Paper 8851

ISSN (Online) 2581-9429
IJARSCT
International Journal of Advanced Research in Science, Communication and Technology (IJARSCT)
Volume 3, Issue 2, March 2023

Impact Factor: 7.301
Lumpy Virus and Skin Infection: A Review

Akanksha Omprakash Deshmukh1, Khushbu Sudhakar Tiwari2, Shubham Kale3,
Suraj B. Rathod4, Nitin B. Kohale5
Student1,2, Faculty3,4 and Principal5
Vardhman College of Pharmacy, Koli, Karanja (Lad), Washim, Maharashtra, India
[email protected]
Abstract: Lumpy skin disease (LSD) responsible for losses in the lives of animals. It is caused due to the
virus called Lumpy skin disease virus (LSDV). It belongs to the family Poxviridae and genus Capripoxvirus.
It includes sheep pox virusas well as goat pox virus. This disease mainly affect cattle and water buffaloes. The
transmission of virus is through the arthropod vectors. it is manifested by characteristics like skin nodules,
pyrexia, nasal discharge, swelling of superficial lymph node, lachrymation. The disease is first observed in
African and Middle East countries but has started spreading from China and Bangladesh sharing borders
with India. LSD causes in female abortions and in male sterility. It can also cause the milk and beef
production. This review aims to summaries the latest developments in the epidemiology with the focus on
spread, aetiology and transmission, clinical presentations, diagnostics and management of the disease.
Keywords: Lump skin disease, animal, India, Virus
I. INTRODUCTION
Production of livestock is one of the principle of achieving living standards to develop the world. The livestock holds
about 40%value of agriculture globally, itsupports the live hoods and provide food security to a billion of people [1]. The
disease is native to African countries but recently the disease has been reported from all over around the world. The first
case of LSD was reported from Zambiain 1929 [2] and then in southern and northern African countries. Later on, it
spread to Israel, Kuwait, Oman and Yemen [3]. According to OIE, at present thisdisease is prevalent in countries
including various African, European countries [4]. This disease can be diagnosed by transmission electron microscopic
(TEM), immune-peroxidase (IMP) staining, antigen trapping enzyme-linked immunosorbent assay (ELISA) anda
polymerase chain reaction [PCR] test. Thereis no proper treatment for LSD. whereas, relative treatment should be given
to animals which are infected to alleviate analytical indication and to control all secondary issues. Immunization is one
of the effective method for susceptible animals to control the disease in South Africa, and the effective vaccines are
madefrom the Neethling strain virus [5].
AETIOLOGY
Lumpy skin disease virus (LSDV) is responsible for causing Lumpy skin Poxviridae family that holds group of viruses
causing diseases in most of the domestic animals but dog is exceptional here. These contain two
subfamilies:Chordopoxvirinae, it contaminate vertebrate host and Entomopoxvirinae infecting invertebrate hosts [6]. The
subfamily Chordopoxvirinae, it comprises 10 genera and it includes Capri poxvirus genus. Three species of genus
contains viruses of three species they are sheep pox virus (SPPV), goat poxvirus (GTPV)and lumpy skin disease virus
(LSDV) infecting sheep, goat and cattle, respectively [7]. LSDV is a brick shaped enveloped virus and it has 320 × 260
nm size, with double stranded DNA have complex symmetry and replicates in cytoplasm of the host cell (Fig1). The
LSDV genome is 151 kbp large, it containa central coding area surrounded with similar 2.4kbp- inverted terminal
repeats and has156 putative genes. LSDV contains 30 structural and non-structural genesas same as sheep pox and goat
pox virus sharing 97% nucleotide identity [8]. Loss of gene limits the host range of poxviruses in subsequent evolution
and identical pattern has been seen within Capri poxviruses after comparing SPPV, GTPV and LSDV. The terminal
areas of LSDV virus encodes nine genes including IL-1 receptor, vaccinia virus F11L, N2L, K7 L genes, myxoma virus
M003.2 and M004.1, LSDV unique gene LSDV132 with likewise virulence and host range functions disrupted by
accumulated mutations both in SPPV and GTPV. However, this disruption does not affect the sequence length of
genome of three viruses but absence of these genes in SPPV and GTPV suggests the role in host restriction to bovines
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only [9][10]. In comparison with other Chordo pox viruses, LSD virus has146 conserved genes encoding proteins
involved in DNA replication, transcription, mRNA synthesis, nucleotide metabolism, structure formation and stability,
virulence and host range. The central region genes shareaverage of 65% collinearity and amino acid identity with gene
of other poxvirusin particular with sui pox virus, leporipoxvirus, and yata pox virus. The terminal region, there is
difference in the genes involved in viral virulence and host range with either absence or disruption sharing lower
percentage of amino acid identity with an average of 43% only. LSDV contains homologues genes such as interleukin-
10 (IL10), IL-1 binding proteins, G protein-coupled CC chemokine receptor (GPCR), and epidermal growth factor-like
proteinwhich are found in other poxvirus genera [11].

Fig.1. Morphology of LSDV
EPIDEMIOLOGY
Lumpy skin disease has a geographical distribution [12] as the disease was first observed in 1929 in Zambia earlier, it
was considered to be the result either of poisoning or a hypersensitivity due to insect bites as at that time was it the year
when populations of insects biting were highest between 1943 and 1945, cases appeared in Botswana, Zimbabwe [13].
LSD was limited to countries in sub-Saharan Africa from 1929 to 1986 (Fig. 2) and it’s native in most African countries
including Madagascar. This Followed by reports of the virus in the Middle East Since 2012 LSD has been expanded
onan unusually wide range throughout Middle Eastern countries as eventually yearswas reported from Oman, Yemen,
Israel, Kuwait, Bahrain, Egypt, Iran, Saudi Arabia Lebanon, Jordan, and in United Arab Emerate[14]. The data
examinationfrom the national disease outbreak report database during the period 2000-2009 showed that major
epidemic outbreaks of LSD occurred in 2000/2001 in the northern parts of the country in Amhara and West Oromia
regions. Then it lengthen to the central and the southern parts of the country, in 2003 and 2004 covering bulky parts of
Oromia and Southern Nation, Nationalities and Peoples (SNNP) domains. In 2006, 2007 other large outbreak come out
in Tigray, Amharaand Benishangul areas in the northern and north western parts of the country[15]. Therefore from 2007
up to 2009 the outbreak number progressively increased inOromia Region situated in the central part of the country.
According to 2010 annual report of Ministry of Agriculture, Animal and plant health regulatory directorate in the
department of epidemiology prevalence of the disease indifferent regional state of the country shows us; 1.63%, 0.49%,
5.2%, 2.69%, 0.37%, 0.7%, and 3.8% in Addis Abeba, Amhara, Gambela, Oromia, SNNP, Somali and Tigray regions
respectively. The 2011 annual report shows prevalence of; 0.36%, 1.13%, 0.22%, 0.65%, 0.24% and 0.30% in Amhara,
Gambela, Oromia, SNNP, Tigray areas respectively[16].

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Fig.2. Global distribution of LSD
II. TRANSMISSION OF LSDV

Evaluate (Fig.3) the epidemiology of the virus the mechanism of LSDV transmission is useful. This mechanism helps
for a give a strategy and extinction of disease [17,18]. An epitome for possible modes of transmission of LSDV in given
fig.3
Fig.3. Epitome of possible modes of transmission of LSDV
PATHOGENESIS
There have been some (Fig.4) observations held on pathogenesis of LSD in cattles [19]. The basic symptom of LSD are
fever, viremia followed by appearing inflammatory nodules and localisation in skin [20]. LSDV is also detected in saliva,
semen and in nodules of skin at least for 11, 42 and 39 days after development of fever respectively [21,22]. LSD skin
nodules may give serum atthe begining but develop a characteristic inverted greyish pink conical zone of necrosis.
Adjoining tissue gives congestion, hemorrhages and oedema. Thenecrotic cores become isolate from the adjacent skin
and are mention to as ‘sit- fasts’. Multiple virus encoded factors are produced during infection, which influence
pathogenesis and disease [23]. The routes which are used in experimental infections are intravenous, intradermal and
subcutaneous. Severe generalized infection are being developed by intravenous route, 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 nodes, develop after subcutaneous or intradermal inoculation of cattle with LSDV[24].

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Fig.4.Pathogenesis of LSDV
DIAGNOSIS
Field diagnosis (Fig.5) of LSD is often depend on characteristic clinical signs ofthe disease. However, mild and
subclinical forms require rapid and reliable laboratory testing to confirm diagnosis [25]. Molecular diagnosis with the help
ofPCR is most easy, applicable and fast test for the diagnosis of this disease. Convinient and real-time PCR have been
developed for time saving diagnosis ofLSD [26]. Differentiation of LSDV from other Capri poxvirus by real- time
PCRhas been developed [27]. Rapid diagnostic verification of the indefinite field diagnosis is basic for the successful
control and elimination of LSD in native andparticularly in non-native countries. There are some diseases having same
sign asLSD. LSD can be confused with the following diseases:
Pseudo-lumpy-skin disease
Bovine virus diarrhoea/mucosal diseaseDemodicosis (Demodex)
Bovine malignant catarrhal fever (Snotsiekte) Rinderpest
Besnoitiosis Oncocercariasis Insect bite allergies
Fig.5.The diagnostic procedures of the LSD

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III. CLINICAL SIGN AND LESSIONS
The incubation (Fig 6) period of the disease in natural conditions ranges from 2 to 5 weeks, while in experimental
conditions it ranges from 7 to 14 days. There are three forms of LSD: acute, subacute and chronic. The disease beginswith
a biphasic fever. The clinical manifestations of a mild infection are fever, weakness, eye discharge, and massesof one or
two nodules within a few days ofthe onset of anthrax. Subsequently, painful, hyperemic nodular lesions were observed
on the body of the animal, especially on the muzzle, nostrils, back, legs,scrotum, perineum, eyelids, lower ears, mucous
membranes of the nose and mouth, and the skin of the tail [28].
Fig.6. LSD in cattle
ECONOMIC IMPORTANCE
The World Organization for Animal Health (OIE) has classified LSD as a diseaseof note due to its economic impact. It
has been considered an agent of agroterrorism due to its ability to spread from Africa to other parts of the world [29].
Animal degradation affects the entire trade in live animals and animal products. This can lead to huge economic losses in
the meat, dairy, leather and other industries related to livestock and their by-products. in danger. Total losses of milk,
meat, beef, drafts, treatments and vaccines in Ethiopia have beenestimated at $6.43 per person for native Zebus and $58
per person for Holstein Friesians (30).
TREATMENT
Lumpy skin disease is caused due to virus and hence has no identified cure. However, to treat secondary bacterial
infections or to deal with fever 10 or inflammation or to improve animal’s apetite antibiotvs, anti-inflammatory drugs or
shots of vitamins are used.
Vaccination in Endemic Areas:

Immunity gained from natural infection of the disease might be lifelong and vaccination can be used successfully.
Vaccination of cattle every year can controlLSD. It is possible to protect cattle against LSD using strains of Capri
poxvirus derived from either of the sheep or goats as used in Egypt by Romanian sheep pox strain [31].
Vaccination in New Areas:

Risks of introducing of the disease in to the new areas are by infected animals and contaminated materials [32]. Ring
vaccination of cattle, quarantination of animals and movement of animals should be restricted. These two practices of
vaccination were followed by Egypt and Israel and it was effective [33].

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The following vaccines have been used in protection of the animals:
Homologous live attenuated virus vaccine (Neethling strain: immunity conferredlasts up to 3 years).
Heterologous live attenuated virus vaccine (Sheep or goat pox vaccine, but may cause local, sometimes severe
reactions) (Fig 7). This vaccine is not advised in countries free from sheep and goat pox because the live vaccines could
otherwiseprovide a source of infection for the susceptible sheep and goat population.
Fig.7. Vaccine for LSD
IV. CONCLUSION
Lumpy dermatosis (LSD) is a contagious, eruptive and sometimes fatal bovine disease, a systemic skin disease caused
by Tamil virus, a relative of Nicelingpoxvirus in thegenus Capripoxvirus of the family Poxviridae. Cattle andbuffaloes
are important livestock that make a significant contribution to the globaleconomy. Rough skin disease is a serious
disease of cattle and buffaloes. LSD was first reported in Zambia, found in most other African countries, is now
endemic in most African countries and has recently spread from Africa to the Middle East, Asia and Europe. Due to the
economic importance of the disease, the spread of the disease to the wider geographical area of the Indian
subcontinentwill certainly hamper rural economies in particular. LSD may also lead to a decline in livestock and
livestock exports. The reason for the arrival of LSD in India needs to be studied along with random epidemiological
screenings in different regions to get a true prevalence of the disease. Apart from these effective quarantine and vector
control methods, vaccination is the only way to prevent disease.
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[30]. Abutarbush, S.M., 2017. Lumpy skin disease (knopvelsiekte, pseudo- urticaria, neethling virus disease,
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ISSN (Online) 2581-9429

Volume 3, Issue 2, March 2023

Lumpy Virus and Skin Infection: A Review

Keywords: Lump skin disease, animal, India, Virus

Volume 3, Issue 2, March 2023

proteinwhich are found in other poxvirus genera [11].

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Fig.2. Global distribution of LSD

II. TRANSMISSION OF LSDV

Fig.3. Epitome of possible modes of transmission of LSDV

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Fig.5.The diagnostic procedures of the LSD

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Fig.6. LSD in cattle

Vaccination in Endemic Areas:

Vaccination in New Areas:

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Fig.7. Vaccine for LSD

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