F. G.

Davies
Dr F. Glyn Davies is head of the ODA Virology Project, Veterinary Research Laboratories,
PO Box Kabete, Kenya.
Lumpy skin disease (LSD) is an economically important disease of cattle and can produce a
chronic debility in infected cattle comparable to that caused by foot-and-mouth disease
(FMD). Mortality rates as high as 40 percent or more have been encountered but they are
usually lower. Severe and permanent damage to hides results from the skin lesions. Lesions in
the mouth, pharynx and respiratory tract commonly occur, resulting in a rapid deterioration
in condition and sometimes severe emaciation, which can persist for months. Serious
economic losses can follow outbreaks that have a high morbidity.
There is no specific antiviral treatment available for LSD-infected cattle. Two vaccines,
however, Neethling and Kenya sheep and goat pox virus, have been used widely in Africa
with success.
History of lumpy skin disease
The clinical syndrome of lumpy skin disease (LSD) was first described in Zambia (formerly
Northern Rhodesia) in 1929. Initially, it was considered to be the result either of poisoning or
a hypersensitivity to insect bites. Between 1943 and 1945, cases occurred in Botswana
(Bechuanaland), Zimbabwe (Southern Rhodesia) and the Republic of South Africa. The
infectious nature of the disease was recognized at this time. A panzootic in South Africa,
which lasted until 1949, affected some eight million cattle and consequently incurred
enormous economic losses (Thomas and Mare, 1945; von Backstrom, 1945; Diesel, 1949).
LSD was first identified in East Africa in Kenya in 1957 and the Sudan in 1972, and in West
Africa in 1974, spreading into Somalia in 1983. From 1929 to 1986 the disease was restricted
to countries in sub-Saharan Africa, although its potential to extend beyond this range had
been suggested (Davies, 1981).
In May 1988, LSD was recognized clinically in the Suez Governorate of Egypt, where it was
thought to have arrived at the local quarantine station with cattle imported from-Africa. The
disease spread locally in the summer of 1988 and apparently overwintered with little or no
manifestation of clinical disease. It reappeared in the summer of 1989 and, in a period of five
to six months, spread to 22 of the 26 governorates of Egypt. A rapid reaction to the problem
led to the vaccination of nearly two million cattle with a sheep pox vaccine. Morbidity in this
epizootic was low, being 2 percent of the whole cattle population. Approximately 1449
animals died.
In 1989, a focus of LSD was identified in Israel and subsequently eliminated by the slaughter
of all infected cattle as well as contacts. Ring vaccination with a sheep pox strain was carried
out around the focus area and no further clinical cases have occurred.
In sub-Saharan Africa, LSD is now enzootic in all the countries in which it has occurred and
has proved impossible to eradicate. Restrictions on cattle movements have not prevented its
spread within countries and today LSD is liable to extend its range eastward from
northeastern Africa and Egypt into the highly receptive Tigris-Euphrates delta. Further
extension westward from Egypt into North Africa is possible and creates a danger of the

coexistence of LSD with the screwworm infestation. This is of considerable significance as

LSD creates multiple necrotic foci in the skin, which are suitable for oviposition by
Cochliomyia hominivorax.
Clinical disease
LSD is an acute infectious disease of cattle of all ages. There have been five instances of
clinical cases of LSD in Bubalus bubalis, the Asian water buffalo (All et al., 1990). No other
domestic ruminant species becomes infected naturally during field outbreaks. There can be a
pyrexia of 40 to 41.5 C, with lachrymation, possible anorexia, some depression and a
reluctance to move. Shortly afterwards, the characteristic skin lumps develop; they may cover
the whole body or be restricted to the head, neck, perineum, udder, genitalia or limbs. The
lesions first manifest themselves as round circumscribed areas of erect hair, measuring 5 to
50 mm in diameter. They are firm and slightly raised above the surrounding normal skin from
which they are often separated by a narrow ring of haemorrhage. The lesions are of full skin
thickness involving the epidermis, dermis and adjacent subcutis. The regional superficial
lymph nodes are enlarged and oedematous.
There is an increase in nasal and oropharyngeal secretions, which may be associated with the
development of lesions on the muzzle and in the mouth. They may be found anywhere in the
oropharynx and the upper respiratory tract. Lesions can occur throughout the alimentary tract
in the subcutis, muscle fascia and in the muscle itself. The lesions on the mucous epithelium
are round (usually 4 to 40 mm in diameter) and have a ring shape where separation from the
normal tissue has occurred. Necrosis follows quickly and the ulcers become infected. There
are mucopurulent discharges from the mouth and nostrils, persistent dribbling of saliva,
coughing and often stertorous respiration. Conjunctivitis and keratitis may be seen.
Infected cattle may develop oedematous and inflammatory swellings of the brisket and of one
or more limbs. The sheath of bulls can be similarly affected. Secondary infection can develop
as the lesions become hard and necrotic. Lesions may harden and remain in situ. They may
also slough away to leave a hole of full skin thickness, known as "sitfast". Extensive
sloughing of necrotic skin from the udder or limbs can occur when they have become
enlarged and oedematous. It is at this stage that the lesions constitute prime sites for
oviposition by the screwworm fly.
Severely infected animals become emaciated and may require euthanasia. The debility
persists for one to three months and occasionally for up to six months. The mouth lesions
interfere with feeding; milk production ceases and udder and teat lesions may result in serious
infections with the sloughing of necrotic tissue. Limb lesions can severely restrict movement.
Painful lesions on the genitalia of bulls interfere with their ability to serve for many weeks.
Oestrus is suppressed during the periods of severe debility.
Lesions in the skin, subcutaneous connective tissue, and muscles of the limbs, together with
the severe skin inflammation caused by secondary infection of the lesions, greatly reduce
mobility. Under nomadic pastoral conditions, animals affected in this manner may rapidly
succumb to dehydration and starvation, thus increasing losses.
Pneumonia is a common sequel in animals with lesions in the mouth and respiratory tract.
Nodular lesions may have quite extensive surrounding areas of interstitial pneumonia in the
lung, and inhalation pneumonia frequently occurs. The responses to antibiotic therapy are

poor. Abortions often follow outbreaks of LSD and calves have been born with extensive skin
lesions, presumably acquired by intra-uterine infection.
Morbidity, mortality and the economic significance of LSD
The morbidity rates in LSD epidemics vary enormously and the disease occurs in many
different biotypes, from the temperate high altitude grasslands through to the various wet and
dry savannah ecotypes and the very dry semi-desert and thorn scrub. It can also spread
extensively in irrigated lands in the Sudan and Egypt. The differences in morbidity rates are
thought to reflect the distribution and relative abundance of insect vectors in the various
habitats.
Morbidity rates of 1 to 2 percent may be contrasted with those of 80 to 90 percent in different
situations. In southern, West and East Africa and the Sudan, the higher rates have been
encountered in epizootics, yet much lower rates may occur during the same epizootic. In
general, the breeds of Bos taurus, imported into Africa from Europe, are far more susceptible
than the indigenous Bos indicus cattle. Channel Island breeds are particularly severely
affected by LSD. Mortality rates of 10 to 40 percent and even higher have been reported on
occasion but the much lower range of 1 to 5 percent is more usual.
Generalized LSD infection - Dermatose nodulaire gnralise - Infeccin generalizada
de dermatosis nodular contagiosa
LSD lesions on the tail - Lsions sur la queue - Lesiones debidas a la dermatosis nodular
contagiosa en la cola
Severe LSD skin lesions - Graves lsions de la peau - Lesiones cutneas graves de la
dermatosis nodular contagiosa
In any epizootic, economic losses clearly depend on the morbidity rates and are brought
about by mortality, the loss of production, the depression of growth rates and hide damage.
The full skin thickness lesions of LSD punch holes right through the hide, thereby causing
permanent damage (Green, 1959).
Treatment and control
There is no specific antiviral treatment available for LSD infected cattle. Sick animals may be
removed from the herd and given supportive treatment consisting of local wound dressing to
discourage fly worry and prevent secondary infections. Systemic antibiotics may be given for
skin infections, cellulitis or pneumonia, and food and water should be made readily available.
Local applications of insecticides to infected cattle have been made in an attempt to reduce
further transmission, but to no apparent benefit.
Should LSD appear in cattle in another country beyond its previous range, it is recommended
that all infected and contact cattle be slaughtered immediately and the carcasses destroyed in
an attempt to eliminate the focus of infection. A vaccination cover with a 25 to 50 km radius
may then be established around the focus and all cattle movements stopped within that zone.
Alternatively, it might be decided to leave all cattle in the zone unvaccinated, allowing the
manifestation of any- residual infection. The vaccination policy may allow the virus to persist
in some cattle.

When an epizootic occurs in an enzootic area and LSD has already spread extensively,
slaughter policies- are inappropriate and extensive vaccination campaigns are recommended.
The imposition of strict movement controls are suggested because, although these do not
contain outbreaks of LSD, they do prevent new foci from becoming established at a certain
distance. Vaccination will greatly reduce the morbidity and economic effects of an epizootic
but may not completely limit the extension of-LSD. Follow-up vaccination of calves and revaccination programmes over a period-of two to three years will greatly reduce the incidence
of clinical disease. No country in sub-Saharan Africa, however, has succeeded in eradicating
LSD once it has occurred.
Vaccines for LSD control
Two different vaccines have been widely and successfully used for the prevention of LSD in
cattle populations in Africa. In southern Africa, the Neethling strain of LSD was passaged 50
times in tissue cultures of lamb kidney cells and then 20 times in embryonated eggs. The
strain proved to be innocuous and immunogenic for cattle, although local reactions do occur
in a high proportion of animals at the vaccination site. No generalization of infection has ever
followed its use. It is produced in tissue culture and issued as a freeze-dried product (Weiss,
1968).
In Kenya, an effective vaccine has been produced from a local strain of sheep and goat pox
virus (SGPV). This was shown to immunize cattle against LSD (Capstick and Coackley,
1961). The SGPV was passaged 16 times in pre-pubertal lamb testes or foetal muscle cell
cultures and used for vaccination at this level. Local reactions have not been seen, but some
Bos taurus breeds have shown lymphadenitis with signs of mild, generalized LSD-like
lesions following vaccination (approximately 0.02 percent). These reactions were not
reproduced in the laboratory, when up to 1 000 times the field dose was used, and there is a
possibility that they represent needle transmission of the field virus. No such reactions have
ever been observed in Bos indicus cattle so the use of the vaccine in the face of epizootics
should not be prevented.
Two other strains of sheep pox vaccine have recently been used as a prophylaxis against
LSD. The Romanian strain, prepared in the skin of lambs for use against sheep pox, was used
in several million cattle in Egypt and appeared to be immunogenic. Another sheep pox strain,
the RM 65 prepared in tissue culture, was used in Israel. No complications have followed the
use of these strains in cattle.
Studies with both the Neethling and the Kenya SGPV strains show that an immunizing dose
of 103.5 TCID50 is desirable for field vaccination campaigns. Good protection has been
obtained with 102 in the face of an epizootic, although there is some suggestion that this may
not be the case with all strains.
Serological studies with vaccinated cattle have shown that many animals resist challenge with
virulent LSD when they have no detectable fluorescent or neutralizing antibody to the virus.
Most animals do show a serological response after field infections with LSD, however. There
is an important cellular component of the immune response to LSD in cattle, as there is to
other pox viruses. This formed the basis for a hypersensitivity test, developed by Capstick
and Coackley (1962), to determine the susceptibility of cattle to LSD for use in vaccination
studies. This test can be used to determine the responses to vaccination.

LSD, Kenya SGPV, Romanian sheep pox and Gorgon goat pox (from Iraq) have all been
shown to be serologically identical by fluorescent antibody and serum virus neutralization
tests (Davies and Atema, 1981). Therefore, it is likely that many of the sheep or goat pox
vaccine strains available in different parts of the world would prove suitable for the
prophylaxis of LSD. It is suggested that ten to 50 times the sheep immunizing dose be used
for this purpose, however.
Recent restriction enzyme analyses of the genome of these virus strains have shown that the
Kenya SGPV and LSD appear to be identical. The other strains of sheep or goat pox do show
differences in their DNA from that of LSD (Gershon and Black, 1988), but this is not
reflected in their serological and immunological properties.
Diagnosis of LSD
The rapid and precise identification of LSD is essential to mobilize resources quickly and
effectively should it appear in new non-enzootic areas outside Africa. The clinical diagnosis
of LSD is not difficult for those familiar with the disease, but those who are not so
experienced can readily confuse the lesions with many other conditions: for instance, bovine
herpes virus 2 (Allerton) infections; delayed hypersensitivity reactions following foot-andmouth disease vaccinations; insect bites; streptothricosis, globidiosis, or demodicosis.
Laboratory confirmation is desirable.
The early skin lesions contain large numbers of virus particles which can be readily seen with
an electron microscope. Simple negative staining of a few small skin fragments taken from
the lesions with phosphotungstic acid will show large numbers of the roughly brick-shaped
pox virus particles. Herpes virus particles may also be seen in such skin fragments, and they
may be of the bovine herpes type 2 or 3. The latter are termed orphan viruses and are often
seen in normal and LSD-infected tissue. They may be present in such numbers that they mask
the larger pox viruses, which may also be present. Diagnostic errors may therefore arise from
this method. Parapox virus particles of an oval shape and with a spiral matrix may also be
seen in an electron microscopy of bovine skin.
Histopathological sections of the skin lesions show changes peculiar to LSD. There is a
vasculitis and perivascular infiltration with white cells which causes a thrombosis of the
vessels in the dermis and subcutis. The cells infiltrating the lesion are of a predominantly
epithelioid type, known as the celles claveleuses, which Borrel (1903) described in sheep
pox. There are also eosinophilic intracytoplasmic inclusions in the epidermal elements of the
lesion and the inflammatory cells (Burdin, 1959). The lesions gradually become necrotic as a
result of the thrombosis. The differential diagnosis from some of the conditions mentioned
above can readily be made by a histopathological examination of the lesions.
Virus isolation may be attempted and is best carried out in primary or secondary prepubertal
lamb testis cell cultures. They are more sensitive than kidney, muscle, lung, skin, thymus or
endothelial cells, although these can be used. Cultures are infected with suspensions of the
early skin lesions, preferably in tubes or wells with cover slips. These can then be stained at
48 to 56 hours to show the eosinophilic intracytoplasmic inclusions, or the viral antigen may
be identified by immunological methods with fluorescent or peroxidase conjugated
antibodies. This may be possible as early as 24 hours after inoculation of the cultures (Davies
et al., 1971). There is a cross-relationship with the cowpox virus which may be detected by
this method, but it is only demonstrable at low titres. The presence of BHV 2 or 3 in the

specimen may result in their rapid growth to mask the simultaneous presence of the Capripox
virus. Early fluorescent or immunoperoxidase staining may allow the diagnosis to be made. It
is suggested that lesions be collected from several animals and processed separately to reduce
the possibilities of such a complication. Cytopathic effects resulting from the LSD virus
develop at five to 14 days in most primary cultures, but it is recommended that they be frozen
and thawed and that one blind passage be carried out. This process will detect LSD strains
that adapt slowly to the cultures or that were present only in very small amounts in the
original sample.
Epidemiology and transmission
The virus of LSD does not spread readily among animals held in insect-proof pens. While
infection by contact can occur, this is thought to occur only at a low rate and is not considered
a major component of transmission during epizootics. Most infection is thought to be the
result of insect transmission of the virus (von Backstrom, 1945; Thomas and Mare, 1945;
Diesel, 1949; MacOwan, 1959; Weiss, 1968). Pox viruses are highly resistant and may
remain viable in infected tissue for at least four months, and probably longer. Virus is also
present in blood, nasal and lachrymal secretions, semen and saliva, which may be sources for
transmission.
There is little hard data incriminating any particular insect species as a vector of LSD. Virus
has been isolated from Stomoxys spp., commonly associated with cattle, and from the
Biomyia fasciata mosquito species, found in large numbers and associated with LSD-infected
cattle. Tabanidae, Glossina and Culicoides spp. have all been found in situations where there
has been ongoing LSD transmission and have been suspected to be involved. Stomoxys spp.
have been shown to transmit SGPV successfully (Kitching and Mellor, 1986). The role of all
these insects in the transmission of LSD remains to be evaluated in the laboratory and under
field conditions. Transmission is likely to be mechanical, as was found to occur with Rift
Valley fever and many of the above insect genera. Fowl pox is transmitted mechanically by
mosquitoes and it is likely that many insects could transmit LSD in this manner. Plant pox
viruses are frequently involved in biological cycles within insect vectors. This is a possibility,
but it would be remarkable for a mammalian pox virus.
LSD is a Capripox virus and these differ from Orthopox viruses by having a narrow
vertebrate host range, infecting only sheep, goats and cattle. Some wild species (giraffe,
impala and Thomson's gazelle) have been infected by parenteral inoculation with LSD virus
and have developed characteristic lesions. Lesions of LSD have not been seen on these
animals when they have been present during epizootics of the disease. Sheep and goats do not
become infected during outbreaks of LSD even when held in close contact with infected
cattle. African buffaloes (Syncerus caffer) do not show lesions in the field during epizootics
of LSD, and nor did the majority of Asian water buffaloes, Bubalus bubalis, exposed during
the Egyptian LSD epizootic. Five cases of LSD-like lesions in buffaloes were reported in
Egypt. Both buffalo types may suffer an inapparent infection and seroconvert, however. This
point has not been examined. In an enzootic area for LSD in Kenya, many African buffaloes
had high titres of antibody to Capripox virus; in another area, no antibody was found. This
may have been specific for LSD or the result of infection with another unknown Capripox
virus. The same sera were screened against cowpox virus and no neutralization of this virus
occurred, suggesting that the antibody detected was specific.

Sheep were found to be infected with Kenya SGPV on the farm where the first outbreak of
LSD occurred in Kenya. The DNA of these viruses is identical according to restriction
endonuclease analysis. It was suggested that the cases originated from a strain of Kenya
SGPV which had an altered level of host adaptation for cattle. The virus strains are identical
in every way in the laboratory, differing only in their ability to produce LSD in one host and
sheep and goat pox in the other. In the alternate host, the viruses produce a local lesion at the
inoculation site with some regional lymph node enlargement. No sheep pox has ever occurred
in southern Africa during the LSD epizootics there, despite the presence of 40 million sheep.
Importance of LSD
Economically, LSD is a significant cattle disease and high mortality rates of 40 percent or
more have been encountered. Skin lesions result in severe and permanent damage to hides,
while lesions in the mouth, pharynx and respiratory tract cause a rapid deterioration in
condition and sometimes severe emaciation, which may persist for months.
LSD has occurred in a wide range of ecotypes in Africa where, in the last 20 years, it appears
to have spread to virtually all countries on the continent. It has recently extended its range to
include Egypt where, in one summer, it spread thousands of kilometres throughout the whole
of the country and also into Israel. Movement restrictions do not control the disease. Insect
movement in air currents is uncontrollable, so there is little way of preventing further
extension into the Near East and North Africa. LSD, furthermore, has the potential to spread
throughout the Mediterranean region.
The basic scientific studies necessary to define the transmission mechanisms for LSD have
not been carried out. This is an embarrassing gap in our knowledge of the disease and calls
for a serious research effort. Information is required on the prevalence of the different biting
flies associated with cattle in the various biotypes of countries that are potentially receptive to
LSD. Subsequently, a judgement may then be made regarding the likelihood of an LSD
epizootic.
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