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An
Overview of Lyme Disease in Dogs
Lyme disease
has been recognized in Europe for nearly a century but was not described
in humans in the United States until 1975. We have since learned that
clinical disease also occurs in dogs and, to a lesser extent, in horses,
cattle, and cats, while many wildlife mammals and birds become subclinically
infected and serve as reservoirs for tick infection. During the 1980s
the disease incidence in both dogs and humans increased dramatically;
Lyme disease is now the most common arthropod-borne disease of humans
in the United States, and one of the most common in dogs.
What causes Lyme disease?
Lyme disease
is caused by Borrelia burgdorferi, a corkscrew-shaped bacterium
of the spirochete group. Among the spirochetes, it is most closely related
to B. hermsii, which causes tick-borne relapsing fever in the
southwestern United States. Better known but more distantly related
spirochetes cause such diseases as leptospirosis and syphilis.
How is the disease transmitted?
Deer ticks,
hard-shelled ticks of the genus Ixodes, transmit B. burgdorferi
by attaching to and feeding on various hosts. Other bloodsucking insects
may be involved, but there is little evidence that they are important
vectors. The
primary way in which an animal or human becomes infected is by tick
bite.
After
a tick attaches and begins to feed, spirochetes residing in the midgut
of the tick begin to migrate to the salivary glands and from there move
into the host. The danger of infection increases when ticks are allowed
to feed for prolonged periods and become engorged. There is believed
to be little danger of infection during the first 12 hours of tick feeding.
Beyond this point, risk of infection increases exponentially.
Ixodes
ticks require three hosts and four different developmental steps to
complete their two-year life cycle. The female ticks lay about 2000
eggs in the spring. The larvae that emerge from the eggs do not carry
sufficient bacteria to induce infection. In the northeastern United
States, the larvae feed mainly on the white-footed mouse, Peromyscus
leucopus. Many infected mice harbor B. burgdorferi for
long periods of time without developing disease themselves. The larvae
become infected by ingesting the blood of persistently infected mice,
then drop off the host and enter a resting stage for the winter.
The larvae
molt into nymphs
the following spring. Up to 25 percent of unfed nymphs in the northeastern
United States are infected with B. burgdorferi. During spring
and early summer the nymphs feed on new hosts, again white-footed mice
or any of a wide range of animals, including dogs and humans. An infected
nymph may infect its new host during the four-day feeding period. Conversely,
an uninfected nymph becomes infected by feeding on a previously infected
animal. Our studies of dogs indicate that nymphs are less effective
vectors than adult ticks.
In the
fall of the second year, nymphs molt again and enter the adult stage.
An average of 50 percent of the adult ticks in infested areas of the
Northeast may be carrying B. burgdorferi, and infected adult
ticks are the most important source of infection for dogs. As long as
temperatures remain above 2°C (35°F), adult ticks can be found
on shrubs, where they are high enough off the ground to attach to the
white-tailed deer and other larger animals.
Adult
ticks mate on the host. Male ticks tend to stay on the host and die,
but the females engorge for five to seven days and then drop off into
the leaves, where they live through the winter. The following spring
they lay eggs and complete the two-year cycle. Adult ticks that do not
find a host in the fall may survive over the winter and become active
again from early spring until about mid-May.
Discoveries
by Cornell investigators indicate that exposure to B. burgdorferi-infected
adult ticks in the fall and early spring months is more dangerous for
dogs than exposure to infected nymphs later in the spring. Only repeated
exposure to nymphs induces infection and disease.
In the
southern United States, I. Scapularis larvae and nymphs feed
primarily on lizards, which do not maintain infection with B. burgdorferi.
Consequently, nymphal and adult infection rates are low, often less
than one percent. Rates of infection with B. burgdorferi are
also low (between one and five percent) in California.
What are the disease signs in dogs?
In contrast
to human cases of Lyme disease, where three different stages are well
known, Lyme disease in dogs is primarily and acute or subacute arthritis.
The acute form may be transient and may recur in some cases. The devastating
chronic stage in humans with systemic disease has rarely been seen in
dogs.
Dogs show
sudden lameness and sometimes signs of severe pain. One or more joints
may be involved. Joints are often swollen, hot, and painful upon manipulation.
Dogs may have fever and be off-feed and lethargic. Some become severely
depressed and are reluctant to move. Lameness may recur after a period
of recovery lasting several weeks.
Work at
the Baker Institute has shown that the incubation period in dogs is
longer than previously believed. Lameness in dogs occurs an average
of two to five months after tick exposure.
The first
stage of human Lyme disease, a skin rash called erythema chronica
migrans, is rarely seen in dogs. Some symptoms associated with
the later stages of Lyme disease in humans have also been reported in
rare instances in dogs. They include heart block, kidney failure, and
neurological changes such as seizures, aggression, and other behavior
changes.
How likely is it that a dog will get Lyme disease?
The proportion
of infected dogs that develop clinical disease is far smaller than it
is for humans. Serological studies suggest that while more than 75 percent
of the dog population in hyper-endemic areas may be exposed to infected
ticks, only about five percent of those exposed actually develop clinical
signs that might be attributable to Lyme disease. Within endemic areas,
“hot spots” of tick infestation where dogs have a much greater
probability of acquiring an infection are intermingled with non-infested
areas where the habitat is not favorable to the vector tick. There may
be age, breed, and genetic differences in the susceptibility of dogs
to Lyme disease, but little is known yet about these factors.
Our studies
indicate that bitches that become infected while pregnant do not transmit
infection to their fetuses. Furthermore, our studies have shown no evidence
that the pups of an infected bitch acquire the infection from her after
birth.
How
can Lyme disease in dogs be diagnosed?
There
are several ways to examine the immune response of dogs to B. burgdorferi
infection. The enzyme-linked immunsorbent assay (ELISA)
performed by our collaborates in the Diagnostic Laboratory of the College
of Veterinary Medicine is very useful if the dog has not yet been vaccinated
against Lyme disease – many vaccinated dogs develop antibodies
that the ELISA and other tests cannot distinguish from a dog’s
antibody response to tick exposure. Our colleagues have found through
ELISA testing that antibody can first be detected in dogs between four
and six weeks after exposure to infected ticks. Antibody titers, which
are the measurement of an immune response, increase for several weeks
and then remain constant for at least 18 months in the absence of re-exposure.
Despite high ELISA titers, viable B. burgdorferi organisms
can be shown to persist in dogs for at least 18 months, the longest
period studied. It is possible that antibody and organisms persist together
in dogs for several years.
The western
blot is a technique that determines antibodies against
multiple antigens of B. burgdorferi. In dogs as in humans,
this method can identify specific antibodies to the organism. The western
blot can distinguish between dogs that have been or are infected with
B. burgdorferi and dogs that have been vaccinated against Lyme
disease. It can also detect the dog that has been both infected and
vaccinated. While the ELISA is a quantitative determination of all the
antibodies produced against many antigenic components of B. burgdorferi,
the western blot determines the unique pattern of antibodies produced
against antigens of a tick-induced infection, which is different than
the pattern produced following vaccination.
There
are now several kits available commercially that allow veterinarians
to test for Lyme antibody in dogs without sending samples to diagnostic
laboratories. However, well-controlled ELISAs and western blots run
in reputable diagnostic laboratories are probably the most reliable
option.
Is it possible to isolate the organism itself?
The definitive
means for diagnosing bacterial infections is to isolate the causative
organism. In veterinary and human studies, B. burgdorferi has
been extremely difficult to culture from body fluids and tissues, apparently
because of the lack of organisms in the samples. In our experimental
studies, the only locus from which B. burgdorferi was consistently
isolated over a period of several months after tick exposure was the
site of bites by infected ticks. If the site of a tick bite is known,
a skin biopsy from that area provides the best chance for successful
isolation of the organism. Even if the area of the bite is not known,
there is a better chance of isolating the organism from the skin, even
from sites distant from the bite, than from the blood or urine. This
approach is not recommended however, because isolation of the organism
is time-consuming and expensive.
What are the criteria for diagnosing Lyme disease?
We consider
four criteria important in establishing the diagnosis of Lyme disease
in dogs:
- History
of exposure to ticks in an endemic area.
- Typical
clinical signs (lameness with or without fever).
- A positive
antibody test.
- A prompt
response to antibiotic therapy.
One or
two of these criteria alone are usually not sufficient to confirm a
diagnosis. For example, if a dog has never been in an area known to
be infected with Ixodes ticks carrying B. burgdorferi,
it is very unlikely that the dog will have Lyme disease. A diagnosis
based on clinical signs often remains questionable, for there are several
other conditions, such as immune-mediated disease and rheumatoid arthritis,
that cause lameness and pain in dogs. A positive antibody titer alone
tells very little. Many dogs with high antibody titers fail to have
clinical signs. The presence of a specific type of antibody (IgM) is
a good indicator of recent infection with some diseases, but in cases
of Lyme disease, IgM antibodies persist. The diagnosis of Lyme disease
is strengthened by a good response to antibiotic therapy, but other
infectious diseases that mimic Lyme disease, such as Rocky Mountain
spotted fever and Ehrlichia canis infection, also respond to
antibiotics.
Can an infected dog be treated?
Antibiotics
are the treatment of choice for Lyme disease in dogs, as in humans.
Several tetracyclines, such as doxycycline, and penicillin-like antibiotics,
including amoxicillin and ceftriaxone, are very effective. Tetracyclines
should not be given to growing dogs. Because B. burgdorferi
has the tendency to persist in dogs, antibiotics should be given for
three or four weeks, even though a beneficial effect can be seen after
a few days of treatment. The long duration of therapy is also warranted
because of the very slow multiplication rate of the organism, which
takes 12 hours or more to double in number, as opposed to the minutes
in which most bacteria do the same. Considering the fact that Lyme disease
appears to be self-limiting, the need for a long-duration therapy may
be arguable. However, there are now reports that tetracyclines may have
a direct ameliorating effect on arthritis.
Dogs with
recurrent episodes of Lyme disease, whether acquired from reinfestation
with infected ticks or a relapse from an initial infection, are highly
responsive to antibiotics given at the same doses as for a primary episode.
Humans in the chronic stage of Lyme disease do not respond as favorably
to antibiotics as dogs do.
Corticosteroids
and other anti-inflammatory drugs are sometimes used for treatment of
Lyme disease in dogs. Although the initial result may be impressive,
these drugs do not have a true healing effect and can mask the diagnostic
value of antibiotic treatment.
Should antibiotic treatment be initiated on dogs found carrying
Ixodes ticks?
The question
is only relevant in endemic areas. If dogs are exposed frequently to
ticks, treatment is impractical. Besides, infection of dogs only occurs
after at least partial engorgement of ticks. The risk of infection,
therefore, is greatly reduced if the ticks are removed from dogs on
a daily basis. Because treatment in dogs is highly effective, many veterinarians
initiate treatment only after the onset of clinical signs.
What is the prognosis for dogs with Lyme disease?
Dogs respond
very well to antibiotic treatment. There may be recurrent disease, but
dogs again respond well to treatment. Complete recovery can be expected
in the vast majority of cases. As noted above, chronic disease, which
can be devastating in humans, has rarely been seen in dogs. Furthermore,
our studies have shown that dogs may recover spontaneously without antibiotic
therapy.
Can humans get the disease from dogs?
Some have
speculated that B. burgdorferi in the saliva or urine of infected
dogs may be transmissible to humans. Experiments however have failed
to provide any evidence of urine or saliva shed. Organisms are rarely
found in the kidneys of infected dogs. Borrelia organisms also deteriorate
quickly in the urine and saliva, and there is so far no evidence of
human infection resulting from contact with dogs. It has also been speculated
that dogs might carry home loosely attached infected ticks, which could
then transfer to human hosts and induce infection. No such instance
has been documented.
How can the disease be prevented?
There
are two approaches to preventing infection in dogs. One is to limit
tick engorgement on dogs by controlling the tick population, using tick
repellents, and/or grooming daily. The other is vaccination.
Attempts
to reduce the deer tick population by radically reducing the deer population,
even by as much as 70 percent, have been only partially successful.
Other wildlife can replace the deer as hosts, and efforts to reduce
the population of white-footed mice are not feasible.
Selective
chemical control of ticks appears to be more promising, although only
relatively small areas can be covered. The Boston-based company Eco
Health, Inc. has developed one approach, biodegradable tubes containing
permethrine-treated cotton batting (Damminix®) that can be placed
in infested areas. Mice use the cotton for nesting material. The acaricide-covered
nesting material rapidly kills exposed I. scapularis larvae
and nymphs. Contradictory reports have appeared about the effectiveness
of this approach.
The Borrelia
burgdorferi Bacterin from Ford Dodge Laboratories is currently
the only licensed Lyme disease vaccine for dogs. Several million doses
have been sold, and, other than transitory fever, dogs do not appear
to have any immediate adverse reactions to its use. In a limited field
study it was concluded that the incidence of disease (4.7 percent in
infected, non-vaccinated dogs) was reduced to about one percent. However,
the vaccine does not protect against actual infection. We do not yet
have experimental data to show whether B. burgdorferi persisting
in dogs vaccinated after tick exposure might cause later disease.
The fact
that dogs showing antibody response only to vaccination, not to tick-induced
vaccination, have been observed to develop classical signs of Lyme disease
may indicate that the risk of vaccination with the whole-cell bacterin
is greater than previously thought. If only one or two percent of vaccinated
dogs in endemic areas experience this phenomenon, the possible advantages
of the vaccine, which is reported to reduce cases of Lyme disease from
about four and one-half percent to one percent of dogs at risk, would
probably be offset by the risk of its use. However, the basis for the
observation that vaccinated dogs develop Lyme disease is not understood
and must be investigated further before firm conclusions can be drawn.
We cannot
recommend vaccination of dogs in endemic areas with the whole-cell bacterin
until questions are resolved about clinical Lyme disease developing
in dogs that have been properly vaccinated. The risk of not vaccinating
is minimal since the disease in dogs is probably self-limiting in the
majority of cases and is effectively treated with antibiotics, even
in cases of recurrent disease. Furthermore, the risk of ever developing
clinical Lyme disease appears to be relatively low.
A recent
vaccine trial at the Baker Institute furnished strong preliminary evidence
that a distinctly different approach to vaccination is effective in
protecting dogs against subsequent exposure to Lyme disease. Task force
member Dr. Yung-Fu Chang engineered a recombinant preparation of Osp
A, an outer surface protein of B. burgdorferi, in the common
bacterium E. coli. Osp A holds promise as a human vaccine as
well as a canine vaccine. Further study will be needed to confirm our
findings.
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