1 In 1974, a scientific report
described a previously unreported nervous disease
of goats which was believed to be caused by a virus.
This was followed by a report of an arthritic disease
in goats presumably caused by the same agent. Shortly
afterward the viral cause of these conditions was
confirmed and the virus characterized. The development
of a diagnostic serologic test was soon reported along
with the observation that a high percentage of goats
in the United States appeared to have experienced
the virus. Investigation into the transmission of
the disease suggested that virus was spread through
colostrum and milk of infected dams and that virus
free herds might be maintained by raising kids in
isolation.
2 Nomenclature The nervous disease
first reported in 1974, was named Viral Leukoencephalomyelitis
of Goats (VLG). When it became apparent that arthritis
could also result from the same virus infection, the
name of the disease was changed to Caprine Arthritis
Encephalitis Syndrome (CAE). It is now apparent that
the virus also produces changes in the lung and udder.
The name CAE however still remains in place.
3 The Causative Virus The virus which
causes CAE is very closely related in structure to
the virus which causes Ovine Progressive Pneumonia,
a common respiratory ailment of sheep in the western
US, and to the virus which causes Visna, a nervous
disease of sheep first reported from Iceland. These
agents, called retroviruses, are classified as slow
viruses which means that they usually produce disease
only after a very long incubation period and that
once an animal is infected, the infection persists
throughout the animal's life. This fact is important
in regard to interpretation of diagnostic tests. CAE
virus has not been shown to cause any disease problems
in man.
4 Transmission of CAE Virus Knowledge
of how a disease is transmitted is often the key to
developing a successful program for preventing the
spread of infection. To date, all published reports
suggest that goats become infected with CAE virus
as newborn kids. Experimental evidence for this is
persuasive. Kids delivered either naturally or taken
by cesarean-section, but deprived of colostrum and
fed cow milk remain free of the virus despite the
fact that their dams are infected. If taken by cesarean-section
or delivered naturally, but allowed to nurse colostrum
or milk from an infected doe, kids will show evidence
of virus infection. These findings indicate that kids
are not infected in utero or during passage through
the birth canal; but do pick up infection when nursing
colostrum or milk from infected dams. This suggests
that control of the spread of new infections might
be achieved by separation and artificial rearing of
kids at birth.
5 Prevalence of CAE One aspect of
the CAE syndrome which has proven most troubling to
the US goat industry was a published report that a
high percentage of goats tested from all over the
United States showed serological evidence of infection
with CAE virus. Of 1160 goats tested from 24 states,
81 howed antibody to CAE virus using the agar gel
immunodiffusion (AGID) test. It can be assumed that
animals with antibody to CAE virus have been exposed
to and infected by the virus. The only exception to
this could be young kids with detectable antibody
picked up from the dam's co lostrum. Unlike most bacterial
diseases, where a strong antibody response means that
the animal has cleared itself of the invading organism,
infections with CAE and other retroviruses are likely
to persist in the animal despite a high antibody titer.
Therefore, it is probably true that a large percentage
of antibody positive goats carry persistent infections.
However, it does not necessarily follow that the majority
of these goats are likely to show clinical signs of
the CAE syndrome. The factors which contribute to
the onset of clinical signs in animals infected with
the virus are unknown.
6 The major problem associated with
this high prevalence of infected US goats is not the
actual incidence of clinical disease so much as the
negative perception of prospective goat buyers and
regulatory officials confronted with a positive AGID
test. Already some countries importing US goats, like
Kenya, have refused or destroyed shipments of goats
which turned out to be antibody positive. Economic
restraints such as this increase pressure on the goat
industry to aggressively tackle the CAE problem.
7 The Clinical Signs of CAE Two separate
distinct syndromes are caused by the CAE virus, a
neurological disease in the spinal cord and brain
of young kids and a joint infection of older goats
resulting in arthritis. How individual animals infected
with CAE virus escaped one or the other or both syndromes
remains a mystery. The clinical signs of the two syndromes
are as follows.
8 The Nervous Form of CAE -- The
nervous form of CAE was the first to be described.
All breeds of goats can be affected as can both sexes,
and most individuals first show signs between one
and four months of age. The problem is one of progressive
weakness (paresis) of the hind limbs leading to eventual
paralysis. The early paresis may be perceived as lameness,
incoordination or weakness in one or both rear legs.
Knuckling over of the feet and difficulty in rising
may follow until such time that the animal is unable
to rise at all. The course of the disease is from
several days to several weeks. Despite the progressive
paralysis, the kid will usually remain bright and
alert and continue to eat and drink. Mild pneumonia
may be present. If the correct diagnosis is made,
the animal is often euthanized since there is no known
treatment for the condition.
9 The development of these signs
results from inflammation in the spinal cord induced
by the virus. Nerves which control motor function
of the hind limbs are progressively destroyed. In
spite of the ongoing inflammation, there is little
or no change observed in the cerebrospinal fluid on
CSF tap nor in the complete blood count (CBC). Diagnosis
is based on recognition of the clinical signs and
confirmation depends on observation of the characteristic
changes seen microscopically in the spinal cord at
the time of postmortem examination.
10 In older goats, a clinical variation
of the nervous form of CAE has been observed which
is clinically indistinguishable from Listeriosis.
Signs include circling, head tilt and facial nerve
paralysis. On postmortem examination, the characteristic
lesions of CAE virus are found in the brain stem rather
than the cervical spinal cord.
11 The Arthritic Form of CAE -- The
joint form of CAE most often appears clinically between
one and two years of age. There can be great variability
in the progression and severity of signs. Some goats
can be severely crippled within a few months while
others may show only intermittent lameness or stiffness
for years without ever becoming completely debilitated.
A ''typical'' case would fall somewhere in between.
The disease is usually first recognized as a gradually
developing lameness accompanied or followed by swelling
of the joints. Swelling is most often noted in the
front knees (carpi) and can also be seen in the hock
and stifle joints. As the condition progresses, joint
pain and stiffness become more apparent. The animal
may spend a good deal of time lying down, will begin
to lose weight and develop a rough hair coat. In severely
affected joints, the range of motion may become limited
and goats are forced to walk around on their carpi.
No specific cure is known for CAE arthritis. The well-being
of affected goats may be improved by proper foot trimming,
extra bedding and administration of anti-inflammatory
drugs such as aspirin.
12 As in the nervous form, the complete
blood count in goats with CAE arthritis will most
likely be normal. Fluid taken from affected joints,
however, may show changes suggestive of CAE. These
include a reddish brown discoloration, increased volume,
low viscosity and an increase in mononuclear cells.
All joint fluid aspirates should be cultured for bacteria,
chlamydia and mycoplasma since these organisms can
also cause arthritis in goats. In addition to these
infectious causes, traumatic injury and poor conformation
can also lead to joint problems. Keep in mind, that
not all swollen joints or stiff limbs are CAE arthritis.
13 Other Clinical Syndromes of CAE
-- Young kids with the nervous form of CAE may show
a concurrent pneumonia. On postmortem examination,
goats with either the nervous form or the arthritic
form may show characteristic changes in the lungs
attributable to CAE virus infection. These changes
are described as interstitial infiltration of mononuclear
cells. Pneumonia due to CAE virus however is rarely
seen as the only clinical sign in infected goats.
14 Another interesting microscopic
finding from postmortem examination is a similar mononuclear
infiltration of the mammary gland of infected does.
There is some speculation, but no certain confirmation,
that the well known condition of hard udder seen in
some does at freshening may be due to CAE virus. This
mysterious condition is often misdiagnosed as udder
edema or mycoplasma mastitis.
15 In arthritis of goats due to CAEV,
clinical signs are limited to the joints and surrounding
structures. Affected goats may initially show soft
fluid swellings over the joints, especially in the
bursae of the front knees. Over a period of weeks
to months pronounced lamenss may develop and progress
to the point where animals are unable to extend the
limbs and may walk on their knees. Radiographs may
reveal extensive calcification of the soft tissues
surrounding the joint. Joint fluid will contain excessive
numbers of mononuclear cells. Postmortem examination
will reveal extensive proliferation of the synovial
membrane. In other animals the advance arthritic signs
may not be so severe and these animals show only intermittent
pain, reluctance to move and progressive weight loss.
16 A serum test can be run which
demonstrates that the goat has been exposed to the
virus, but the test will not absolutely confirm that
arthritis is due to the virus infection. No treatment
or vaccine is available for arthritis due to CAEV.
A separate chapter on CAE follows because of its importance.
17 Prevention and Control Suggestions
for the control of CAE infection and plans for the
establishment of CAE free herds have been published.
These plans are based on current knowledge concerning
the transmission of the virus and controversy has
arisen regarding the practicability and effectiveness
of these programs. Perceptions of how reasonable these
suggestions are, may depend largely on the interest
to establish a CAE virus free herd. A hobbyist with
two grade does in the backyard for home milk consumption
may not be motivated sufficiently to change the management
in order to raise CAE free kids. On the other hand,
an internationally reputable breeder with sales of
registered stock may in fear of a positive AGID test
want strongly to establish and maintain a CAE free
herd. A control plan would include the following:
1. A serologic survey of all animals presently in
the herd.
2. Culling of all AGID positive animals if economically
feasible.
3. Repeated AGID testing at 6 month intervals to insure
that all positive individuals were identified.
4. If some or all AGID positive animals are maintained
for the time being, the strategy then shifts to the
creation of a new CAE free herd founded with the next
kid crop.
5. At the next kidding season all births are observed
and the kids are removed from their does immediately.
These kids are either deprived of colostrum, fed only
frozen colostrum from does previously identified as
AGID negative, or fed pasteurized colostrum. Only
experienced herdsmen with a strong background in kid
rearing should attempt to raise colostrum deprived
kids since these animals are susceptible to a variety
of dangerous infections if not given protective immunoglobulin
injections. Pasteurization of colostrum is considered
a poor alternative because heating to 161F causes
the liquid colostrum to congeal. Slow pasteurization
at 131F for 1 hour may minimize this problem but this
is time consuming. Feeding colostrum from AGID test
negative does may be the best compromise although
it must be pointed out that an occasional seronegative
doe may actually be shedding the virus and a small
number of new kids may be infected.
6. Kids should be raised in separate quarters from
does and fed cow milk or milk replacer until weaning.
7. All kids should be tested at 6 months of age and
periodically thereafter to insure their seronegative
status. Seropositive animals should be culled immediately.
8. As the new replacement herd matures, older previously
seropositive animals, still in the herd, should be
systematically culled. Any animal showing clinical
signs of CAE should be culled immediately.
9. In this manner the incidence of CAE in a herd can
be dramatically reduced in one generation and possibly
eliminated in a few generations. For this to occur,
conscientious adherence to the program is necessary.
18 Hopefully research into the workings
of CAE virus will continue at the same dynamic pace
observed over the last eight years. Clarification
of the mechanisms of transmission and the animal's
responses to infection could lead to better recommendations
for control of the disease and
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