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Strangles is hardly a new
disease, having been recognized as a contagious bacterial problem in
horses since the late 18th century. Yet, it still remains a troublesome
and persistent issue in the horse world and is identified worldwide.
Research has been directed toward developing effective vaccines to control
its spread through the horse population, but management strategies are
equally important in limiting its presence.
What is Strangles?
Strangles is
the colloquial name given to an infection caused by a bacterial organism
known as Streptococcus equi. This bacteria invades the respiratory tract
of horses, donkeys, and mules and causes swelling of the lymph nodes
around the head and neck. In some cases, the swelling around the pharynx
can become so severe that the horse's airway is obstructed; the audible
respiratory stridor and potential for suffocation spawned the name
"strangles." Up to ten percent of strangles cases may result in death.1
Fortunately, most cases
of strangles do not become this extreme. An affected horse may stand
listless in the paddock and be inappetant. A fever may develop along with
myalgia. Most horses that are sick with this disease eventually develop a
mucopurulent nasal discharge and/or a cough. The submandibular and/or
retropharyngeal lymph nodes often swell to varying degrees. There may be
some edema around the face, and breathing may be labored or stertorous. At
the onset, the lymph nodes may be very firm and painful to touch, long
before they soften and break open to drain a creamy mucopurulent
discharge. Typically the lymph node abscesses rupture within a couple of
weeks subsequent to the horse showing initial clinical signs of infection.
Only half the time do the draining lymph nodes culture positive for the
Streptococcus equi organism.1 Identification of the disease is based on
clinical signs and probabilities since few other illnesses infect the
lymph nodes.
Who Is At Risk?
Any age horse
can be affected, but it is the very young and the very old who usually
suffer the worst. Young horses may not have yet developed sufficient
immunity through natural exposure in their short lives, while the immune
system of the geriatric horse may be less functional due to age-related
decline. It takes about 3-14 days for the disease to incubate once the
horse has been exposed until he shows clinical signs of infection. Not all
infected horses develop obvious symptoms of disease yet these asymptomatic
individuals may serve as carriers and shed the organism through their
respiratory secretions and saliva and spread it to other susceptible
horses.
Strangles is a highly
contagious disease, particularly in conditions of stress. This includes
situations where horses are housed in crowded areas, or with poor hygiene,
or with inadequate nutrition. Transmission occurs via direct contact with
nasal secretions or saliva. Flies also spread the disease, as do
contaminated fomites such as feed buckets, rakes, and human hands and
clothing. The organism can survive in the environment for a couple of
months, particularly if shielded from the sun inside of dark barns or
within the soil.2 Once established on a property, another outbreak may
occur on that farm a year or two later. The infection keeps cycling
through horses to the environment and back to horses to become a
persistent and frustrating management issue.
Once a horse has been
infected with strangles, it is possible for him to continue to shed the
organism through nasal secretions for months. Most horses stop shedding
within about 6 weeks, but the potential exists for a previously sick horse
to carry the infection to others despite appearing to be fully recovered.
Nasopharyngeal swabs of suspected carriers or of previously infected
horses can help identify those that may be shedding S. equi organisms yet
are not exhibiting clinical signs. In one study, the average period of
shedding from carriers was 9.2 months, with one horse shedding for as long
as 42 months.3 Sixty-eight percent of horses continued to shed for at
least four weeks following resolution of clinical signs.3 Seventy-five
percent of horses infected by strangles develop a long-lived immunity once
they recover from the disease.2
Treatment
This disease is labor intensive, requiring supportive nursing care. The
disease must run its course, but hot packs applied to the swollen glands
help point the abscesses for drainage. Surgical lancing of the affected
lymph node hastens drainage and speeds the horse on its way to recovery.
The opened abscess should be irrigated with a 3-5 % povidone iodine
solution on a daily basis. Supportive care is essential: The horse should
be encouraged to eat by providing pelleted gruels, and food and water
should be accessible in a way that a horse can reach comfortably.
Non-steroidal anti-inflammatory medications make the horse more
comfortable, control swelling, control fever, and encourage eating and
drinking by reducing pain and inflammation.
Antibiotics may actually
be counter-productive, particularly in the early stages of disease.
Antibiotics often suppress the bacteria within the lymph nodes
sufficiently for a time, only to have a simmering infection flare when the
antibiotics are discontinued. Then the abscesses return and the horse
appears sick again. Antibiotic therapy is indicated in certain instances
when an affected horse remains persistently off feed and is depressed
despite other supportive care, or if the fever remains elevated (greater
than 104 degrees Fahrenheit), or if the airway is being obstructed by
lymph node swelling, contributing to dyspnea. Once the abscesses rupture,
then antibiotic treatment is appropriate to enable the horse's immune
system to eliminate the disease. Procaine penicillin (22,000IU/kg bid)
still remains the drug of choice in addressing S. equi infections,
although tetracyclines, erythromycin, and ampicillin may be useful.
Control and Prevention
Once a horse is recognized with strangles, the ideal means of containment
is to isolate any sick or suspect individuals for about six weeks.
Excellent sanitation and good common sense are important to control the
disease from spreading through a herd. Fly control measures are important.
Contaminated bedding should be composted beneath a layer of plastic so
flies cannot access the bedding. Use separate halters, water and feed
buckets, cleaning utensils and wheelbarrows, and brushes to manage the
sick horses. Advise horse owners of sound management principles: Always
handle the sick horses last, taking care of the healthy horses first;
change clothing after being in contact with any sick ones; wash hands with
antiseptic soaps. Also, it is a good idea to scrub down the fences, stall
walls, and anything that may have been contaminated by respiratory
secretions, using materials known to kill the Streptococcal organisms.
These include phenolic products, iodophors, chlorhexidine, or
glutaraldehyde disinfectants.2
In the face of an
outbreak, it has been demonstrated that vaccinating non-sick animals can
decrease the morbidity by half. This strategy may have limited usefulness
in horses that have never before been vaccinated against strangles since
in order to ensure the maximum protective effect, the non-sick horses need
to receive the full protocol of two vaccines spaced 2-3 weeks apart. This
may be too long a time-frame for the horses to develop sufficient
protective immunity when directly challenged by the bacteria; it is
possible that disease may occur before the second vaccine in the series is
given. Horses that have been on a previous strangles vaccine program can
be "boosted" with one dose of vaccine, and this should effect some
immunity at least to limit the severity of the infection. Pregnant mares
should be vaccinated with approved products about a month prior to foaling
so the newborn foal will receive protective antibodies in the colostrum.
It is good common sense
to isolate any newcomers to a farm for 2-3 weeks just in case they may be
carrying a bacterial infection or virus to which the resident horses have
not previously been exposed. This allows the new horses to incubate and
break with disease before they've had a chance to co-mingle and infect all
the others on the farm. Then a disease process can be identified and
controlled before too much damage is done. This is especially important
where foals, weanlings, and yearlings are involved. In managing herd
health for any farm and to minimize casual spread of disease, it is
prudent that a new horse be examined and given a health certificate prior
to entry on the new premises. Rectal temperatures of new arrivals should
be checked twice daily. If S. equi is suspected or is a concern,
nasopharyngeal swabs are useful to identify a carrier horse. Ideally, a
horse is considered to not be a carrier if it has three negative
nasopharyngeal swabs for S. equi over a two to three week period.
Nasopharyngeal swab bacterial cultures detect 60 percent of carrier horses
while combining this test with PCR (polymerase chain reaction) testing
increases detection of carriers to 90 percent. The PCR test detects DNA
from both living and dead bacteria so is more sensitive than a bacterial
culture which only detects live bacteria that grow on laboratory media.
Complications
Besides the frustration experienced in dealing with horses affected by the
acute disease, strangles is not without its set of complications that
arise subsequent to infection. About 20 percent of horses infected with
strangles develop other problems than the basic upper respiratory signs.4
Some of the complications may even be life-threatening, so an infected
horse should be monitored closely for a time following the first clinical
signs. As an example, the Streptococcal organism can seed itself within
the lung tissues creating a bacterial pneumonia.
One of the more
difficult-to-identify complications is called bastard strangles. In these
cases, the organism spreads to other internal lymph nodes (particularly
those of the gastrointestinal tract) or to other organs like the spleen,
liver, kidney, lungs, or even the brain. It is often hard to recognize
that a horse has bastard strangles until there is an on-going problem with
unthriftiness, continued weight loss, poor performance, and listlessness
that cannot be explained by any other causes. The results of a complete
blood count and fibrinogen level may strongly point to a systemic
infection. A rectal exam, an abdominal ultrasound exam, or an abdominal
tap may identify the location of an internal abscess. These are hard cases
to treat, requiring long term antibiotic therapy.
Another complication that
may not become apparent for a time is an infection of the guttural pouch
with the development of empyema or chondroids. This could be a
life-threatening problem if the infection erodes through the large blood
vessels that course through the guttural pouch. Major nerve branches may
also be affected in this area creating neurologic problems referable to
the cranial nerves. Often the mucopurulent debris that accumulates within
the guttural pouch is swallowed as it drains into the pharynx, but
sometimes it is visible as a nasal discharge from one or both nostrils. An
endoscopic exam and radiographs of the head are useful to detect this
problem. Most asymptomatic carrier horses harbor S. equi within their
guttural pouches.
Some horses infected with
strangles develop myocarditis. This can be a source of exercise
intolerance and poor performance. An EKG and ultrasound of the heart are
useful diagnostic tools to screen for this problem. Chronic anemia can
also be a complication of a strangles infection, but once the primary
disease is resolved, the heart problems usually resolve with time.
The Streptococcal bacteria can also create an immune-mediated syndrome
known as purpura hemorrhagica that leads to abdominal edema, limb edema,
head edema, scrotal edema, and hives. The protein antigens of the
bacterial organism combine with antibodies to set up an allergic response
in the horse, causing vasculitis. This only occurs in one to two percent
of infected horses.2 The horse may seem to be well on the mend, only to
suffer a severe set-back about 2-4 weeks following a strangles infection.
Gravity dependent areas swell, like the legs, abdomen, and head. The horse
is depressed, off feed, and petechiations are present on the mucuous
membranes of the gums, conjunctiva, and nasal mucosa. Often serum
exudation and skin necrosis are associated with pronounced limb edema.
Since this syndrome arises due to an immune-mediated complex stimulated by
components of the bacteria, the horse needs to be treated with both
corticosteroids and systemic antibiotics for a lengthy period of time.
Vaccination|
Because the site of entry of this organism is through contamination of the
upper respiratory tract, the most ideal method of stimulating immunity is
by eliciting a secretory antibody response (IgA and IgG) in the local
respiratory tissues. The intranasal vaccine (Pinnacle I.N.) recently
developed by Fort Dodge Laboratories takes advantage of this mechanism of
protective immunity.
Previously, all
vaccination strategies against strangles have relied on intramuscular
injections that elicit a systemic immune response. These vaccines have had
limited efficacy, only curtailing disease in 60-70 percent of those cases
challenged by the organism. In addition, many times the intramuscular
injections are accompanied by sore muscles, malaise, and a fever. These
secondary vaccine reactions may last for as long as a week. Although these
complications occur in a small percentage of horses, many horse owners are
concerned by these adverse reactions. Having weighed the risks, many have
considered that the intramuscular vaccine is seemingly as bad as the horse
contracting the disease. For that reason, use of the strangles vaccine has
been limited by horse owners until the advent of the intranasal form.
The intranasal strangles
vaccine is given as a series of two doses spaced 2-3 weeks apart. The
material is a live avirulent S. equi organism that is freeze dried and
then reconstituted with a special diluent just prior to administration.
The 2 ml dose is squirted through a nasal canula into a nostril to reach
the local area of the upper respiratory tract. This provides the best
protective response since it stimulates the production of locally produced
antibody at the level of an infectious invasion into the system. This
prevents attachment of the organism to tonsil receptors, and may prevent
tissue invasion of the organism if it does manage to adhere to the
receptive respiratory tissues.
In the clinical trials
associated with this product, there was a reduction in the clinical
disease observed in vaccinated horses. However, despite "protection"
derived from the intranasal vaccine, 40 percent of horses challenged with
the organism did still develop clinical signs of disease as opposed to 60
percent of unvaccinated horses that were challenged with the organism.
Morbidity was decreased, and of those that did get sick, the clinical
signs were reduced by 65 percent as compared to unvaccinated horses. Just
as with the intramuscular vaccines, no horse can receive complete
protection from the strangles organism when challenged. However the
intranasal vaccine shows promise in reducing the number of horses affected
and the severity of the infection if it occurs.
There is some concern
that giving a modified live organism via the nasal passages could result
in shedding from the vaccinated individuals to those who were not. The
safety studies performed by
Fort Dodge
indicated that any slight shedding that may occur does so only during the
first day and the organism is not shed to any significant degree. This
company feels that "the use of the vaccine is safe in vaccinated horses
and for those horses kept in contact with vaccinates." Currently, the
vaccine is not yet approved for use in pregnant mares although preliminary
data indicates there are as yet no problems.
It is recommended that
the intranasal strangles vaccine be administered following vaccination of
other intramuscular products during routine inoculations. This strategy
may prevent inadvertent contamination of other intramuscular inoculation
sites with the avirulent S. equi organisms that could result in the
development of injection site abscesses. |