Lumpy Skin Disease

An Emerging Transboundary Disease

What is lumpy skin disease?

Cattle and water buffalo are susceptible to the infectious illness Lumpy Skin Disease (LSD). The Chordopoxvirinae subfamily of Poxviridae contains the genus Capripoxvirus, which is frequently transmitted to ruminants. The Sheep Pox Virus (SPPV), Goat Pox Virus (GTPV), and Lumpy Skin Disease Virus (LSDV) are three of the genera in this genus that, respectively, infect ovine, caprine, and bovine animals. The etiological agent of the globally significant lumpy skin condition is LSDV. A lipid envelope surrounds LSDV, a double-stranded DNA with around 151kilobase pairs (kbp) and diameters between 230 and 260 nm.The virus's brick- or oval-shaped capsid or nucleocapsid contains the genome and lateral bodies).

Fig 1: Morphological structure of Lumpy skin disease virus (source; Haftu et al., 2012)

(Fig 1This virus may survive at room temperature for up to 18 days in air dried hides and up to 35 days in dry necrotic nodules. However, the virus is rendered inactive by exposure to sunshine, lipophilic substances, and very alkaline or acidic environments for 2 hours at 55^oC or 30 minutes at 65^oC. The virus is highly sensitive to ether (20%), chloroform, formalin (1%), phenol (2% for 15 min), sodium hypochlorite (2-3%), iodine compounds (1:33 dilution), and quaternary ammonium compounds (0.5%) and stays stable in a pH range between 6.6 and 8.6 at 37^oC for 5 days. The isolation of the virus can be done after 6 months from the infected tissue culture stored at refrigeration, and even after 10 years from the infected skin nodules stored at -80 ºC.

Epidemiology

LSD was first detected in Zambia around the start of 20th century, but due to the country's high insect population at the time, it was mistaken for poisoning cases or any allergic reaction to an insect bite. But when it extended to Zimbabwe, Botswana, and the Republic of South Africa from 1943 to 1945, the disease's contagiousness was identified. With the exception of Algeria, Libya, Tunisia, and Morocco, it then quickly spread across the cattle population in several African nations, and the virus persisted in Sub-Saharan Africa until 1984. As the world's nutritional demands grew, importing animal-based foods from African countries became crucial. Geographically, Egypt, which shares a border with the Sahara Desert and the Arabian Peninsula, had the highest possibility of a transnational LSD emergence and was also the closest to it. Due to unfettered cattle movement from other nations, this country initially reported an epidemic of LSD in 1988 and its re-emergence in 2006. The fly Stomoxyscalcitrans was reported to be the vector responsible for the disease transmission from Egypt after the role of vectors in LSD transmission was fully investigated. Middle Eastern nations including Kuwait, Lebanon, Yemen, the United Arab Emirates, Bahrain, and Oman have reported LSD since 1990. In the next years, outbreaks were noted in Iran, Cyprus, and Azerbaijan in 2014, as well as Jordan, Iraq, and Turkey in 2013. LSD entered Russia in 2015 and remained there during 2019. The virus then migrated to South East Asia, where Bangladesh reported the first LSD outbreak in July 2019 with 66 cases.

The state of Odisha saw the country's first LSD outbreak in August 2019 during the monsoon season, when there was a high vector population. Since the primary insect vectors during the monsoon season in the coastal region of Odisha include mosquitoes, flies, biting midges, and ticks, it's possible that cyclone FANI, which passed through the area before this epidemic, was the reason for the virus' entry and vector-mediated dissemination. The government recently informed the RajyaSabha that over 1.55 lakh cattle have died recently in the country this year owing to lumpy skin disease (LSD). The most cattle deaths were reported in Rajasthan (75,819), followed by Maharashtra (24,430), Punjab (17,932), Karnataka (12,244), Himachal Pradesh (10,681), Gujarat (6,193), Haryana (2,937), and Jammu & Kashmir (2,698). According to information acquired from the states/UTs, in 2022 there were 29,45,863 cases and 6,28,84,366 vaccines administered.

Transmission

Broadly, the mode of transmission of LSDV can be classified in two ways viz. Non-vector and Vector transmission. There are very little evidence that showed LSDV can be spread through direct contact. Although ineffective, non-vectored LSD transmission happens when clinically afflicted animals come into contact with contaminated materials, without the need of biological or mechanical vectors. Infectious LSDV is excreted in saliva, nasal and ocular discharges, contaminating communal eating and drinking areas and spreading the disease. Spread of infection to calves from infected dam has been assumed to be through excretion of virus in milk and via skin abrasion. Transmission through contaminated needles during vaccination, dispersion through infected semen during coitus, ingestion of infected milk, and intrauterine transmission may also act as a source of infection.

LSDV is primarily spread through arthropod vectors by mechanical transmission. In most of the sub-Saharan African region an abrupt increase in the incidence of disease is observed as weather continues to get warm and humid. This phenomenon is due to the peak activity of vectors involved in transmission of LSDV. Contrary to that, clinical cases of the disease decrease considerably as weather continues to get cooler and spike again as spring and summer approaches.Several blood-sucking hard ticks, for instance, Rhipicephalusappendiculatus (brown ear tick),Rhipicephalusdecoloratus(blue tick), and Amblyommahebraeum, mosquito Aedesaegyptiand flies Stomoxyscalcitrans, Haematobiairritans and Muscadomestica have been implicated in the spreading of LSDV. In the tick host, LSDV is trans-stadially and transovarially transmitted during cold temperatures. Therefore, it is suggested that quarantine could not be the only method to prevent the spread of LSD as movement of vector can blow out the disease. Fig 2 describes the transmission of LSD.

Fig 2: Transmission of Lumpy skin disease

Pathogenesis

In the generalized disease there is viremia and fever as the spread of viral particles takes place through the blood and subsequently there is development of generalized lymphadenitis. Viremia occurs after the early febrile condition for almost 4 days and is followed by localization of virus in the skin and development of inflammatory cutaneous nodules. Following skin lesions due to the replication of the virus in certain cells such as fibroblasts, pericytes, and, endothelial cells of lymphatic and blood vessels, lesions are produced in those sites. Histopathological changes in acute skin injuries include lymphangitis, vasculitis, thrombosis, infarction, edema and necrosis. A special structure called ‘sit-fasts’ (necrotic cores detached from the adjacent skin) is usually seen indifferent parts of the body, which may ulcerate.

Clinical signs

The incubation period of disease in natural condition is between 2 and 5 weeks but in experimental condition, the duration ranges from 7 to 14 days. Lumpy skin disease is clinically presented in three forms; acute, subacute and chronic form. The illness begins with biphasic fever. The clinical manifestations in mild form of infection appears as one or two lumps of nodules within 2 to 3 days of onset of fever, emaciation, ocular discharge, agalactia. Later on, nodular lesions, which are painful and hyperemic may be observed on the animal body especially in the skin of the muzzle, nares, back, legs, scrotum, perineum, eyelids, lower ear, nasal and oral mucosa, and tail. In severe condition, more than hundred nodules develop on skin all over the body and this stage persist for 7 to 12 days. With time lesions develop on mucous membranes of nostrils, respiratory tract, mouth and vulva. After 2-3 weeks, the cutaneous lesions become harder and necrotic causing discomfort to animals and they become reluctant to move. The sloughing of the lesions may create hole form “sitfast”, the characteristic lesion, which subsequently cause invasion by screwworm fly and bacterial invasion that can further lead to septicaemia. Severe form is characterized by emergence of hundreds of nodules all over the skin, lasting for about a week until they become firm and narrow hemorrhagic ring on the skin start to encapsulate them. The lesions continue to scab and may spread to other mucosae. Histopathology of these nodules has revealed that at this point in time, the dermis and musculature have attachments to these wart-like structures with observable ballooning degeneration pattern along with presence of eosinophilicintracytoplasmic inclusions bodies. These superficial structures desiccate and become harder within two to three weeks causing animal discomfort upon movement. Constant degeneration of these areas along with poor re-epithelialization leads to formation of fistulas commonly referred to as “sit fast”. These wounds are reported to be commonly infested with fly maggots or screw worm fly larvae. Furthermore, suppuration and secondary bacterial infections may lead to severe septicemia followed by death.

Diagnosis

Diagnosis due to lack of logistic and familiarity of the exotic diseases is always a challenging task. A differential diagnosis is required to ascertain LSD from demodicosis of skin or Foot and mouth disease. Therefore, histopathological and molecular evidence is needed to confirm LSD diagnosis. The diagnosis of LSD can be established based on the typical clinical signs, enlarged superficial lymph nodes and generalized nodular skin lesions in animals combined with laboratory confirmation of the presence of the virus or antigen. Histopathological analysis of infected tissue samples has distinct vascular thrombosis and neutrophilicinfiltration in dermis and subcutis, furthermore cytoplasmic inclusion bodies called “cellesclavelauses”. Prior studies have established the comparative effectiveness of PCR and viral culturing whereby viremia was detected 4–11 days using PCR and 1–12 days using virus isolation. Samples obtained from the skin lesions yield more positive results in PCR than the blood or those collected from septic viscera due to the greater load of viral particles sheltered in the nodule. Fluids like saliva, nasal swab, or whole blood can be collected from clinically infested animals for viral isolation and molecular testing. Additionally, the disease can be detected using serological tests using Enzyme-linked Immunosorbent Assay (ELISA), Indirect Fluorescent Antibody test (IFAT), Indirect Immunofluorescence test, Virus Neutralization Test (VNT) and Serum Neutralization Test (SNT). A fairly new assay called Immuno-peroxidase Monolayer Assay (IPMA) has been identified for potential use in LSD diagnosis. It is a cheap and convenient test, adapted to low biosafety levels, and has higher sensitivity and specificity than VNT and commercial ELISA.

Vaccination

The virus that causes lumpy skin disease has no recognised treatment. To treat secondary bacterial infections, fever, inflammation, or to increase the animal’s appetite, antibiotics, anti-inflammatory medications, or an injection of vitamins are often administered. In addition to movement restrictions and the evacuation of sick animals, vaccination is the only method that may successfully control the sickness in endemic areas. Veterinary professionals and everybody who works with cattle need to be educated so they can recognise clinical cases immediately and halt the spread of disease. Both homologous (the Neethling LSDV strain) and heterologous (the sheeppox or goatpox virus) live attenuated vaccines can effectively protect cattle against LSD infection. Additionally, eradication methods including quarantine, slaughtering of infected and in-contact animals, proper disposal of carcasses, cleaning and sanitising of the facilities, and insect control must be implemented as soon as possible during the outbreak. So, prevention is better than cure. Recenlty, the indigenous vaccine Lumpi-ProVacInd has been developed to protect livestock from Lumpy Skin disease.  The vaccine has been developed by the National Equine Research Center, Hisar (Haryana) in collaboration with the Indian Veterinary Research Institute, Izzatnagar (Bareilly). The Vaccine was officially launched by the Ministry of Agriculture & Farmers Welfare on 10 August 2022.

Conclusions

The disease's rapid spread into disease-free areas is a sign of its importance from an economic and epidemiological perspective. Animal movements should be carefully regulated by veterinary authorities.  Additionally, careful study of the disease's transmission and epidemiology as well as the application of efficient preventative interventions like immunisation may lead to improved disease control. Therefore, effective measures to stop further spread include accurate and prompt diagnosis in endemic areas, vaccination with the homologous strain of the LSDV, vector control, animal movement restrictions, and LSDV testing of bulls used for breeding.

Dr.AbrarUlHaq

Assistant Professor

Dept. of Veterinary Medicine

Guru AngadDev Veterinary and Animal Sciences University, Ludhiana

Dr.BiswaRanjan Jena 

Ph.D. Scholar

Dept. of Veterinary Medicine

Guru AngadDev Veterinary and Animal Sciences University, Ludhiana