INTRODUCTION:

Lumpy skin disease is an infectious viral illness caused by the Lumpy skin disease virus (LSDV), which belongs to the family Poxviridae, subfamily Chordopoxvirniae, and genus Capripoxvirus. The condition is referred to by many names, including "LSD," "Pseudo-urticaria, "Exanthema nodular is bovis, Neethling virus disease likewise "knopvelsiekte" (Al-Salihi K.2014).

Cattle and water buffalo can get acute or sub-acutesickness from LSD, a serious threat to stockbreeding. Cattle of all ages and types are impacted, although young animals and those lactating at their peak are particularly vulnerable. The World Organization for Animal Health (OIE) has classified this transboundary disease as a noteworthy disease with the potential for rapid spread because to its significant economic losses.

Given that the disease has recently expanded to previously disease-free nations, controlling and eradicating the sickness is crucial. The double-stranded DNA of the lipid-enveloped lumpy skin disease virus (LSDV) is a reasonably large 150 kilo base pairs (kbp) in size (230–260nm). It is a member of the Capripox virus genus, which shares genetic ancestry viruses with the cause sheep pox (SPPV) and goat pox (GTPV). Despite the common misconception that capripox viruses are host-specific, SPPV and GTPV strains can infect and injure both host species when they cross naturally or artificially. LSDV has the capacity to infect sheep in an experimental setting, however no cases of naturally occurring LSDV infection in sheep and goats have been reported or made public (Namazi F et al. 2021).

Skin lesions have been found following experimental infection in sheep, but natural infection of sheep and goats, even in close proximity to diseased cattle and buffaloes, has not been recorded. Goat, giraffe, impalas, and giant gazelles (Davies FG. 1991). LSD is blamed for high morbidity and low fatality rates (Abutarbush SM. et al. 2015). High fever, lymphadenitis, severe emaciation, bilateral epiphora, decreased milk production, sterility, skin erythema, and nodules are among the illness's notable symptoms. Ineffective reproduction, term loss reduced milk production, decreased hide quality, and ongoing degenerative emaciationthe most significant economic ramifications of animal farmers living in endemic zones of LSD (Rgbe H. 1991).

Egypt and Israel saw the first LSD outbreak outside of sub-Saharan Africa between 1988 and 1989(Beard PM. 2016). According to OIE, this disease is currently widespread in a number of African, European, and Asian nations (Tuppurainen ES, et al 2015). Although the mechanisms of the disease's introduction to India are unknown, they may be connected to the translocation of animals over borders or the migration of vectors from nearby countries. LSD has reportedly been used in recent years from India's neighbours, namely China and Bangladesh. Consequently, comprehension the epidemiology of exotic sickness makes it vital to promptly arrange the efficient illness control. This review highlights the most recent updates regarding the LSD Viruses can be promptly destroyed by sunlight and lipid detergents, but they can survive for several months in dim environments like feed warehouses and animal shelters. Virus inactivation occurs at 55°C. Temperature for 2 hours and 30 minutes at 65°C. It is susceptible to extremely acidic or alkaline pH but can sustain 6.6 to 8.6 for five days at 37°C without noticeably lowering virus titres. Formalin, chloroform, and ether (20%) are among the viruses that are susceptible to these chemicals. Sodium hypochlorite (2-3%), phenol (2% for 15 minutes), and (1%), Iodine compounds with quaternary ammonium (1:33 dilution) substances (0.5%) (Tuppurainen ES, et al 2015).

It is a disease that must be reported and has a terrible impact on international cattle trade as well Africa has an endemic case of the disease however, recent reports of the disease have come from new areas all over the place. The first LSD case was documented in Congo in 1929. The OIE has determined that LSD is a transboundary disease that must be reported on international forums since it has terrible and long-lasting impacts on world trade in livestock. The illness was once believed to be endemic, exclusively in African nations, but recently, there have been reports from additional geographical areas of the world. According to OIE, LSD is common in practically all African, Asian, and European nations European (Tuppurainen ES, et al 2015).

Numerous studies have indicated that this disease is more prevalent in crossbred young animals that participate in community grazing and during the rainy season, when arthropod vectors are active. Another important step that introduces risk is the introduction of new animal species (Kononov, A. et al. 2019). Although LSD has spread to many nations, it is still unclear whether strain or mutations will provide the best candidates for vaccine development. Contrarily, during the illness outbreak in Russia, vaccination strains were also discovered, casting more doubt on the vaccine candidate and its efficiency (Giasuddin M et al. 2019). In the middle of 2019, Bangladesh's local veterinary services administration reported an epidemic of an unexplained syndrome with nodular skin lesions. In the population of commercial and backyard cattle in a few Chattogram neighbourhoods (Anwara, Karnaphuli, and Patiya) district (Anonymous, 2019). (Anonymous, 2019). The same clinical onset pattern was reported thereafter in various regions of the nation (Quinn PJ et al. 2015). Although the reasons for the disease's spread to India are unknown, they might be connected to the transnational movement of animals or the migration of vectors from nearby countries. LSD has reportedly been used in recent years from India's neighbours, including China and Bangladesh. Consequently, comprehension the epidemiology of exotic sickness makes it vital to promptly arrange the efficient illness control. This review highlights the most recent updates regarding the LSD.

Figure No. 1. Lumpy skin disease and raised circumscripted nodular lesions

AETIOLOGY:

The virus that causes lumpy skin disease (LSDV), which affects all domestic animals besides dogs, is a member of the Poxviridae family of viruses. The two subfamilies make up the family: Chordopoxvirinae, infecting Entomopoxvirinae infecting an invertebrate and a vertebrate as its host (King AM et al.2015). There are ten genera in the Chordopoxvirinae subfamily, including Capripox virus. Three viral species, including the sheeppox virus (SPPV), goatpox, and human both the lumpy skin disease virus and the GTPV) sheep, goats, and cattle, in that order (King AM et al. 2015). Lumpy skin condition might show up frequently or suddenly. Far from the site of the first outbreak, other foci of infection frequently appear. Although it can happen in the winter, its occurrence is greater in humid summer conditions. It is mainly common on low-lying areas and beside waterways. Biting insects have been implicated as mechanical vectors since quarantine measures meant to stop the spread of infection frequently fail; nonetheless, outbreaks have happened in situations when insects could feasibly be excluded. Three types of African hard ticks have been demonstrated in experiments to biologically spread the virus. Contact infection is a different possible method of infection because the illness has been experimentally shown to be spread by infected saliva. In Africa, African buffalo are thought to serve as maintenance hosts, although other (Tulman ER et al. 2002).

LSDV is a 320 x 260nm brick-shaped enveloped virus that replicates in the cytoplasm and possesses double-stranded DNA with complicated symmetry. The LSDV genome measures 151 kbp, comprised of identical 2.4's on either side of the core coding section. Comprises 156 putative genes and kbp-inverted terminal repeats. 30 homologous structural and non-structural genes are present in LSDV. Sheeppox and goatpox viruses share 97% of their nucleotides identity (Tulman ER et al. 2001). Poxviruses' host range is restricted in later evolution as a result of gene loss; comparable trends have been observed within Capripox viruses when comparing LSDV, SPPV, and GTPV. The IL-1 receptor, the F11L gene for the vaccinia virus, N2L, K7 L genes, M003.2 and M004.1 of the myxoma virus, and LSDV are among the nine genes encoded by the terminal regions of the LSDV virus. With respect to potential pathogenicity and host range capabilities, the unique gene LSDV132 has been impacted by accumulating mutations in both SPPV and GTPV. However, the sequence is unaffected by this interruption. Three viruses' genomes are long, yet none of them contain these SPPV and GTPV genes may have a role in host limitation to only cattle¹⁵. Thirty structural and nonstructural genes make up this virus. Infected cells' cytoplasm is where viral DNA is replicated. Structurally both sheep pox and goat pox have similar non-structural genes. virus. Additionally, these genes share about 97% of the same nucleotides in both viral species (Mulatu, E. and Feyisa, A., 2018).

Unlike other Chordopoxvirniae members, the LSD virus has 146 conserved genes that code for information needed for host diversity, transcription, pathogenicity, DNA replication, nucleotide metabolism, and other functions. Leporipox, Suipox, and Yatapox viruses are examples of pox viruses. Viruses share 65% collinearity and the core region's amino acid composition. Virus-carrying LSD genes. However, there are big discrepancies between their genome's terminal regions, as these genes are implicated in hostrange and pathogenicity of a virus. More base pairs than 43% of the nucleotides in this case are common. The existence of similar genes, however, that are responsible for producing substances such as IL-1 binding proteins, IL-10, epidermal growth factor-like protein, G protein-coupled CC, and chemokine receptor (GPCR), indicate that poxvirus genera have a common genetic past (Tuppurainen ES, et al 2015).

LSDV'S VIRAL STABILITY:

The virus can survive for a very long time in an environment. It has a minimum survival time of 18 days in air-dried hides, 33 days in necrotic nodules, and 35 days in crusts of dehydrated skin. Viruses can be promptly destroyed by sunlight and lipid detergents, but they can survive for several months in dim environments like feed warehouses and animal shelters. At a temperature of 65°C for 2 hours and 30 minutes, viruses are inactivated. Although it is sensitive to extremely acidic or alkaline pH, it can maintain 6.6 to 8.6 for five days at 37°C without noticeably lowering titres. The virus is susceptible to the formalin, chloroform, and ether (20%). Sodium hypochlorite (2-3%), phenol (2% for 15 minutes), and (1%), Iodine compounds with quaternary ammonium (1:33 dilution) substances (0.5%). Even after ten years, skin nodules preserved at -80°C may be utilised to recover LSDV, while infected tissue culture fluid can achieve the same thing after six months at 4°C (Tuppurainen ES, et al 2015). UV radiation has the ability to render the virus that causes lumpy skin disease inactive. Due to the vaccinations' susceptibility to sunlight, lumpy skin disease vaccines should be manufactured in dark glass vials. The lumpy skin disease virus may endure 35 days at 28°C in phosphate buffered saline (Tuppurainen, E. Et al 2017).

PHATOGENISITY:

Following LSDV infection, the virus replicates, viremia develops, fever sets in, the virus localises to the skin, and nodules form (Tuppurainen, E. et al 2017). In an experiment, following intradermal vaccination the following incidents related to the virus:

· Localized swelling as 1-3cm nodules or plaques at the site of inoculation occurs 4 to 7 days post-infection (DPI).

· Viral shedding via oral and nasal discharge occurs 6 to 18 DPI.

· Regional lymphadenopathy and the occurance of generalised cutaneous nodules occur 7 to 19 DPI.

· Virus found in semen 42 days after fever.

Infected tissues develop vasculitis and lymphangitis as a result of the virus' intracellular reproduction in fibroblasts, macrophages, pericytes, and endothelial cells (El-Nahas et al. 2011).

Evidently, humoral immunity is compromised in younger calves, breastfeeding cows, and underweight animals, making them more vulnerable to common diseases (Annandale et al. 2010). Recovery by the animal from the virus's naturally have demonstrated lifetime immunity. Due to acquired maternal antibodies, calves from infected dams are immune towards illness for about 6 months. Animals affected recover from the infection, and the carriers of lumpy skin disease virus is not known at this time (Annandale et al. 2010).

TRANSMISSION:

Lumpy skin disease can affect ruminants of various kinds, including cattle, water buffalo, and wild animals. It appears that the virus does not affect sheep and goats. LSDV may endure the environment for a very long time at normal temperatures, mainly in scrabs. The virus reportedly continues to exist in nodules on necrotic skin. For a minimum of 33 days, for a minimum of 35 days, in desiccated crusts, then it should be air dried for about 18 days in air- dried hides (Khwannimit, B. and Bhurayanontachai, R., 2009). Since the virus can live for a long period in lesions or scabs, skin lesions are believed to be the primary sites of infection. Blood, milk, saliva, semen, nasal, and lachrymal secretions all help to get rid of the infection (transmissible to suckling calves).Arthropods, notably spiders, spread the LSDV. Blood-sucking bugs contaminated food, water, and other resources directly transmit LSD by saliva and nasal secretions in its later stages and sperm (Kahana‐Sutin et al. 2017). Research has shown that indirect transmission is more significant in starting phase than direct transmission of ilthe virus, as there is no correlation between the density of the cattle and infection rates (Lubinga et al. 2014).

Since LSD outbreaks are more active in the summer, when arthropod activity is at its peak, this could mean that different types of vectors, particularly those that feed on blood, are involved in the propagation of the virus (Gupta et al. 2020). The saliva and several tick organs, such as the haemocytes, salivary glands, and mid-gut, were discovered to have the virus and viral antigen that causes lumpy skin disease(Gupta et al. 2020). The main means through which diseases are disseminated is mechanical transmission by vectors. When the seasonal rains and summertime arrive in the majority of the endemic nations, such as sub-Saharan Africa, Egypt, and Ethiopia, and coincide with the peak vector activity, disease occurrences significantly rise (Tuppurainen et al.2015). With the coming of winter, incidents drastically decline before resuming in the spring and summer. Observations revealed that despite limited. Egyptian animal movements, a virus spreading to Israel, through the airborne movement of biting insects, 80 to 200 kilometres away (Ali et al. 1977). Mechanical parasites include the ticks Amblyomma spp., Rhipicephalusdecoloratus, Rhipicephalusappendiculatus, and Amblyommahebraeum viral reservoirs and vector (Niesche, R. and Haase, M., 2012.).

Additionally, the mechanical transmission of disease is facilitated by biting flies (such as Biomyiafasciata and Stomoxycalictrans) and mosquitoes (such as Culexmirificens and Aedesnatrionus).

The following is proof of LSDV direct transmission: however, the field observations and experimental research of Weiss 1968 draws a conclusion about the low rate of direct transmission route. However, investigations have found that direct interaction of animals plays no part in the spread of viruses (Lubinga et al. 2014). LSD can be caused via milk, nasal secretions, saliva, blood, and lachrymal secretions, providing animals that are close to one another with an indirect source of infection (Annandale et al. 2014). The virus is thought to be transmitted from a mother who is infected to her calf by milk secretions and skin abrasions (Annandale et al. 2010). 43 days after infection, the LSDV virus may be cultured from semen. The iatrogenic pathway is another potential route for virus transmission from the crusts or scabs on the skin when same needle is utilized to provide mass vaccinations that can transfer LSD (Tuppurainen et al. 2015). It is generally known that quarantine cannot be the exclusive method of disease control, given the variety of vectors that this virus may use to spread (Al-Salihi 2014).

HOST RANGE:

Cattle and buffalo are the two most susceptible hosts to LSDV. However, compared to Bosindicus cattle, Bos Taurus animals have a somewhat higher propensity to develop LSD. Animals of all ages are equally vulnerable to this viral infection, while calves are much more susceptible also immune-deficient animals. According to reports, mucous Lesions appear in calves between 23 and 48 hours (Al-Salihi K.2014). Wild animals are immune to infection in their natural habitat, but a giraffe's experimental infection resulted in clinical lesions (Giraffecamelopardalis) as well as the impala (Aepycerosmelampus), the Arabian oryx (Oryx), springbok (Antidorcasmarsupialis), leucoryx, and oryxthomson's gazelle and (Oryx gazelle) The prevalence of wild and feral animals is thought to play a negligible part throughout the spread of illness (Davies FG. 1991).

TRANSBOUNDARY SPREAD:

In 1929, Zambia was where the sickness was first discovered. The disease quickly spread across the entire continent of Africa after this finding. Only a small number of nations, including Algeria, Libya, Tunisia, and Morocco, have escaped the wrath and devastation of this disease (Ali et al. 1990). Middle Eastern nations have boosted the shipping of animals from their neighbours in response to the region's rising food needs. Due to the transportation of infected animals from afflicted African nations, Egypt contracted LSD in 1988. Again in 2006, the disease reappeared as a result of unrestricted cow movement from nations producing African horn (Yeruham et al. 1995, Abutarbush et al. 2015).Because of restrictions of trade between Israels and the majority Arab nations, breakouts in Israel initially surprised most academics, but the situation became clear when importance of vectors in LSD transmission was thoroughly investigated. Scientist stated that LSD was transmitted by the stomoxycalcitrans vector originated in Egypt (Panel, E.A., 2016). The condition first manifested from 2012 to 2013 for the first time ever in Lebanon, Jordan, and Syria. The epidemic Israel and Syria's border appeared in Jordan demonstrating the global spread of illness (Gupta et al. 2020). In 2013 and 2014, the disease further spread to adjacent nations including Iran and Turkey. Later, LSD reports also came from Turkey, Azerbaijan, and Cyprus (Zhugunissov et al. 2020). The spread of LSD from Bangladesh to India served to confirm the notion that this illness is transponder (Sudhakar et al. 2020). A strict immunisation schedule may lower the prevalence of disease, according to earlier studies. As comparable circumstances are documented, lax measures against this sickness could lead to the recurrence in 2019. Epidemiological studies demonstrate that illness entered China across the border with Kazakhstan close to the village of Illi Kazakh in 2019 saw the reporting of 65 sick animals.

The condition Kazakhstan had previously been informed by 2016. Likewise, soon with the first-ever reporting of about 68 cases on july 2019 in Bangladesh, India was infected with the lumpy skin condition. LSD has persisted in farmers in eastern Russian areas and southern Turkish provinces are in hardship (Abutarbush, S.M., 2017). During the monsoon season August 2019 in the surrounding districts of Orissa, India recorded its first LSD epidemic. Lumpy skin disease outbreaks were observed in three separate locations concurrently in various parts of Orissa and odisha. The primary occurrences of 182 animals in India were discovered to have the sporadic illness lumpy skin. Negative for the illness. There were fatalities and non-fatal morbidity rates. In excess of 7.1% The virus isolated from Indian samples underwent phylogenetic analysis. Animal samples that have been affected have shown similarity of European strains versus southern part of Africa (Niesche, R. and Haase, M., 2012.).

SIGN AND SYMPTOMS:

The illness has a two - five week incubation period in living things, however under experimental circumstances, this time has been found to be reduced to seven - fourteen days. Clinically, LSD is exhibited in following forms: chronic, acute and sub-acute. At its mildest with the illness, there is initially sporadic fever followed by development of one or two skin nodules. Epiphora as well as malnutrition and the most challenging clinical signs to manage are agalactia. Erythema, Later stages of pruritis and nodular lesions become noticeable on the sepidermis. Sore wound on the groin, perineal, and or-nasal mucosae becomes obvious (Khan et al. 2021,).

Several lesions appear on the epidermis in the severe type, which lasts for approximately a week before they harden up and a narrow haemorrhagic loop on outer part of the body begins enclosing them. The wound are still healing, it could escalate to other part. These nodules' histopathology showed that they currently contained structures with an apparent ballooning degeneration pattern and eosinophilicintra cytoplasmic inclusion bodies. These wart-like lesions eventually develop attachments to the dermis and muscle(Salib et al. 2011).

Within two to three weeks, these exposed components dry out and harden, causing pain for moving animals. continual deterioration of these regions and poor re-epithelialization cause their development of "sit fast" fistulas, as they are sometimes called. These abrasions are reportedly frequently infected by screw worm flies or fly maggets larvae. In addition, secondary bacterial infections and suppuration may result in fatal septicaemia and severe septic shock (Gari et al.2010, Alemayehu et al. 2013). In certain situations, lymphadenitis is also seen. These nodules continue to slough necrotic material into the lungs as they infiltrate the respiratory mucosae, which resulting in pneumonia In severe circumstances, LSD has been linked to infertility and female bovine foetal abortion. unpleasant nodules on the male animals surrounding genitals could impair fertility( Al-Salihi K.2014).

IMPACT ON ECONOMY:

Lumpy skin is under the Office International des Epizooties (OIE) classification. A disease's propensity to spread internationally makes it a notifiable outbreak with agro terrorism as a threat[40]. The lumpy skin condition does not high mortality rate, hence the effects on the economy are much more indirect. Significant losses are experienced after the occurrence of this disease because conceal physical harm and body mass loss(Salib et al. 2011).The decline in animal quality has an impact on the entire market.. This could have significant financial consequences losses to the industries who gain from diary and for sectors of the industry depending on this animals, its leftovers. Industries, but also struggling farmers holding the dilemma that the livestock must endure as a result of disease. Losses overall due to milk, meat, beef, ethiopian draught authority, healthcare, and immunisation in local zebu, were expected about 6.42 USD. The illness significantly decreases milk quality. Additional effects like harmed skins and a reduction in cattle growth, abortion, and infertility death of afflicted animals and expenses for treatment and vaccination(Heine et al. 1999). The cost of supportive antibiotic treatment for an outbreak in Jordanper person was found to be 27.8 pound(Gari et al. 2010). Sheeppox and goatpox can also be caused by the causal agent, capripoxvirus, and both illnesses have economic relevance because they provide a significant barrier to trade between nations and the potential for economic bioterrorism agent.

DIAGNOSIS:

Lack of logistical support and familiarity with rare diseases prevent proper diagnosis is usually a difficult task. To make a differential diagnosis distinguish LSD from skin demodicosis or foot-and-mouth disease to confirm the diagnosis of LSD, histological evidence is required to accomplish this, samples should be kept in phosphate buffer immediately after collection, 20–50% saline and glycerol (Orlova et al. 2006). Skin samples also exhibit typical histological alterations, such as perivascular infiltration of white cells that results in thrombosis and vasculitis in the subcutis and dermis of the vessel. Cellular invasion of the "Cellesclavelauses," or epithelial cells, are the lesion of which are described as sheep fox. Gel precipitation from agar since the LSDV antigen is shared, the test is not specific for LSD along with other parapox and capripoxviruses.

It is possible to employ virus isolation to provide a definitive diagnosis at fresh new niches. the prepubescent lamb and cattle testicles, principal Additionally, secondary culture is most vulnerable to virus isolation.

PCR is the most effective and quick method for molecular diagnostics test to determine a disease's diagnosis. traditional and in-the-moment PCRs were created for quick diagnosis(Mangana-Vougiouka et al 1999). Vascular thrombosis, neutrophilic infiltration in the dermis and subcutis, as well as the presence of cytoplasmic inclusion bodies known as "cellesclavelauses" help to distinguish BHV-2 from LSDV, where syncytia and intranuclear inclusion bodies are seen.

PREVENTION:

Currentlytreatment of LSD doesnot exists anti-inflammatory and antibacterial medications are used to treat symptoms. To control the illness, efficient management and implementing preventive measures is necessary, such as:

a) Limit movement: Avoid allowing diseased animals to travel.To avoid the spread of international disease, restriction or banning of lumpy skin disease can be a major step. Animals should be isolated for inspection if they have such lesions within a country and can quickly slow down the diseasespread.

b) Restrict vector vectors may move as a result of the current winds cause the spread of disease. Methods of vector control, such as the in addition to using insecticides and vector traps, prevention methods include the illness.

c) Immunization: A live, attenuated vaccination accessible for LSD Depending on various LSD virus strains (Tuppurainen et al. 2015)

CONCLUSION:

Important livestock like cattle and buffaloes plays and important role in the global economy. Cattles and buffaloes are susceptible to the dangerous disease lumpy skin disease. Before recently spreading to India and other previously disease-free Asian nations, the disease was confined to Africa and a small number of other nations. This is concerning for the livestock rearing industry because the economics of the majority of these nations are built on agriculture. The expansion of this disease to more extensive geographic areas of the Indian subcontinent will undoubtedly have huge involvement on all sectors of the economy, but the rural economy in particular. LSD may also result in a decline in the export of cattle and livestock-related goods. To determine the true disease prevalence, the causes of LSD's introduction into India must be looked into, combined with epidemiological random screening in various areas. Besides, the only way to avoid the disease is through immunisation, efficient vector control measures, and quarantine.

REFERENCE:

1. Abutarbush, S.M., Ababneh, M.M., Al Zoubi, I.G., Al Sheyab, O.M., Al Zoubi, M.G., Alekish, M.O. and Al Gharabat, R.J. Lumpy Skin Disease in J ordan: Disease Emergence, Clinical Signs, Complications and Preliminary‐associated Economic Losses. Transboundary and Emerging Diseases. 2015; 62(5): 549-554.

2. Abutarbush, S.M., 2017. Lumpy skin disease (knopvelsiekte, pseudo-urticaria, neethling virus disease, exanthema nodularis bovis). Emerging and re-emerging infectious diseases of livestock. 2017; 309-326.

3. Al Rammahi, H.M. and Jassim, A. Epidemiological and diagnostic study of first lumpy skin disease outbreak in southern Baghdad district. Asian Academic Research Journal of Multidisciplinary. 2015; 1(30): 196-205.

4. Ali, A.A., Esmat, M., Attia, H., Selim, A. and Abdel-Hamid, Y.M., 1990. Clinical and pathological studies of lumpy skin disease in Egypt. Veterinary Record. 1990; 127(22): 549-550.

5. Ali, B.H. and Obeid, H.M. Investigation of the first outbreaks of lumpy skin disease in the Sudan. British Veterinary Journal. 1977; 133(2): 184-189.

6. Al-Salihi, K., 2014. Lumpy skin disease: Review of literature. Mirror of research in veterinary sciences and animals. 2014; 3(3): 6-23.

7. Alemayehu, G., Zewde, G. and Admassu, B. Risk assessments of lumpy skin diseases in Borena bull market chain and its implication for livelihoods and international trade. Tropical Animal Health and Production. 2013; 45: 1153-1159.

8. Annandale, C.H., Holm, D.E., Ebersohn, K. and Venter, E.H Seminal transmission of lumpy skin disease virus in heifers. Transboundary and Emerging Diseases. 2014; 61(5): 443-448.

9. Annandale, C.H., Irons, P.C., Bagla, V.P., Osuagwuh, U.I. and Venter, E.H. Sites of persistence of lumpy skin disease virus in the genital tract of experimentally infected bulls. Reproduction in Domestic Animals. 2010; 45(2): 250-255.

10. Beard, P.M. Lumpy skin disease: a direct threat to Europe. The Veterinary Record. 2016; 178(22): 557.

11. Biswas, P.K., Rahman, M.H., Das, A., Ahmed, S.S.U., Giasuddin, M. and Christensen, J.P. Risk for highly pathogenic avian influenza H5N1 virus infection in chickens in small‐scale commercial farms, in a high‐risk area, Bangladesh, 2008. Transboundary and Emerging Diseases. 2011; 58(6): 519-525.

12. Davies, F.G., Krauss, H., Lund, J. and Taylor, M. The laboratory diagnosis of lumpy skin disease. Research in Veterinary Science. 1971; 12(2): 123-128.

13. Davies, F.G. Lumpy skin disease of cattle: a growing problem in Africa and the Near East. World Animal Review. 1991; 68(3): 37-42.

14. El-Nahas, E.M., El-Habbaa, A.S., El-Bagoury, G.F. and Radwan, M.E. Isolation and identification of lumpy skin disease virus from naturally infected buffaloes at Kaluobia, Egypt. Global Veterinaria. 2011; 7(3): 234-237.

15. Gari, G., Waret-Szkuta, A., Grosbois, V., Jacquiet, P. and Roger, F., 2010. Risk factors associated with observed clinical lumpy skin disease in Ethiopia. Epidemiology & Infection. 2010; 138(11): 1657-1666

16. Giasuddin, M., Yousuf, M.A., Hasan, M., Rahman, M.H., Hassan, M.Z. and Ali, M.Z. Isolation and molecular identification of Lumpy Skin Disease (LSD) virus from infected cattle in Bangladesh. Bangladesh Journal of Livestock Research. 2019; 26(1-2): 15-20.

17. Gupta, T., Patial, V., Bali, D., Angaria, S., Sharma, M. and Chahota, R. A review: Lumpy skin disease and its emergence in India. Veterinary Research Communications. 2020; 44: 111-118.

18. Heine, H.G., Stevens, M.P., Foord, A.J. and Boyle, D.B. A capripoxvirus detection PCR and antibody ELISA based on the major antigen P32, the homolog of the vaccinia virus H3L gene. Journal of Immunological Methods. 1999; 227(1-2): 187-196.

19. Kahana‐Sutin, E., Klement, E., Lensky, I. and Gottlieb, Y. High relative abundance of the stable fly Stomoxys calcitrans is associated with lumpy skin disease outbreaks in Israeli dairy farms. Medical and Veterinary Entomology. 2017; 31(2): 150-160

20. King, A.M., Lefkowitz, E., Adams, M.J. and Carstens, E.B. eds., 2011. Virus taxonomy: ninth report of the International Committee on Taxonomy of Viruses (Vol. 9). Elsevier.

21. Khan, Y.R., Ali, A., Hussain, K., Ijaz, M., Rabbani, A.H., Khan, R.L., Abbas, S.N., Aziz, M.U., Ghaffar, A. and Sajid, H.A. A review: Surveillance of lumpy skin disease (LSD) a growing problem in Asia. Microbial pathogenesis. 2021; 158: 105050

22. Khwannimit, B. and Bhurayanontachai, R. The epidemiology of, and risk factors for, mortality from severe sepsis and septic shock in a tertiary-care university hospital setting. Epidemiology & Infection. 2009; 137(9): 1333-1341.

23. Kononov, A., Byadovskaya, O., Kononova, S., Yashin, R., Zinyakov, N., Mischenko, V., Perevozchikova, N. and Sprygin, A. Detection of vaccine-like strains of lumpy skin disease virus in outbreaks in Russia in 2017. Archives of Virology. 2019; 164(6): 1575-1585.

24. Liang, Z., Yao, K., Wang, S., Yin, J., Ma, X., Yin, X., Wang, X. and Sun, Y. Understanding the research advances on lumpy skin disease: A comprehensive literature review of experimental evidence. Frontiers in Microbiology. 2022; 13.

25. Lubinga, J.C., Clift, S.J., Tuppurainen, E.S., Stoltsz, W.H., Babiuk, S., Coetzer, J.A. and Venter, E.H. Demonstration of lumpy skin disease virus infection in Amblyomma hebraeum and Rhipicephalus appendiculatus ticks using immunohistochemistry. Ticks and tick-borne diseases. 2014; 5(2): 113-120.

26. Mangana-Vougiouka, O., Markoulatos, P., Koptopoulos, G., Nomikou, K., Bakandritsos, N. and Papadopoulos, O. Sheep poxvirus identification by PCR in cell cultures. Journal of Virological Methods. 1999; 77(1): 75-79.

27. Mulatu, E. and Feyisa, A., 2018. Journal of Veterinary Science & Technology.

28. Namazi, F. and Khodakaram Tafti, A. Lumpy skin disease, an emerging transboundary viral disease: A review. Veterinary Medicine and Science. 2021; 7(3): 888-896.

29. Niesche, R. and Haase, M., Emotions and ethics: A Foucauldian framework. 2012.

30. Orlova, E.S., Shcherbakov, A.V., Diev, V.I. and Zakharov, V.M. Differentiation of capripoxvirus species and strains by polymerase chain reaction. Molecular Biology. 2006; 40(1).

31. Panel, E.A. Statement: Urgent advice on lumpy skin disease. EFSA Journal. 2016; 14(8): 4573.

32. Quinn, P.J., Markey, B.K., Leonard, F.C., FitzPatrick, E.S. and Fanning, S. Concise Review of Veterinary Microbiology. 2015.

33. Salib, F.A. and Osman, A.H. Incidence of lumpy skin disease among Egyptian cattle in Giza Governorate, Egypt. Veterinary World. 2011; 4(4).

34. Sudhakar, S.B., Mishra, N., Kalaiyarasu, S., Jhade, S.K., Hemadri, D., Sood, R., Bal, G.C., Nayak, M.K., Pradhan, S.K. and Singh, V.P. Lumpy skin disease (LSD) outbreaks in cattle in Odisha state, India in August 2019: Epidemiological features and molecular studies. Transboundary and Emerging Diseases. 2020; 67(6): 2408-2422.

35. Tulman, E.R., Afonso, C.L., Lu, Z., Zsak, L., Sur, J.H., Sandybaev, N.T., Kerembekova, U.Z., Zaitsev, V.L., Kutish, G.F. and Rock, D.L. The genomes of sheeppox and goatpox viruses. Journal of Virology. 2002; 76(12): 6054-6061.

36. Tulman, E.R., Afonso, C.L., Lu, Z., Zsak, L., Kutish, G.F. and Rock, D.L. Genome of lumpy skin disease virus. Journal of Virology. 2001; 75(15): 7122-7130.

37. Tuppurainen, E.S., Lubinga, J.C., Stoltsz, W.H., Troskie, M., Carpenter, S.T., Coetzer, J.A., Venter, E.H. and Oura, C.A. Evidence of vertical transmission of lumpy skin disease virus in Rhipicephalus decoloratus ticks. Ticks and Tick-borne Diseases. 2013; 4(4): 329-333.

38. Tuppurainen, E.S., Venter, E.H., Coetzer, J.A. and Bell-Sakyi, L. Lumpy skin disease: attempted propagation in tick cell lines and presence of viral DNA in field ticks collected from naturally-infected cattle. Ticks and Tick-borne Diseases. 2015; 6(2): 134-140.

39. Tuppurainen, E., Alexandrov, T. and Beltrán-Alcrudo, D.J.F.A.P., Lumpy skin disease-a manual for veterinarians. FAO Animal Production and Health Manual. 2017; 20.

40. Yeruham, I., Nir, O., Braverman, Y., Davidson, M., Grinstein, H., Haymovitch, M. and Zamir, O. Spread of lumpy skin disease in Israeli dairy herds. Veterinary Record. 1995; 137: 91-91.

41. Zhugunissov, K., Bulatov, Y.E., Orynbayev, M., Kutumbetov, L., Abduraimov, Y.E., Shayakhmetov, Y.E., Taranov, D., Amanova, Z.H., Mambetaliyev, M., Absatova, Z.H. and Azanbekova, M. Goatpox virus (G20-LKV) vaccine strain elicits a protective response in cattle against lumpy skin disease at challenge with lumpy skin disease virulent field strain in a comparative study. Veterinary Microbiology. 2020; 245: 108695.

Received on 27.12.2022 Modified on 17.03.2023

Asian J. Res. Pharm. Sci. 2024; 14(1):43-50.

DOI: 10.52711/2231-5659.2024.00007