Lumpy Skin Disease in Cattle: Transmission, Impact, and the Role of Lumpi-ProVacInd Vaccine
Dr. Moatoshi Ozukum and Dr. Ashish Soni
Abstract
Lumpy skin disease (LSD), a viral disease in cattle caused by the lumpy skin disease virus (LSDV), is primarily spread by arthropod vectors, especially during warmer, humid months that promote vector activity. LSD has significant economic impacts on the cattle industry, leading to weight loss, hide damage, infertility, mastitis, decreased milk production, and mortality rates up to 20%. Transmission typically occurs via blood-sucking insects, although direct contact, contaminated feed or water, and iatrogenic methods (such as shared needles) can also spread the virus. Clinically, LSD manifests with fever, lymphadenopathy, and characteristic skin nodules. Diagnosis relies on clinical signs and laboratory methods like PCR, electron microscopy, and antibody tests. Treatment is symptomatic, aiming to prevent secondary bacterial infections, while vaccination remains the most effective preventive strategy in endemic areas. Lumpi-ProVacInd, a recent vaccine developed by the Indian Council of Agricultural Research (ICAR), is a homologous live-attenuated vaccine derived from a local LSD strain isolated in Ranchi, Jharkhand. Field trials showed 100% efficacy in controlled settings and an 85.18% seroconversion rate by day 30 post-vaccination. The vaccine, containing 10^3.5 TCID50 of LSD virus, induces both antibody-mediated and cell-mediated immunity. With ongoing outbreaks in India, the vaccine’s commercialization has been fast-tracked, receiving approval from the Central Drugs Standard Control Organization (CDSCO) for production by Biovet Pvt Ltd.
Keywords: LSD; Transmission; Diagnosis; Lumpi-ProVacInd; Vaccine
Introduction
Lumpy skin disease is caused by lumpy skin disease virus (LSDV), with arthropod vectors serving as the primary means of mechanical transmission (Tuppurainen, 2012). Temporally LSD tends to cluster during the warm and humid months of the year, a pattern directly linked to vector activity (Gari et al., 2010).
The host range of the lumpy skin disease virus (LSDV) is restricted, and it is unable to complete its replication cycle in hosts other than ruminants (Shen et al., 2011). Besides, LSD has not been reported in sheep and goats even when kept in a close contact with infected cattle (Davies, 1991). Both sexes and all ages of cattle breeds are susceptible to LSDV, although evidence suggests that younger animals may be more vulnerable to severe disease forms (Jameel, 2016). LSD leads to significant economic losses due to weight loss, hide damage, infertility, mastitis, reduced milk production, and mortality rates reaching up to 20% (Alexander et al., 1957).
Transmission and pathogenesis
The primary mode of transmission for LSD is through arthropod vectors, particularly blood-sucking insects.These insects can mechanically transmit the virus from infected cattle to healthy ones, especially during warmer months when insect activity peaks. The virus is present in high concentrations in the skin nodules and other bodily fluids of infected animals, which facilitates this transmission (Spryginet et al., 2019). A study investigating the risk factors associated with the spread of LSD in Ethiopia showed that warm and humid agro-climate, conditions supporting abundance of vector population, was associated with a higher prevalence of LSD (Gari et al., 2010). The most important source of infection to healthy animals is considered to be skin lesions or nodules since the virus persists in the lesions or scabs for long periods of time and has strong tropism to dermal tissues. Though rare, transmission also occurs through direct contact, and can also spread from contaminated feed and water (Prozeesky and Barnard). Transmission or spread can also occur iatrogenically during mass vaccination in which single syringe and needle are used in several animals.
Intravenous, intradermal and subcutaneous routes are used in experimental infection. The intravenous route develops severe generalized infection, while the intraepidermal inoculation develops only 40% to 50% of animals may developed localized lesions or no apparent disease at all. A localized swelling at the site of inoculation after four to seven days and enlargement of the regional lymph nodes, develop after subcutaneous or intradermal inoculation of cattle with LSDV (Vorster and Mapham 2008). LSDV replicates inside the host cells such as macrophages, fibroblasts, pericytes and endothelial cell in the lymphatics and blood vessels walls lead to developing vasculitis and lymphangitis, while thrombosis and infarction may develop in severe cases.
Clinical signs
The incubation period for LSD typically ranges from 4 to 14 days, but can extend up to 5 weeks in naturally infected animals High Fever: The disease often begins with a high fever, exceeding 40°C, which may persist for about a week Swollen Lymph Nodes: Enlargement of superficial lymph nodes, particularly subscapular and prefemoral nodes, is common and easily palpable.
Characteristic nodules appear on the skin, ranging from 10 to 50 mm in diameter. These lesions can be found on various body parts, including head, neck, udder, scrotum and perineum limbs
The nodules are typically firm, raised, and may ulcerate over time. They involve all layers of the skin and can lead to necrotic changes125. Ulceration and Scabbing: The center of the nodules may ulcerate, leading to scab formation. These lesions can persist for several months. Other clinical signs involve lachrymation and nasal discharge, depression and anorexia excess salivation and milk production drop (Tuppurainen et al., 2017).
Diagnosis
The diagnosis of LSD can be established based on the typical clinical signs or generalized nodular skin lesions and enlarged superficial lymph nodes in affected animals combined with laboratory confirmation of the presence of the virus or antigen.
The gold standard method for the detection of capripox viral antigen and antibody are electron microscopy examination and serum or virus neutralization tests, respectively (Tuppuraine et al., 2011).
The clinical diagnosis of LSD can be confirmed using conventional or real-time PCR methods (Tuppuraine et al., 2005). The host immunity against LSDV is mainly cell mediated and therefore, serological testing may not be sensitive enough to detect mild and long-standing infections or antibodies in vaccinated animals. Antibody ELISAs have been developed with limited success (Tuppuraine et al., 2011). Indirect fluorescent antibody test (IFAT) can be used for LSD diagnosis and screening however, the test requires longer time and may be more costly as compared to ELISA technique (Gari et al., 2008).
Treatment, prevention and control
The treatment of LSD is only symptomatic and targeted at preventing secondary bacterial complications using antimicrobial therapy (Abutarbush et al. 2013). Sick animals should be removed from the herd and follow supportive treatment such as antibiotics, anti-inflammatory drugs, and vitamin injections. These therapies are usually the chances for the development of secondary bacterial infection, inflammation and fever, and thus improving the appetite of the animal (Capstick et al., 1959). However, the treatment of LSD (its complications) is costly as well as does not ensure full recovery therefore; prevention is more beneficial to avoid the substantial economic losses due to hide damages, loss of milk due to mastitis and loss of animal product due to death, abortion, fever and myiasis. Therefore, vaccination is the only effective method to control the disease in endemic areas as movement restrictions and removal of affected animals alone are usually not effective. Effective vaccines against LSD exist and the sooner they are used the less severe the economic impact of an outbreak is likely to be (Tuppuraine et al., 2017).
The biting flies and certain tick species are probably the most important method of transmission of the disease, control by quarantine and movement control is generally not very effective. In endemic areas, control is therefore essentially confined to immunoprophylaxis (Coetzer, 2004).
Two approaches to immunization against LSD have been followed. In South Africa, the Neethling strain of LSD was attenuated by 20 passages on the chorio-allantoic membranes of hens’ eggs, but the vaccine virus is now propagated in cell culture (Nawthe et al., 1982).
Current breakthrough in vaccine development in India
Lumpi-ProVacInd was developed by the Indian Council of Agricultural Research (ICAR) through a joint effort between the National Research Centre on Equines (ICAR-NRCE) in Hisar, Haryana, and the Indian Veterinary Research Institute (IVRI) in Izatnagar, Uttar Pradesh. The vaccine was produced using a local strain of the LSD virus, isolated from infected cattle in Ranchi, Jharkhand, in 2019. LSD was first reported in India that same year and has since spread across numerous states, resulting in considerable morbidity and mortality in cattle. Prior to Lumpi-ProVacInd, only heterologous vaccines, such as those derived from the Goat Pox and Sheep Pox viruses, were available, offering limited protection (approximately 60-70%) against LSD (Kumar et al., 2023).
Lumpi-ProVacInd is a homologous live-attenuated vaccine designed specifically for cattle, utilizing a weakened form of the LSD virus. Under controlled conditions, the vaccine has shown 100% efficacy in protecting against LSD. Field trials reported a seroconversion rate of approximately 85.18% by day 30 post-vaccination (Kumar et al., 2023). Each dose of Lumpi-ProVacInd contains 103.5 TCID50 of the live-attenuated LSD virus, effectively stimulating both antibody-mediated and cell-mediated immunity to provide full protection against lethal LSD challenges (Wikipedia, 2024). In response to the ongoing LSD outbreaks in various states, efforts are being made to accelerate the vaccine’s commercial availability for farmers. In 2024, the Central Drugs Standard Control Organization (CDSCO), Government of India, approved Biovet Pvt Ltd, Bengaluru, to commercially produce Lumpi-ProVacInd (Wikipedia, 2024).
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