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Lumpy Skin Disease

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Lumpy skin disease
Previous authors: J A W COETZER

Current authors:
J A W COETZER - Professor Emeritus, BVSc, BVSc (Hons), M Med Vet (Path), Faculty of Veterinary Science,
University of Pretoria, Private, Bag X04, Onderstepoort, Gauteng, South Africa, 0081
E TUPPURAINEN - Self Employed, DMV, MSc, PhD, 20 Wolseley Road, Aldershot, GU11 1NE, Hampshire, United
Kingdom
S BABIUK - Research Scientific, PhD, National Centre for Foreign Animal Disease, 1015 Arlington Street,
Manitoba, Canada, R3E 3MA
D B WALLACE - Senior Researcher, PhD, Agricultural Research Council, Onderstepoort Veterinary Research, Old
Soutpan Road, Pretoria, Gauteng, 0110, South Africa

Introduction
Lumpy skin disease (LSD) is a viral disease of cattle and possibly Asian domestic buffaloes (Bubalus
bubalis) caused by lumpy skin disease virus (LSDV). It is characterized by fever and multiple firm, well-
circumscribed and deep-seated skin nodules and necrotic plaques in the mucous membranes, chiefly of
the upper respiratory tract and oral cavity. Mastitis, orchitis and swelling of peripheral lymph nodes are
also common. Lumpy skin disease virus is a capripoxvirus first isolated in the 1940s; however, the first
widespread outbreak was reported from Zambia in 1929.5, 15
Despite the fact that its origins are obscure LSD was until recently believed to be a disease confined to
Africa. The disease that was initially termed pseudo-urticaria, but now presumed to have been LSD,81,
82 was thought to be the result of insect bites and later ascribed to plant poisoning.81 Lumpy skin disease

was first recognized as an infectious condition in 1943 following an outbreak in Ngamiland (northern
Botswana).119 Towards the end of 1944 LSD was reported from South Africa105 where it spread rapidly
throughout the country despite enforcement of control measures. The disease subsequently spread
northwards and was reported from Central and East Africa in 1956; since then it has occurred widely in
Africa and in Madagascar.39, 52, 91, 92 It was first reported from Ethiopia in 198383 and in Egypt in
1988.64 Lumpy skin disease was recorded for the first time outside Africa/Madagascar in 1989 in Israel,37,
123 followed by outbreaks in Bahrain and Reunion in 1993, although those outbreaks were not confirmed

by virus isolation.10
In 2006 and 2007 LSD was reported again in Egypt98 and Israel and in 2009 occurred in Oman.25 The
disease reappeared in northern Israel in 201220 and then spread swiftly in the Middle East, being reported
in Lebanon, the Palestinian Autonomous Territories and Jordan.1 The disease also spread into
Turkey,106 Kuwait, Saudi Arabia and Iraq in 2013.4 In 2014 outbreaks of LSD were reported in Iran99 and the
northern part of Cyprus as well as in Saudi Arabia and Bahrain.103 It then spread northeast through the
Caucasus, affecting Azerbaijan (2014), Armenia and the Russian Federation (2015) and Georgia and
Kazakhstan (2016).
Lumpy skin disease was reported for the first time in the European Union from Greece in 2015; it
probably originated in Thrace (Turkey). The Greek outbreak occurred in two beef herds situated in the
Evros River Delta from August 2015 to December 2015, i.e. within 15 km of the closest confirmed LSD
outbreak in Turkey. The Evros River Delta is a National Park and a wetland with high temperatures and
humidity. The disease emerged again in Greece from April to November 2016.3, 49
In 2016 LSD spread to Bulgaria, the former Yugoslav Republic of Macedonia (FYROM), Serbia,
Montenegro, Kosovo and Albania (www.oie.int WAHIS Interface).49 In the same year it was reported again
in Iran and Iraq as well as Azerbaijan.126
The number of reported LSD outbreaks in Balkan countries was substantially less in 2017 (385) than in
2016 (7,483) and most occurred in Albania (379) in areas where vaccination was not applied in all cattle
herds, indicating that the virus is still present in the environment and/or in the cattle population and may
re-emerge again.49 In contrast, Bulgaria, Serbia, Montenegro and Kosovo reported no outbreaks,
providing field evidence of the effectiveness of mass vaccination campaigns conducted at regional
levels.49
Since the beginning of the LSD epidemic in south Eastern Europe (excluding Turkey) in 2015 more than
7900 outbreaks and approximately 13 650 cases have been reported.49
It appears that LSD spread rapidly and more or less unpredictably during the recent outbreaks in Greece
and the Balkan countries. Current information on its distribution can be obtained from the OIE (World
Organisation for Animal Health) website (www.oie.int) under the WAHIS interface’s disease distribution
maps and the Food and Agriculture Organization of the United Nations (FAO EMPRES-I
website, www.fao.org). Information is also provided by FAO on the incursion risk of LSD to Central Asia
and Europe51 and distribution maps of recent outbreaks (2013-2017) in the Middle East, Turkey, the
Balkans and Eastern Europe/ Central Asia.51
Lumpy skin disease can be considered a ‘neglected disease’ because since it was first confirmed as a
poxvirus infection in South Africa in 1944, research has been limited. Until recently, LSD was not a
research priority for developed countries because it was exotic. Consequently, there are still gaps in
information about the disease including:

• the role of different potential insect vectors, including ticks, in different epidemiological settings
and the persistence of LSDV in some of these potential vectors in interepidemic periods;
• the susceptibility of different wildlife species to LSDV and their role in the epidemiology of the
disease;
• the proportion of animals that develop subclinical infections and their role in transmitting
disease and infecting potential vectors;
• the importance of fomites such as saliva-contaminated feed and water troughs in the
transmission of the disease;
• the level and duration of virus excretion in milk, semen, saliva and nasal secretions and their role
in transmission of LSD;
• the level and duration of viraemia in animals vaccinated with attenuated LSD viruses and the
potential for transmission;
• determinants of immunity and its duration following vaccination with attenuated LSD viruses;
and
• the usefulness of improved serological tests, including ELISAs.

Socio-economic impact
Because LSD is ‘listed’ by the OIE, member countries are obliged to report its occurrence promptly.
Although the disease does not incur high mortality (usually less than 10 per cent), it is economically
important because of its prolonged debilitating effects in severely afflicted animals including reduced
weight-gain, temporary or permanent cessation of milk production, sometimes accompanied by mastitis,
temporary or permanent infertility or even sterility in bulls as a consequence of orchitis, as well as
permanent skin damage. Abortion may follow infection in approximately 10 per cent of pregnant cows.58,
63

In the outbreak reported in Albania in 2017, the morbidity had a median value of 0.8 per cent with values
up to 7.2 per cent while mortality median value was 0.3 per cent with values up to 2.9 per cent. Similar
ranges were reported in 2016 in Albania, when morbidity median value was 0.7 per cent up to 4.8 per
cent and the mortality upper values was 0.7 per cent.49
During the outbreaks of LSD in the Balkans in 2016 the disease resulted in severe socio-economic
consequences for small-scale farmers whose livelihoods are highly dependent on the production of their
few dairy cows. In addition to the above-mentioned impacts, losses were also ascribed to costly control
measures such as total or partial stamping-out (see Control) and the resultant need for compensation,
cleaning and disinfection measures on affected farms, vaccination, supportive medical treatments and
nursing of affected animals, vector control and increased laboratory activity (e.g. diagnostic kits, reagents
and equipment) as well as more intensive monitoring and surveillance costs.
In African countries where cattle are often used for other purposes, such as for draught power and social
and religious ceremonies, restrictions of such traditional practices result in economic and social
disruption.
The most dramatic effects of LSD in endemic as well as newly infected areas are often indirect, resulting
from market exclusion due to bans on movement and sale of cattle and commodities derived from them.
That is particularly so if trade restrictions are unreasonable, i.e. do not accord with international trade
standards set out in the OIE’s Terrestrial Animal Health Code chapter on LSD (i.e. Chapter 11.9
– www.oie.int), according to which meat (beef), hooves, horns, casings, tallow, gelatine and collagen are
not considered a significant trade risk.51 Infection through milk and semen is possible.8, 9, 51 Hides are more
likely to be contaminated with virus than meat or milk and the OIE Terrestrial Animal Health Code made
certain recommendations for the importation of hides from LSD-infected countries.

Aetiology
Lumpy skin disease virus is a member of the genus Capripoxvirus within the
family Poxviridae (subfamily Chordopoxvirinae); see Introduction to the Poxviridae for a more general
overview of poxviruses. The other members of the genus include sheeppox virus (SPPV) and goatpox
virus (GTPV).
Mature capripox virions (Figure 1) have a similar morphology to those of orthopoxviruses (prototype,
vaccinia virus) when viewed using transmission electron microscopy, although capripox virions tend to be
less symmetrical in shape,120 with average dimensions of 320 × 260 nm, giving an axis ratio of
approximately 1:2.88 A cross-sectional analysis of the virions reveals a pair of lateral bodies (Figure 2)
common to all poxviruses.88
Compared to other poxviruses, the double-stranded DNA genomes of capripoxviruses are relatively small,
averaging around 150 kilo-base pairs (kbp) (compare with avipoxvirus genomes of around 300 kbp). Their
genomes are highly conserved between the three genus members, with LSDV containing two unique
genes compared to sheeppox or goatpox viruses.109 The viruses share around 97 per cent sequence
identity.108, 109 Centrally located “house-keeping” genes (coding for structural proteins, proteins involved in
replication, transcription etc.) are the most highly conserved, in line with other poxviruses, with inclusion
of less conserved “virulence” genes (coding for proteins involved in pathogenesis) towards the termini, a
number of which have putative immunomodulatory functionality for host immune response.70, 108
Available evidence suggests that there is only one serotype of LSDV. Virus isolates collected over an
extended period from a large number of natural cases originating from outbreaks of the disease in South
Africa, Kenya and Malawi,96, 120 showed reciprocal cross-neutralization with the prototype Neethling
strain.40-42, 73 Complete genome sequencing of recent LSDV isolates SERBIA/Bujanovac/2016 and
Evros/GR/15 demonstrated 99.5 per cent and 99.8 per cent homology respectively with the LSDV field
isolate Neethling Warmbaths LW isolated in South Africa in 2000, indicating genetic stability of LSDV as
well as providing genetic evidence in support of a single serotype.2, 107
Existence of only one serotype is further supported by studies in which cross-neutralisation of
capripoxviruses is possible using sera containing neutralising antibodies generated in animals inoculated
with a different capripoxvirus. This fact has been utilized to demonstrate that capripoxviruses can afford
varying degrees of cross-protection.10, 22, 74 For example, the Kenyan sheep- and goatpox (KSGP) O-240
vaccine strain has been successfully used for the immunization and protection of sheep and goats against
sheeppox and goatpox and cattle against LSD in many regions in Africa.30, 38 This vaccine strain was
originally believed to be a SPPV but was later shown to be LSDV using DNA sequencing.116 This error in the
original classification of the vaccine as a sheeppox virus illustrates the need to use DNA sequencing to
properly identify capripoxviruses as all other identification methods are insufficiently specific (see
Diagnosis).
Culturing capripoxviruses in cell cultures is relatively simple, although they replicate more slowly and
grow to lower titres (up to 106 TCID50/ml) in permissive cells than the orthopoxvirus vaccinia virus, and
thus for new LSDV isolations in cell cultures up to 11 days, and more than one passage may be required
before cytopathic effects (cpe) become evident (www.oie.int Lumpy skin disease chapter). The highest
titres are achievable in a variety of primary cell cultures of ovine or bovine origin, most commonly kidney
or testes cells, but cells from other organs, including adrenal, thyroid, muscle, lung and skin, may also be
utilized.5, 10, 96 Additionally, there are several transformed cell lines that are permissive to LSDV
propagation, including Madin-Darby bovine kidney (MDBK) and ovine testes (OA3.Ts) cells.16, 21 The
development of cpe may be observed as early as three days after culture inoculation but it usually
requires longer incubation in the case of primary isolation.5, 94-96, 120, 121 The virus induces discrete viral
plaques in cell monolayers derived from primary cells, characterized by early appearance of discrete foci
of rounded cells, followed by formation of irregular holes in the monolayer as the cells die.88 Virus
replication is accompanied by the formation of intracytoplasmic inclusion bodies similar to those which
occur in a variety of cells in the epidermis and dermis in skin lesions (see Clinical signs and Pathology) of
affected cattle.26, 43, 95

Figure 1 Typical ultrastructural morphology of capripox virions

Figure 2 Line drawings of poxviruses: 1 = double membrane with filaments; 2 = surface protein; 3 = core
with matrix and nucleoid membrane; 4 = lateral bodies. Note arrangement of surface filaments

As is the case with other poxviruses, LSDV is highly stable (see General Introduction: Poxviridae). Virus is
recoverable for at least 18 days from air-dried hides kept at room temperature and from infected tissue
culture fluid stored at 4 °C for six months.120 The virus was reported to persist in necrotic skin nodules for
up to 33 days but this period may be much longer.110, 120, 121
Between pH 6.6 and 8.6 virus preparations showed no significant reduction in titre after exposure to a
temperature of 37 °C for five days. The resistance to physical and chemical actions are summarized in the
OIE manual
(http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/Disease_cards/LU
MPY_SKIN_DISEASE_FINAL.pdf).

Epidemiology
The range of animal species that may be infected and develop clinical disease is uncertain but it is
probably wider than cattle and Asian water buffaloes (Bubalus bubalis); there are conflicting reports
concerning the latter species.46
All ages of cattle and both sexes are susceptible to infection120 although on occasion cows have been only
mildly affected while their calves developed more typical and severe lesions 24 to 48 hours earlier than
their dams.79 More severe disease has been reported in breeds of cattle exotic to Africa, especially those
with thin skins such as Friesians and in other high-producing European dairy breeds. Cows in peak
lactation seem also to be more severely affected.54, 79, 101, 102
Involvement of wildlife in the maintenance and transmission of LSD is uncertain. Disease resembling LSD
clinically has been reported in Arabian oryx (Oryx leucoryx) in Saudi Arabia,12 springbok (Antidorcas
marsupialis) in Namibia75 and oryx (Oryx gazella) in South Africa, although there is no record of isolation
of LSDV from these species. According to Hedger and Hamblin61 wildlife play no significant part in the
epidemiology of the disease. Birds have been postulated as possible vectors27, 63 but there is likewise no
objective evidence for that.
Serological studies on wildlife have provided inconsistent results. Sera from 440 culled African buffalo
(Syncerus caffer), 1-20 years of age, in the Kruger National Park (KNP) in South Africa were all found to be
negative in serum virus neutralizing tests against the prototype Neethling strain and a more recent field
isolate.65 Conversely, antibodies to capripoxvirus were demonstrated in African buffalo in an area of
Kenya where LSD is believed to be endemic.39 In South Africa, blue wildebeest (Connochaetes taurinus),
black wildebeest (Connochaetes gnou), springbok and eland (Taurotragus oryx) have been reported to
show serological evidence of infection.18
Experimental studies have provided equally equivocal results. Giraffe (Giraffa camelopardalis) and impala
(Aepyceros melampus) were found to be highly susceptible to experimental infection125 but two African
buffalo calves infected during the same study did not develop disease.125 In a subsequent study a group of
nine sero-negative African buffalo comprising five adults and four calves were experimentally infected by
subcutaneous inoculation with increasing doses (103 to 106 TCID50) of cell culture-passaged virus derived
from a virulent field isolate.65 No skin nodules appeared at the site of inoculation or elsewhere on the skin
or mucosae of the animals. Furthermore, seroconversion did not occur within 42 days of infection, while
two susceptible control cattle that received 103 and 105 TCID50 respectively, developed skin nodules 12
days later. Both cattle also seroconverted.
In southern Africa LSD is usually more prevalent during the wet summer and autumn months, particularly
in low-lying areas and along water courses,6, 7, 33, 44, 60, 63, 81, 87, 90, 119, 122but outbreaks have also occurred during
dry seasons and winter months.60, 90 In this regard, in Albania and other Balkan countries, outbreaks were
reported from high mountainous areas where arthropods are not as abundant as in low-lying areas and
also during the winter months. According to OIE’s WAHIS database, Albania reported 580 outbreaks in
December 2016, 104 outbreaks in January and 17 in February 2017. Greece reported an outbreak in late
February 2017 in Corfu and the FYROM reported one outbreak in early January 2017. Most outbreaks
were, however, reported between May and August, in common with the typical seasonality of LSD. 49
In African countries, spread of LSD apparently follows road, rail or cattle migration routes.7, 60, 82 In Sudan,
for example, it covered a distance of more than 1 000 km across the country in 35 days.7 In Israel, air-
borne spread of disease by vectors over more than 100 km has been suggested.123 Although there is as yet
no clear evidence of the role of Culicoides midges in the transmission of LSD it is known that these
midgescan be carried for long distances by wind currents.
A mathematical model fitted to Albanian data suggested that LSD spreads mostly up to 4 km (i.e. via
vectors), but some transmission occurred over much longer distances (i.e. through animal movement).49
Lumpy skin disease’s mode of transmission has not clearly been established although there is
circumstantial evidence suggesting that haematophagous arthropods are largely responsible for
mechanical transmission of the infection. Carn and Kitching32 concluded that the low levels of viraemia
that occur in infected cattle would be insufficient to support mechanical transmission by biting flies
feeding on blood alone and it would therefore be necessary for biting flies to feed on skin lesions to
enable ingestion of sufficient virus for transmission to occur. Subclinical infection is common (possibly
around 50 per cent of infected animals),111 but the role of sub-clinically infected animals in transmission is
uncertain.
Attempts to isolate LSDV from insects, including Culex and Aedes spp., Culicoides spp., and flies belonging
to the Muscidae, have mostly been unsuccessful. However, the virus was recovered from Stomoxys spp.
and Musca confiscata,45 although attempts to transmit the infection with those flies were
unsuccessful.45 In this respect, Stomoxys spp. (stable flies) (Figure 3) have been shown to be capable of
transmitting related sheeppox virus.84 An abundance of the Stomoxys flies was associated with outbreaks
of LSD in Israel.69Experimentally, female Aedes aegypti (L.) mosquitoes were shown to transmit the
infection from infected to susceptible cattle.35 Lumpy skin disease viral DNA was detected in non-
engorged female midges (Culicoides punctatus) from affected areas within a radius of two km from LSDV-
infected herds in Turkey.101 Further indirect evidence that a vector(s) is involved in the transmission of LSD
was the failure of control measures such as quarantine to halt the spread of the disease in South
Africa120 and Kenya.90
Figure 3 Stable fly: Stomoxys calcitrans

Recently, transmission studies have been conducted on the potential of some common African tick
species to transmit LSDV. Interrupted feeding is a natural behaviour pattern in male Rhipicephalus
appendiculatus (brown ear tick) and Amblyomma hebraeum (African bont tick). Experimentally, R.
appendiculatus males were shown to transmit LSDV mechanically from infected to naïve cattle.112 There is
less evidence that A. hebraeum males80, 114 behave similarly but it is likely they do. Infected African blue
tick, R. (Boophilus) decoloratus), females were shown to transmit the virus via their eggs to larvae that, in
turn, were able to infect naïve cattle.113 Sexual transmission, i.e. in addition to vertical transmission, is
also possible although not yet demonstrated. Further work is required to establish whether multiplication
of the virus (i.e. virogenesis) occurs in these tick species as well as precise long-term
persistence/transmission in ticks. No work has yet been done on closely related tick species in the Middle
East such as R. (Boophilus) annulatus, R. praetextatus and Hyalomma extravatum or European tick
species to establish their potential vector competence.
Potential arthropod vectors of LSDV probably vary amongst affected regions, depending on the season,
environmental temperature and humidity as well as type of vegetation that favour the breeding and
survival of different species. For example, in most of sub-Saharan Africa where LSD is endemic, high
densities and prevalence of many tick species may be more important as vectors of LSD than in the
Middle East and European and Balkan countries where there is a lower variety of ticks, usually at lower
densities. In Albania, most dairy cattle are kept indoors in a small confined space and up to four animals
may share the same feeding and water troughs. In this setting, ticks would seem to play a minor if any
role in the transmission of the disease while saliva and nasal secretions that contaminate hay and
drinking water may be more important in transmission of the disease.
In Greece it has been shown that the risk of contracting LSD was six times higher where cattle were kept
outdoors than where animals were housed indoors, independent of vaccination status, possibly because
of higher exposure to arthropod vectors.49
Lumpy skin disease may spread in the absence of insects although direct transmission by contact
between animals would seem to be inefficient in most instances.60, 63 Deliberate attempts to infect
susceptible animals by handling them immediately after handling infected animals were
unsuccessful.120 However, transmission did occur when common drinking and feeding troughs were used,
thus confirming the suspicion that infected saliva may contribute to the spread of the disease.60,
63Particularly in severely affected animals numerous necrotic lesions are present in the oral and nasal
cavities and it is known that high levels of virus are found in lesions. Although more work needs to be
done, LSDV can be found in saliva and nasal discharges for up to 18 days in clinically affected animals.15
The disease is transmissible to suckling calves through infected milk and infected cows have been
reported to give birth to calves with skin lesions.97
Iatrogenic transmission via contaminated needles during vaccination or other injections may also occur.51
In a study by Weiss (1968)120 LSDV was isolated from the semen of experimentally infected bulls for 22
days after infection. A more recent study by Irons et al.(2005) 68demonstrated the persistence of live virus
in bovine semen for up to 42 days after infection and viral DNA was detected for up to 159 days. In both
studies the virus was isolated from the semen of bulls without apparent disease. The epididymis and
testis were identified as the sites of persistence of LSDV, viral DNA being detected in all fractions of
semen.9Vaccination of bulls with the South African live attenuated Neethling strain prevented shedding
of LSDV in the semen of animals subsequently challenged with wild-type LSDV, and vaccinated animals
did not shed vaccine virus in their semen.93 Transmission of LSDV via artificial insemination has also been
shown experimentally.8
Lumpy skin disease virus was shown to replicate in sheep by recovery of virus from animals inoculated
intradermally or subcutaneously with different field isolates of LSDV. The inoculated animals developed
localized erythematous swellings at the site of inoculation, as well as enlarged regional lymph nodes from
which LSDV was isolated.17

Pathogenesis
Subcutaneous or intradermal inoculation of cattle with LSDV usually results in the development of a
localized swelling at the site of inoculation after four to seven days and enlargement of the regional
lymph nodes while generalized eruption of skin nodules usually occurs seven to 19 days after
inoculation.120 Animals inoculated intravenously are more inclined to develop generalized lesions and
more severe disease.17, 33, 120 However, clinical signs and pathology are variable following both natural and
experimental infection; obtaining consistent experimental results is therefore problematic.
Initial experimental investigation indicated that viraemia persisted for about four days.120 However, in
more recent studies that employed more sensitive diagnostic methods, viral genomic material could be
detected by PCR for up to eight days.115
After experimental infection LSDV was present in skin nodules, lymph nodes, liver, kidneys, saliva, nasal
mucosa and semen of infected animals.15, 28, 60, 95, 105, 120 Skin nodules contain high levels of virus (up to
106 TCID50/ml). High levels and shedding of virus were also found in the nasal mucosa of affected animals.
The virus has been demonstrated electron microscopically in keratinocytes in the epidermis, and
fibroblasts and endothelial cells and pericytes of blood vessels in the dermis in affected parts of the
skin.95 Immunohistochemistry revealed that several different cell types may contain LSDV antigen,
including keratinocytes, hair follicle epithelium, and fibroblasts and macrophages in the dermis, subcutis
and lymph nodes.13, 15

Clinical signs and pathology

The clinical signs and pathology of LSD in naturally and artificially infected cattle are well documented.27, 32,
39, 42, 63, 81, 104, 115, 119 Morbidity rates of five to 45 per cent on affected farms is usual while mortality rates may

be as high as 10 per cent even among indigenous cattle.60, 104

Typically, cattle develop a febrile response one to two weeks after exposure to the virus.15, 32, 60, 115 Animals
remain febrile for four to 14 days, during which time excessive salivation, lachrymation and a mucoid
nasal discharge are evident. The nasal discharge later becomes mucopurulent. Lachrymation may be
followed by conjunctivitis, and in a few cases erosions are present in the mucosae of the conjunctivae,
ultimately resulting in corneal opacity and blindness (Figure 4). In the majority of affected cattle the
superficial lymph nodes are enlarged.

Figure 4 Severe keratitis and necrotic skin lesions on the eyelids (Courtesy of Dr Massimo Scacchia,
Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via Campo Boario, 64100
Teramo, Italia)

Skin nodules, the characteristic feature of the disease, usually appear two to five days after the initial
febrile response (Figures 5 to 8). The nodules, which are randomly distributed and range in diameter
from 10 to 30 mm, involve both the skin and subcutaneous tissues and sometimes even the underlying
musculature. The size of the nodules is usually fairly uniform but several nodules may fuse to form large,
irregularly circumscribed nodules or plaques. The number of nodules may range from a few to several
thousand in severely affected animals. The nodules are well-circumscribed, firm, round and raised (Figure
9) and are particularly conspicuous in short-haired animals. In long-haired cattle the nodules are often
only recognized when the skin is palpated or moistened.63 In most cases, nodules are particularly
noticeable on the perineum and the vulva.120 On cross-section, the skin nodules in acute or subacute
stages of infection are reddish-grey and the dermis and subcutaneous tissues oedematous.104 The
subcutis is often infiltrated with a reddish-grey serous fluid.120 Skin lesions either resolve, become
indurated (in which case they persist as hard lumps or ‘sitfasts’ for 12 months or longer) (Figure 9) or
sequestrate to leave deep ulcers (Figure 10), partly filled with granulation tissue that often suppurates.
In severe acute cases, the ventral parts of the body, for example the dewlap, brisket and the legs (Figure
11) may be slightly too severely oedematous one to two days before the appearance of the nodules and
remain so for a week or more.
Figure 5 Severe case of subacute lumpy skin disease: randomly distributed nodules in the skin (Courtesy
of Dr Massimo Scacchia, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via
Campo Boario, 64100 Teramo, Italia)

Figure 6 Severe case of subacute lumpy skin disease: numerous nodules in the skin (Courtesy of Dr
Massimo Scacchia, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via
Campo Boario, 64100 Teramo, Italia)
Figure 7 Severe case of subacute lumpy skin disease: note numerous variable-sized skin nodules
Figure 8 Mild case of lumpy skin disease: few nodules randomly distributed over the body (Courtesy of Dr
Massimo Scacchia, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via
Campo Boario, 64100 Teramo, Italia)

Figure 9 Chronic lumpy skin disease: fibrotic and indurated skin lesions (Courtesy of Dr Massimo Scacchia,
Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via Campo Boario, 64100
Teramo, Italia)
Figure 10 Subacute lumpy skin disease: desquamation of necrotic skin lesion (Courtesy of Dr Massimo
Scacchia, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via Campo Boario,
64100 Teramo, Italia)

Figure 11 Acute lumpy skin disease: note severe oedematous swelling of the dewlap, brisket, ventral
abdomen and thorax and legs
Figure 12 Desquamating lesions on coronary band of the hoof (Courtesy of Dr Massimo Scacchia, Istituto
Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via Campo Boario, 64100 Teramo,
Italia)

Figure 13 Necrotic well-circumscribed ulcers on the muzzle (Courtesy of Dr Massimo Scacchia, Istituto
Zooprofilattico Sperimentale dell’Abruzzo e del Molise "G.Caporale" Via Campo Boario, 64100 Teramo,
Italia)

Nodular skin lesions may extend into underlying tissue such as tendons and tendon sheaths resulting in
lameness in one or more legs (Figure 12). Most affected animals have multifocal, roughly circular,
necrotic areas 10-20mm in diameter on the muzzle (Figure 13) and in the respiratory tract (nasal cavity,
larynx, trachea and bronchi) and buccal cavity (the inside of the lips, gingivae and dental pad); these
lesions may also be present in the fore-stomachs, abomasum, uterus, vagina, teats (Figures 14 and 15),
udder, and testes (Figure 16).
In the upper respiratory tract (e.g. larynx and trachea) multiple, well-circumscribed, necrotic areas of
about 10-20mm in diameter are common in severe clinical cases (Figures 17 to 19). These necrotic tissues
may dislodge and be inhaled, resulting in pneumonia. Stenosis of the trachea may follow healing of these
lesions (Figure 19) with scar tissue formation some weeks or months after the acute stage of the
disease.42
In bulls, lesions may occur on the scrotum, prepuce, preputial mucosa, the glans penis and in the
parenchyma of the testes (Figure 16).63 Acute orchitis may progress to fibrosis and atrophy of the testes,
resulting in temporary or permanent infertility or more rarely, sterility. Similarly, lesions in the
reproductive tract of cows may result in infertility.
Nodules, necrotic plaques or scabs, 10-20mm in diameter, are commonly present in the skin of the udder
and teats (Figures 14 and 15), and, when the parenchyma of the udder is involved, as it frequently is, the
gland becomes swollen and tender due to mastitis. Secondary bacterial mastitis may be severe and
complicate the udder lesions. Occasionally, parts of the udder may become sequestrated and slough.
Involution of the udder as a result of mastitis often causes severe economic losses on dairy farms. Lesions
on and in the teats may cause distortions of the teat canal, leading to ascending bacterial infections.

Figure 14 Subacute lumpy skin disease: Numerous ulcerative lesions on the teats and the skin of the
udder (Courtesy of Dr Massimo Scacchia, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise
"G.Caporale" Via Campo Boario, 64100 Teramo, Italia)
Figure 15 Subacute lumpy skin disease: note skin lesions on the teats

Figure 16 Chronic lumpy skin disease: note atrophy of testes following orchitis
Figure 17 Subacute lumpy skin disease: greyish-yellow foci of necrosis in the pharynx and larynx
(Courtesy of Dr Massimo Scacchia, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise
"G.Caporale" Via Campo Boario, 64100 Teramo, Italia)

Figure 18 Subacute lumpy skin disease: Note necrotic areas in trachea

Figure 19 Chronic lumpy skin disease: Stenosis of trachea

Microscopically the lesions vary considerably depending on the stage of development. In the acute stage
of the disease, vasculitis is sometimes accompanied by thrombosis and infarction, as well as perivascular
fibroplasia and infiltration by macrophages, some lymphocytes and eosinophils in the dermis and
subcutis particularly. The keratinocytes in the epidermis reveal ballooning degeneration and may show
evidence of lysis, intra- and intercellular oedema with vesicle formation, as well as some degree of
acanthosis, parakeratosis and hyperkeratosis.
During the acute and subacute stages of the disease eosinophilic intracytoplasmic inclusions (Figure 23)
that range in size from 1 µm to almost the size of the nucleus may be present, particularly in
macrophages and keratinocytes in the skin, but may also be seen in endothelial cells, pericytes, and the
acinar and ductal epithelial cells of mucus and serous glands. Ultrastructurally, the viroplasms
(inclusions), appear as well-delineated areas of finely granular to fibrillar deposits that contain developing
virions, mature viral particles and, occasionally, groups of tubular structures.95 Mature viral particles are
apparently randomly distributed in the cytoplasm of affected cells (Figures 20 and 21).95
Figure 20 Numerous viral particles in the cytoplasm of a macrophage

Figure 21 Numerous viral particles in the cytoplasm of a macrophage

Diagnosis
A presumptive diagnosis of LSD can be made on the characteristic clinical signs but it is advisable to
confirm the diagnosis by submitting appropriate samples to a suitably equipped laboratory.
Classical methods for laboratory diagnosis include serology using the gold standard serum/virus
neutralization test, virus isolation on cell culture or histopathology. However, these tests have certain
shortcomings including being relatively insensitive, time-consuming and expensive to perform. Thus,
more modern molecular-based tests such as polymerase chain reaction (PCR) assays have been
introduced to most diagnostic laboratories and are well described in the OIE Manual of Diagnostic Tests
and Vaccines for Terrestrial Animals, Chapters 13/14 on LSD) (www.oie.int).

Sampling
A detailed history including vaccination status of the herd should accompany the specimens. Biopsies of
nodules or scabs on ice, as well as in 10% buffered formalin, are the preferred samples for
histopathology, immunohistochemistry (IHC) and transmission electron microscopy (TEM). Fresh skin
biopsies or scabs in virus transport medium, both kept on ice, are preferred samples for molecular
studies and virus isolation. Although blood in ethylenediaminetetraacetic acid (EDTA) can be used for
virus detection by polymerase chain reaction (PCR) and collected in heparin for virus isolation, detection
of viraemia is unreliable because it is frequently of short duration. Oral and nasal swabs can also be taken
for PCR or virus isolation. Sera should be collected for serum or virus neutralization testing (the current
gold standard assays) and enzyme-linked immunosorbent assay (ELISA) (not yet routinely available) two
to three weeks after the first appearance of skin lesions.

Virus isolation
The diagnosis of LSD can be confirmed by isolation of the virus on different cell cultures (see Aetiology).
Confirmation is obtained by subjecting the virus to techniques such as PCR and sequencing or fixing and
staining the cell monolayer for immunohistochemical analysis.

Serological tests
Serum or virus neutralisation testing (SNT or VNT): The SNT and VNT are essentially the same test, with
minor differences, and are used to measure the levels of neutralising antibodies in a serum sample, as an
indicator of prior exposure to the virus, either through natural infection or vaccination. However, in
general, the immune status of a previously infected or vaccinated animal doesn’t directly correlate to the
levels of serum neutralizing antibodies. For example, some animals following natural infection or
vaccination may remain seronegative, even though fully protected. In those animals that do develop
neutralizing antibodies, levels start to rise approximately one week after detection of fever and reach the
highest levels approximately two to three weeks later and then start to decline, eventually dropping
below detectable levels. The interpretation of serological results may thus sometimes be difficult.10, 72
Enzyme-linked immunosorbent assay (ELISA): After many attempts to develop an indirect antibody ELISA
[Bowden, Coupar 2009 24, Carn, Kitching 1994 34] the first validated ELISA has recently become
commercially available, facilitating large-scale sero-surveillance for LSD in unvaccinated cattle
populations. This ELISA (manufactured by IDVet) is able to detect antibodies against capripoxviruses
(LSDV, SPPV and GTPV) from approximately 20 days until seven months post-vaccination. Its sensitivity is
therefore better than the SNT and its specificity is 99.7 per cent. Individual animals with low antibody
levels such as those in the early stage of infection or with mild disease or a low antibody response to
vaccination may not be identified. [European Food Safety 2018 49] In addition, another serological assay,
the immunoperoxidase monolayer assay (IPMA) [Haegeman, Zro 2015 59] has been developed for LSDV.
This assay is comparable to the SNT, but it is labour-intensive and requires experienced personnel to
interpret the result. Live virus is used and therefore the assay should be performed in high bio-
containment laboratories in areas where the disease is non-endemic. The assay is not suitable for large-
scale testing.
It is not possible to distinguish antibody responses resulting from infection with wild-type LSDV from
those following vaccination with currently available attenuated LSDV vaccines (DIVA testing).
An antigen-trapping ELISA has been developed to detect viral antigen in skin lesions.10, 31 However, the
molecular methods described have made this assay obsolete.
Pathology
The macroscopic lesions of a typical severe case of LSD will leave little doubt as to the true identify of the
disease, but less typical and milder cases should be differentiated from other conditions (see Differential
diagnosis). Although the intracytoplasmic inclusion bodies in keratinocytes in haematoxylin and eosin-
stained sections of acute skin nodules may support a diagnosis of LSD, these inclusions are not always
present in all acute cases (see Clinical Signs and Pathology) and are not discernible in subacute and
chronic skin lesions.
More specific immunohistochemical methods, for example immunoperoxidase staining of tissue sections,
can be used to demonstrate the virus in formalin-fixed skin lesions and tissues. Immunohistochemistry
using a monoclonal antibody was used to detect LSDV antigen in skin nodules from animals with acute
LSD, as well as in some subacute or chronic cases of the disease. The sensitivity of this assay was
comparable to PCR.13

Transmission electron microscopy (TEM)

In specialized laboratories the diagnosis can be confirmed within a few hours of receipt of specimens by
TEM demonstration of virus in negatively-stained preparations of biopsies or scabs taken from affected
skin.40

Polymerase chain reaction (PCR)

As stated previously (see Aetiology), members of the genus Capripoxvirus (SPPV, GTPV and LSDV) are
genetically similar with nucleotide homology greater than 96 per cent.109 This genetic similarity has
enabled rapid, sensitive and validated conventional10, 62, 67 and real-time (RT) group-specific PCR23 assays to
be developed that are gaining acceptance in an ever increasing number of national reference
laboratories. There are also several PCR-based commercial diagnostic kits available for the detection of
capripoxviruses (e.g. Techne quantitative PCR [qPCR] test, Genesi Standard and Advanced Kit, Tetracore,
Biosellal).49 Some assays are also able to differentiate between SPPV, GTPV and LSDV75-78 and a one-step
multiplex RT-qPCR assay has recently become available for simultaneous detection of peste des petits
ruminants virus, capripoxviruses, Pasteurella multocida and Mycoplasma
capricolum subspecies capripneumoniae.100
Polymerase chain reaction assays are also available to differentiate between wild-type LSDV and
attenuated vaccine strains of LSDV when clinical signs are detected in animals following vaccination.2, 3, 49, 71,
85, 86, 118

Sometimes during an outbreak of LSD, characteristic clinical signs may be detected in cattle vaccinated
with attenuated SPPV or GTPV-containing vaccines. Species-specific genotyping PCR methods can be used
to determine if the vaccine virus or wild-type LSDV is the cause of disease in these cases.56, 57 These same
PCR assays are suitable to confirm the presence of SPPV or GTPV in certain wild antelope species that are
susceptible to these viruses.
Four loop-mediated isothermal amplification (LAMP) assays36, 89, 117, 127 are available for diagnostic purposes.
The advantage of these LAMP assays is that they can be performed inexpensively compared to real-time
PCR and do not require expensive equipment. Recently the first PCR assay utilizing a portable
thermocycler has been described.11

Sequencing
As the price for sequencing is continually being reduced, sequencing of whole viral genomes is now
relatively cheap, fast and simple and provides a wealth of information. Sequencing of virulent and
vaccine isolates of LSDV revealed a number of differences between the isolates,55, 70 with the field isolates
being more highly conserved, as expected, compared to the multiple cell-passaged vaccine strains.

Differential diagnosis
The skin lesions of LSD can be confused with pseudo-lumpy skin disease caused by bovine herpesvirus-2
(BVH-2) infection. Generally, the latter causes more superficial lesions affecting only the epidermis while
in LSD the lesions are deep-seated, involving the epidermis, dermis and other subcutaneous tissues as
well as other tissues and organs. Pseudo-lumpy skin disease is a mild disease and apart from a brief
febrile reaction, affected animals show no signs of systemic illness and full recovery is usual. In LSD on
the other hand, the disease is characterized by prominent signs of systemic disease in severely affected
animals (see Clinical signs and pathology). Molecular and other appropriate diagnostic methods should
be applied to confirm the diagnosis (see Diagnosis). In contrast to the intracytoplasmic inclusions in LSD,
intranuclear inclusion bodies (Figure 22) are found in keratinocytes in pseudo-lumpy skin disease caused
by BHV-2 infection.120
Skin lesions caused by allergic reactions, nodular lesions resulting from arthropod bites such as ticks as
well as Demodex infection, dermatophilosis, onchocercosis and besnoitiosis also need to be
differentiated from LSD skin lesions.

Figure 22 Bovine herpesvirus 2 infection: intranuclear inclusion bodies

Figure 23 Lumpy skin disease: intracytoplasmic inclusion bodies in keratinocytes

Control
Control of LSD in endemic countries in Africa
In most African countries, LSD control has relied mainly on vaccination, with no movement control or
stamping-out. Vaccination is voluntary and aimed at clinical protection rather than decreasing and
eventually eliminating the circulating virus. In endemic situations, outbreaks of LSD occur intermittently,
consequently vaccination is often neglected in interepidemic periods. Although preventative vaccination
(see below) should be conducted annually, that is usually only carried out in relatively few commercial
dairy and beef herds. Most subsistence or small-scale farmers do not routinely vaccinate their cattle
against LSD and may only do so in the face of an outbreak.
In most instances mildly affected animals with only a few skin nodules will recover without any treatment
while those that are severely affected should be provided with quality palatable feed and should be well
cared for. Prolonged supportive treatment with antibiotics and anti-inflammatory drugs should also be
given to combat secondary infections, pneumonia, mastitis and orchitis. The prognosis of severely
affected animals is grave as they will most probably not recover fully and will die or remain unthrifty
notwithstanding proper care and therapy and should preferably be culled to avoid ongoing losses.

Control of LSD in non-endemic countries

(epidemic situations)
During the widespread outbreaks of LSD in 2015/16 in Greece, western Balkan and Caucasus countries, it
became evident that vaccination, in combination with cattle movement control, were crucial in halting
the spread of the virus and that a range of other interventions were also required to diagnose and
control the disease.51 Lumpy skin disease was a “new” disease for this region and it was considered a
regional problem, involving many countries, and consequently it could best be dealt with through a
coordinated multi-national effort.51 The following actions were taken in these countries in an attempt to
combat the devastating consequences of the disease:

Vaccination
All of the Balkan countries affected by LSD in 2016 used one of the attenuated Neethling strain LSDV
vaccines, either obtained from the European Commission vaccine bank or directly sourced from the
manufacturers. In the early stages of the outbreaks, some of the countries experienced severe delays in
acquiring LSD vaccines due to lack of financial resources, legal or bureaucratic obstacles and cumbersome
tender procedures.
The live attenuated LSD vaccines are not registered for use within the European Union. In order to use
these vaccines, a Member State needed to provide a detailed vaccination plan to the European
Commission to obtain authorization to apply vaccination. Also, preemptive vaccination affects the official
disease-free status of the country, resulting in restrictions to trade in live cattle and their products. For
this reason, competent veterinary authorities and farmers of those countries neighbouring the infected
areas were unwilling to adopt vaccination. Later, the Commission Implementing Decision (EU) 2016/2008
was changed to allow the movement of vaccinated animals, under specified conditions and under bi-
lateral agreements, that reduced some of these drawbacks. The European Union also provided specific
rules for movement of cattle products, such as dairy products, semen, ova and hides that were
considered to be risks for transmitting LSD. A distinction was made between zones where animals were
vaccinated preventively, i.e. in the absence of disease (free zones with vaccination) and zones where
disease had been reported (infected zones with vaccination). Milk and dairy products from free zones
with vaccination were not restricted with specific conditions but certain restrictions were implemented in
infected zones with vaccination. In both free and infected zones, it was required that at least 28 days
should lapse after vaccination before any movement of animals or their products could take place. The
aim was to attain 100 per cent vaccination coverage and to carry out clinical surveillance in these zones.
In Balkan countries it became evident that vaccination of the entire cattle population, including pregnant
animals and calves, was the most effective measure to prevent the spread of LSD, especially if it was
applied before the virus entered the region or a country. It has been shown that if vaccination is properly
done, the additional benefits derived from stamping-out are limited.47 Achieving the highest vaccination
coverage in the shortest period of time is therefore recommended for the control of LSD outbreaks,
coupled with good clinical surveillance for detection of clinical cases caused by wild-type virus from cases
resulting from vaccine virus.49
The following vaccines are currently commercially available for the control of LSD:
Attenuated LSDV vaccines: In 1963 Weiss produced the first attenuated LSDV vaccine by 60 serial
passages of the LSDV prototype Neethling strain in lamb kidney cells, followed by 20 serial passages in
the chorio-allantoic membranes of eight day-old embryonated hen’s eggs. According to Weiss, this
attenuated LSDV was safe when inoculated into cattle of all ages and was more effective when applied
subcutaneously than intradermally. A local swelling (nodule) developed at the inoculation site in 50 per
cent of cattle but did not generalize or cause ill-health of vaccinated animals. The local nodules
disappeared within four to six weeks without complications.120
According to the recommendations of the LSD vaccine manufacturer, Onderstepoort Biological Products
(OBP, South Africa), susceptible adult cattle should be vaccinated annually to ensure adequate
protection. Under field conditions approximately 50 per cent of cattle may develop a swelling 10 to 20
mm in diameter at the point of inoculation and this may be accompanied by a temporary drop in milk
yield in dairy cows. The swelling disappears within a few weeks. Calves whose dams were either naturally
infected or immunized should be vaccinated at four to six months of age to preclude interference by
maternal antibody. However, calves born to non-vaccinated cows are highly susceptible and should be
vaccinated irrespective of age in the face of an outbreak.
In Israel a low percentage (0.5 per cent) of animals vaccinated with the attenuated Neethling strain of
LSDV showed a vaccine reaction referred to as “Neethling disease” (see below).20 In Balkan countries,
following vaccination of cattle with attenuated Neethling strain LSDV vaccine, adverse reactions were
apparently more frequent and severe compared with the potential adverse effects described by the
manufacturer on the information leaflet that accompanied the vaccine namely “swelling at vaccine
injection site” and “temporary decrease in daily milk yield”. In Greece, a decreased daily milk yield,
lasting for more than two weeks, was reported by farmers. Most of the reactions occurred 10-14 days
after vaccination and were characterized by a fever lasting a couple of days and a small nodule at the
injection site, sometimes lasting for more than 15 days. Some animals developed a few to many nodules
all over the body. In some of these cases PCR assays were performed and these confirmed that the ”LSD-
like signs” were indeed caused by attenuated LSDV vaccine. Occasionally a large oedematous swelling
occurred at the injection site that gravitated to the ventral parts of the neck and abdomen that lasted up
to 30 days.71, 103 (Although no explanation for these swellings was given, they could have been due to the
use of contaminated needles).
So-called “Neethling disease” is a rare condition for a short period after vaccination and is clinically much
milder than LSD. Its true occurrence is difficult to estimate with accuracy as in most instances vaccination
campaigns were initiated when outbreaks were already ongoing. However, data collected from Croatia,
which was the first non-affected country that applied preventive vaccination campaigns against LSDV in
high-risk regions showed that only 0.09 per cent of vaccinated cattle developed adverse reactions.48 A
recent study claimed that the incidence of side effects following vaccination was underestimated.19
Table 1 lists currently available commercial vaccines.
Table 1 Commercially available attenuated LSDV vaccines

Name Strain Producer

Lumpy skin disease Live attenuated Neethling Onderstepoort Biological Products,
vaccine for cattle strain of LSDV (OBP), South Africa
Live attenuated LSDV field
Lumpyvax MSD Animal Health, South Africa
strain(SIS)
Bovivax LSD Live attenuated LSDV MCI Sante Animale, Morocco
National Veterinary Institute of
Attenuated LSDV vaccine Live attenuated LSDV
Ethiopia
Live attenuated LSDV Kenya Veterinary Vaccines Production
Lumpivax-TM
vaccine Institute-KEVEVAPI

Attenuated sheeppox- and goatpoxvirus vaccines: Several SPPV and GTPV vaccines have been used to
protect cattle against LSD in countries where these diseases overlap.20, 53 The so-called Kenyan sheep and
goat pox O-240 and O-180 strains have been used as vaccine strains in Kenya and elsewhere to control
LSD.28-30, 82, 124 Recently, this O-240 vaccine strain was shown using sequencing to have been derived from
LSDV.116
Attenuated SPPV or GTPV vaccines have often been used at increased dosages compared to the doses
that are recommended for small ruminants to vaccinate cattle against LSD. For example, in Israel in 2013
the attenuated Neethling strain LSDV vaccine was shown to be more effective in preventing LSD than the
RM65 SPPV vaccine used at ten times the small ruminant dose.20 Yugoslavian RM65 SPPV vaccine has
been used in cattle in the Middle East at 10 times the dose that is prescribed in sheep. Romanian SPPV
vaccine has been used to control LSD in Egypt, Bakirköy SPPV was used in cattle in Turkey at 3 or 10 times
the dose in sheep and in Russia a local SPPV strain was used to control LSD.
Immunity after recovery from natural infection is believed to be lifelong in most cattle.120 After
vaccination, antibodies appear within 15 days and reach the highest level in 30 days, dropping gradually
to below detectable levels. Some vaccinated animals did not seroconvert although they are fully
protected.120 Annual revaccination is recommended by vaccine manufacturers. By 28 days after
vaccination, animals will have a protective immunity.14, 66

Stamping-out
In Greece and most affected Balkan countries, total stamping-out was carried out before vaccination with
live attenuated vaccines was approved for use. Greece and Bulgaria applied total stamping-out of all
infected and in-contact animals throughout the epidemics. The negative impact of total stamping-out on
peoples’ livelihoods, food security and welfare should not be underestimated, particularly as it concerns
the most vulnerable producers whose few animals are often their main source of income. According to
the European Food Safety Authority (EFSA) Urgent Advice on LSD, vaccination has a greater impact in
reducing LSDV spread than stamping-out and that when vaccination was properly undertaken, the
additional benefits of stamping-out were limited.47
In some affected countries, culling of severely affected animals (modified or partial stamping-out) from
the herd was recommended as they were regarded as a more important source of virus for
haematophagous insects than subclinically infected animals and a full recovery of the former was unlikely
(Figure 24). In order for farmers to cooperate, compensation was paid for those cattle that died or were
culled due to LSD.

Figure 24 Outbreak of lumpy skin disease in Albania: disposal of a carcass following euthanasia

Culling of animals should be done in a humane and safe manner with prompt and appropriate disposal of
carcasses, which should be sprayed with disinfectant and insect repellent prior to disposal to prevent
insects feeding on them. Cleansing and disinfection of holdings are important measures to prevent
spreading of the virus by indirect means. FAO has provided practical recommendations for
decontamination of premises, equipment and the environment in the Animal Health Manual on
Procedures for Disease Eradication by Stamping Out.50
Although not clearly specified, LSDV like other poxviruses can survive for prolonged periods in the
environment and therefore restocking should be done after a minimum waiting period of 21 days, as
specified in the current EU legislation (Council Directive 92/119/EEC), and the restocked animals
vaccinated at least 28 days before introduction into formerly infected locations.

Movement control
Movement of unvaccinated cattle for trade, slaughter or communal or seasonal grazing is the major risk
for spreading the disease. Implementing effective movement control is challenging and not always
successful.
The guidelines by OIE specify that protection (3 km), surveillance (20 km) and restriction (at least 50 km)
zones need to be established around outbreaks. Commission Implementing Decision (EU) 2016/2008
requires the establishment of an increased surveillance area of at least 20 km around the area where
vaccination is practised, in which intensified surveillance is conducted and the movement of cattle is
subject to official controls. A recent recommendation is to establish a vaccination zone of at least 50 km
radius around the infected area, with at least 90 per cent vaccination cover.51

Vector control
Efforts should be made to institute vector control on the animals or in the barns and stables where the
animals are kept. Spot-on products, dipping or spraying of cattle with acaricides and insect repellents can
be used in an attempt to reduce transmission by vectors.
Other measures: Large-scale awareness campaigns on the importance and other aspects of LSD to all
stakeholders are crucial to ensure success in the implementation of effective surveillance, monitoring,
control and eradication of LSD. Particular effort should be made to detect and report LSD as early as
possible through active clinical surveillance, followed by sample collection from infected and suspected
animals. Diagnostic capacities of local laboratories should be capable of dealing with the large number of
specimens received.

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