Lumpy Skin Disease – An Emerging Threat
Sanjana1, Nancy Jasrotia1*, Komal1 and Ayush Ranjan2
1PhD Scholar, ICAR-IVRI, Bareilly
2MVSc Scholar, BVC, BASU, Patna
Abstract
Lumpy skin disease is an economically important disease affecting bovine, which is endemic in most African countries and some Middle East ones, spreading the disease into the rest of Asia and Europe. Understanding the restrictions and channels of distribution is crucial given the recent rapid spread of disease in nations that are currently disease-free. The causative agent, Capripoxvirus, can also induce sheeppox and goatpox. Given that they pose a threat to worldwide trade and could be exploited as tools of economic bioterrorism, the economic impact of these diseases is a major worry. Due to poor conditions in farming communities and limited availability to efficient immunizations, the dissemination of capripoxviruses appears to be expanding.
Key words: Lumpy skin disease, transboundary disease, Capripox
Introduction
Lumpy skin disease (LSD) is an emerging transboundary viral infection of cattle and water buffalo. It is caused by the Lumpy skin disease virus (LSDV) which belongs to the genus Capripoxvirus of the family Poxviridae and subfamily Chordopoxvironae. All breeds of cattle and age group are susceptible to the disease however, it is more severe in case of young animals and cows during lactation period. The incubation period varies from 4 days to 5 weeks. The disease is characterized by fever, excessive salivation, enlarged superficial lymph nodes, nasal discharge, lachrymation and pox lesions in the skin and mucous membranes of the digestive and respiratory tracts. The disease comes under the Notifiable Diseases of the World Organization of Animal Health (OIE) because of its fast spread. Morbidity rate of the disease varies between 10 and 20% with a mortality rate of 1-5%.
The LSDV serotype, “Neethling,” was discovered in South Africa and shares antigenic characteristics with goat and sheep pox virus. The virus often remains constant between pH 6.6 and 8.6 and is resistant to many physical and chemical stimuli, but it is more likely to thrive in environments with higher alkalinity. The virus is susceptible to the extremely alkaline or acidic solutions, as well as detergents with lipid solvents. The virus is highly host specific and not zoonotic.
Epidemiology
The disease has been reported in several countries starting from Zambia (1929) to different regions in Africa and spread rapidly to the Middle-Eastern countries (1990), South-eastern European countries and Russia. Recently the disease has been reported in significant number of Asian countries and the initial source of the virus spread has yet to be determined.
Clinical signs
Clinical signs include a fever of 40–41°C, reluctance to move, inappetence, salivation, lachrymation, and nasal discharge. The superficial lymph nodes (subscapular and pre-crural) of infected cattle are enlarged and skin nodules vary in number and size in clinical cases of LSD.
Transmission
The LSDV is mainly transmitted through arthropods, particularly blood‐sucking vectors, contaminated food and water and direct transmission in the later stages of the disease via saliva, nasal secretions and semen. Vectors mainly include biting flies of genus Stomoxys, blood-sucking hard ticks e.g., Rhipicephalus appendiculatus and Amblyomma hebraeum and mosquitoes of the genus Aedes.
Diagnosis
Diagnosis is mainly dependent on the clinical signs but can be confirmed through PCR and RT-PCR techniques. Additionally, a real-time PCR method has been developed to distinguish between the LSDV, sheep, and goat poxviruses. Restriction Fragment Length Polymorphism (RFLP) has also been utilized to distinguish the pathogenic LSDV from the vaccination strain. Several other methods used for LSDV detection include electron microscopy, virus isolation, virus neutralisation, and serological methods. The only currently validated test among serological methods is the viral neutralisation test, which is slow and expensive with a high specificity and low sensitivity.
Prevention and Control
Capripoxviruses appear to be spreading more widely because to the scarcity of efficient vaccines, poverty in farming communities in endemic areas, rising legal and illegal trade in live animals, as well as global climatic changes. In addition to mobility limitations and removal of diseased animals, vaccination is the only strategy that can effectively manage the disease in endemic areas.
Currently, most commercially available vaccines against LSD are live attenuated vaccines based on a LSDV strain, sheeppox virus (SPPV), or goatpox virus (GTPV). The first inactivated vaccine has recently entered the market. At present, live attenuated vaccinations based on LSDV strains, sheeppox virus (SPPV), or goatpox virus (GTPV) represent the majority of commercially available LSD vaccines. Live vaccines effectively stop the spread of disease by eliciting a potent and long-lasting immune response. Live vaccinations, however, can result in localised inflammation and a minor illness with skin sores. Inactivated vaccines are expensive and require multiple injections, but they are safe and can be combined with other antigens to create polyvalent vaccinations that can be used in places without outbreaks. Moreover, as part of the strategy that uses live vaccines first, inactivated vaccines could be used in the ultimate stage of disease eradication.
Treatment
The treatment of LSD is only symptomatic and it uses a combination of antimicrobials, anti-inflammatory drugs, supportive care, and antiseptic treatments to prevent further bacterial problems. The culling of affected animals, movement restrictions and compulsory and consistent vaccination have been recommended as control strategies. However, given the significance of arthropod vectors, eradicating the disease is highly challenging, and any delays in removing diseased animals raise the chance of LSD spread. Additionally, risk considerations must to be taken into account in control efforts. Educating veterinarians and livestock workers would enable them to perform timely diagnoses of clinical cases, helping to slow the spread of disease.
References
Chihota, C. M. , Rennie, L. F. , Kitching, R. P. , & Mellor, P. S. (2001). Mechanical transmission of lumpy skin disease virus by Aedes aegypti (Diptera: Culicidae). Epidemiology and Infection, 126, 317–321.
Hamdi, J. , Boumart, Z. , Daouam, S. , El Arkam, A. , Bamouh, Z. , Jazouli, M. , Tadlaoui, K. O. , Fihri, O. F. , Gavrilov, B. , & El Harrak, M. (2020). Development and evaluation of an inactivated lumpy skin disease vaccine for cattle. Veterinary Microbiology, 245, 108689.
Namazi, F., & Khodakaram Tafti, A. (2021). Lumpy skin disease, an emerging transboundary viral disease: A review. Veterinary medicine and science, 7(3), 888–896.
Sevik, M. , & Dogan, M. (2017). Epidemiological and molecular studies on lumpy skin disease outbreaks in Turkey during 2014–2015. Transboundary and Emerging Diseases, 64(4), 1268–1279.
Tuppurainen, E. S. M. , Alexandrov, T. , & Beltran‐Alcrudo, D. (2017). Lumpy skin disease field manual ‐ A manual for veterinarians. FAO Animal Production and Health Manual, 20, 1–60.
https://www.pashudhanpraharee.com/lumpy-skin-an-emerging-transboundary-disease/
https://pubmed.ncbi.nlm.nih.gov/21749675/
