Lumpy Skin Disease of Springbok

Dr R D Last – BVSc; M.Med.Vet (Pathology)

Specialist Veterinary Pathologist

 

Introduction.

Lumpy skin disease (LSD) is a well-known, presumed insect transmitted, capripox viral infection of cattle, endemic to most African countries, although since 2012 there has been rapid spread through the Middle East, Southeast Europe, the Balkans, Caucasus, Russia and Kazakhstan. Clinical lumpy skin disease has now been confirmed in springbok in South Africa, and suspected in springbok from Namibia. A disease suspected to be LSD has also been described in water Buffalo (Egypt), Arabian oryx (Saudi Arabia) and oryx (South African), while giraffe and Impala are highly susceptible to experimental infection. Natural infection of African buffalo remains controversial and current available evidence suggests that they are probably not / or only slightly susceptible.

 

The Virus.

LSD is caused by lumpy skin disease virus (LSDV), which is a virus from the family Poxviridae, genus Capripoxvirus. Sheeppox virus and Goatpox virus are the other two species in this genus and closely related to LSDV. Currently only one immunological type of LSDV is thought to occur in natural disease, which shows complete cross reaction with the prototype “Neethling” strain. LSDV is remarkably stable, surviving for long periods at ambient temperature especially in dried scabs, desiccated crusts, necrotic skin nodules and air-dried hides.

 

Pathogenesis.

The primary mode of transmission of the virus is believed to be via arthropod vectors, although this has not yet been fully established. The virus has been recovered from biting flies (Stomoxys spp and Musca confiscate) and mechanical transmission has been demonstrated with Aedes egypti mosquitoes. Three common African tick species namely brown tick (Rhipicephalus appendiculatis), bont tick (Amblyomma hebraeum) and African blue tick (Rhipicephalus (Boophilus) decolaratus) were experimentally able to transmit the virus mechanically (brown tick, bont tick) as well as trans-ovarially (blue tick). Bont ticks overwinter as nymphal stages while African blue ticks overwinter in gravid females and eggs. Therefore, such a scenario might in part explain how lumpy skin disease virus survives between disease outbreaks. Skin nodules, crusts and scabs contain extremely high levels of LSDV and are deemed to be the primary source of virus material for mechanical transmission by arthropods.

 

Direct animal to animal transmission through close contact plays a minor, if any, role in virus transmission and such transmission is believed to be highly inefficient. There have however, been reports of transmission occurring when common drinking troughs were used indicating that saliva may contribute to the spread of the disease. Disease transmission to suckling calves via infected milk has been reported in cattle. Virus has also been isolated from semen in cattle, but venerial transmission of the disease is not known to occur. It is unknown if such scenarios occur in springbok, but they would be considered likely.

 

Following innoculation of the virus there is a viremic phase with skin nodules usually developing around 28 days later. Skin nodules usually appear within 48 hours of the febrile reaction.

 

Clinical Signs and Pathology.

Cutaneous nodules, lymphadenopathy and pyrexia are the lesions most commonly described in springbok. The cutaneous lesions are firm, circumscribed, nodules ± 0.5-5.0 cm in diameter with lesion distribution being similar to that described in cattle namely head, neck, limbs, other, genitalia and perineum (figure 1 and figure 2). Nodules affecting the scrotum, perineum, udder, vulva, glans penis, eyelids, and conjunctiva are usually flatter (figure 2 arrow). Typically, nodules undergo necrosis and sequestration, but some may resolve rapidly and completely, while a few may become indurated and persist as hard intradermal lumps for many months. There is a high risk of secondary bacterial infection during the period of necrosis and sequestration.

Figure 1 Springbok – Lumpy skin disease  with cutaneous nodules over the face, neck and trunk. (Courtesy Dr Martin Malan)

Figure 2 Springbok – Lumpy skin disease demonstrating nodules on the eyelids have a faller appearance (arrow). (Courtesy Dr Martin Malan)

Diagnosis.

Collection of skin biopsies into 10% buffered formalin for histopathology and subsequent immunohistochemistry forms the basis of disease diagnosis. Immunohistochemistry (IHC) for LSDV is a rapid, specific and sensitive procedure for disease diagnosis, as it enables demonstration of the virus within the histological lesions allowing for confident confirmation of clinically disease. Polymerase chain reaction (PCR) has largely replaced virus isolation as a diagnostic procedure for detection of the virus. The preferred samples for PCR analysis include fresh skin nodules, scabs or dried swabs thereof, as these tissues carry high concentrations of virus. The PCR analysis is also effective on saliva and nasal secretions (dry swabs) as well as blood collected into EDTA.

 

Histological examination of H&E stained sections enables detection of the characteristic pathology of ballooning epidermal degeneration, follicular epithelial hyperplasia, deep dermal thrombosis and ischemic necrosis in conjunction with the demonstration of eosinophilic intracytoplasmic, viral inclusion bodies in keratinocytes of the epidermis and follicular epithelium as well as macrophages, endothelial cells, pericytes, acinar and ductal epithelial cells of the mucous and serous glands, and skeletal and smooth muscle cells.

 

Immunohistochemistry enables detection of LSDV within histological sections and facilitates demonstration of the virus within histological lesions enabling definitive confirmation of the diagnosis (figure 3 and figure 4).

Figure 3 Springbok skin – Lumpy skin disease IHC stain.  Note the ballooning degeneration of the epidermis and follicular epithelium with strong, dark brown positive labelling of viral antigen including the intra-cytoplasmic inclusions in epidermal and follicular keratinocytes, and dermal macrophages (arrows).

Figure 4 Springbok skin – Lumpy skin disease IHC staining.  Note the positive labelling of virus in sebaceous glands, macrophages and smooth muscle cells (asterix).

Prevention and Control.

The cornerstone of prevention and control in cattle revolves around implementation of an effective vaccination program. “Neethling” strain vaccines as well as of live attenuated Sheeppox or goatpox vaccines (utilizing cross protection), have effectively been used to control LSD in cattle. There is currently no data available for the use of these vaccines in springbok. Vector control appears to have minimal effect on preventing disease.

 

References:

  1. Coetzer JAW & Tuppurainen E. Lumpy Skin Disease. http://www.afrivip.org/sites/default/files/02_lsd_eeva_epidemiology.pdf
  2. World Organization for Animal Health (2017) – Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. OIE, Paris.
  3. Jubb & Kennedy (2016). Pathology of Domestic Animals 6th

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