Hi mattmcgreevy,
Thank you for your clarification! Your vet is correct - there is not
much information on this topic!
You may by now, know about this condition, but I will explain the
meaning of the diagnosis ?idiopathic eosinophilic syndrome? and the
function of eosinophils.
Idiopathic refers to an unknown cause. Eosinophils are a form a white
blood cell, that circulate in the blood, whose job it is to protects
us (and animals) from allergens and parasites. The cell is covered
with tiny granules, that take up red stain, eosin, in a
laboratory?hence the name eosinophils - red stain lovers! The granules
contain toxins, specifically histamine and other lysosomal enzymes,
good for killing off parasites and allergens, but harmful to tissue
should too much be released. A collection of symptoms and conditions
is known as a syndrome. Idiopathic eosinophilic syndrome simply means
your dog has an elevated eosinophil count, along with certain symptoms
(skin rash, asthma, lung infiltrates, colitis, etc.), whose cause is
unknown.
http://nic.sav.sk/logos/books/scientific/node14.html
Numerous things can elevate an eosinophil count. (In the lab, we call
eosinophils, ?eos? for short). Allergies, parasites (particularly
helminths), snakebite, colitis, other conditions, such as
polyarteritis nodosa, tuberculosis, and radiation are among some of
the causes of eosinophilia, also called eosinophilic Leukocytosis or
hypereosinophilia. Eosinophilia are associated also with eczema,
rhinitis, nasal allergies, asthma, leukemia, and autoimmune diseases.
http://www.provet.co.uk/health/diagnostics/eosinophilia.htm
You can view some photos of eos here:
http://www.mcl.tulane.edu/classware/pathology/Krause/Blood/Eosinophils.html
This University of California, San Diego site discusses a case of
hypereosinophilic syndrome in a 4 year old English setter.
?A diagnosis of hypereosinophilic syndrome including pulmonary
infiltrates with eosinophilia (PIE) and eosinophilic myositis was
determined based on the demonstration of eosinophils within aspirates
of a solitary pulmonary nodule, bronchoalveolar lavage and aspirate
smears of lung containing eosinophils, circulating eosinophilia, and
localization of eosinophilic infiltrates within a limb muscle biopsy.
A reversible megaesophagus was also present.?
?Differentials for acquired megaesophagus include myasthenia gravis,
hypoadrenocorticism, polymyositis, polyneuropathy, hypothyroidism (?),
and idiopathic causes.?
?Esophageal dilatation was resolved within 14 days of treatment with
prednisone. Since PIE may be associated with allergy, and this dog was
found to be sensitive to numerous antigens on allergy testing,
densensitization treatment was initiated.. The dog continues to be
symptom free 3 months after clinical diagnosis.?
?Intravenous dexamethasone sodium phosphate (0.25 mg/kg) was given
post bronchoscopy followed by subcutaneous injections of prednisone
acetate (1 mg/kg BID). A PEG tube was placed for facilitation of
feeding and medications including Carafate. Other treatments included
Timentin and Baytril for an aspiration pneumonia, Zantac for reflux
esophagitis, and Terbutaline for bronchodilatation. Repeat thoracic
radiographs 14 days later showed resolution of the megaesophagus.
Eosinophilia was no longer present on repeat CBC. Based on results of
an allegery test panel, hypersentization treatments were initiated.?
http://medicine.ucsd.edu/vet_neuromuscular/cases/1999/jul99.html
Other case studies:
Idiopathic eosinophilic meningoencephalitis
in Rottweiler dogs: three cases (1992-1997)
?Idiopathic forms of eosinophilic meningitis have been reported in six
dogs, of which three were Golden Retrievers. The idiopathic form of
the disease has also been seen in cattle. Eosinophilic meningitis has
been seen as a suspected type I sensitivity reaction in the cat,25 and
in dogs with protozoal (Toxoplasma or
Neospora),protothecal,cryptococcal2, or parasitic (Dirofilaria,
Toxocara, Angiostrongylus, Ancylostoma, and Cuterebra)34 infections.
The dog was treated with prednisone at 1.5 mg/kg every 12 h for six
weeks and was given three doses of fenbendazole at 50 mg/kg to try and
rule out parasitic disease. There was no improvement with this
treatment and the dog was euthanased.?
Another dog ? was treated with intravenous dexamethasone at 1 mg/kg
every 24 h. This dosage was reduced to 0.25 mg/kg every 24 h for the
next 3 days, then oral treatment with prednisone was commenced at 1
mg/kg every 24 h. The dog made a slow recovery, but still had
significant neurological abnormalities 3 weeks later. The gag reflex
returned within 2 days. A left-sided facial paralysis was seen for a
few days during the first 2 days of treatment. The dog continued to
circle for 2 weeks and remained depressed during this time. The dog
showed some side effects to prednisone treatment and an alternate-day
therapy was started at the same dose after 3 weeks of treatment. At
the time of writing (4 months after treatment) the dog has almost
fully recovered, but has reduced vision in the left eye and a dislike
of sudden changes in position, possibly suggesting a residual
vestibular lesion. The dose of prednisone has been reduced to 0.1
mg/kg every 48 h."
http://www.ava.com.au/content/avj/9711/97110786.pdf
Another case study: In this study, the fecal tests were negative for
parasites. ?An 11-year-old desexed female crossbred dog weighing 21
kg was referred with a 2-week history of recurrent vomiting,
diarrhoea, abdominal discomfort and mild persistent cough. The owner
reported previous episodes of intermittent, recurrent vomiting,
diarrhoea and coughing extending over 2 years. The
cough had been diagnosed without investigation as allergic bronchitis
and was partially controlled with a preparation containing
prednisolone and chlorpheniramine. Additional testing was undertaken
to identify potential causes of eosinophilia. A heartworm antigen test
was negative. Faecal flotation and faecal sedimentation tests for
endoparasites were negative. Cytological evaluation of fine needle
aspirates of the
subcutaneous masses indicated they were lipomas. As signs of illness
had abated, the dog was sent home on enrofloxacin and
amoxycillin-clavulanate for suspected localised peritonitis. The
chlorpheniramine-prednisolone combination was withdrawn, because of
concern that prednisolone might exacerbate pancreatitis, and
dexchlorpheniramine was substituted. Stilboestrol and thyroxine were
also withdrawn, in case the eosinophilia was induced by a drug
reaction.?
This case study goes on to further explain the function of eosinophils:
? Eosinophils are tissue-dwelling cells, found in loose connective
tissue of organs that serve as entry points for foreign substances,
such as the skin and respiratory and gastrointestinal tracts. They are
secretory cells containing several cytotoxic and neurotoxic
proteins.These proteins although important for defence against
parasites can contribute to tissue destruction. Eosinophils have the
potential to produce cytokines, act as antigen-presenting cells, and
contribute to chronic inflammation and fibrosis.15 It is these effects
which cause multi-organ damage in HES.
A diagnosis of HES is made by excluding all known causes of
eosinophilia. The most common cause of eosinophilia in the dog is
parasitism. This may occur with both endoparasites and ectoparasites,
although the response is greater with endoparasites because of the
prolonged host-tissue contact. Sensitised T-lymphocytes initiate and
maintain eosinophilia by production of IL-5. Inflammation or local
hypersensitivity reactions in mast cell rich sites, such as skin and
alimentary, respiratory and genitourinary systems, also cause
eosinophilia.
Treatment:
The stimulus for eosinophil accumulation at sites of inflammation may
be success reported with glucocorticoid therapy alone in feline and
human HES patients, treatment was begun with a combination of
hydroxyurea (25 mg/kg) and prednisolone (1.5 mg/kg), given twice
daily. Omeprazole 20 mg was given once daily as prophylaxis against
corticosteroid-induced gastrointestinal ulceration. Pancreatic enzyme
supplementation was continued.
The dog responded well to treatment and clinical signs ceased almost
immediately. After 7 days the peripheral eosinophil count was zero.
Prednisolone and hydroxurea doses were slowly tapered over a 4-month
period. Clinical signs and eosinophil count were stabilised at final
doses of hydroxyurea 15 mg/kg and prednisolone 0.8 mg/kg, given on
alternate days. Omeprazole was given only while the dog was receiving
high prednisolone doses. Onychomadesis (sloughing of nails), a known
side-effect of hydroxyurea, occurred on two occasions
soon after treatment began. Mild anaemia developed and persisted while
hydoxyurea dosages were high, but resolved as it was reduced.?
http://www.ava.com.au/content/avj/0110/01100686.pdf
Cases on this site discuss dogs(Case 1 discusses a Rottweiler) with
eosinophilia from a Bartonella septicemia (infection of the blood).
Your vet could draw blood cultures to check for this or other
organisms, if deemed possible.
http://vetclinpathjournal.org/VOL32_OPEN/VCP3203_147-149.pdf
?The etiology of this disorder remains unknown, although the presence
of eosinophils and the response to corticosteroids suggests an
immune-mediated pathogenesis?
http://www.ivis.org/special_books/Braund/braund27/chapter_frm.asp?LA=1#Eosinophilic
Canine allergies:
Dogs can be allergic to inhalants such as grass and pollen, flea
saliva, mold and dog food.
http://www.canismajor.com/dog/allergy.html#Inh
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/60204.htm
About the use of prednisone in canines
?Prednisone and other corticosteroids have a lot of different effects
on the digestive tract. It is well documented that glucocorticoids,
including prednisone, increase the risk of gastric ulcers. This
happens due to a combination of effects of the corticosteroids. The
stomach produces a protective mucous layer that helps it defend itself
against the acid it produces. Corticosteroids interfere with
production of this mucous layer because they suppress the growth of
the gastric mucin cells that produce the mucous. In addition,
corticosteroids inhibit the
production of mucous in the cells that remain. Eventually, this leads
to a thinning of the protective layer and a greater risk of ulcer. The
rate of ulceration has not been established in dogs, at least that I
know of, but it is about 5% in humans with long term use of
corticosteroids. This may be a little higher than in animals because
people probably have an increased susceptibility to Helicobacter
infections while on prednisone and the role of Helicobacter in dog and
cat ulcers is still unclear. Long term prednisone use also decreases
the absorption of minerals (especially calcium and iron) from the
digestive tract and increases the absorption of fat. It may increase
the risk of pancreatitis. On the plus side, glucocorticoids decrease
inflammation, which can be very beneficial in some gastrointestinal
disorders, such as lymphocytic/plasmacytic enteritis and they may
offer some protection against stress related ulcers.?
And
?It usually takes very long term use of prednisone or other corticosteroid
medications before side effects that might lead to kidney damage occur. If
prednisone is helpful for your rottweiler's problem it is probably best to
go ahead and use it as your vet advises.?
http://www.vetinfo.com/dpred.html#Glucocorticoids,%20including%20prednisone%20and%20gastric
Have you considered a food allergy? Many dogs are allergic to wheat
and corn in some dog foods. Switching to a rice and lamb based food
may help.
?The number of offending food allergens varies from 1 to 5 ingredients
per animal. The most frequently identified causative allergens in
canine food allergy include beef, chicken, corn, wheat, soy, and milk.
Once the offending allergens are identified, control of the food
allergy is by strict avoidance of these offending allergens.
Concurrent diseases (such as atopy or flea allergy) may complicate the
identification of underlying food allergies. Infrequently, the dog
will react to new food allergens as it ages. Response time to the
elimination diets varies from 1 to 9 wk. Time until relapse of
pruritus after challenge with the offending food varies from 15 min to
10 days. The most frequently identified food allergens in cats include
fish, beef, and chicken. Avoidance of the offending allergens will
control the clinical signs associated with the food allergy. ?
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/70400.htm
Rat and vermin urine are allergens to dogs, as well as wood chips in
dog beds and pillows. ?Plicatic acid (in wood chips) has been shown to
cause an array of pathological changes consistent with inflammatory
and allergic reactions. However, no one knows the mechanism by which
plicatic acid induces these changes, which include increased
concentrations of eosinophils?
http://allergies.about.com/gi/dynamic/offsite.htm?site=http%3A%2F%2Fwww.trifl.org%2Fcedar.shtml
I would follow your vet?s instructions for prednisone, and ask her/him
about concurrently taking some sort of H2 blocker such as Tagamet,
Zantac of Pepcid to prevent esophageal reflux. Prednisone makes dogs
more likely to get infected with H. pylori (stomach) and can cause an
excess amount of stomach acid. Predisone can also raise blood glucose,
making your dog thirstier than usual, so keep plenty of fresh water
available. Finally, it is important to taper the dose at the end of
the regimen. Your vet should explain how to do this, and stress to you
the importance of tapering off prednisone. Your dog may need an
allergy medication (antihistamine) once he is recovered as well!
?Antihistamines can be used with relative safety in dogs. About one
third of owners report success with them. The major drawback, as with
people, is sedation. Dr. Ackerman recommends that a minimum of three
different types of antihistamines be tried before owners give up on
this therapy. According to Dr. Johnson, the most common problem with
this type of treatment is
that owners give the drugs at doses that are too low. Check with your
vet on correct dosing. Examples of antihistamines commonly used for
dogs include: Tavist, Benadryl, Chlortrimeton, Atarax and Seldane.
Personally, I have seen the best results with Atarax.?
http://www.faqs.org/faqs/dogs-faq/medical-info/canine-allergies/
Has your dog been tested for heartworms?
http://education.vetmed.vt.edu/curriculum/vm8754/X.html
Skin testing:
http://allergies.about.com/gi/dynamic/offsite.htm?site=http%3A%2F%2Fwww.peteducation.com%2Farticle.cfm%3Fcls%3D2%26articleid%3D504
You may find this off-topic article interesting as well:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=339300
Please keep in mind that this answer is for information purposes only,
and is not intended to diagnose, treat or replace sound medical advice
from your veterinarian.
I hope this has explained IES (idiopathic eosinophilic syndrome) to
you adequately. If any part of my answer is unclear, please use the
Answer Clarification button, before rating. This will enable me to
assist you further, if possible.
Wishing your rottweiler a speedy recovery!
Sincerely,
crabcakes
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