Three-day fever
A.J. Akakpo
B.P. 12 104 Dakar-Yoff, Senegal
E-mail: ayia11612@gmail.com
Summary
Three-day fever is a viral disease caused by an Ephemerovirus of the family
Rhabdoviridae, transmitted by arthropod vectors. It is common in tropical and sub-
tropical regions, where it affects mainly domestic cattle and buffaloes, especially
in intensive dairy or fattening production systems. It is of economic importance
because it reduces milk production and fertility and causes abortion. The disease
is generally benign. It manifests in several susceptible subjects simultaneously,
with a sudden episode of fever accompanied by muscle involvement with arthritis,
stiffness of the limbs, and lameness, followed by rapid recovery. The presence of
a serofibrinous exudate in the joints is indicative of the disease. Clinical diagnosis
is often difficult in the absence of pathognomonic signs. Epidemiological factors
(proliferation of arthropod vectors), associated with a short-lived fever and the
presence of many immature neutrophils, point strongly to three-day fever. In the
absence of any specific treatment, the symptoms are treated with antibiotics and
anti-inflammatories. Medical prophylaxis currently uses live attenuated vaccines,
pending the development of recombinant vaccines, which are giving promising
results.
Keywords
Arbovirosis – Buffalo – Cattle – Ephemorovirus – Rhabdoviridae – Three-day fever –
Tropical region.
Rev. Sci. Tech. Off. Int. Epiz., 2015, 34 (2), 533-538
Introduction
Three-day fever (also known as bovine ephemeral fever,
bovine epizootic fever, three-day stiffsickness, three-day
sickness and dengue of cattle) is a virulent, inoculable and
non-contagious viral infectious disease of domestic cattle
and buffaloes. It is caused by an RNA virus belonging
to the family Rhabdoviridae, transmitted by arthropod
vectors. Clinical signs of the disease include mild fever
associated with joint pains, muscular weakness, stiffness
of the limbs and lameness, sometimes accompanied by
anorexia and depression. Although morbidity may affect
100% of the herd, mortality is generally low (1–2%). In
most cases the disease resolves itself suddenly within
three days. This disorder is of considerable importance for
intensive dairy farms because of its impact on reproduction
and because it can lead to a decrease, or even complete
cessation, in milk production.
Background
and geographical distribution
Three-day fever is most often reported in countries close
to the equator and in tropical and subtropical regions of
Africa, Asia and Australia, as well as in a few temperate
zones of Asia.
In 1878, Schweinfurth (1) wrote a brief description of the
disease in Africa. However, it was Piot (2) who gave us the
first scientific description in his excellent report on the
Egyptian epidemic of 1895. He referred to the disease as
epizootic dengue fever of cattle to mark the similarity between
the signs of the disease in animals and those of dengue
fever in humans. In 1907, Bevan (3) described the clinical
signs of the disease in former Northern Rhodesia (now
Zambia). In 1910, Freer (4) highlighted two important
points:
– the need for intravenous inoculation of a healthy animal
with blood taken from a sick animal to reproduce the
disease
– the intervention of arthropod vectors in the transmission
and spread of the disease.
In 1967, Van der Westhuizen (5) succeeded in isolating and
characterising the causal agent as a member of the family
Rhabdoviridae. In 1974, Davies and Walker (6) demonstrated
the possibility of viral replication in biting arthropods, by
isolating the virus from a mixture of Culicoides during an
epizootic outbreak of the disease in cattle in Kenya.
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Between 1936 and 1940, the disease spread beyond Africa
to other countries. Subsequently, the disease has been
reported in the Near and Middle East (Israel, Syria, Iran,
Iraq), Central Asia (Pakistan, India, Bangladesh, People’s
Republic of China), Southeast Asia, Australia and later
Japan (1968) (7, 8, 9, 10, 11).
In Senegal, despite the lack of scientific reports, the disease
is well known to Fulani herders, who refer to it as ‘rainy
season fever’. Rural veterinarians are also well acquainted
with it.
The disease is unknown in New Zealand, Europe and the
Americas.
Affected species
Species belonging to the genus Bos (taurine cattle, zebu) and
domestic buffaloes are responsive and susceptible to three-
day fever. Experimentally infected goats and sheep and many
wild herbivores, such as wildebeest (Connochaetes taurinus),
buffalo (Syncerus caffer), hartebeest (Alcelaphalus buselaphus),
waterbuck (Kobus ellipsiprymnus), kudu and giraffes, are
responsive but not susceptible because they experience a
silent infection with seroconversion (12, 13, 14).
Importance
The importance of three-day fever is largely economic in
nature. While it does not cause significant mortality, apart
from during the rare epizootics reported in Egypt and South
Africa (15, 16), on intensive dairy farms the disease leads
to abortion and a very sharp drop in milk production (8,
13, 17, 18).
Aetiology
The three-day fever virus is a cone-shaped capsule with a
spiky surface, similar to the rabies virus. The nucleocapsid,
180 nm in length and 73 nm in diameter, is formed of a
negative-sense single-stranded RNA and proteins and is
helical in structure. The lipoprotein envelope has fine
projections on its surface called spicules.
The virus contains five major proteins (19). These are:
– the glycoprotein envelope (G protein), which is
immunogenic because it induces neutralising antibodies
that aid resistance
– four non-membranous proteins: the N protein, generally
associated with the nucleocapsid, the L protein, which is a
polymerase, and the matrix proteins M1 and M2.
There are four serotypes of this virus, only one of which is
pathogenic. In 1986, a fifth serotype was reported to have
been isolated in Japan, but this was unconfirmed (20).
Culture is possible on cell lines (BHK-21 and Vero), as well
as on young mouse brains.
The virus is vulnerable under external conditions. It is stable
at a pH of between 5 and 10 and inactivated by the meat
maturation process, during which the pH falls below 5. The
virus is very sensitive to disinfectant chemicals and to lipid
solvents.
The pathogenicity of the three-day fever virus is variable;
as a general rule it is not particularly pathogenic, making
the disease fairly mild, but there are some strains with quite
high pathogenicity that cause more serious sickness in
lactating females and fattening animals.
The three-day fever virus belongs to the genus
Ephemerovirus. It belongs to the group Lyssavirus in the
family Rhabdoviridae (21). As it belongs to the group
Lyssavirus, the three-day fever virus shares antigens with the
Adelaide River, Kimberley and Berrimah viruses, as well as
with the Puchong and Malakal viruses. This can cause cross-
reactions and problems interpreting serological reactions.
According to Nandi & Negi (13), a subacute infection with
the Kimberley virus induces weak production of antibodies
that neutralise the three-day fever virus, but confers no real
protection.
The most powerful protection comes from the strong and
lasting immunity that develops in animals that recover.
This humoral immunity is based on neutralising antibodies
directed against the glycoprotein of the envelope. It seems
that this confers relative, rather than absolute, immunity
because relapses in cured animals have been reported by
St Georges in Australia (17). The author also speculates
on the possible role of related rhabdoviruses, such as the
Kimberley virus, which triggers the initial appearance of
non-protecting xenogenic antibodies, leading to possible
confusion with specific antibodies during serological testing.
Pathogenesis
After entering the body, the three-day fever virus produces
polynuclear neutrophils in the blood 24 hours after
infection. Infection of endothelial cells, which is associated
with hypocalcaemia, leads to the development of clinical
signs and lesions (8). Inflammation and toxaemia in
the blood vessels, joints and mucosa are linked with the
massive production of interferon in cells infected with the
virus, with plasma fibrinogen found in the joints and the
peritoneal, pleural and cardiac cavities. A sharp fall in blood
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calcium levels is responsible for the signs of nerve paralysis
observed.
Clinical signs
The incubation period under normal conditions is very
short: 36–48 hours. Under experimental conditions,
this may vary from 29 hours to 10 days, but the average
is three to four days.
The disease causes a sudden rise in temperature and affects
the general state of health. There is a similar sudden fall
in temperature, culminating in a general recovery after
three to five days without complications. Hyperthermia
generally occurs in two phases (22, 23). During the first
peak of fever, the clinical signs are discreet and hard to
detect. In more severely affected animals there is sudden
fever with temperatures reaching 40–41°C, as well as
depression, loss of appetite, anorexia, stiff gait, salivation
and nasal discharge, inflammation of the joints, rapid
pulse and respiration rate, shivering and oedema of the
subcutaneous muscles, eye sockets and head. The animal,
sometimes lying in sternal recumbency and sometimes on
its side, shows some reflexes, but these gradually disappear
as the disease progresses. Loss of the swallowing reflex,
lack of rumination, constipation and profuse salivation
become evident. Total loss of reflexes followed by coma
leads to the death of the laterally recumbent animal. It
should be noted, however, that these clinical signs may
also disappear as suddenly as they appeared. The second
peak of fever occurs 12–24 hours after the first, affecting
the lungs (tachypnea, rattling) and causing lacrimation.
Secondary complications may include signs of pneumonia
and pulmonary emphysema, abundant discharge, stiffness
of the limbs, arthritis, lameness and lasting paresis, forcing
the animal into prolonged sternal recumbency. This phase
of hyperthermia may last from two to four days.
In addition to hyperthermia, other clinical signs may appear
or persist, such as subclinical mastitis leading to a sharp
reduction in milk yield, abortion in 5% of pregnant females
and infertility in bulls. Generally speaking, animals in good
physical condition (fat, good milkers) show more severe
signs than lean animals and non-lactating females.
The disease can lead to death in some individuals following
a gradual loss of reflexes, or to cessation of swallowing and
rumination. But other individuals recover in five to six days
without complications (pulmonary emphysema, locomotor
ataxia, persistent stiffness of the limbs). Milk yield in
recovered milking cows is always lower than it was prior
to the disease.
Lesions
Serofibrinous polyserositis, of varying degrees, in the
articular synovial membranes and in the thoracic and
peritoneal cavities is characteristic of the disease (23).
Serous surfaces may also show signs of bleeding and
oedema to varying degrees. The oedema fluid in the
thoracic or abdominal cavity contains fibrin. In the joints,
this periarticular inflammatory fluid is yellow or brown and
gelatinous in appearance.
Other lesions may also occur, such as pulmonary and
lymph node oedema, inflammation of the parietal and
visceral pleura, pericarditis (especially at the base of the
heart), necrosis at certain points of the skeletal muscles,
and, sometimes, emphysematous lesions of the lungs,
mediastinum and subcutaneous connective tissue.
Epidemiology
Three-day fever is especially common in tropical and sub-
tropical regions of Africa, Asia and Australia, as well as
in certain temperate regions of Asia. It affects intensively
reared domestic cattle and buffaloes and has a significant
economic impact. The disease is seasonal, with increased
prevalence in the hot, wet season (rainy season in tropical
and subtropical zones, summer and autumn in temperate
zones), when conditions favour the proliferation of
arthropod vectors.
The main sources of infection are sick live animals and
asymptomatic carriers of the virus, as well as arthropod
vectors. Owing to its vulnerability (low resistance to
desiccation, heat and ultraviolet rays, etc.), the virus is non-
persistent in the external environment.
The responsiveness and susceptibility of individuals are
influenced by both intrinsic and extrinsic factors. One of
the intrinsic factors that has a significant influence is the
species of the animal. Three-day fever is pathogenic mainly
to domestic cattle and buffaloes. Wild ruminants (eland,
buffalo, wildebeest) often show no signs of infection. Heavy
animals and dairy cows are more susceptible and succumb
to severe forms of the disease. As demonstrated by Momtaz
et al. in Iran, in a given herd, the prevalence of the disease
is higher in females than in males and it also increases with
age (14). Extrinsic factors include: a warm, wet season;
heavy rain; physical fatigue; low-lying, wet swampy areas;
flood plains and irrigation zones.
Direct transmission of three-day fever is unknown;
transmission is exclusively indirect via vector-borne
hematophagous arthropods belonging to various species
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of mosquitoes or Culicoides (24), particularly the family
Culicidae, which includes the genera Culex, Aedes and
Anopheles (Culex annulirostris and Anopheles bancrofti are the
prime suspects), and the family Ceratopogonidae (Culicoides
brevitarsis and C. imicola) (16, 25).
Three-day fever develops in an enzootic or sporadic form
in infected countries where the vectors survive throughout
the year. Prevalence increases with the proliferation of
arthropod vectors in favourable seasons (the rainy season in
tropical zones or summer and autumn in temperate zones).
Prevalence decreases once again with the arrival of the less
conducive dry or cold season. During epizootic outbreaks,
morbidity may be high (50–100%), but mortality is always
low (2–3%). When the disease appeared in Saudi Arabia,
morbidity of 59% and mortality of less than 1% were
recorded (26).
Diagnosis
Three-day fever can be diagnosed either in the field or in
the laboratory. The first cases are difficult to diagnose in
areas previously free from the disease, and diagnosis is not
always any easier in areas where the disease is well known,
because of its non-characteristic appearance and its discreet
early clinical signs.
In the field, diagnosis of the disease relies on
epidemiological and clinical elements and lesions. In
general, three-day fever may be suspected in an enzootic
zone or in the season conducive to the proliferation of
arthropod vectors (hot, wet season, low-lying, wet, swampy
areas, delta or flood plain). It should also be suspected in
an intensive dairy or fattening cattle system with improved
breeds if several animals simultaneously present with fever,
stiffness of the limbs and lameness, and subsequently
recover rapidly. The presence of a serofibrinous exudate in
the joints is also highly indicative of the disease.
A differential diagnosis may be necessary, depending on
the location, for hyperthermic and nervous or respiratory
disorders. Diseases that induce hyperthermia include
Rift Valley fever and bluetongue. The ability to induce
hyperthermia is not the only similarity between these
two diseases: both are caused by viruses transmitted
by arthropod vectors (arboviroses), and both occur
mainly in the hot, wet season, which is conducive to
the proliferation of arthropod vectors. Diseases causing
nervous and respiratory symptoms include botulism,
ehrlichiosis of ruminants, intoxication by poisonous plants
(genera Crotalaria, Diplodia), hypocalcaemia, pulmonary
emphysema and acute pulmonary oedema.
In general, three-day fever evolves benignly towards a cure
in three to four days if there are no complications.
In the field, the disease cannot be diagnosed with certainty
if there are no pathognomonic signs, making it necessary to
resort to laboratory tests to confirm or invalidate a clinical
suspicion.
Laboratory diagnosis entails both direct and indirect
microbiological testing of blood samples taken from animals
in the hyperthermic phase, to identify the virus and specific
antibodies.
Direct microbiological diagnosis involves the isolation and
detection of the pathogenic agent. Blood collected during
the hyperthermic phase in a tube with an anticoagulant can
be used for direct examination, as well as to isolate the virus
in a culture and identify the viral genome.
– Histological analysis of a blood smear on a slide can be
used for a blood cell count, as well as immunofluorescence.
a) A cell count is used to determine the number of formed
elements in the blood. The presence of neutrophilia
(neutrophils significantly higher than 30%) associated with
many immature forms strongly indicates three-day fever.
This test can be used for rapid diagnosis in the field.
b) Immunofluorescence can be used to detect and identify
the virus or its antigens on the smear using immune
serum (the virus-specific antibodies are marked with a
fluorochrome).
– The virus is isolated either in a culture of blood leukocytes
on cell lines (BHK-21 or Vero) or by intracerebral inoculation
of newborn mice. The virus is identified by neutralisation of
the viral culture in the presence of the specific antiserum or
immunofluorescence on the cell lawn. A result is obtained
after three to four days using this costly reaction.
– The viral genome can be identified using the classic
reverse transcription polymerase chain reaction (RT-PCR).
In 2011, Zheng et al. (27) described a real-time loop-
mediated isothermal amplification (RT-LAMP) assay used to
detect the three-day fever virus. This test is more sensitive
than isolation and identification of the virus using traditional
RT-PCR and thus allows earlier detection of the virus.
Indirect microbiological diagnosis aims to detect neutralising
antibodies using viral neutralisation tests or an enzyme-
linked immunosorbent assay (ELISA). The detection of
antibodies in the second of two blood samples taken after
an interval of two to three weeks demonstrates infection by
the three-day fever virus. However, the existence of antigens
in common with other lyssaviruses, such as the Kimberley
virus, can make it difficult to interpret serological responses
because of cross-reactions. The blocking ELISA test can
overcome this problem because the reaction is more specific
than viral neutralisation. It can also differentiate between
infection with the three-day fever virus and infection with
other similar viruses (22, 28).
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Treatment
There is no specific treatment for infection with the three-
day fever virus. Nevertheless, the symptoms can be treated
and hygiene measures implemented.
Anti-inflammatories and antibiotics can be used to reduce
the severity of the disorder, as was done in India (29). The
intravenous administration of calcium, taking care not
to overdose, can remedy signs of hypocalcaemia such as
constipation, rumen atony, muscle tremors or paresis.
Hygiene measures are implemented to avoid or remedy
situations conducive to the disease. It is important to rest
sick animals because, if they go in search of water or food
in a pastoral system, this could exacerbate the clinical signs
and increase mortality. Convalescent animals must also be
nursed to enable them to regain their health.
In Senegal, Fulani herders make febrile cattle take cold baths
in order to lower their body temperature. Ousseynou Diouf,
Doctor of Veterinary Medicine, treats seriously sick animals
with antipyretics, anti-inflammatories and antibiotics,
in particular tetracyclines, which results in a spectacular
improvement in their condition (personal communication).
Prophylaxis
Efforts to prevent infection are based on controlling
arthropod vectors and implementing livestock hygiene
measures to reduce the impact of favourable conditions.
The results are limited, especially in countries where
livestock rearing is pastoral and vector control programmes
are not entirely satisfactory.
In enzootic countries, strengthening the immune defences
of susceptible organisms can offset the inadequacies of
prophylactic measures.
Medical prophylaxis relies on active immunisation to make
animals produce their own defences. The immunising
component of the virus structure is the glycoprotein of the
envelope. The vaccines used are based on the inactivated
or attenuated whole virus. Vaccines inactivated by
ethyleneimine and adjuvanted with aluminium hydroxide
have given mixed results in the field. Attenuated virus
vaccines, combined with an immunostimulant and
administered twice at 15-day intervals have given better
results in Australia. The conferred immunity lasts one
year and protects against severe forms of the disease, but
not against infection (30). Experiments with recombinant
vaccines (insertion of the G protein gene or envelope
glycoprotein) in an expression vector (poxvirus) have given
promising results (31) and are therefore vaccines of the
future.
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