Epidemiological investigation of lumpy skin disease in Jhenaidah district of Bangladesh

Lumpy Skin disease (LSD) is an economically important disease in cattle caused by the LSD virus (LSDV) of the genus Capripoxvirus, while pseudocowpox (PCP) is a widely distributed zoonotic cattle disease caused by the PCP virus (PCPV) of the genus Parapoxvirus. Though both viral pox infections are reportedly present in Nigeria, similarities in their clinical presentation and limited access to laboratories often lead to misdiagnosis in the field. This study investigated suspected LSD outbreaks in organized and transhumance cattle herds in Nigeria in 2020. A total of 42 scab/skin biopsy samples were collected from 16 outbreaks of suspected LSD in five northern States of Nigeria. The samples were analyzed using a high-resolution multiplex melting (HRM) assay to differentiate poxviruses belonging to Orthopoxvirus, Capripoxvirus, and Parapoxvirus genera. LSDV was characterized using four gene segments, namely the RNA polymerase 30 kDa subunit (RPO30), G-protein-coupled receptor (GPCR), the extracellular enveloped virus (EEV) glycoprotein and CaPV homolog of the variola virus B22R. Likewise, the partial B2L gene of PCPV was also analyzed. Nineteen samples (45.2%) were positive according to the HRM assay for LSDV, and five (11.9%) were co-infected with LSDV and PCPV. The multiple sequence alignments of the GPCR, EEV, and B22R showed 100% similarity among the Nigerian LSDV samples, unlike the RPO30 phylogeny, which showed two clusters. Some of the Nigerian LSDVs clustered within LSDV SG II were with commonly circulating LSDV field isolates in Africa, the Middle East, and Europe, while the remaining Nigerian LSDVs produced a unique sub-group. The B2L sequences of Nigerian PCPVs were 100% identical and clustered within the PCPV group containing cattle/Reindeer isolates, close to PCPVs from Zambia and Botswana. The results show the diversity of Nigerian LSDV strains. This paper also reports the first documented co-infection of LSDV and PCPV in Nigeria.

Detection of lumpy skin disease (LSD) virus and distribution of blood-sucking insects as potential vector in Indonesia.

Lumpy skin disease (LSD), an economically significant disease in cattle caused by lumpy skin disease virus (LSDV), is endemic to nearly all of Africa. Since 2012, LSDV has emerged as a significant epizootic pathogen given its rapid spread into new geographical locations outside Africa, including the Middle East, Eastern Europe, and Asia. To assess the genetic diversity of LSDVs in East Africa, we sequenced and analyzed the RPO30 and GPCR genes of LSDV in twenty-two archive samples collected in Ethiopia, Kenya, and Sudan before the appearance of LSD in the Middle East and its incursion into Europe. We compared them to publicly available sequences of LSDVs from the same region and those collected elsewhere. The results showed that the East African field isolates in this study were remarkably similar to each other and to previously sequenced field isolates of LSDV for the RPO30 and GPCR genes. The only exception was LSDV Embu/B338/2011, a field virus collected in Kenya, which displayed mixed features between the LSDV Neethling vaccine and field isolates. LSDV Embu/B338/2011 had the same 12-nucleotide insertion found in LSDV Neethling and KS-1 vaccines. Further analysis of the partial EEV glycoprotein, B22R, RNA helicase, virion core protein, NTPase, and N1R/p28-like protein genes showed that LSDV Embu/B338/2011 differs from previously described LSDV variants carrying the 12-nucleotide insertion in the GPCR gene. These findings highlight the importance of the constant monitoring of genetic variation among LSDV isolates.

BackgroundLumpy skin disease (LSD) is an infectious viral disease of cattle caused by a Capripoxvirus. LSD has substantial economic implications, with infection resulting in permanent damage to the skin of affected animals which lowers their commercial value. In Uganda, LSD is endemic and cases of the disease are frequently reported to government authorities. This study was undertaken to molecularly characterize lumpy skin disease virus (LSDV) strains that have been circulating in Uganda between 2017 and 2018. Secondly, the study aimed to determine the phylogenetic relatedness of Ugandan LSDV sequences with published sequences, available in GenBank.ResultsA total of 7 blood samples and 16 skin nodule biopsies were screened for LSDV using PCR to confirm presence of LSDV nucleic acids. PCR positive samples were then characterised by amplifying the GPCR gene. These amplified genes were sequenced and phylogenetic trees were constructed. Out of the 23 samples analysed, 15 were positive for LSDV by PCR (65.2%). The LSDV GPCR sequences analysed contained the unique signatures of LSDV (A11, T12, T34, S99, and P199) which further confirmed their identity. Sequence comparison with vaccine strains revealed a 12 bp deletion unique to Ugandan outbreak strains. Phylogenetic analysis indicated that the LSDV sequences from this study clustered closely with sequences from neighboring East African countries and with LSDV strains from recent outbreaks in Europe. It was noted that the sequence diversity amongst LSDV strains from Africa was higher than diversity from Eurasia.ConclusionThe LSDV strains circulating in Uganda were closely related with sequences from neighboring African countries and from Eurasia. Comparison of the GPCR gene showed that outbreak strains differed from vaccine strains. This information is necessary to understand LSDV molecular epidemiology and to contribute knowledge towards the development of control strategies by the Government of Uganda.

Lumpy skin disease virus (LSDV) infection poses a significant threat to global cattle farming. Currently, effective therapeutic agents are lacking. TMP269, a small molecule inhibitor of class IIa histone deacetylase inhibitor, plays a vital role in cancer therapy. In this study, we demonstrated that TMP269 treatment inhibits the early-stage replication of LSDV in a dose-dependent manner. RNA sequencing data revealed that metabolism-related signaling pathways were significantly enriched after LSDV infection. Furthermore, untargeted metabolomics analysis revealed that lysophosphatidic acid (LPA), a key metabolite of the glycerophospholipid pathway, was upregulated following LSDV infection and downregulated after TMP269 treatment. In addition, exogenous LPA promotes LSDV replication by activating the mitogen-activated protein kinase (MEK)/extracellular-signal-regulated kinase (ERK) signaling pathway and suppressing the host's innate immune response. Furthermore, treatment with the LPA receptor inhibitor Ki16425 suppressed LSDV replication and promoted the host's innate immune response. These findings suggest that LSDV infection can induce LPA expression and aid viral activation of the MEK/ERK signaling pathway and escape of the host's innate immune response, whereas TMP269 treatment can inhibit LPA production and limit its promotion of LSDV replication. These data identified the antiviral mechanism of TMP269 and a novel mechanism by which LSDV inhibits host innate immune responses, providing insights into the development of new preventive or therapeutic strategies targeting altered metabolic pathways.IMPORTANCELumpy skin disease virus (LSDV) poses a significant threat to global cattle farming. Owing to insufficient research on LSDV infection, pathogenesis, and immune escape mechanisms, prevention and control methods against LSDV infection are lacking. Here, we found that TMP269, a class IIa histone deacetylase inhibitor, significantly inhibited LSDV replication. We further demonstrated that TMP269 altered LSDV infection-induced host glycerophospholipid metabolism. In addition, TMP269 decreased the accumulation of lysophosphatidic acid (LPA), a key metabolite in glycerophospholipid metabolism, induced by LSDV infection, and exogenous LPA-promoted LSDV replication by activating the mitogen-activated protein kinase (MEK)/extracellular-signal-regulated kinase (ERK) signaling pathway and suppressing the host innate immune response. Our findings identified the antiviral mechanism of TMP269 and a novel mechanism by which LSDV manipulates host signaling pathways to promote its replication, offering insights into the development of novel antiviral agents against LSDV infection.

Lumpy skin disease (LSD) has emerged as a threat to cattle production in Asia, and India has been facing LSD epidemics since 2019. Although water buffalo (Bubalus bubalis) is susceptible to natural LSDV infection, there have been no confirmed reports of LSDV infection in water buffalo in India. In this study, we investigated suspected cases of LSD in water buffaloes from 12 Indian states and one union territory during 2020-2023. Buffaloes showed mild to moderate clinical disease with fever and nodular skin lesions, but most remained asymptomatic. Eighteen of 177 (10.18%) buffaloes in 12 districts in three states tested positive for LSDV by real-time PCR, while 22 of 57 (38.59%) from nine districts in six states tested positive for LSDV-neutralizing antibodies, demonstrating the prevalence of LSDV infection in buffaloes over a wider geographic area. Successful virus isolation and nucleotide sequencing confirmed natural LSDV infection in buffaloes. Phylogenetic analysis of complete GPCR, RPO30, and EEV gene sequences revealed the presence of wild-type strains of two divergent LSDV lineages (1.2.1 and 1.2.2) in buffaloes. The 1.2.2 strains were closely related to the dominant LSDV strain (subcluster 1.2.2, KSGP-like) circulating in India, while the 1.2.1 strains clustered with strains from the Middle East, Europe, and the Balkans, confirming that there have been multiple introductions of LSDV into India. The detection of viruses with identical sequences in buffaloes and local cattle implied that the LSDV strain found in buffaloes is probably of cattle origin. We also found evidence of cocirculation of LSDV 1.2.1 and 1.2.2 wild-type strains in the same area, highlighting the importance of LSDV surveillance and genetic analysis. This is the first confirmed report of natural LSDV infection in water buffaloes in India. Further investigations are needed to assess the impact of LSDV infection in buffalo production and the role of buffalo in LSD epidemiology.

Introduction. Lumpy skin disease (LSD) is currently a matter of veterinary concern due to the significant economic losses of the live stock in dustry. The risk of LSD spread and penetration into the disease-free countries is increasing every year. Therefore, timely monitoring of the infection spread for the development a strategy for this disease control becomes of current importance. Description of thedisease manifestations and course, evaluation of historical and statistical data on LSD spread in the Middle Eastern countries as well as the further joint actions at the international level are presented in this review.Objective. Analysis of historical and statistical data on clinical lumpy skin disease in the Middle Eastern countries.Materials and methods. The following electronic databases were used for relevant data searching and collection: PubMed, Web of Science, eLIBRARY.RU, mdpi.com, frontiersin.org, researchgate.net, etc. English literature data for 10 years were analyzed.Results. In 1988 LSD spread outside the African continent then LSD stayed for a short time within the MiddleEastern countries and two years later spread further to the west and east. Despite the further spread, recurrent LSD outbreaks were reported in the Middle Eastern countries over the next few years. Many countries in the Middle East still face the problem of uncontrolled livestock movement, lack of high-quality laboratory diagnostics, and irregular contacts with international health and surveillance organizations aggravated by the unstable political situation in the region. These problems indicate the importance of LSD control at the international level, the significance of regional and international cooperation and effective biosafety policies.Conclusion. Role of the Middle East region in LSD virus spread, probable causes of LSD infection in the region, trends for further actions for LSD control were determined.

BackgroundLumpy skin disease (LSD) is a contagious viral disease of cattle caused by lumpy skin disease virus (LSDV). LSD has recently spread in Asia following outbreaks in the Middle East and Europe. The disease emerged in Bangladesh in July 2019 in the Chattogram district, then rapidly spread throughout the entire country. We investigated six LSD outbreaks in Bangladesh to record the clinical signs and collect samples for diagnostic confirmation. Furthermore, we performed the molecular characterization of Bangladesh isolates, analyzing the full RPO30 and GPCR genes and the partial EEV glycoprotein gene.ResultsClinical observations revealed common LSD clinical signs in the affected cattle. PCR and real-time PCR, showed the presence of the LSDV genome in samples from all six districts. Phylogenetic analysis and detailed inspection of multiple sequence alignments revealed that Bangladesh isolates differ from common LSDV field isolates encountered in Africa, the Middle East, and Europe, as well as newly emerged LSDV variants in Russia and China. Instead, they were closely related to LSDV KSGP-0240, LSDV NI2490, and LSDV Kenya.ConclusionsThese results show the importance of continuous monitoring and characterization of circulating strains and the need to continually refine the strategies for differentiating vaccine strains from field viruses.

Lumpy skin disease virus (LSDV) causes lumpy skin disease in cattle and buffaloes, which is associated with significant animal production and economic losses. Since the 2000s, LSDV has spread from Africa to several countries in the Middle East; Europe; and Asia; including, more recently, several south-east Asian countries. In November 2020, Myanmar reported its first LSD outbreak. This study reports on the first incursion of LSD in Myanmar and the molecular analysis of the LSDV detected. Staff from the Livestock Breeding and Veterinary Department (LBVD) of the Ministry of Agriculture, Livestock, and Irrigation collected samples from cattle with suspected LSD infection. The Food and Agriculture Organization (FAO) of the United Nations’ Emergency Centre for Transboundary Animal Diseases (ECTAD) and the Joint International Atomic Energy Agency (IAEA)/FAO program’s Animal Health and Production laboratory provided LSDV diagnostic support to two regional veterinary diagnostic laboratories in Myanmar. Samples from 13 cattle tested positive by real-time PCR. Selected samples underwent sequence analysis in IAEA laboratories. The results show that the Myanmar LSDV sequences clustered with LSDV isolates from Bangladesh and India, LSDV Kenya, and LSDV NI-2490. Further characterization showed that the Myanmar LSDV is 100% identical to isolates from Bangladesh and India, implying a common source of introduction. These findings inform diagnosis and development of control strategies.

Madin-Darby bovine kidney (MDBK) cells are a suitable cell line for the propagation and study of the bovine poxvirus lumpy skin disease virus

Since 2012, lumpy skin disease virus (LSDV) has been spreading from the Middle East to south-east Europe and Russia. Although vaccination campaigns have managed to contain LSDV outbreaks, the risk of further spread is still high. The most likely route of LSDV transmission in short distance spread is vector-borne. Several arthropod species have been suggested as potential vectors, but no proven vector has yet been identified. To check whether promiscuous-landing synanthropic flies such as the common housefly (Musca domestica) could be involved, we carried out entomological trapping at the site of a recent LSDV outbreak caused by a vaccine-like LSDV strain. The presence of vaccine-like LSDV DNA was confirmed by the assay developed herein, the assay by Agianniotaki etal. (2017) and RPO30 gene sequencing. No evidence of field LSDV strain circulation was revealed. In this study, we discovered that M.domestica flies carried vaccine-like LSDV DNA (Ct >25.5), whereas trapped stable flies from the same collection were negative for both field and vaccine LSDV. To check whether flies were contaminated internally and externally, 50 randomly selected flies from the same collection were washed four times and tested. Viral DNA was mainly detected in the 1st wash fluid, suggesting genome or even viral contamination on the insect cadaver. In this study, internal contamination in the insect bodies without differentiation between the body locations was also revealed; however, the clinical relevance for mechanical transmission is unknown. Further work is needed to clarify a role of M.domestica in the transmission of LSDV. To our knowledge, this is the first report demonstrating that an attenuated LSD vaccine strain has been identified in Russian cattle given the ban on the use of live attenuated vaccines against LSDV.

Lumpy Skin Disease (LSD) is caused by Lumpy Skin Disease Virus (LSDV), a member of the Capripoxvirus genus of the Poxviridae family. LSD was first introduced in Zambia in the 1920s, Since then LSD has been transported to parts of Asia, the Middle East, and Europe and presents a real danger to livestock. It is mainly spread by biting insects, such as mosquitoes, ticks, flies, and direct contact. LSD can be diagnosed clinically by features like fever, enlarged lymph nodes, punched-out skin lesions that slough or ulcerate, as well as respiratory and gastrointestinal involvement. Animals affected by this disease have lower milk yields, sterility, and secondary infections that lead to substantial economic losses. Morbidity is often high and may differ widely between species and herds, while mortality is usually low but may rise in cases of serious outbreaks in animals with weak immunity. PCR, serological tests, or viral isolation often do confirmation of the diagnosis. Several strategies can be implemented, such as improving stewardship, including biosecurity measures, controlling vectors, and vaccinations. For controlling LSD outbreaks, live attenuated and recombinant vaccines are most commonly used, with certain difficulties in reaching coverage in affected areas. Direct economic losses caused by LSD are attributed to a decrease in output, restrictions on trade, and an increase in veterinary costs. A qualitative study of the geographical spread of LSD indicates that there is a growing need for better surveillance activities as well as cooperation among countries. This review aims to understand the papers on LSD from epidemiology, clinical presentations, diagnostic techniques, and lastly, addressing the principles of control of LSD with a focus on preventive methods.

Lumpy skin disease (LSD) is an economically devastating emerging viral disease of cattle. Lumpy skin disease is currently endemic in most African countries and has recently spread out of Africa into the Middle East region. In this article, we review the putative mechanisms of spread of LSD into the Middle East and the risks of further spread into Turkey, Europe and Asia. We also review the latest findings on the epidemiology of LSD, its mechanisms of transmission, the potential role of wildlife in its maintenance and spread and the diagnostic tests and control methods currently available.

Lumpy skin disease (LSD) is a viral disease of cattle caused by lumpy skin disease virus (LSDV). LSDV shares high degree of sequence homology with goatpox virus (GTPV) and sheeppox virus (SPPV), the two other members of the genus Capripoxvirus of the family Poxviridae. Genetically LSDV is a double-stranded DNA genome of approximately 151 kbp. LSD is an economically important and notifiable animal disease by the World Organisation for Animal Health (OIE). Clinically LSD is characterized by fever and the appearance of nodules on the skin and mucous membranes. In severe and chronic cases, nodular skin lesions cover the entire body and become deep scab and eroded. Transmission of the disease occurs predominantly by insects possibly through mechanical vectors, contaminated feed and water, infected saliva, and rarely natural contact. LSD is endemic in many African countries and mostly coexists with sheeppox and goatpox. Recently, LSD has been rapidly spreading to the Middle East, Turkey, and Russia, the Balkan and European Union countries. Diagnosis is mainly based on observation of clinical signs and the detection of virus genome using conventional and real-time PCR methods. In Africa, prevention and control of LSD relies on vaccination using live attenuated vaccines derived from Kenyan or South African LSDV strains. Vaccine that can allow the differentiation of infected from vaccinated animals (DIVA) and high-throughput serological method for the detection of specific antibody need to be developed. Alternatively, a 12 nucleotide deletion that exists only on the G-protein-coupled chemokine receptor gene of LSDV field isolates can be used to differentiate wild-type from vaccine strains by sequencing and real-time PCR.

Lumpy skin disease (LSD) is a devastating viral disease of cattle which has recently spread from Africa into the countries of the Middle East. The aim of the present study was to investigate the relationships among lumpy skin disease viruses (LSDV) isolated from different regions of Iran and the origin and spread of these viruses. In this study, a total of 234 blood samples from clinically affected animals from four provinces in the northwest of Iran were screened for LSDV using polymerase chain reaction (PCR). From 80 positive samples for LSDV detected by PCR, the partial P32 gene (759bp) of 12 isolates were sequenced and phylogenetically analyzed. LSD viruses were grouped in three subclusters with an overall 97.1-100% nucleotide identity. LSDVs isolated from Gilan showed lowest nucleotide identity with the other LSDVs. Four isolates of LSDV including KO-1, EA-1, EA-3, and WA-3 showed 100% similarity with each other and also with the Neethling strain. Phylogenetic analysis indicated that the identified LSDVs were closely related to each other and had high-sequence homology with other LSDV isolates from Africa. It was concluded that LSD outbreak probably occurred in the northwest of Iran by LSDVs entering the country from Iraq and P32 nucleotide sequence information obtained in the present study is a valuable resource in understanding the genetic nature and molecular epidemiology of local LSDV isolates which can be used for future vaccine development based on the circulating strains in the region.