LUMPY SKIN DISEASE
Anu Malik1 and Vaishali2
1Department of Veterinary Microbiology, Lala Lajpat Rai University of Veterinary and Animal Sciences, Hisar-125004, Haryana
2Department of Public Health & Epidemiology, Lala Lajpat Rai University of Veterinary and Animal Sciences, Hisar-125004, Haryana
Lumpy skin disease is a poxvirus infection of cattle caused by virus belonging to genus Capripoxvirus. The disease has synonyms such as Neethling virus disease, Pseudourticaria exanthema nodularis bovis, knopvelsiekte. The virus has tropism for epithelial cells of the host and cutaneous nodules or lymphadenitis develop with infection of LSD virus. Lumpy skin disease is having sporadic occurrence in African countries with low prevalence and seasonal incidences. Lumpy skin disease can affect any dairy cattle including exotic breed or indigenous breeds. The signs of disease include fever, oedema and nodules on skin, internal organs and mucous membranes, swollen lymph nodes and occasionally death. The lesions are 0.5–5 cm in diameter, firm, multiple, well circumscribed to coalescing with flat-topped. The nodules are confined to epidermis, dermis and may extend to the underlying subcutis and less commonly to the adjacent striated muscle. In the early stages initially lesions are painful and exude a little serous fluid but after sometime usually (2 weeks) skin lesions regress and centre of the lesion becomes dry, hard and necrotic – the so-called “sitfast”. After 3 to 4 weeks, formation of granulation tissue occurs which heals after 2 to 3 weeks unless complicated by pyogenic bacteria.
The poxvirus is hardy and stable virus that may persist in the environment for prolonged periods of time and remains infective for long duration. Introduction of infected animal into or in close proximity to a herd of susceptible animals could be the probable cause of infection usually. Virus can persist in cutaneous lesions and bodily secretions such as saliva, nasal discharge, milk and semen. Disinfectants like sodium hypochlorite, iodine, quaternary ammonium disinfectants, ether, chloroform, formalin, phenol, and detergents containing lipid solvents render the virus less infective. The virus is susceptible to heating at 65°C for 30 minutes or 55°C for 2 hours. The virus can remain viable for up to 35 days in desiccated crusts. There is no carrier state known for LSDV. Movement of animal is associated with the spread of the infection. LSD causes temporary reduction in the milk yield, temporary and permanent loss of fertility in bulls, damage to hides and may cause mortality in animal that pose a potential threat to animal health and economy associated to animal husbandry and livestock sectors. Permanent damage to the joints, tendons, teats and mammary gland may occur due to secondary bacterial infections. The disease may lead to abortion in pregnant cows and temporary or permanent sterility in bulls is possible. LSD was first described in 1929 in Zambia (then Northern Rhodesia) and moved northwards through sub-Saharan West Africa through a series of epizootics through the 1960s. Owing to high rainfall, there was a resurgence of the disease in southern Africa during the 1990s. Turkey served as a gateway for trade, migration and introduction of exotic diseases from Asia to Europe. The precise source from which the LSD infection was introduced to Turkey in 2013 has not been identified with certainty. It has been speculated that cattle trafficking, coupled with the influx of more than two million refugees from war-torn adjacent countries, resulted in the introduction of an uninvited “guest” that has affected the naïve population of cattle. Though, lumpy skin disease has been recognized since 1929 but the exact mechanism for transmission route has not been fully understood till now. That vectors were involved was clear, but to what extent and how had not been answered. The LSD should be differentially diagnosed from the pseudo-LSD caused by bovine herpesvirus 2 (BoHV-2). Pseudo-LSD is a milder clinical condition characterised by superficial nodules. BoHV-2 infection could be differentiated from LSD on basis of presence of histopathological characteristics such as intra-nuclear inclusion bodies and viral syncytia in BoHV-2 . Other differential diagnoses (for integumentary lesions) include: dermatophilosis, dermatophytosis, bovine farcy, photosensitisation, actinomycosis, actinobacilosis, urticaria, insect bites, besnoitiosis, nocardiasis, demodicosis, onchocerciasis, pseudo-cowpox, and cowpox.
Differential diagnoses for mucosal lesions include: foot and mouth disease, bluetongue, bovine viral diarrhoea, malignant catarrhal fever, infectious bovine rhinotracheitis, and bovine popular stomatitis.
The postmortem lesions are characteristic and develop as grayish-pink, deep nodules with necrotic centers in the skin. These nodules often extend into the subcutis and underlying skeletal muscle, and the adjacent tissue exhibits congestion, hemorrhages and edema. The regional lymph nodes are typically enlarged. Flat or ulcerative lesions may be found on the mucous membranes of the oral and nasal cavities, pharynx, epiglottis and trachea. Nodules or other lesions can occur in the gastrointestinal tract (particularly the abomasum), udder and lungs, and sometimes in other tissues such as the urinary bladder, kidneys, uterus and testes. Lesions in the lungs are difficult to see and often appear as focal areas of atelectasis and edema. The mediastinal lymph nodes may be enlarged in severe cases, and pleuritis may be evident. Some animals have additional complications, such as synovitis and tendosynovitis. Some aborted fetuses and premature calves may have large numbers of skin nodules. They can also have lesions on internal organs.
The diagnosis of LSDV include isolation of nucleic acids, antigen detection in biopsy or necropsy samples of skin nodules, lymph nodes, nodular fluid, scabs, and skin scrapings, lesions on internal organs. In the early stages of viremia, LSDV can be isolated from blood samples also. For detection of virus from tissue samples, PCR assays can be followed. Dot blot hybridization a loop-mediated isothermal amplification assays (LAMP) also used for diagnosing LSDV. Transmission electron microscopy, which can detect the typical capripoxvirus morphology in biopsy samples or desiccated crusts, is sometimes employed in diagnosis. In endemic areas, the presumptive diagnosis of disease is attained with a history of consistent clinical signs. Variety of serological tests are available including virus neutralization, an indirect fluorescent antibody test, ELISAs, and immunoblotting (Western blotting), can detect antibodies to LSDV, but some of these tests have not yet been validated.
The lumpy skin disease can be treated with supportive care as there is no specific treatment available, also administration of antibiotics and regular dressing of wound is essential to prevent secondary bacterial infections and reduce fly strike. In case of any incidence of the LSD, veterinarians should report to desired higher authorities following the national and/or local guidelines. Lumpy skin disease could be introduced into a new area by infected animals, contaminated hides and other animal products or infected insects. Outbreaks recognized early have been eradicated with quarantines, depopulation, cleaning and disinfection of infected premises, but vaccination was an important component of eradication plans in some large outbreaks. Quarantines and movement controls are unlikely to prevent transmission completely when LSDV is being spread by vectors; however, they can stop infected animals from introducing the virus to distant foci. Insect control is generally employed during lumpy skin disease outbreaks. In endemic areas, the disease can be controlled by live attenuated vaccines a decrease or eliminate virus shedding in semen. Killed vaccines are also available in some areas. The vaccines differ in terms of their efficacy.
