Adult, female, crossbred goatThe owner of a goat/sheep ranch (open to the public) had previous history of contagious ecthyma (Orf). The owners animals suffered from a pustular-like skin disorder with mortality around 50% during May to June of 2008.
The goat submitted for necropsy showed good nutritional condition.Â The skin had slightly raised, 0.5~3 cm, white to red, round papules widely spread over sparsely haired areas.Â The mucocutaneous junction of the muzzle, nares, conjunctiva, lingual mucosa and vaginal mucosa had variably raised nodules with occasional ulcers.Â The lungs were discolored with a mottled, patchy, dark purple to dark grayish red appearance.Â Trachea and bronchi were filled with froth and white-tinged edema fluid.Â
The mucosal membranes and skin follicles consisted of thickened, hyperplastic epithelium with ballooning degeneration, vesicle formation and necrosis, where intracytoplasmic eosinophilic inclusion bodies were clearly visible (Fig.Â 3-1 and 3-2).Â The superficial epidermal layers and the lingual ulcerated areas had fibrin, necrotic cellular debris, extravasated erythrocytes, and necrotic epithelium.Â The dermal layer was characterized by fibroplasia with a moderate infiltrate of lymphocytes, plasma cells, histiocytes, and some neutrophils.Â Capillaries were highly congested and some arterioles showed degeneration and perivascular infiltrates of histiocytic cells, lymphocytes, plasma cells, some neutrophils, admixed with fibroblastic cells.Â Intracytoplasmic eosinophilic inclusion bodies were also found in histiocytic cells and fibroblasts in the dermis in association with fibroplasia and vasculitis.Â
The bronchi, bronchioles, and terminal bronchioles showed varying degrees of epithelial hyperplasia, necrosis, and ballooning degeneration, with squamous metaplasia.Â In severely affected areas, alveolar septa were thickened as a result of pneumocyte hypertrophy.Â Alveolar spaces were commonly filled with fibrin, proteinaceous exudates, necrotic cellular debris, macrophages, edematous fluid with foci of alveolar septal necrosis, and septal vascular thrombi with vasculitis (Fig.Â 3-3).Â Peribronchiolar and perivascular lymphocytic infiltrates were evident in some areas.Â Similar inclusion bodies were also detected in histiocytes, fibroblasts, epithelial cells and pneumocytes.Â There was lymphoid depletion along with histiocytosis in the spleen and lymph nodes, with necrosis and numerous inclusion bodies in histiocytic cells.
1.Â Skin: Dermatitis, hyperplasia, severe, multifocal, chronic, with vesicles, papules, ballooning degeneration, vasculitis and eosinophilic intracytoplasmic inclusion bodies.
2.Â Lung: Bronchointerstitial pneumonia, hyperplasia, severe, multifocal, chronic, with ballooning degeneration, vasculitis, and eosinophilic intracytoplasmic inclusion bodies.
PCR results were positive for capripoxvirus.
Capripoxvirus, the causative agent of sheep/goat pox, belongs to the family Poxviridae.Â It is usually more severe in goats than in sheep.Â All goat age groups are susceptible to the virus.Â The disease is endemic in Africa, the Middle East, the Indian subcontinent, and much of Asia.Â This disease had never been reported in Taiwan.Â As a result, this will be the first confirmed sheep/goat pox
outbreak in Taiwan.
Clinically, infected animals can have acute to chronic disease characterized by generalized pox lesions throughout the skin and mucous membranes accompanied with persistent fever, lymphadenitis, and often a focal viral pneumonia.Â
The differential diagnosis should include contagious pustular dermatitis (Orf), peste des petits ruminants, and bluetongue.Â Orf is an endemic disease in Taiwanese goat herds.
PCR for detecting Capripox or Orf virus by the primer pair CPVS, CPVA (413 bp) and OVS, OVA (708 bp) (Zheng M.Â et al) respectively was employed for final diagnosis of this case.Â The source of the outbreak, however, is inconclusive.
Haired skin: Dermatitis, proliferative and necrotizing, subacute, focally extensive, moderate, with intraepidermal vesicles, ballooning degeneration, intracytoplasmic eosinophilic inclusion bodies, and periadnexal and perivascular histiocytic inflammation.
Lung: Pneumonia, bronchointerstitial, proliferative, subacute, multifocal, moderate, with intraepithelial intracytoplasmic eosinophilic inclusion bodies.
The family Poxviridae is divided into two subfamilies: Chordopoxvirinae which infects vertebrates, and Entomopoxvirinae which infects insects.Â Poxviruses are double stranded DNA viruses that cause disease in numerous living organisms.Â Most poxvirus virions have a characteristic brick shape and are very large viruses measuring up to 250 x 200 x 200 um, with a complex structure with lateral bodies, an outer membrane, and are sometimes enveloped.Â The genera of the subfamily Chordopoxvirinae include: Orthopoxvirus, Capripoxvirus, Suipoxvirus, Leporipoxvirus, Molluscipoxvirus, Yatapoxvirus, Avipoxvirus, and Parapoxvirus.Â This table is a brief summary of some of these viruses.Â
|Orthopoxivirus|| Variola virus (smallpox)
Humans, cattle, swine, rabbits
Humans, cattle, cats, rats
Humans, non-human primates
|Capripoxivirus|| Sheeppox virus
Lumpyskin disease virus
| Sheep, goats
Cattle, cape buffalo
|Leporipoxvirus||Molluscum contagiosum virus||Humans, horses|
|Yatapoxvirus|| Yabapox virus and
|Humans, non-human primates|
|Avipoxvirus||Fowlpox virus||Chickens, turkeys|
|Parapoxvirus|| Orf virus
Bovine papular stomatitis virus
| Sheep, goats, humans
Poxviruses are epitheliotropic viruses, and in some instances, such as with smallpox, sheeppox, goatpox monkeypox, or ectromelia, they can cause generalized, severe, or fatal disease.Â Grossly, poxvirus lesions progress from an initial macule, to a papule, to a vesicle, ending in pustule and and crust formation.Â Histologically, poxvirus infection often causes proliferation of cells within the stratum spinosum with ballooning degeneration and eosinophilic intracytoplasmic inclusions.(2,4)
1.Â Bhanuprakash V, Indrani BK, Hosamani M, Singh RK: The current status of sheep pox disease.Â Comp Immunol Microbiol Infect Dis 29:27-60, 2006
2.Â Ginn PE, Nasell JEKL, Rakich PM: Skin and appendages.Â In: Jubb, Kennedy and Palmers Pathology of Domestic Animals, ed.Â Maxie MG, 5th ed., pp.Â 297-298.Â Elsevier Limited, Edinburgh, UK, 2007
3.Â Kitching RP, Hammond JM, Black DN: Studies on the major common precipitating antigen of capripoxvirus.Â J Gen Virol 67:139-148, 1986
4.Â Murphy FA, Gibbs EPJ, Horzinek MC, Studdert MJ: Poxviridae.Â In: Veterinary Virology, 3rd ed., pp.Â 277-291.Â Academic Press, San Diego, California, 1999
5.Â Parthiban M, Govindarajan R, Manoharan S, Purushothaman V, Chandran NDJ, Koteeswaran A: Comparative sequence analysis of diagnostic PCR amplicons from Indian sheeppox virus.Â Vet Arhiv 75:203-209, 2005
6.Â Zheng M, Liu Q, Jin N, Guo J, Huang X, Li H, Zhu W, Xiong Y: A duplex PCR assay for simultaneous detection and differentiation of Capripoxvirus and Orf virus.Â Mol Cell Probes 21:276-81, 2007