Lumpy Skin Disease (LSD): A Dreadful Emerging Disease in Cattle

Lumpy Skin Disease (LSD): A Dreadful Emerging Disease in Cattle

¹Indian Veterinary Research Institute, Bengaluru-Karnataka

² Indian Veterinary Research Institute,Mukteswar-Uttarakhand

³Project Directorate of Foot and Mouth Disease, Bengaluru-Karnataka

⁴Indian Veterinary Research Institute, Palampur-Himachal Pradesh

Synonyms: Pseudo-urticaria, Neethling virus disease, Exanthema nodularisbovis, Knopvelsiekte

Introduction:

Lumpy skin disease (LSD) is atransboundary, viral disease caused by Lumpy skin disease virus (LSDV) of Capripoxvirus genus, subfamily Chordopoxvirniae, family Poxviridae. LSD has limited host range and found only in ruminants viz. cattle and water buffaloes.Natural infection of sheep and goat has not been reported even in close contact with infected cattle and buffaloes but skin lesions have been seen after experimental infection in sheep, goat, giraffe, Giant gazalles, impalas. LSD is non-zoonotic and a vector borne disease. The arthropod vectors which are responsible for disease spread include mosquitoes, biting flies and ticks.

The world organization for animal health (OIE) categorizes LSD as a notifiable disease due to its economic impact. LSD has been considered as agro-terrorism agent due to its ability to spread from Africa to other parts of the world. The economic implications of the disease are high due to morbidity rather than mortality. The significant losses are due to severe emaciation, hide damage, infertility in males and females, mastitis, drop in milk production and abortions. Due to reduction in quality of the animal, the effect can be seen in overall trade of the live animals and animal products. LSD is responsible for huge financial losses to meat industry, milk industry, leather industry and other industries associated with livestock and its by-products.

Virus Characteristics:

LSDV is a brick shaped, enveloped virus, 320 × 260 nm size, with double stranded DNA and replicates in cytoplasm of the host cell. The LSDV genome is 151 kbp large, consisting of a central coding region surrounded by identical 2.4 kbp-inverted terminal repeats and contains 156 putative genes. LSDV contains 30 structural and non-structural genes homologous to sheeppox and goatpox virus sharing 97% nucleotide identity. The virus is stable in ambient conditions for long period. It can persist in desiccated skin crusts for 35 days, in necrotic nodules for 33 days and in air-dried hides for at least 18 days.LSDV is very stable and can be recovered even after 10 years from the skin nodules kept at -80ºC and after 6 months from the infected tissue culture fluid kept at 4ºC. Sunlight and lipid detergents can destroy LSDV quickly but virus can persist for many months in dark environment like animal sheds and feed stores. Virus gets inactivated at 55ºC temperature for 2 hours and 65ºC for 30 minutes. It is susceptible to highly alkaline or acid pH but can sustain pH range 6.6–8.6 for 5 days at 37°C without significant reduction in titres. The virus is susceptible 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%).

Host range:

Cattle (Bosindicus and Bostaurus) and buffalo (Bubalusbubalis) are major susceptible hosts. Bostaurus is more susceptible than indigenous cattle breeds. Animals of all ages are susceptible but calves are more susceptible and develop lesions within 24 to 48 hours. Wild animals under natural conditions, are resistant to infection but experimental infection produced clinical lesions in Giraffe (Giraffe camelopardalis), impala (Aepycerosmelampus), Arabian oryx (Oryx leucoryx), springbok (Antidorcasmarsupialis), oryx (Oryx gazelle) and Thomson’s gazelle. Normally the role of wildlife in the transmission and maintenance of LSDV has been found to be almost negligible. Humans are also resistant to LSDV.

Epidemiology and transboundary spread:

The disease is endemic in African countries but recently the disease has been reported from new territories around the world. The first case of LSD was reported from Zambia in 1929 which later on spread to whole African continent except Libya, Algeria, Morocco and Tunisia. Later on, it spread to Middle eastern countries such as Kuwait,Israel, Oman, Jordan, Syria, Lebanon, Iran, Iran, Turkey and Yemen. The first outbreak in Israel in 1989 was thought to be due to the movement of infected Stomoxycalcitrans from Egypt. According to OIE, at present this disease is prevalent in various countries of Africa, Europe and Asia. The reasons of the disease spread to India are unknown but it may be due to livestock movement across international borders or may be due to vectors movement from the neighbouring countries. In recent years, LSD has been reported from neighbouring countries of India such as China and Bangladesh. Therefore, understanding the epidemiology of exotic diseases becomes necessary for timely planning the effective disease management.

In India, first outbreak of the disease was reported in Odisha in August, 2019, in monsoon season with high humidity and vector density. The first incident started in Khairbani, Betnoti, Mayurbhanj districts of Orissa. Then after few days, second outbreak was reported from the same region at new place Patalipura. The third case outbreak was reported in Rajendrapur, Bhandaripokhari and Bhadrak in Odisha. On the basis of phylogenetic analysis, the strain present in India was genetically close to South African NI2490/KSGP-like strains rather than European strains.

Transmission:

Mechanical transmission by vectors is the prime route of spread of disease. In most of the endemic countries, the disease incidences significantly increase with the onset of seasonal rainsand summer season, coinciding with the peak activity of the vectors. The tick Amblyomma spp., Rhipicephalusdecoloratus, Rhipicephalusappendiculatus and Amblyommahebraeum have been reported as a mechanical vectors and reservoirs of LSDV. The bitting flies (Stomoxycalictrans and Biomyiafasciata) and mosquitoes (Culexmirificens and Aedesnatrionus) are also involved in mechanical transmission of the disease. Hence, it is suggested that quarantine alone could not be the only method to prevent the spread of LSD as movement of vector can blow out the disease. Experimental studies and field observations conclude the low rate of transmission by direct route. Virus is secreted in milk, nasal secretions, saliva, blood and lachrymal secretions forming indirect source of infection for animals sharing feeding and watering troughs. LSD virus transmission through intrauterine route has been documented. The infection has also been transmitted from infected mother to calf via milk secretions and skin abrasions. The virus persists in the semen for up to 42 days post infection.

Clinical Signs and lesions:

The incubation period of LSD is between 2 and 5 weeks. LSD takes either of the 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 form, more than hundred nodules develop on skin all over the body and this stage persist for 7 to 12 days. The nodules are firm and slightly raised from surrounding skin, separated by narrow haemorrhagic ring. The nodules involve dermis, epidermis, subcutis and musculature. The lesions then progress towards papules, vesicles, pustule with exudation and then slowly to scab formation. Healing of the lesions is very slow. 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 and this characteristic lesion is known as “sit fast”, which subsequently gets invaded either by screwworm fly or bacterial infectionwhich can lead to septicemia. Generalized lymph node swelling is also observed in infected animals. The sequela of LSD is pneumonia due to the inhalation of necrotic material by the animal itself. Abortion occurs in acute phase of infection. Recovery is very slow due to secondary bacterial infection, pneumonia, mastitis and fly strike in necrotic lesions leaving deep holes in the body

Diagnosis:

Tentative diagnosis can be made on the basis of skin nodules observed on face, eyelid, neck, muzzle, nostrils, udder, limbs. However, clinical signs can be confused with other diseases like foot and mouth disease, buffalopox, demodicosis, hypersensitivity and insect bite. Hence, laboratory diagnosis is a must for confirmation of the disease. Skin biopsy sample can be collected for further confirmation of disease. Samples should be transported in transport medium with 20 to 50% glycerol in phosphate buffer saline. Skin samples can be checked by electron microscopy to identify LSDV. Samples of skin also show characteristic histopathological changes, which include vasculitis and perivascular infiltration with white cells causing a thrombosis of the vessel in the dermis and subcutis. Cells infiltrating the lesion are epithelial cells, known as “cellesclavelauses”, which are also described in sheep pox. Virus isolation can be used for the confirmatory diagnosis of LSDV. Bovine testes and pre-pubertal lamb, primary and secondary culture is most sensitive for isolation of LSDV. Molecular diagnosis using conventional and real-time PCR has been developed for rapid diagnosis. Differentiation of LSDV from other Ccpripoxvirus is made possible by real-time PCR.

Treatment:

Anti-inflammatory and antibiotics are used for symptomatic treatment since no effective treatment against LSD has been developed till date.

Prevention and control:

In order to control the disease, movement of infected animals should be restricted. Within countries, if animal with lesions are observed, they should be quarantined in order to prevent the spread of LSD. Moreover, there should be restriction in vector movement. Vectors movement due to prevailing winds may cause disease transmission. The use of vector control methods like theuse of insecticides and the use of vector traps can also be tried for disease prevention. The use of vaccination is another method used for prevention. Live attenuated vaccines are currently available for LSD. For effective control and prevention of disease, long term vaccination with 100% coverage should be made mandatory as LSD virus being stable survives in environment for long time. Before introducing new animals to the affected farm, they should be immunized. Calves should be immunized at the age of 3 to 4 months. Pregnant cows and breeding bulls can be vaccinated annually.

Based on different strains of LSD virus, several vaccines are available such as the Neethling strain based Lumpy Skin Disease Vaccine made available by Onderstepoort Biological Products (OBP) of South Africa where Neethling strain is passaged 60 times in lamb kidney cells and 20 times on the chorioallantoic membrane of embryonated chicken eggs and this vaccine provides immunity for 3 years. Another vaccine termed Bovivaxis made available by MCI Sante Animale of Morocco. Based on SIS Neethling type, Lumpyvax vaccine is made available by MSD Animal Health-Intervet of South Africa.

Vaccines against sheeppox and goatpox can also be used for prevention of LSD since LSD is closely related to sheeppox and goatpox virus.Sheeppox vaccines used against LSD includes Romanian sheeppox virus and Yugoslavian RM 65 sheeppox and GTPV Gorgon strains. These heterologous vaccine strains cause some local reactions. However, live attenuated Gorgan goatpox strain provides good protection in cattle with practically no side effect.

Selected References

1. Kumar, N., Chander, Y., Kumar, R., Khandelwal, N., Riyesh, T., Chaudhary, K.,.. . Tripathi, B. N. (2021).Isolation and characterization of lumpy skin disease virus from cattle in India. PLoS One, 16(1), e0241022.
2. Sudhakar, S. B., Mishra, N., Kalaiyarasu, S., Jhade, S. K., Hemadri, D., Sood, R.,.. . Singh, V. P. (2020).Lumpy skin disease (LSD) outbreaks in cattle in Odisha state, India in August 2019: Epidemiologicalfeatures and molecular studies. Transbound Emerg Dis, 67(6), 2408–2422
3. Tuppurainen, E. S. M., Venter, E. H., Shisler, J. L., Gari, G., Mekonnen, G. A., Juleff, N.,.. . Babiuk, L. A.(2017). Review: Capripoxvirus Diseases: Current Status and Opportunities for Control. Transbound Emerg Dis, 64(3), 729–745. doi:10.1111/tbed.12444.
4. (2018). Lumpy skin disease. chapter 3.04.12. In P. Beard & B.A. Lubisi (Eds.), OIE terrestrial manual (pp. 1158-1171). Paris, France: World Organization for Animal Health.
5. Tuppurainen, E. S., & Oura, C. A. L. (2012). Review: Lumpy skin disease: An emerging threat to Europe, the Middle East and Asia. Transboundary and Emerging Diseases, 59, 40-48.
6. Tuppurainen, E., Alexandrov, T., & Beltrán-Alcrudo, D. (2017). Lumpy skin disease eld manual –A manual for veterinarians. FAO Animal Production and Health Manual No. 20. (pp. 60).
7. Tuppurainen ES, Pearson CR, Bachanek-Bankowska K, Knowles NJ, Amareen S, et al. (2014) Characterization of sheep pox virus vaccine for cattle against lumpy skin disease virus. Antiviral Res 109: 1–6. pmid:24973760.
8. Binepal YS, Ongadi FA, Chepkwony JC (2001) Alternative cell lines for the propagation of lumpy skin disease virus. Onderstepoort J Vet Res 68: 151–153. pmid:11585094.
9. Sprygin A, Pestova Y, Wallace DB, Tuppurainen E, Kononov AV (2019) Transmission of lumpy skin disease virus: A short review. Virus Res 269: 197637. pmid:31152757.
10. Woods JA (1988) Lumpy skin disease—a review. Trop Anim Health Prod 20: 11–17. pmid:3281337.

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