Lumpy Skin Disease (LSD): An Emerging Transboundary Viral Disease
Kanchan Arya1, G P S Sethi2
1Phd scholar, Department of Veterinary Medicine, Lala Lajpat Rai University of Veterinary and Animal Sciences, Hisar,Haryana
2Assistant Professor, Animal Science, Krishi Vigyan Kendra, Fatehgarh Sahib
Introduction
Lumpy skin disease is a re-emerging bovine viral illness that is widespread in the majority of African and some Middle Eastern nations, with a high risk of spreading to the rest of Asia and Europe. The recent rapid spread of disease in disease‐free countries indicates the importance of understanding the limitations and routes of distribution. Lumpy skin disease (LSD), a major threat to stockbreeding, can cause acute or subacute disease in cattle and water buffalo (Givens, 2018). Cattle of all ages and breeds are affected, although young and lactating animals are particularly vulnerable (Tuppurainen et al., 2011). Lumpy skin disease virus (LSDV) is a double‐stranded DNA containing around 150 kilobase pairs (kbp) with relatively large sizes (230–260 nm), enclosed in a lipid envelope, and belongs to the genus Capripoxvirus, which is genetically related to the sheep pox (SPPV) and goat pox (GTPV) viruses (Buller et al., 2005; Givens, 2018). Although capripoxviruses are normally considered host-specific. The strains of the sheep pox virus (SPPV) and goat pox virus (GTPV) have been known to naturally or artificially cross-infect both host species and cause disease. In contrast, LSDV can experimentally infect sheep and goats, but no natural infection of sheep and goats with LSDV has been reported.
33 districts of Rajasthan in India have been affected by the lumpy disease. 26 of Gujarat’s 33 districts have been devastated by this illness. While it has taken control of all 22 of Haryana’s districts, all 23 of Punjab’s and 21 of Uttar Pradesh’s districts. Lumpy skin disease has resulted in significant economic losses. Due to the high fever and secondary mastitis caused by the illness, milk production is significantly reduced (by 10 per cent to 85 per cent). Milk production has declined by 30 percent in the five most lumpy-affected districts of Rajasthan followed by 10 percent in Gujarat while in Punjab milk production has decreased by 7 percent. Damaged hides, decreased beef cattle growth, abortion, temporary or permanent infertility, high treatment, and immunization expenditures, and the death of affected animals are some significant effects of the disease. (Alemayehu et al., 2013; Sajid et al., 2012; Sevik and Dogan, 2017).
Risk factors and Transmission
Warm and humid climate, factors that encourage a plethora of vector populations, such seasonal rains, and the introduction of new animals to a herd are the risk factors in the spread of LSD. The herd size, vector populations, migration of herd, transport of infected animals into disease‐free areas, and common pasture and water sources have all been considered as other risk factors, which may increase the disease prevalence (Gari et al., 2010; Sevik and Dogan, 2017).
The most likely vectors for LSDV transmission are blood-sucking arthropods such as stable flies (Stomoxys calcitrans), mosquitoes (Aedes aegypti), and hard ticks (Rhipicephalus and Amblyomma species). Within a short period of time, the disease has the potential to spread hundreds of kilometres from the initial (focal) outbreak sites. The mobility of infected animals appears to be a major factor in the long-distance spread of LSDV, but specific seasonal patterns suggest that the illness is most likely spread quickly and aggressively over short distances by arthropods. Cattle sharing feed or water troughs that have been contaminated by the saliva or nasal discharge of infected animals may indirectly transmit the LSDV (Ali et al, 2012). After infection of 12–18 days, oral and nasal secretions only showed trace amounts of the virus. It should be observed that these experimental animals only showed a moderate form of LSD, with nodules covering just around 25 per cent of their skin’s surface (Babiuk et al., 2008). Recent studies have shown that LSDV can be transmitted intra-uterine (Rouby and Aboulsoud, 2016). However, experimental verification of this hypothesis is required. Transmission from mother to calf via contaminated milk or skin lesions on the mother’s udder and teats are also likely to occur (Tuppurainen et al., 2013).
Pathophysiology and Symptoms
Following LSDV infection, virus replication, viremia, fever, cutaneous localization of the virus and development of nodules occur (Constable et al., 2017). The spread of the virus occurs after the early febrile condition through blood and form generalized lymphadenitis followed by viremia for almost 4 days.
- 4 to 7 days post‐infection (DPI): localized swelling as 1–3 cm nodules or plaques at the site of inoculation
- 6 to 18 DPI: viremia and shedding of the virus via oral and nasal discharge
- 7 to 19 DPI: regional lymphadenopathy and development of generalized skin nodules
- 42 days after fever: presence of virus in semen (Coetzer, 2004).
The clinical signs are following:
- Fever, inappetence, nasal discharge, salivation and lachrymation, enlarged lymph nodes, a considerable reduction in milk production, loss of body weight and sometimes death (Abutarbush et al., 2013; Tasioudi et al., 2016).
- Firm, slightly raised, circumscribed skin nodules that are 2–7 cm in diameter and typically appear on the neck, legs, tail and back, after the beginning of fever (Sevik and Dogan, 2017).
- Oedema of the legs and lameness (Tuppurainen and Oura, 2012).
- Abortion (Radostitis et al., 2006), mastitis and orchitis (Awadin et al., 2011) is also occur in LSDV infection.
- On necropsy, lung oedema and congestion, nodules throughout the lungs and gastrointestinal tract were often observed (Zeynalova et al., 2016). Muzzle, nasal cavity, larynx, trachea, dental pad, gingiva, abomasum, udder, teats, uterus, vagina and testes might be affected.
Treatment and Prevention
LSD is solely symptomatically treated, with an emphasis on preventing additional bacterial problems with a combination of antimicrobials, anti-inflammatory drugs, supportive care, and antiseptic treatments (Salib and Osman, 2011). It is essential that a clinical diagnosis is prompt so that eradication measures, such as quarantine, culling of affected animals, proper disposal of carcasses, cleaning and disinfecting the area, and vector control can be brought into place as soon as possible during the outbreak (Constable et al., 2017). The culling of affected animals, movement restrictions and compulsory and consistent vaccination have been recommended as control strategies (OIE WAHIS, 2016). Members of the capripoxvirus are known to provide cross‐protection hence, homologous (Neethling LSDV strain) and heterologous (sheeppox or goatpox virus) live attenuated vaccines can all be used to protect cattle against LSD infection (OIE, 2013). In India, after the first LSD outbreak in 2019, heterologous live attenuated GTPV (Uttarkashi strain) vaccine has been officially permitted for emergency use in cattle and buffaloes. Also, ICAR-NRCE, Hisar in collaboration with IVRI has developed homologous live attenuated LSD vaccines commercially available as- “LumpiProVacInd”. The safety of the vaccine has also been ascertained in the field in cattle and buffaloes of all age groups including lactating and pregnant ones.
Conclusion
The disease’s rapid spread into previously disease-free areas is a sign of its significance from an economic and epidemiological perspective. As a result, focusing adequate attention to the various components of the disease, such as transmission and epidemiology, and practicing efficient preventative measures, like vaccination, could lead to better disease control. Therefore, to prevent future spread, it is strongly advised that accurate and prompt diagnosis be made in endemic areas, vaccination with the homologous strain of the LSDV, vector management, restrictions on the movement of animals and LSDV testing of bulls used for breeding are highly recommended as tools to control further spread.
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