from 2 to 8 mm in diameter were present over the goat's entire body, affecting the mucocutaneous junctions, nasal planum, periocular skin, interdigital spaces, both pinnae, and dorsum (Figure 1). Visual examination of the coat and microscopic examination of a deep skin scraping revealed no ectoparasites. Punch biopsy specimens of several skin lesions were collected. Owing to the severity of the goat's lesions and the herd health implications, the owners elected euthanasia the day after the initial evaluation. The goat was rendered unconscious with xylazine hydrochloride and ketamine hydrochloride, and then magnesium sulfate solution was administered IV. Following euthanasia, a complete necropsy was performed.

Figure 1—
Figure 1—

Photographs of the right side of the face (A) and the right pinna (B) of a young adult female Boer goat that was evaluated because of severe skin lesions of approximately 1 to 2 months' duration. Notice the multifocal to coalescing pustular and crusting lesions (2 to 8 mm in diameter). Nineteen other goats in a herd of 750 goats and sheep were similarly affected. In each panel, bar = 1.0 cm.

Citation: Journal of the American Veterinary Medical Association 255, 3; 10.2460/javma.255.3.313

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

Histopathologic Findings

Microscopic examination of sections of affected skin revealed that the epidermis was markedly hyperplastic and formed rete pegs. The epidermis was covered by a thick serocellular crust composed of alternating layers of orthokeratotic and parakeratotic hyperkeratosis, viable and degenerate neutrophils admixed with serum protein and fibrin, karyorrhectic debris, and fragmented hair shafts (Figure 2). Within the crust were numerous 1- to 2-μm-diameter and paired bacterial cocci arranged in parallel rows (railroad track appearance) that formed branching filaments. In sections around the mucocutaneous junctions, the keratinocytes had clear cytoplasmic vacuoles interpreted as ballooning degeneration with rare eosinophilic, oval (2- to 6-μm-long), cytoplasmic viral inclusions. Multifocally, the superficial dermis had small areas of hemorrhage and was infiltrated by a small number of neutrophils, macrophages, lymphocytes, and plasma cells. Vessels were congested and lined by hypertrophied endothelial cells.

Figure 2—
Figure 2—

Photomicrographs of a section of the epidermis obtained from an affected area in the goat in Figure 1. A—Notice the thick serocellular crust that has formed from alternating layers of keratin and degenerate neutrophils. H&E stain; bar = 200 μm. B—Within the crust, paired cocci are arranged in parallel rows (railroad track appearance [arrow]) and have formed branching filaments. H&E stain; bar = 2 μm. C—Viral inclusions are visible within the cytoplasm of keratinocytes (arrows). Some keratinocytes are undergoing ballooning degeneration (asterisk). H&E stain; bar = 2 μm.

Citation: Journal of the American Veterinary Medical Association 255, 3; 10.2460/javma.255.3.313

Results of Ancillary Testing

Formalin-fixed paraffin-embedded haired skin biopsy specimens were further evaluated by molecular methods in 2 laboratories.a,b A universal bacterial 16S rRNA PCR assay followed by sequencinga detected Dermatophilus congolensis. Orf virus was detected by use of a real-time quantitative PCR assay.b

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: severe, chronic, multifocal to coalescing, proliferative, and neutrophilic dermatitis with marked hyperkeratosis, intralesional filamentous and coccoid bacteria, and rare intracytoplasmic viral inclusions.

Case summary: Dermatophilus congolensis and parapoxvirus of contagious ecthyma (orf virus) coinfection in a goat.

Comments

Differential diagnoses for goats with pustular and crusting lesions around the mucocutaneous junctions and pinnae include contagious ecthyma, pemphigus foliaceus, photosensitization, zinc-responsive dermatosis, and dermatophilosis. On the basis of the histologic features and minimal viral inclusions, dermatophilosis was the primary diagnosis in the case described in the present report.

Dermatophilus congolensis is a gram-positive facultative actinomycete bacterium that causes pustular skin lesions. The disease is known as cutaneous streptothricosis, cutaneous actinomycosis, rain scald, rain rot, strawberry foot rot, and lumpy wool.1 Dermatophilus congolensis has been documented worldwide and has a wide host range, including goats, cattle, horses, sheep, camels, dogs, cats, pigs, alpacas, reptiles, and humans.1 Infections can substantially impact livestock production through wool loss in sheep, hide damage in cattle, and decreased milk production in sheep and cattle.1–3 Predisposing factors for spread of and infection with D congolensis among host animals include environmental humidity, tick infestation, impaired immune status, and skin wounds.1,2,4 Dermatophilus congolensis is transmitted as zoospores and through direct contact with an infected host, ectoparasites, and occasionally the environment.2,4

Infection with D congolensis begins at sites of mechanically damaged skin and continues as wet conditions and warm temperatures stimulate the zoospores to germinate, make filaments, and spread to areas of viable epidermis and to outer root sheaths of hair follicles. Lesions progress from small papules to large, circular, nonpruritic, coalescing scabs. As keratinocytes begin to cornify, neutrophils accumulate beneath those cells. The epidermis regenerates with cells from adjacent external hair follicle sheaths and is subsequently invaded by the bacteria; the bacterial invasion induces a neutrophilic response and separation of epidermis and dermis. The repetition of this cycle leads to the formation of pustules that progress to thick laminar and parakeratotic crusts. Lesions are restricted to the skin and can be acute, subacute, or chronic.1 Secondary infections of staphylococci, streptococci, and Corynebacterium spp have been reported.1,2

In D congolensis-infected goats, 2- to 3-mm-diameter crusty lesions are typically located on the pinnae and tail of kids and on the dorsal midline region, lateral aspects, and caudal thigh regions of adults; the scrotum of adult males can be affected. The initial clinical signs are small pustules, which can progress to severe exudative purulent dermatitis, followed by the formation of crusts and a classic so-called paintbrush lesion when entangled in hair.2,5

Diagnosis of infection with D congolensis typically includes a combination of clinical signs and cytologic, histopathologic, and bacteriologic findings. For all affected animals, microscopic examination of direct impression smears or histologic sections of affected skin reveals bacteria with branching filaments and transverse and longitudinal septa, which form parallel rows of small, coccoid bodies.2 Stains that can be used to better visualize the organisms in those preparations include H&E, Gram, Giemsa, periodic acid-Schiff, and Grocott stains.2 Results of microbial culture of samples of the lesions and morphological identification of D congolensis spores can confirm the diagnosis.1 A real-time quantitative PCR assay that specifically detects D congolensis is useful to confirm the diagnosis, and assay results are especially helpful in diagnosis of dermatophilosis in animals that have concomitant infections with other organisms.6 Serologic tests, including an indirect fluorescent antibody assay and an ELISA, are also available for use in research studies and epidemiological surveys.7

Regardless of species, mild dermatophilosis may be resolved by removal of crusts, moisture, and parasites from the skin of affected animals. Topical treatments may be useful in cases of greater disease severity. Povidone-iodine or lime-sulfur soaks of affected skin areas can be performed every day for 1 week, and then repeated every week for 3 or 4 weeks. Systemic administration of antimicrobials is also very effective. Dermatophilus congolensis is typically susceptible to ampicillin, cephalosporin, cloxacillin, lincomycin, tetracycline, tylosin, and penicillin.7 Given the ability of the bacteria to survive for long periods in the crusts of affected hosts, it is critical that affected animals are thoroughly treated to prevent re-infection and spread of disease to other animals.1

Dermatophilus congolensis and orf virus coinfections in goats have previously been documented, although the exact mechanism of coinfection is unknown.8 The skin forms the first line of defense against both infections; the presence of one infection is likely to predispose an affected animal to the other infection. Similar to infection with D congolensis, pox viral infections increase keratinocyte production and are known to suppress the host immune response by the release of immunomodulatory proteins.1,8–10 Lesions on the pinnae and dorsum, which are common in cases of dermatophilosis, are also features of parapoxvirus infection, as are lesions at mucocutaneous junctions and on the face, flanks, coronary bands, teats, and scrotum.11,12 Parapoxvirus-associated skin lesions are brown and pustular, and their histologic characteristics include epidermal hyperplasia and parakeratotic and orthokeratotic hyperkeratosis with intracytoplasmic viral inclusion bodies in degenerated keratinocytes.1

For the goat of the present report and the other 19 affected herd mates, the source of infection was unknown. In any outbreak of dermatophilosis, potential contributing factors include stress, husbandry practices that result in skin trauma, and the merging of animals from different sources, all of which may increase a herd's exposure to vectors and introduce chronically infected yet clinically unaffected carriers.

Footnotes

a.

Pennsylvania State University Animal Diagnostic Laboratory, University Park, Pa.

b.

Washington Animal Disease Diagnostic Laboratory, Washington State University, Pullman, Wash.

References

  • 1. Jubb KVF, Kennedy PC, Palmer N, et al. Integumentary system. In: Maxie MG, ed. Jubb, Kennedy & Palmer's pathology of domestic animals: 3-volume set. 6th ed. San Diego: Elsevier Health Sciences, 2015;616618, 632–634.

    • Search Google Scholar
    • Export Citation
  • 2. Loria GR, La Barbera E, Monteverde V, et al. Dermatophilosis in goats in Sicily. Vet Rec 2005;156:120121.

  • 3. Ambrose N, Lloyd D, Maillard J-C. Immune responses to Dermatophilus congolensis infections. Parasitol Today 1999;15:295300.

  • 4. Yeruham I, Elad D, Perl S. Dermatophilosis in goats in the Judean foothills. Rev Med Vet 2003;154:785788.

  • 5. Scott DW. Bacterial skin diseases. In: Color atlas of farm animal dermatology. Ames, Iowa: Blackwell, 2007;104106.

  • 6. García A, Martínez R, Benitez-Medina JM, et al. Development of a real-time SYBR green PCR assay for the rapid detection of Dermatophilus congolensis. J Vet Sci 2013;14:491494.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Merck Veterinary Manual. Dermatophilosis. Available at: www.merckvetmanual.com/mvm/integumentary_system/dermatophilosis/overview_of_dermatophilosis.html. Accessed Oct 28, 2016.

    • Search Google Scholar
    • Export Citation
  • 8. Munz E. Double infection of sheep and goat in Kenya with orf virus and Dermatophilus. In: Dermatophilus infection in animals and man. London: Academic Press, 1976;5767.

    • Search Google Scholar
    • Export Citation
  • 9. Zaria LT. Dermatophilus congolensis infection (dermatophilosis) in animals and man! An update. Comp Immun Microbiol Infect Dis 1993;16:179222.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Haig DM, McInnes CJ. Immunity and counter-immunity during infection with the parapoxvirus orf virus. Virus Res 2002;88:316.

  • 11. Nandi S, De UK, Chowdhury S. Current status of contagious ecthyma or orf disease in goat and sheep— a global perspective. Small Rumin Res 2011;174:663664.

    • Search Google Scholar
    • Export Citation
  • 12. Ndikuwera J, Odiawo GO, Usenik EA, et al. Chronic contagious ecthyma and caseous lymphandenitis in two Boer goats. Vet Rec 1992;131:584585.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Photographs of the right side of the face (A) and the right pinna (B) of a young adult female Boer goat that was evaluated because of severe skin lesions of approximately 1 to 2 months' duration. Notice the multifocal to coalescing pustular and crusting lesions (2 to 8 mm in diameter). Nineteen other goats in a herd of 750 goats and sheep were similarly affected. In each panel, bar = 1.0 cm.

  • Figure 2—

    Photomicrographs of a section of the epidermis obtained from an affected area in the goat in Figure 1. A—Notice the thick serocellular crust that has formed from alternating layers of keratin and degenerate neutrophils. H&E stain; bar = 200 μm. B—Within the crust, paired cocci are arranged in parallel rows (railroad track appearance [arrow]) and have formed branching filaments. H&E stain; bar = 2 μm. C—Viral inclusions are visible within the cytoplasm of keratinocytes (arrows). Some keratinocytes are undergoing ballooning degeneration (asterisk). H&E stain; bar = 2 μm.

  • 1. Jubb KVF, Kennedy PC, Palmer N, et al. Integumentary system. In: Maxie MG, ed. Jubb, Kennedy & Palmer's pathology of domestic animals: 3-volume set. 6th ed. San Diego: Elsevier Health Sciences, 2015;616618, 632–634.

    • Search Google Scholar
    • Export Citation
  • 2. Loria GR, La Barbera E, Monteverde V, et al. Dermatophilosis in goats in Sicily. Vet Rec 2005;156:120121.

  • 3. Ambrose N, Lloyd D, Maillard J-C. Immune responses to Dermatophilus congolensis infections. Parasitol Today 1999;15:295300.

  • 4. Yeruham I, Elad D, Perl S. Dermatophilosis in goats in the Judean foothills. Rev Med Vet 2003;154:785788.

  • 5. Scott DW. Bacterial skin diseases. In: Color atlas of farm animal dermatology. Ames, Iowa: Blackwell, 2007;104106.

  • 6. García A, Martínez R, Benitez-Medina JM, et al. Development of a real-time SYBR green PCR assay for the rapid detection of Dermatophilus congolensis. J Vet Sci 2013;14:491494.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Merck Veterinary Manual. Dermatophilosis. Available at: www.merckvetmanual.com/mvm/integumentary_system/dermatophilosis/overview_of_dermatophilosis.html. Accessed Oct 28, 2016.

    • Search Google Scholar
    • Export Citation
  • 8. Munz E. Double infection of sheep and goat in Kenya with orf virus and Dermatophilus. In: Dermatophilus infection in animals and man. London: Academic Press, 1976;5767.

    • Search Google Scholar
    • Export Citation
  • 9. Zaria LT. Dermatophilus congolensis infection (dermatophilosis) in animals and man! An update. Comp Immun Microbiol Infect Dis 1993;16:179222.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Haig DM, McInnes CJ. Immunity and counter-immunity during infection with the parapoxvirus orf virus. Virus Res 2002;88:316.

  • 11. Nandi S, De UK, Chowdhury S. Current status of contagious ecthyma or orf disease in goat and sheep— a global perspective. Small Rumin Res 2011;174:663664.

    • Search Google Scholar
    • Export Citation
  • 12. Ndikuwera J, Odiawo GO, Usenik EA, et al. Chronic contagious ecthyma and caseous lymphandenitis in two Boer goats. Vet Rec 1992;131:584585.

    • Search Google Scholar
    • Export Citation

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