Introduction

Food adverse reactions may be immunologic (type I hypersensitivity being most common in humans) or non-immunologic (food intolerance, pharmacologic, toxic or metabolic food reactions).¹ The underlying mechanisms may be different, but the diagnosis and treatment of food reactions is typically not influenced by this. Most patients will react to only a few allergens, the mean number of reactions in one study including dogs was 2.4.² In dogs there is no classical set of signs for food adverse reactions (FAR), this disease cannot be differentiated from non-seasonal atopic dermatitis clinically. Thus, any dog or cat with pruritus possibly due to environmental allergens should also be considered to be potentially reacting to food antigens. The major complaint is pruritus, which is non-seasonal and sometimes poorly responsive to glucocorticoids. However, corticosteroids may be highly effective. Pruritic bilateral otitis externa and secondary seborrheic skin disease and/or pyoderma are commonly seen in conjunction with FAR. Concurrent gastrointestinal disturbances have been reported in a minority of the cases.¹ Studies report a wide variety in the age of onset and concurrent other allergies in a minority of these patients. Points to note include:

 Pruritus is the hallmark of the disease, but dogs with recurrent pyoderma due to food allergy have been reported that were not pruritic during antibiotic therapy.

 Otitis externa was the only sign of food allergy in 30% of the cases in one study.

 The feet and inguinal area were other sites commonly seen.

 A papular rash was reported in half of the cases.

Siamese cats seem to be predisposed to food adverse reactions according to Rosser⁶. The most common signs in the cat are miliary dermatitis and facial pruritus.¹ Head or neck pruritus and eosinophilic plaques or indolent or eosinophilic ulcers may be seen. 'Bald belly syndrome' or seemingly noninflammatory alopecia have also been caused by food adverse reaction. Onset is often abrupt and explosive and can be as early as two months of age and as late as 13 years. There may be subtle or prominent gastrointestinal signs such as diarrhoea, vomiting or often just frequent defecation or flatulence. Thus, in many pruritic patients, an elimination diet is the second or third tier of diagnostic tests after skin cytology and scrapings and subsequent ectoparasite control to rule out infections, mite infestation or flea allergy.

Diagnosis

There are three possibilities to diagnose food adverse reactions:

1.  Serum testing: absolutely useless^3,4

2.  Skin testing: absolutely useless^3,5

3.  Elimination diet: only realistic alternative

Elimination Diet

To get an owner to perform a home-cooked elimination diet is hard work in most cases and to keep the compliance up all the way through the 6-8 weeks or longer^1,6 needed to make the diagnosis is even more difficult. An elimination diet for canine patientsconsists of a protein source and a carbohydrate source previously not fed. These are home-cooked and usually fed in a ratio of three parts of the carbohydrates and one part of the protein. Possible proteins are deer, rabbit, buffalo, shark, salmon, horse or kangaroo, but any protein source not previously fed is suitable. Similarly, carbohydrate sources may be rice, potato, sweet potato, kidney beans, tofu or yam. The protein part can be increased, but should not fall below 25%. Nothing else is included in the diet. In cats, only the protein source is fed, as most cats are not extremely eager to eat rice, potatoes or beans.⁷

If owners previously have fed treats, we need to provide options for them to continue these habits without violating the diet. Depending on the diet, jerky of the used meat, rice cakes, potato chips or little pieces of fried or grilled meat are all possibilities to allow the feeding of snacks without adding proteins potentially causing pruritus and masking the success of the elimination diet.⁷

An elimination diet should be started gradually, initially just added to the normal food, to increase the chance of acceptance. This holds particularly true for cats. In dogs, some dermatologists recommend 2-3 days of fasting to increase acceptance and response time. If pets still do not like the food, spices such as salt or garlic may increase palatability. Warming the food in the oven or microwave may also increase acceptance.⁷

Rechallenge

After a period of eight weeks or longer the patient is reevaluated. If the animal is in remission, a rechallenge with the previously fed diet is performed. If there is significant improvement, the diet can be continued for another 6-8 weeks to evaluate the full degree of possible improvement on the diet. However, with a difficult owner, rechallenge may be indicated right away. If there is no improvement after 8 weeks or longer, or if clinical signs do not return after a few days or at the most two weeks on the old diet, food adverse reaction is ruled out.

Ideally, we then start a sequential rechallenge with individual proteins to identify the offending protein. In the author's practice, beef mince is fed then lamb mince, then chicken, then add cheese or milk in the diet for dairy products and finally add pasta to check the wheat proteins. Each protein is fed for approximately one week. One can 'guestimate' the time until deterioration by how quickly the symptoms returned after the rechallenge previously. If there was deterioration within two days, it is very likely that this pattern will be repeated. Once the offending protein is identified, it is avoided in the future. Most dogs and cats react to only one or two protein in our experience, even though some animals deteriorate on several different ones. However, other dermatologists feel they see food adverse reactions involving many allergens more frequently.²

Some owners refuse to perform the sequential rechallenge. In these cases, the author tries several commercial diets containing a limited number of or unusual or hydrolyzed proteins and if no deterioration occurs, these continue to fed. If the home-cooked diet is chosen as a permanent solution, it needs to be balanced, preferably by a nutritionist, to avoid long-term problems.

Commercial elimination diets with unusual proteins/carbohydrates (rabbit, duck, venison, kangaroo, potato, oats, etc.) or hydrolyzed proteins are available on the market. In hydrolyzed diets, protein size is decreased by hydrolysis to decrease or abolish allergenicity of the protein. In humans, the most common hydrolyzed proteins are milk proteins; in pet food, hydrolyzed soy and chicken products are currently marketed. It is important to remember that commercial diets will not cause remission in all patients with food adverse reactions and are thus only the second best option! In the authors' clinic, home-cooked diets are proposed. If owners chose commercial diets and no improvement is seen, and subsequent intradermal testing or testing for serum allergen-specific IgE is unsatisfactory, a home-cooked diet is proposed again to rule out food adverse reaction!

Long-term Management

One can identify the exact allergenic protein(s) and avoid that over the long term. This is the ideal solution, but will sometimes be met with owner resistance due to the long duration of the trial and involves timely and emotional effort. Of course, one can maintain the dog on a commercial elimination diet that the pet tolerates well without knowing which allergen(s) is/are the culprit(s). Similarly, one can feed the home-cooked elimination diet long-term, but should then consult a nutritionist to make sure the diet is balanced and complete, which typically requires adding fatty acids and some vitamins and minerals.

Food adverse reactions are not common in the author's experience. However, if you have the rare patient with food adverse reactions in your consult room, then statistics are meaningless to that particular owner and don't help the pet either. Thus, an elimination diet, despite all its drawbacks, is an essential tool in the work-up of patients with chronic pruritus. In addition, there may be a local variation in the incidence and prevalence of food adverse reactions.

References

1.  Scott DW, Miller WH, Griffin CE. Small animal dermatology. 6th ed. Philadelphia: W B Saunders, 2001.

2.  Jeffers JG, Meyer EK, Sosis EJ. Responses of dogs with food allergies to single-ingredient dietary provocation. J Am Vet Med Assoc 1996 209: 608-611.

3.  Jeffers JG, Shanley KJ, Meyer EK. Diagnostic testing of dogs for food hypersensitivity. J Am Vet Med Assoc 1991 198: 245-250.

4.  Mueller RS, Tsohalis J. Evaluation of serum allergen-specific IgE for the diagnosis of food adverse reactions in the dog.Veterinary Dermatology 1998 9: 167-171.

5.  Kunkle G, Horner S. Validity of skin testing for diagnosis of food allergy in dogs. J Am Vet Med Assoc 1992 200: 677-680.

6.  Rosser EJ, Jr. Diagnosis of food allergy in dogs. J Am Vet Med Assoc 1993 203: 259-262.

7.  Mueller RS. Dermatology for the Small Animal Practitioner. Jackson: Teton NewMedia, 2000.

Introduction

Certain skin lesions are highly characteristic of specific diseases, 'diagnostic entities' or pathophysiologic phenomena and may be used as clinical markers or strong visual clues. The clinical presentation of some of these lesions comes very close to being pathognomonic. These clinical clues can be used to prioritize our index of suspicion when generating differential diagnoses and this allows us to take diagnostic short-cuts when considering the most appropriate clinical and laboratory diagnostic procedures.

Other somewhat less characteristic lesions may be used as visual markers if the lesions are seen in conjunction with strongly supportive data such as breed, sex or age predilections.

Clinical Markers

The following will be illustrated:

1.  Ventral alopecia of rapid onset in a cat with the exposed skin becoming shiny.

2.  A well-demarcated band of erythema, papules or comedones extending from the scrotum to the tip of the prepuce in an intact male dog with skin disease.

3.  Darkly colored, greasy or waxy, tightly adherent debris that mats the facial hair in a Persian or Himalayan cat.

4.  Severe erosive and ulcerative skin disease where when vesicles or bullae rupture, the lesion formed is larger than the intact vesicle or bullae.

5.  Severe erosive and ulcerative skin disease where when vesicles or bullae rupture; the lesion formed is the same size as the intact vesicle or bullae.

6.  Large comedo located on the ventral abdomen of a young German shepherd dog.

7.  Well-demarcated region of alopecia on the shoulder or dorsal thorax of a toy or miniature poodle or Bichon frise.

8.  Adult onset excessively fragile, tissue paper thin skin on a previously normal cat.

9.  Focal coalescing loss of pigmentation occurring on the lips, planum nasale or elsewhere on the muzzle in a dog.

10.  Gradually enlarging and coalescing lesions affecting the dorsal muzzle of a dog that do not violate the planum nasale.

11.  Localized patches of thin, atrophic skin sometimes accompanied by large comedo present on the relatively glabrous skin of the ventral abdomen of a dog.

12.  Well-demarcated circular plaques with umbilicated centers especially affecting the medial aspects of the ear pinnae in a dog.

13.  Well-demarcated ulcerated nodule or nodules located on the ear pinnae or head of a short-coated dog. Especially in a boxer dog!

14.  Well-demarcated, circular, erythematous, alopecic nodules located on the face or distal extremities of a dog which when examined closely reveal minute fistulous tracks.

15.  Well-demarcated alopecic area of erosion or ulceration with or without palpable nodules located near the axilla on the lateral body wall of a middle-aged or older dog. Lesions are not pruritic but elicit grooming.

16.  Coalescing nodules with draining fistulous tracts located on the muzzle of a cat.

17.  Generalized alopecia with exfoliation with areas of increased severity affecting the head and neck in a cat. Facial skin commonly is thickened with narrowing of the eyelid margins.

18.  Painful, focal or multifocal, eroded coalescing alopecic plaques located ventral to the ear, or elsewhere on the face of a golden retriever.

19.  Syrup-like viscid fluid emanating from a traumatized bleb or skin biopsy hole in a dog.

20.  Depressed puppy less than 4 months of age initially presented with a remarkably exudative otitis externa.

21.  Symmetric non-draining deformed enlargement of the planum nasale in a dog.

22.  Asymptomatic, multicentric ulcerated, cavitated, crateriform masses in the skin of a dog.

23.  Firm, well-demarcated, sometimes gritty alopecic plaques with a whitish 'feathery' look to the margin of the lesion.

24.  Coalescing nodular dermal lesions with patchy alopecia and broken hairs in a Persian cat.

25.  Partial or complete alopecia markedly restricted to areas with certain hair color.

Please do not view the answers until you have viewed the presentation!

Clinical Markers of Selected Dermatoses: Visual Clues--Answers

1.  Feline paraneoplastic alopecia

2.  Linear preputial erythema--Sertoli cell tumor

3.  Facial dermatitis of Persian and Himalayan cats

4.  Pemphigus vulgaris (autoimmune skin diseases affecting intercellular bridges)

5.  Bullous pemphigoid (autoimmune skin diseases affecting the basement membrane zone)

6.  Demodicosis comedones

7.  Post rabies vaccination alopecia

8.  Feline skin fragility syndrome

9.  Facial depigmentation (DLE, VKH, vitiligo, MF)

10.  'Do not violate planum'--follicular diseases (dermatophytosis, demodicosis, pyoderma)

11.  Topical application corticosteroid reaction

12.  Adverse drug reaction (with umbilicated lesions)

13.  Canine leproid granuloma

14.  Kerion dermatophytosis

15.  Sweat gland adenocarcinoma

16.  Sporotrichosis

17.  Degenerative mucinotic mural folliculitis

18.  Pyotraumatic furunculosis

19.  Mucinosis

20.  Juvenile cellulitis (juvenile sterile granulomatous dermatitis & lymphadenitis)

21.  Histiocytosis of the planum nasale (clown nose disease!)

22.  Subgroup of cutaneous lymphosarcoma

23.  Calcinosis cutis

24.  Dermatophytic pseudomycetoma

25.  Black-hair follicle dysplasia (color dilution alopecia)

Introduction

Malassezia pachydermatis (Pityrosporum pachydermatis, P. canis) is a lipophilic, non-mycelial yeast with characteristic thick-walled elongated oval shape and unipolar budding. It is a commensal organism in the dog, residing on or in the skin, ear canals, anal sacs, vagina and rectum. It is considered as a 'secondary' pathogen in canine otitis externa.

Malassezia pachydermatis was recently reported as an opportunistic nosocomial pathogen in a human intensive care nursery. Pityrosporum ovale (a related organism that colonizes humans) is considered to be both a commensal and an opportunistic pathogen.

Pathogenesis

Malassezia pachydermatis was controversially implicated by Mason as a cause of localized or generalized pruritic and inflammatory skin disease in dogs (1987). Mason hypothesized:

1.  Alterations in host defense mechanisms and skin surface microclimate allow the organism to become a pathogen--a facultative pathogen?

2.  Excessive sebum production, moisture accumulation and disruption of normal barrier function may lead to yeast proliferation.

3.  Lipases produced by the yeast may further alter the sebum film and zymosan in the yeast cell wall may activate mammalian complement leading to loss of epithelial integrity and the clinical signs of inflammation and pruritus. (A similar pathogenesis has been proposed in humans).

Role of Hypersensitivity

Atopic dogs with Malassezia dermatitis developed an IgE-mediated, type 1 hypersensitivity to intracellular protein extracts of M. pachydermatis. Immediate hypersensitivity reactions occurred in 30.4% of 46 dogs and delayed hypersensitivity in 6.9% of 29 dogs with seborrheic dermatitis by intradermal skin testing. Seborrheic dermatitis in humans may be partially due to a Type I hypersensitivity reaction to Pityrosporum ovale.

Number of Organisms Required to Cause Clinical Disease

Still not clearly defined. Apparently, surface yeast colonization without tissue invasion can lead to clinical disease. Concurrent colonization or infection with Staphylococcus intermedius may enhance the inflammation seen with Malassezia dermatitis.

Predisposing Causes

1.  Allergic disease--especially atopic dermatitis

2.  Diseases of cornification

3.  Chronic or recurrent inflammatory skin disease

4.  Previous treatment with antibiotics or corticosteroids?

5.  Marked breed predilections--basset hounds, springer spaniel, German shepherd dog, West Highland white terrier, silky, Maltese, Chihuahua, poodle, Shetland sheepdog, dachshund, Australian terrier, Newfoundlands?

Clinical 'Syndromes' and Features

Three distinct syndromes are described by Mason:

1.  Secondary Malassezia Dermatitis--associated with chronic, inflammatory skin disease, characterized by a strong 'seborrheic' odor and severe pruritus (common).

2.  Primary Malassezia Dermatitis--generalized, inflammatory skin disease with a strong 'seborrheic' odor, rapid onset, rapid therapeutic response and lack of reoccurrence, (rare).

3.  Severe Pruritus and Self-trauma--localized to the muzzle or perianal area (pruritus out of proportion to the visual severity of the skin lesions), owners perceive as seizures!, rapid response, (very rare!).

Lesions are focal, multifocal or generalized with erythema, hyperpigmentation, alopecia, lichenification, scaliness and/or greasiness. Exudative dermatitis and a 'musty' seborrheic odor occur. Pruritus is a common unifying clinical feature. Lesions may be sharply demarcated, closely adjacent skin may be un-inflamed and normally haired. Alopecic, greasy, lichenified lesions gradually expand peripherally to involve previously normal adjacent skin. Site predilections are ventral neck, ventral abdomen, axilla, face, ears (pinna), feet, forelegs, any skin folds.

Diagnostic Procedures

1.  Yeast culture--not recommended as a diagnostic procedure due to difficulty in interpreting non-quantitative results.

2.  Skin biopsy--not a very helpful diagnostic procedure, histopathology of lesions with large numbers of organisms identified by cytology may not exhibit organisms. This seeming discrepancy could be explained by a non-linear distribution of organisms or removal of organisms during automatic processing. However, other characteristics of Malassezia dermatitis besides the presence of organisms may be present and increase the index of suspicion for this disease.

3.  Skin cytology--diagnostic method of choice--controversy still exists as to the best method of obtaining a reproducible number of organisms. Skin scraping, cotton swabs, direct impression smears, tape stripping and 'sticky' glass slides have been recommended.

a.  Dry skin scraping--material obtained is smeared onto a glass slide.

b.  Dry cotton swabs--harvest debris and transfer it to glass slides.

c.  Direct impression smears--in regions where a glass slide can be firmly pressed against the affected area.

d.  Clear cellophane tape stripping--to acquire debris with the tape being used as a cover slip applied to ribbon of stain on a glass slide.

e.  Sticky glass slides--(Durotak®--Delasco Dermatologic Supply).

4.  Microscopic evaluation--heat fixed on the glass slide, stained with Dif Quik® or new methylene blue and examined under oil.

5.  Malassezia--oval to peanut-shaped budding organisms that stain blue varying from faint to dark. The presence of at least three or four organisms per oil emersion field is considered significant by most dermatologists.

Diagnosis

1.  Identification of the organism in sufficient number to be considered a pathogen.

2.  Identification of predisposing underlying causes--if Malassezia dermatitis is treated simply as the pathogenic proliferation of yeast, than reoccurrence after therapy is the rule rather than the exception since in most cases, Malassezia dermatitis is a secondary disease.

Therapy

Ongoing management of documented underlying disease(s) or predisposing causes that may be the predisposing cause for the opportunistic pathogen:

Systemic Therapy

Antifungals--most likely to both induce speedy resolution of skin lesions and markedly diminish the number of organisms that can be harvested by cytology. The availability of generic ketoconazole has greatly diminished the cost of therapy (200 mg. tablets--$0.75 to $1.50 each, wholesale in the United States.) However, systemic therapy is still expensive, especially in larger dogs.

1.  Ketoconazole (Nizoral®--Janssen, or generic)--orally, 5mg/kg once daily--current drug of choice, given for a minimum of thirty days. (Some of the dramatic improvement seen with this therapy may be due to anti-inflammatory effects, plus the effect on the cornification process seen with ketoconazole). Some dermatologists advocate monitoring liver enzymes during therapy due to the controversy of possible hepatotoxicity in humans. Monitoring of healthy dogs probably is not necessary.

2.  Itraconazole (Sporonox®--Janssen)--orally, 5mg/kg given once daily for at least thirty days, itraconazole lacks anti-inflammatory effect seen with ketoconazole.

3.  Fluconazole (Diflucan®--Roerig, or generic)--orally, 5mg/kg once daily.

Topical Therapy--Shampoos

Adjunct to systemic therapy, can be used as sole therapy if financial constraints, minimum of twice weekly for at least six weeks, (ideal product does not exist!--degreasing, anti-fungal, residual).

1.  Miconazole/chlorhexidine gluconate--Malaseb® (DVM)

2.  Ketoconazole/chlorhexidine gluconate--KetoChlor^TM (Virbac)

3.  Acetic acid/boric Acid--MalaAceticR (DermaPet)

Topical Therapy--Rinses

1.  Miconazole--ResiZole® (Virbac)

2.  Chlorhexidine--ResiChlor® (Virbac)

3.  Acetic acid and water 1:1 (white vinegar & water)

4.  Enilconazole (Imaverol®--Janssen), side effects?

Overview

Control or cure underlying causes, kill the yeast, combine systemic and topical therapy, hope no recurrence!

Recurrent Malassezia Dermatitis

Similar to recurrent pyoderma, persistent underlying skin disease is the most commonly diagnosed cause of recurrent Malassezia dermatitis, frequently occurs together! Recurrent secondaryMalassezia dermatitis is a frustrating problem both in general practice and in specialty dermatology referral practice. Recurrent secondary Malassezia dermatitis is more likely to occur when multiple predisposing causes are present in a predisposed breed. Consider the likelihood of a West Highland white terrier with multiple allergies and a defect in cornification developing secondary Malasseziadermatitis!

Prevention of Recurrent Malassezia Dermatitis

1.  Goals of long term management--prevent or diminish frequency of recurrence.

2.  Long-term management of underlying skin diseases or other predisposing causes. (especially. canine atopic dermatitis).

3.  Topical therapy--shampoos and rinses.

4.  Systemic therapy--antifungals, extended regimens:

a.  Ketoconazole (generic)--5 mg/kg three days per week

b.  Fluconazole (generic)--orally, 5mg/kg 3 days per week

Introduction

Dilated cardiomyopathy (DCM) is prevalent in certain breeds of dog and is rare in cross breeds. Indeed, DCM contributes to a large proportion of the overall mortality in certain large breed dogs <10>

Presentation

DCM is defined as a primary myocardial disease characterized by cardiac enlargement and impaired systolic function in the absence of other cardiac or non-cardiac causes. The clinical presentation may be subtle and include the gradual development of exercise intolerance and weight loss. However, more commonly, these early indications are overlooked and the diagnosis of DCM is not established until congestive heart failure (CHF) develops and the patient is presented for coughing, dyspnea, tachypnea, wasting, arrhythmia and sometimes ascites. For the symptomatic patient, it is important for the clinician to rule out other possible causes for the clinical signs, such as pericardial effusion, pneumonia, neoplastic disease, undiscovered congenital heart disease. For the asymptomatic patient, the challenge lies in differentiating normal variation and cardiac or non-cardiac pathologies from DCM.

In a proportion of boxers and Dobermans (not all), ventricular tachyarrhythmias may cause fainting and weakness, whereas the cardiac dilatation and systolic dysfunction is not apparent. Histopathological characterization of dogs with DCM has shown that there are two histopathological phenotypes that presumably precipitates different clinical presentations. The Dobermans and boxers presenting with ventricular tachyarrhythmias have myocardial lesions that include myocytolysis, myofibre degeneration, vacuolization and myocyte atrophy with extensive fibrosis and fatty infiltration. presenting with systolic dysfunction. Cardiac dilatation may also present with an arrhythmia, most commonly atrial fibrillation, but the histopathological findings include myocytes that are thinner than normal with a wavy appearance that are separated by a clear space, indicating edematous fluid that is generally free from cellular infiltrates; there may also be diffuse infiltration of subendocardial fibrosis.

Diagnosis

Although DCM is currently believed to be a genetic disease, there are currently no genetic tests available for establishing early diagnosis and the diagnosis is, therefore based on phenotype characterization. Because of the two histopathological phenotypes, dogs of different breeds are screened differently for preclinical disease. Most breeds are screened using echocardiography, whereas Dobermans and boxers are also screened with 24-h (Holter) recordings because a single ECG trace is not useful, since it corresponds to a small fraction of the dog's rhythm over a 24 hour period, and identification of abnormalities may be entirely fortuitous. Evidence of ventricular arrhythmia precedes echocardiographic evidence of DCM in the Doberman by some months or even years. Guidelines for diagnosing DCM were suggested in 2003 by the European Society of Veterinary Cardiology (ESVC) Taskforce Group. The echocardiographic diagnosis of DCM is based on the identification of myocardial (predominantly but not solely systolic) dysfunction with the active exclusion of other acquired or congenital cardiac disease. Evaluation of diastolic function may be valuable for determining prognosis as it has been shown in dogs that a restrictive pattern on mitral inflow and a short E wave deceleration time (<80>

The suggested criteria for diagnosing DCM are likely to be changed in the future as new findings and new techniques become available to a broader veterinary community. New techniques that appear particularly promising are the Tissue-Doppler Imaging (TDI) and Tissue Tracking Imaging (TTI) techniques. These techniques allow characterization of global and regional myocardial function, which not only gives insight to the pathophysiology and characterization of myocardial disease in dogs, but appears to allow identification of diseased individuals before conventional echocardiography. Furthermore, the biomarker N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) appears very promising in correctly identifying dogs with preclinical DCM.

Treatment

Preclinical Cases

There are very few studies addressing the potential benefit of treating preclinical DCM. In dogs with cardiac dilatation, ACE-inhibitors (0.5 mg/kg q12-24h is the usual dose for most of the ACE-inhibitors) and/or the inodilator pimobendan (0.25 mg/kg q12h) are often introduced. Although reasonable, there is very little evidence that these drugs are beneficial at this stage. Many experts initiate antiarrhythmic therapy once an arrhythmia, such as atrial fibrillation or ventricular tachycardia, is discovered. In the case of ventricular tachycardia in boxers or Dobermans, commonly used antiarrhythmics include sotalol (2 mg/kg q12h), amiodarone (8-10 mg/kg q12h and reduce to 5 mg/kg q24h after 6 months; should be used with caution due to irreversible hepatoxicity), or a combination between mexiletine (5-8 mg/kg q8h) and a low dose atenolol. A significant (85%) reduction of number of ventricular complexes is considered a therapeutic success, but it is not proven that this leads to improved survival. In the case of atrial fibrillation, therapy is usually aimed at reducing ventricular rate by introducing digoxin (0.22mg/m² q12h or lower), or a beta-blocker (carvedilol (maximum dose 0.5 mg/kg q12h), metoprolol (maximum dose 1 mg/kg q8h), atenolol (maximum dose 1 mg/kg q12h), or propranolol (maximum dose 1 mg/kg q8h)). Caution should be used when introducing an antiarrhythmic drug with negative inotropic actions (such as beta-blockers) in a dog with a hypocontractile heart or in a dog with fluid retention (heart failure). The dose should be slowly titrated upwards starting with approximately ¼ to ½ of the recommended dose.

Symptomatic Cases

The minimal database required for managing the symptomatic DCM patient includes, in addition to echocardiography, a complete case history (including previous diagnostic tests and previous/current medication), a thorough physical examination, thoracic radiographs (to identify cardiomegaly and pulmonary edema and exclude other disease), abdominal radiographs and ultrasound examination in case of ascites, ECG recording (to identify and characterize an arrhythmia), and routine hematological tests and urinalysis (to exclude other disease and identify prerenal azotemia and disturbances in the fluid electrolyte balance). Therapy should be started once a tentative diagnosis has been established.

Moderately to severely symptomatic dogs should preferably be hospitalized and subject to intensive therapy that includes: minimizing stress, absolute rest, oxygen supplementation, intravenous injections of furosemide at a comparably high dose (initially 2-6 mg/kg, and then 2-3 mg/kg q1-2 h until pulmonary edema has improved). Severely symptomatic patients may require, in addition to the measures listed above, nitroglycerine ointment, pimobendan, or infusions of sodium nitroprusside and/or dobutamine (the latter two requires careful monitoring in a specialized clinic).

Mildly symptomatic dogs or those with stabilized CHF may be managed at home. Successful CHF therapy is always based on a good collaboration between pet owner and veterinarian. It is important that the owner is educated on the following issues: how to monitor heart rate and respiratory rate at home; importance of regular habits and medication; the possibility to modify diuretic dose within a fixed range; avoid strenuous exercise; diet; possible complications; and importance of rechecks.

Chronic medical therapy includes diuretic therapy (furosemide) at a dose of 1-4 mg/kg q8-24h. Spironolactone at a dose of 2 mg/kg q 12-24h and/or hydrochlorothiazide at a dose of 2-4 mg/kg q12h may be added in cases where the fluid retention is refractory to furosemide alone. Pimobendan and/or and ACE-inhibitor are often added to the diuretic therapy once the diagnosis of DCM has been established. Many dogs with DCM are tachycardic and may potentially benefit from heart rate control by adding digoxin or a beta-receptor blocker. However, introduction of a beta-receptor blocker should be done with care to avoid adverse side reactions and the dose should preferably be titred upwards slowly. The above mentioned drugs are often added stepwise as the severity of clinical signs progress. Neutraceuticals such as taurine/L-carnitine and omega-3 fatty acid supplementation may be considered.

The strength of evidence for clinical efficacy of different heart failure drugs in canine DCM is not strong owing to few published clinical trials. ACE-inhibitors have shown to improve quality of life variables in two clinical trials comprising clinical (symptomatic) DCM cases, but they have never been shown to improve survival. Pimobendan has been shown to improve quality of life variables and survival in a population of different breeds and in Dobermans when compared to placebo. The combined alpha- and beta-receptor blocker carvedilol was recently studied in DCM, but the authors could not detect any clinical or laboratory effect of the drug. Furthermore, the median survival time in propranolol treated DCM dogs was recently reported similar to DCM cases without beta-receptor blockade.

Summary

Dilated cardiomyopathy is a common disease in some large bred dogs, in which the disease leads to increased mortality. There are at least two distinct phenotypes of DCM: one that is characterized by systolic dysfunction and histopathological evidence of attenuated wavy fibers; and one characterized by ventricular tachyarrhythmias and histopathological evidence of myocyte degeneration, fibrosis and fatty infiltration. In the absence of genetic tests, dogs are currently screened for DCM in affected breeds using echocardiography and/or 24h-Holter ECG recordings. Suggested criteria for diagnosing DCM has been suggested, but these are likely to be changed in the future as new diagnostic techniques are developed. There is very little published evidence that any type of therapy has a prophylactic effect in preclinical DCM, even in arrhythmic patients. Therapy of symptomatic dogs varies in composition and intensity depending on severity of clinical signs and presence of arrhythmia, but chronic therapy should preferably include furosemide and pimobendan ± ACE-inhibitor.

Disturbances of Sinus Impulse Formation

Sinus Arrest

Sinus arrest is a period where there is no evidence of atrial activity for a period in excess of the two preceding R-R intervals, and implies that there is a depression in automaticity within the sinus node. It is usually recognised in dogs with high vagal tone such as brachycephalic dogs or dogs with underlying respiratory disease. Periods without evidence of any sinus node activity may be prolonged enough to result in syncope.

Sinus Bradycardia

May be a normal rhythm. It may also be recognised in patients with hypothermia, hyperkalaemia, CNS lesions, or drug related, e.g., digoxin, opioids, beta blockers, calcium channel antagonists.

Atropine Response Test

If these bradyarrhythmias are genuinely related to high vagal tone, they should be easily abolished by the administration of atropine. The recommended protocol is to record an ECG trace, then administer atropine (0.04 mg/kg by subcutaneous injection) and after 30 minutes record a further ECG trace.

Sinus Tachycardia

Sinus tachycardia is probably the most common rhythm detected in small animal cardiac patients due to the excited state of most patients. Animals with incessant tachycardia may well have underlying congestive heart failure with high sympathetic drive. Animals in pain or with pyrexia may also show a persistent sinus tachycardia.

Disturbances of Supraventricular Impulse Formation

Supraventricular Premature Complexes (SVPC)

These are supraventricular complexes that occur early and arise from a focus in the atria or the AV node junctional area rather than from the sinus node. The P waves may be positive, negative or hidden in the QRS complexes. The QRS complexes are narrow upright complexes in lead II and look similar to the sinus complexes.

Supraventricular Tachycardia (SVT)--Atrial or Junctional

This is characterized by a tachycardia where the P wave configuration differs from the sinus P waves. The rate is rapid. The QRS morphology is normal. The rhythm is regular unless a multifocal tachycardia is present. The origin may be atrial or junctional. In junctional tachycardia an ectopic focus in the AV junction acts as the primary pacemaker. The P waves are usually inverted and may precede, be superimposed on or follow the QRS complex. It is frequently impossible to differentiate atrial tachycardia from a junctional tachycardia. SVT may be paroxysmal or sustained.

Atrial Fibrillation (AF)

Is recognised by an irregular chaotic ventricular rhythm. In the majority of cases there are no recognisable P waves preceding the QRS complex. Sometimes fine irregular movements of the baseline are seen as a result of the atrial fibrillation waves--referred to as F waves. They may be indistinguishable from baseline artefact. The ventricular rate in dogs and cats is nearly always fast, as most cases are in congestive heart failure and therefore there is a compensatory sympathetic drive. Slower rates are sometimes seen in the giant breed dogs.

Atrial Flutter

Is seen as a rapid and regular, 'saw toothed' type movement of the baseline, at a rate of 300-500/min. These are referred to as F waves; the QRS complexes are normal, and occur at a more normal and regular heart rate, often at a set frequency to the F waves.

Disturbances of Ventricular Impulse Formation

Ventricular Premature Beats (VPC)

These beats occur early. They are not related to a P wave and they are usually wide and bizarre in appearance. If they originate high up in the interventricular septum they may have a narrow upright conformation and may be confused with a supraventricular premature complex.

Ventricular Tachycardia (VT)

Ventricular tachycardia is a continuous series of VPCs resulting from stimulation of an ectopic ventricular focus. It may be intermittent or persistent. Ventricular tachycardia may be a life threatening arrhythmia. The ventricular rate is usually above 160 bpm. A ventricular rhythm between 100-160 bpm is termed an idioventricular rhythm. P waves that are seen are of normal configuration. There is no relationship between the P waves and the QRS complexes. The P waves may precede, follow or be hidden in the QRS complexes. QRS complexes are wide and bizarre. Ventricular fusion and capture complexes occur commonly in ventricular tachycardia.

Ventricular Fibrillation (VF)

This is a nearly always a terminal effect, and causes cardiac arrest. The depolarisation waves occur randomly throughout the ventricles. There is therefore no significant coordinated contraction to produce any cardiac output. If the heart is visualised, fine irregular movements of the ventricles may be seen. The ECG shows coarse (larger) or fine (smaller); rapid, irregular and bizarre movement; no normal wave or complex can be seen. VF often follows ventricular tachycardia.

Disturbances of Impulse Conduction

Sinus Block

Sinus block is diagnosed where there is no P wave for a duration equal to the two preceding R-R intervals. Like sinus arrest it is usually recognised in dogs with accentuated sinus arrhythmia, often those with high vagal tone such as brachycephalic dogs or dogs with underlying respiratory disease.

Atrioventricular (AV) Block

Atrioventricular (AV) block describes an abnormality affecting conduction from the normally depolarized atria to the ventricles. The block occurs at the level of the AV node or the bundle of His.

 1st degree: In 1st degree AV block, conduction across the AV node or the bundle of His is merely slowed--the P-R interval is thus prolonged.

 2nd degree: In second degree AV block, some of the atrial depolarisation (P wave) does not result in a QRS complex--i.e., the P:QRS ratio is >1:1.

The P-R interval may be variable, usually tending to increase prior to the block (Mobitz type I; the Wenckebach phenomenon)--this is another manifestation of high vagal tone. In other cases of second degree AV block, there is a constant P-R interval. This is Mobitz type II block and is generally more serious, indicating disease of the conduction system.

 3rd degree: In third degree AV block, none of the P waves are responsible for ventricular depolarisation. There tends to be a constant and regular P rate, and the ventricular rate depends upon junctional or ventricular escape or rescue beats. The overall ventricular rate is slow. The shape of the ventricular escape complexes will depend on where they originate in the ventricles.

Persistent Atrial Standstill

Persistent atrial standstill is recognised with a slow regular escape focus and no evidence of atrial activity. No P waves can be identified on any lead system. The condition is seen with certain forms of muscular dystrophy. In the Siamese cat and some breeds of dogs atrial standstill is seen without any skeletal muscle involvement. Hyperkalemia produces a temporary reversible atrial standstill.

Atrioventricular Dissociation

This term refers to complete dissociation of the atria and ventricles. The atria and ventricles are being excited by two separate and independent foci. Usually normal sinus node activity depolarises the atria and a junctional rhythm depolarises the ventricles. There is no regular P-R interval. On ECG, P waves appear to wander in and out of the QRS complexes.

Disturbances of Impulse Formation and Conduction

Sick Sinus Syndrome (SSS)

Sick sinus syndrome may result in a variety of ECG abnormalities. The syndrome probably should be called sick conduction syndrome as the sinus node, AV node and escape rhythms are all affected. A variety of arrhythmias are seen including sinus bradycardia, sinus arrest with no escape rhythm, AV block and paroxysmal episodes of supraventricular tachyarrhythmias.

Ventricular Pre-excitation and Supraventricular Tachycardia

In ventricular preexcitation, an atrial bypass tract outside the AV junction connects the atrium to the ventricle circuiting the AV node, which results in premature activation of the ventricles. An abnormally short P-R interval is seen on the ECG. If the bypass tract circumvents both the AV node and the bundle of His early activation of the ventricles causes a slurring of the upstroke of the QRS, called a (delta) wave. Retrograde conduction may result in supraventricular paroxysmal tachycardia due to a reentry mechanism. This is called the Wolff-Parkinson-White syndrome (WPW).

Escape Rhythms

Escape Beats

In general, the escape beats apparent in the various bradyarrhythmias look like ventricular premature complexes, as they arise from a similar focus. However they are not premature; they are late or escape complexes and should never be suppressed.

Treatment of Arrhythmias

Bradyarrhythmias

Animals with bradyarrhythmias such as sinus arrest, sinus bradycardia, 2nd or 3rd degree AV node block, atrial standstill, sick sinus syndrome should be carefully checked for electrolyte imbalances, systemic disease causing high vagal tone or history of drug ingestion. Bradyarrhythmias due to high vagal tone may respond to medication with vagolytic or sympathomimetic drugs. If there is no response to medication then pacemaker implantation is the only option.

 Vagolytic drugs: Atropine, proantheline, glycopyrrolate

 Sympathomimetic drugs: Isoprenaline, terbutaline, methylxanthine

 Other: Pacemaker implantation

6 settimane = dentatura di latte anteriore completa

2/3 mesi = i denti di latte cominciano a cadere e gli occhi assumono il colore definitivo

3/5 mesi = avviene la sostituzione dei denti incisivi

7 mesi = dentatura completa

2 anni = iniziano a consumarsi gli incisivi inferiori

3 anni = comincia a notarsi il deposito di tartaro sui denti

7/8 anni = può comparire un piccolo orlo periferico chiaro intorno all'occhio (inizio dell'anzianità)

12 anni = comincia a perdere i denti

Classi di displasia:

grado A- nessun segno di displasia.La testa del femore e l'acetabolo sono congruenti.Il margine acetabolare cranio-laterale appare netto e leggermente arrotondato. La rima acetabolare è sottile ed uniforme. L’angolo acetabolare secondo Norberg è di circa 105° o superiore.Nelle anche giudicabili eccellenti il margine acetabolare cranio-laterale include la testa del femore ancora di più in direzione latero-caudale.

grado B -quasi normale. La testa del femore e la cavità acetabolare sono leggermente incongruenti e l’angolo secondo Norberg è di circa 105°, oppure l’angolo di Norberg è inferiore a 105°, ma il centro della testa del femore si trova medialmente rispetto al margine acetabolare dorsale mentre la testa del femore e l’acetabolo sono congruenti.

grado C - leggera. La testa del femore e l’acetabolo sono incongruenti, l’angolo secondo Norberg è di circa 100° e/o sussiste un leggero appiattimento del margine cranio-laterale dell’acetabolo. Sono presenti lievi irregolarità o leggeri segni di artrosi a carico del margine acetabolare craniale, caudale o dorsale od in corrispondenza del collo o della testa del femore.
grado D- media. E' presente un’incongruenza evidente tra testa del femore e cavità acetabolare con sublussazione. L’angolo acetabolare secondo Norberg è compreso tra 90 e 100°. Sono presenti segni riferibili ad osteoartrosi ed è evidente l’appiattimento del margine acetabolare cranio-laterale.

gradoE - grave. Sono presenti modificazioni displastiche evidenti delle articolazioni coxo-femorali quali lussazione o marcata sublussazione, l’angolo acetabolare secondo Norberg è minore di 90°, c’è appiattimento del margini acetabolare craniale, deformazione della testa del femore (testa a fungo, appiattita) o altri segni di osteoartrosi.

Quando arriva a casa, il nuovo cucciolo ha già ricevuto la prima vaccinazione. Se ha sette o otto settimane d’età, non è ancora completamente protetto verso molte malattie e bisogna fare attenzione ai rapporti con gli altri cani finché non ha terminato il suo programma vaccinale. Affinché sia ben protetto, è importante continuare a vaccinarlo per tutta la vita.
Il veterinario adotterà il programma vaccinale più adatto allo stile e all’ambiente di vita di ciascun animale. Alcuni vaccini possono essere somministrati contemporaneamente con la stessa siringa, altri devono essere iniettati in sedi diverse ma nella stessa seduta. Come per i bambini, molte delle vaccinazioni primarie sono effettuate attraverso una serie di iniezioni successive.

PERCHÉ VACCINARE IL CANE?
Il principio su cui si basa la vaccinazione è la stimolazione delle difese dell’organismo verso alcune malattie specifiche. La difesa immunitaria è sostenuta da numerose cellule e molecole, come gli anticorpi. I cuccioli sono protetti contro molte malattie infettive grazie agli anticorpi contenuti in quella parte di latte materno che ricevono nelle prime ore di vita, il colostro. La protezione di origine materna dura meno di tre mesi. Per questo, i programmi vaccinali iniziano attorno ai due mesi d’età con la prima vaccinazione e sono completi dal terzo mese, quando gli anticorpi materni diminuiscono.

PERCHÉ è NECESSARIO RIPETERE LE VACCINAZIONI?
Molte persone credono che, vaccinando il cane da cucciolo, l’immunità ricevuta lo possa proteggere per tutta la vita. Purtroppo non è così. Per mantenere la protezione sono necessari i richiami vaccinali. Il richiamo stimola le difese immunitarie affinché la protezione sia attiva per un ulteriore periodo. In assenza di questi regolari richiami, il sistema immunitario del cane può non essere in grado di proteggerlo da malattie gravi, spesso fatali.

CONTRO COSA POSSIAMO VACCINARLO?
Le principali malattie infettive contro cui si vaccina oggi il cane sono parvovirosi, cimurro, epatite, leptospirosi e bronchite infettiva. Sono tutte altamente contagiose e possono essere difficili da curare. La vaccinazione antirabbica è obbligatoria solo in alcune condizioni particolari e per portare l’animale all’estero, ma può essere ugualmente consigliata dal veterinario.

Parvovirosi canina

La parvovirosi canina è forse la più grave e comune malattia infettiva del cane. Rappresenta un problema serio, con epidemie che possono verificarsi periodicamente. Esordisce improvvisamente con la comparsa di vomito e di diarrea maleodorante ed emorragica che conducono rapidamente a disidratazione e collasso. Anche il cuore può essere raggiunto dal virus. La morte del cucciolo può avvenire entro 24 ore. L’unica protezione contro questa malattia è la vaccinazione.

Cimurro canino
Il cimurro canino è una malattia altamente contagiosa e spesso fatale. I cani che sopravvivono all’infezione virale iniziale spesso convivono con alcuni problemi come deformazione dei denti, tic nervosi e predisposizione ad episodi epilettici. La terapia è spesso inutile perché il periodo di incubazione è lungo - in genere di tre settimane - e, quando esordisce l’infezione è solitamente troppo tardi per vaccinare.

Epatite infettiva canina
L’epatite infettiva canina è una malattia che colpisce il fegato. Le forme acute possono causare la morte del cane entro 24-36 ore. I soggetti che sopravvivono alla malattia possono divenire portatori e diffondere il virus ad altri cani.

Leptospirosi
La leptospirosi è una malattia infettiva sostenuta da differenti sierotipi. E’ trasmissibile direttamente, da animale malato a sano, o indirettamente attraverso l’ingestione di materiale contaminato. Agenti di diffusione sono soprattutto i roditori, che eliminano le leptospire con le urine. Nel cane la leptospirosi si manifesta con differente sintomatologia: gastroenterite emorragica, ittero, nefrite. Oltre ad essere pericolosa per il cane, tale patologia può essere trasmessa all’uomo. Nel cane la prevenzione con la vaccinazione copre i due sierotipi di Leptospirosi più frequentemente riscontrati. E’ consigliabile vaccinare i cani particolarmente esposti prima del periodo a rischio.

Bronchite infettiva o parainfluenza canina
Il virus della bronchite infettiva o parainfluenza canina è uno dei patogeni responsabili della malattia conosciuta come “tosse dei canili”. Come indica il nome, è una malattia respiratoria molto contagiosa, specifica di canili, pensioni, allevamenti e rifugi. All’origine di questa malattia si riscontrano numerosi virus e batteri, tra cui quelli principali e fondamentali sono il batterio Bordetella bronchiseptica e il virus della Parainfluenza. I cani colpiti da questa malattia manifestano una tosse secca che può durare molte settimane, causando disagio tanto al cane quanto a chi vi convive. Esiste un programma specifico di vaccinazione che è consigliabile per i cani che vivono in collettività.

Rabbia
La rabbia è una malattia virale che può essere trasmessa all'uomo (zoonosi) attraverso il morso e il graffio di animali infetti. E’ quindi importante non lasciare liberi i cani nelle regioni in cui questa malattia è diffusa negli animali selvatici. Nel nostro continente la patologia è presente soprattutto in Germania, Francia, Austria, Paesi dell’Est ed Ex Jugoslavia. Si manifesta con sintomi a carico soprattutto del sistema nervoso. La vaccinazione antirabbica è attualmente obbligatoria solo in alcune regioni italiane tra cui il Friuli Venezia Giulia e il Trentino Alto Adige. E' inoltre obbligatoria quando si porta il cane all'estero o in Italia nelle zone sopra indicate e in Sardegna, che è indenne dalla malattia. La vaccinazione antirabbica può tuttavia essere consigliata dal veterinario anche nelle altre zone. Si consiglia di rivolgersi al proprio veterinario per ogni aggiornamento relativo agli obblighi vaccinali per la rabbia.

Le vaccinazioni del cane sono registrate su un apposito libretto, che contiene i dettagli di ciascun vaccino e la data di somministrazione. è firmato dal veterinario dell’animale e costituisce un registro permanente, necessario per dimostrare la storia vaccinale del cane qualora debba essere introdotto in una pensione o debba viaggiare al seguito della propria famiglia adottiva.

Cani di differenti razze, sesso ed età possono sviluppare patologie a carico del legamento crociato.
Retriver, Rottweiler, Mastiff, Amarican Staffordshire Terrier,Akita, San Bernardo e Newfoundland sono razze predisposte.
I maschi castrati e le femmine sterilizzate, mostrano un'aumentato rischio di sviluppare tali patologie, così come le taglie grandi ed i cani obesi.

STORIA
L'esordio è dopo un evento traumatico oppure insidioso, che lentamente evolve verso la zoppia tipica dell'interessamento del crociato.

VALUTAZIONE DELL' ANDATURA
I cani affetti anche da una leggera zoppia tengono l'arto un po' "aperto" ache quando stanno fermi in piedi.Anche in posizione seduta, le zampe non assumono una posizione normale, ma ne assumono una che appare piuttosto scomoda. Spesso spostano il loro peso in avanti quando si siedono e quando si alzano.

ESAME FISICO
Un esame eseguito col cane in piedi,permette di identificare sottili cambiamenti a carico della massa muscolare, delle fibre periarticolari e dell'articolazione.

RADIOGRAFIA
Mostra le condizioni articolari,osteofitosi o spostamento della superficie articolare tibiale.Per fare una diagnosi certa devono coincidere i dati derivanti dalla radiografia, dalla palpazione, dalla presenza o assenz adi dolore e dall'osservazione dell'andatura.

TRATTAMENTO
Nella maggior parte dei casi è chirurgico.Si sostituisce il legamento crociato con tessuto autologo o di materiale sintetico. Recentemente si interviene sulle asperità della superficie tibiale.

INTRODUZIONE
Le malattie infiammatorie intestinali sono le più comuni cause di vomito e diarrea nei cani e nei gatti.Tale termine comprende un gruppo di malattie caratterizzate da : parziale anoressia, diarrea e persistente perdita di peso ( che dura da più di 3 settimane). Dal punto di vista istopatologico, la mucosa gastrointestinale appare infiltrata da cellule infiammatorie ( linfociti, cellule plasmatiche, neutrofili, esinofili, istiociti, ecc) di eziologia sconosciuta.

INCIDENZA
Questo tipo di patologia è più evidente nei cani rispetto ai gatti. Alcune razze come Shar-Pei,Pastore Tedesco e gatto Siamese risultano essere più esposte anche se si riscontrano in altre razze e anche nei meticci.
Il grosso intestino è la parte del sistema digerente più colpita nei cani. Nei gatti lo è il piccolo intestino. In molti casi i linfociti e le cellule plasmatiche sono il tipo predominante di cellule infiammatorie.

FISIOPATOLOGIA
La fisiopatologia delle malattie infiammatorie intestinali rimane un problema scarsamente compreso. E' stato determinato che l'inizio e lo sviluppo di questo tipo di patologie, è attribuito ad una inappropriata risposta immunitaria ad antigeni che normalmente sono tollerati (batteri e cibo).
L'origine delle malattie infiammatorie intestinali è attribuito a molteplici fattori. Ci sono varie ipotesi che propongono la presenza di uno o più fattori che attivano questo processo infiammatorio, quale un'alterazione della permeabilità della mucosa intestinale. una anomala introduzione di antigeni ai linfociti, e una perdita o inibizione del meccanismo di tolleranza antigenica.
L'alterazione della permeabilità della mucosa intestinale causa un aeccessiva entrata di antigeni e., di conseguenza, dei loro mediatori. Questo contesto attiva una risposta infiammatoria, con il rilascio di prostaglandine, leucotrieni, interleukina 1, interleuchina 6, interleuchina 8, e fattore di necrosi tumorale Alfa (meccanismo di esclusione antigenica). La persistenza di alterata permeabilità, o l'esistenza di una anomala risposta immmunitaria, produce infiammazione cronica. Questa alterazione conduce probabilmente a perdita del meccanismo di tolleranza, che genera una risposta immunitaria in presenza di antigeni del cibo e di batteri che normalmente sono tollerati.

SEGNI CLINICI
Variano secondo la porzione o le porzioni di tratto digestivo interessato.
Quando è infiltrato il piccolo intestino i segni sono: parziale anoressia o appetito normale, feci acquose o steatosiche, aumento del volume delle feci, progressiva perdita di peso, può includere vomito sporadico sebbene lo stomaco non sia direttamente coinvolto.
Se è infiltrato il colon, i segni comprenderanno: tenesmo, presenza di muco e sangue fresco nel materiale fecale, aumentato numero di evacuazioni, parziale anoressia o appetito normale e vomito intermittente. In tal caso la perdita di peso è meno frequente.

DIAGNOSI
Per porre diagnosi di malattia infiammatoria intestinale, occorre escludere un gruppo di patologie che inducono vomito e/o diarrea cronica.
A tale proposito deve essere eseguita una coprocultura per escludere la presenza di Nematodi,Cestodi, Giardia, Criptosporidi, ecc..
Gli esami ematochimici dvono essere completi, comprendendo gli esami per la funzionalità epatica ( ALT-AST-FAS), renale (Urea, Creatinina), tiroide (T4), test di stimolazione ACTH.
Si usa il test TLI per ricercare o escludere l' insufficienza pancreatica esocrina.
I valori ematici della B12 (cobalamina) e dei folati per testare l'assorbimento a livello di ileo e digiuno e per determinare la presenza di diarrea da antibiotici.
E' importante valutare proteine totali ed albumina per valutare una enteropatie da deplezione proteica.
L'analisi delle urine è necessaria per valutare se la perdita di proteine avvene per via urinaria o intestinale.

La radiologia è di scarso aiuto.
L' ecografia serve a determinare l'aumento di spessore della mucosa gastrica e intestinale, alterazione degli strati e presenza di linfonodi reattivi.
Come parte della diagnosi differenziale, ai pazienti deve essere somministrata una dieta libera da antigeni per discriminare un allergia ai cibi.
Una volta scartate queste patologie, ma non è stata raggiunta una diagnosi definitiva, si dovrebbe procedere ad una ecografia endoscopica.
Dal punto di vista macroscopico, si determinano le condizioni generali della mucosa intestinale, la diagnosi di tumori,identificazione di stenosi, ulcere, polipi, ecc..
Le bipsie devono essere prese da diverse porzioni di stomaco, piccolo intestino e colon.

TRATTAMENTO
Prevede l'uso di immunososppressori, antibiotici e cambiamenti nella dieta.
Occorre osservare scrupolosamente la terapia per ottenere buoni risultati.
Spesso la sola dieta risolve il problema, a volte vi si associano farmaci. La dieta deve essere altamente digeribile, ipoallergenica, bilanciata, appetibile e povera di grassi. Deve includere proteine che il paziente non ha mai assunto prima ( agnello, soia, pesce, coniglio, ecc). La dieta non deve essere mai abbandonata, se non se ne vedono subito i risultati: essa va continuata in quanto non avvengono cambiamenti prima di 4 settimane e oltre. Sono disponibili diete ipoallergeniche "commerciali" e diete con proteine idrolizzate. Si incoraggiano supplementi di omega3 che contribuiscono a ridurre l'infiammazione del tratto digestivo. Qualunque sia il tipo di dieta scelto ( pronta o fatta in casa), i paziento devono fare almeno 3-4 pasti per facilitare la digestione e l'assimilazione dei nutrienti.


IMMUNOSOPPRESSORI

Glucocorticoidi
In generale prednisone e prednisolone sono i farmaci di scelta nel trattamento di questo gruppo di patologie. la dose varia tra 1-2 mg/Kg ogni ore. Successivamente si riduce la dose della metà ( per 4 settimane) e poi ancora del minimo efficace ( a discrezione del veterinario), fino alla sospensione del trattamento.
Il dexametasone può anche essere somministrato per via orale nei pazienti che dimostrano eccessivi effetti collaterali dopo la somministrazione di prednisolone ( polifagia, poliuria,ecc..).
Corticoidi per via parenterale sono un'alternativa nei pazienti ch epresentano vomito o quando si teme che il processo di assorbimento digestivo sia alterato da fenomeni infiltrativi.
Il budesonide è uno steroide 200 volte più potente dell' idrocortisone. Poichè è ampiamente distrutto (90%) dal fegato,riduce i rischi di Sindrome di Cushing.La dose è di 1-3mg/die.

Sulfasalazina
E' una combinazione di acido 5-aminosalicilico e sulfapiridina.Circa il 70% della dose somministrata raggiunge il colon e la molecola si divide in due parti. La siusa per trattare pazienti con coliti, nei quali da un ottimo risultato. La dos eusata è di 12.5mg/Kg ogni 6 ore per 2 settimane,seguita dalla stessa dose ogni 12 ore per 28 giorni.
Gli effetti collaterali includono anoressia e vomito.I pazienti devono essere strettamente minitorati , con un epatogramma mensile per prevenire possibili danni epatici. Altri possibili effetti collaterali sono la cheratite secca e la dermatite allergica.

Olsalazina
Consta di due molecole di acido 5-aminosalicilico. Dose: 25mg/Kg ogni 8 ore.

Mesalamina
Si usa anche nelle patologie infiammatorie del colon. Dose: 10-20mg/kg ogni 12 ore, per somministrazione orale.


Azatiopirina
lo si usa quando non c'è risposta ai farmaci convenzionali o quando si è costretti a riduzioni di dosaggio per effetti collaterali ai glucocorticoidi. dose:1-1.5mg/Kg al giorno per 2 settimane.Occorre eseguire un monitoraggio periodico, con controllo degli esami del sangue ed epatogramma.

Ciclofosfamide
Poco usato e riservato ai pazienti refrattari ai farmaci di cui sopra.Richiede costanti controlli ematologici ed espone al rischio di cistite emorragica.

Ciclosporina
potente immunosoppressore. Dose: 5mg/Kg/die. 

Antibiotici: metronidazolo
Effetti contro i batteri anaerobi e i protozoi, inibisce la risposta immunitaria cellulo-mediata.Generalmente non lo si usa da solo, ma in combinazione ai glucocorticoidi. Ciò implica una riduzione della dose:10-20mg/Kg ogni 12 ore.

Poichè gli occhi sono ben vascolarizzati e poichè la retina ed il nervo ottico sono considerati parte del SNC, non deve sorprendere che le malattie neurologiche e vascolari possano manifestarsi nell' occhio. In aggiunta a ciò, ricordiamo che la superficie dell'occhio può essere coinvolta in malattie che interessano altre membrane mucose del corpo e del tratto superiore dell'apparato respiratorio. Le palpebre possono essere interessate da malattie dermatologiche generalizzate. L'orbite, i muscoli extraoculari e masticatori possono essere affetti da disturbi sistemici così come da malattie della cavità orale. Qui vedremo una panoramica delle più comuni malattie sistemiche che si manifestano nell'occhio ed attorno ad esso.

1. MANIFESTAZIONI OCULARI DI MALATTIE SISTEMICHE
Superficie oculare e uvea.
E' importante comprendere che gli occhi possono essere il primo e l' unico organo affetto da una malattia sistemica, molto prima che la malattia diena una manifestazione sistemica di se stessa. Pertanto, possibili sottostanti malattie sistemiche devono essere prese in considerazione quando non ci sono altre cause evidenti di un problema oculare. Questo è particolarmente vero in caso di uveiti,la più comune manifestazione oculare delle malattie sistemiche. Dovrebbe essere intrapreso un serio lavoro diagnostico insieme ai proprietari del cane colpito.
Le malattie infettive che possono interessare gli occhi includono virus ( adenovirus, rickettsie, batteri, funghi, protozoi e parassiti.
Gli occhi possono essere interessati anche da malattie metaboliche, come il diabete mellito ( formazione di cataratta) ed ipotiroidismo (in possibile associazione con cheratocongiuntivite secca). L' ipertensione cronica sistemica danneggia la barriera sangue-occhio ep rovoca emorragie intraoculari e distacco della retina con cecità.Un animale in cui si pone diagnosi di emorragia intraoculare senza una evidente storia di traumi o di neoplasia intraoculare, può soffrire di problemi di coaugulazione. Una rapida diagnosi è altamente racconamdata in questi pazienti così che si possa intraprendere al più presto la terapia più apporpriata
La Sindrome uveodermica è una malattia immuno-mediata, dove i melanociti del tratto uveale ed il derma, sono gli organi bersaglio. Questa sindrome può coplire tutte le razze di cani, ma la si vede più comunemente in Akita, samoiedo, Siberian Husky e Cane da Pastore Scozzese. I problemi oculari si manifestano solitamente prima dei cambiamenti dermatologici ed includono uveute e depigmentazione dell' uvea, con secondario distacco di retina e glaucoma. Le manifestazioni oculari includono vitiligine e poliosi.
Il linfosarcoma è la più comune causa di neoplasia secondaria nell' occhio di cani e gatti. I segni clinici più comuni includono : uveite, emorragie intraoculari e malattie ad esse connesse.La maggior parte degli animali con lesioni oculari sono già in stadio avanzato di linfoma.

2. NEUROOFTALMOLOGIA
Si tratta di malattie del sistema neurologico, che coinvolgono le normali funzioni dell'occhio. E' bene acquisire una certa confidenza con le manovre mediche che permettono di localizzare eventuali lesioni, rendendo così più agevole il lavoro del veterinario.
Il sistema visivo si compone di retina,nervo ottico,chiasma,nucleo genicolato laterale,e le radicolazioni ottiche che rilasciano le informazioni alla corteccia.
Perchè la percezione visiva avvenga correttamente,le informazioni devono raggiungere la corteccia visiva, situata nella zona occipitale.Test per la corretta valutazione del sistema visivo includono la risposta alla minaccia,il test col fiocco di cotone ed il test del labirinto.Il riflesso pupillare alla luce non è un test efficacie, in quanto le informazioni sulla luce non hanno bisogno di raggiungere la corteccia, ma rimane comunque importante valutare la risposta oculare alla luce. Tale riflesso interessa la regione del mesencefalo.Il diametro della pupilla è regolato da fibre del nervo simpatico e parasimpatico. I nervi craniali (CN) coinvolti nelle funzioni dell'occhio sono: l' ootico (CN II), l' oculomotore (CN III), il trocleare (CN IV), il trigemino (CN V),l' adducente (CN VI) il facciale (CN VII) ed il vestibolare (CNVIII). Le anomalie pupillari includono un diseguale diametro pupillare delel due pupille o anisocoria.Molte delle possibili cause sottostanti possono avere serie conseguenze sull'animale: paralisi del nervo facciale, cecità centrale,strabismo e nistagmo.

3.MALATTIE DELL' ORBITA
Poichè l' orbita è posta molto vicino alla cavità orale e alla cavità nasale, alle radici dentali e ai seni paranasali, le strutture orbitarie sono suscettibili che partendo da esse si allargano alle pareti ossee e ai tessuti molli.
Le malattie delle orbite possono essere suddivise in quelle che causano esoftalmo (globo oculare più prominente) e quelle che causano enoftalmo (globo oculare infossato). Le più comuni cause di esoftalmo includono: traumi, cellulite o ascesso orbitale, neoplasia orbitale , miositi dei muscoli masticatori ed extraoculari.I problemi infiammatori si pososno riconoscere dal dolore provocato dalla retropulsione del globo oculare e/o all'apertura della bocca.Si tratta di malattie molto comuni. 
Possibili cause di lesioni infiammatorie includono l'estensione delle stesse dalla cavità orale, infezioni dei seni e delle radici dentali.