Dieta la animale

8/13/2019 Dieta la animale

1/7

DIETARY-RESPONSIVE DISEASE

EtiologyDietary-responsive disease is an all-inclusive term thatincludes dietary allergy (a hyperimmune response to a

dietary antigen) and dietary intolerance (a nonimmune

mediated response to a dietary substance). From a clinical

standpoint, there is minimal value in distinguishing betweenthe two unless there are concurrent cutaneous signs of allergic

disease.

Clinical FeaturesAffected patients may have vomiting and/or diarrhea (largeand/or small bowel) as well as allergic skin disease.

Diagnosisiagnosis consists of showing response to feeding an elimination

diet that is appropriate for the patient (see the discussion

of dietary management in !hapter "#). $here is typicallyminimal value in distinguishing between allergy and intolerance.

$ests for %g& antibodies i n the patient's blood to specific

antigens are not as valuable as seeing the response to an

elimination diet. $he diet must be carefully chosen it must

consist of nonallergenic substances or foods to which thepatient has not previously been eposed. *ost animals

respond to an appropriate diet within " weeks, although

some take longer.

Treatment*ost patients that respond can simply be fed the diet towhich they responded in the dietary trial (assuming that it

is balanced). +are patients develop allergies to the elimination

diet and reuire different elimination diets to be fed on

rotating - to "-week cycles.

Prognosis$he prognosis is usually good.

SMALL INTESTINAL INFLAMMATORY

BOWEL DISEASE

Clinical Features% involves idiopathic intestinal inflammation. % canaffect any portion of the canine or feline intestine. Although

the cause of % is unknown, it is speculated to involve aneaggerated or inappropriate response by the immune system

to bacterial and/or dietary antigens as at least part of themechanism. $he clinical and histologic features of % can

closely resemble those of alimentary lymphoma (see p. 01).

2ymphocytic-plasmacytic enteritis (23&) is the most commonlydiagnosed form of canine and feline %. !hronic

small intestinal diarrhea is common, but some patients have

weight loss with normal stools. %f the duodenum is severely

affected, vomiting may be the ma4or sign, and diarrhea can

be either mild or absent. 3rotein-losing enteropathy canoccur with the more severe forms.

&osinophilic gastroenterocolitis (&5&) is usually an allergic

reaction to dietary substances (e.g., beef, milk) and as

such is not %. 6owever, the clinical signs do not always

respond to dietary change and may represent true % insome dogs. %t is less common than 23&. 7ome cats have

eosinophilic enteritis as part of a hypereosinophilic syndrome

(6&7). $he cause of feline 6&7 is unknown, but

immune-mediated and neoplastic mechanisms may beresponsible. 2ess severely affected cats without 6&7 seem tohave a condition similar to canine &5&.

Diagnosisecause % is idiopathic intestinal inflammation, it is adiagnosis of eclusion it is not 4ust a histologic diagnosis.

8o physical eamination, historic, clinical pathology,imaging, or histologic findings are diagnostic of %. iagnosis

reuires elimination of known causes of diarrhea

plus histology showing mucosal inflammatory infiltrates,

architectural changes (e.g., villus atrophy, crypt changes),


2/7

and/or epithelial changes. *ucosal cytologic evaluation is

unreliable for diagnosing lymphocytic inflammation because

lymphocytes and plasma cells are normally present in intestinal

mucosa. 6istologic diagnosis of mucosal inflammation

is unfortunately sub4ective, and biopsy samples are freuentlyoverinterpreted. 9 * i l d 9 23& often refers to essentially normal

tissue. &ven descriptions of 9moderate9 or 9severe9 23& may

be dubious because of substantial inconsistency among

pathologists. %t can be etremely difficult to distinguish awell-differentiated lymphocytic lymphoma from severe 23&,even with full-thickness samples. 7ome animals with intense

dietary reactions have biopsy findings that resemble lymphoma.

%f the biopsy specimens are of marginal uality

(either from the standpoint of si:e or artifacts present), it is

easy to mistakenly diagnose 23& instead of lymphoma if thelatter is causing a secondary tissue reaction. +ecent data

document that biopsy of more than one site (e.g., duodenum

and ileum, as opposed to 4ust duodenum) is sometimes

critical in finding inflammatory (and neoplastic) changes.

iagnosis of feline 23& is similar to that of canine 23&, butit is important to note that cats with % may have mild to

moderate mesenteric lymphadenopathy, and such lymph

adenopathy is not diagnostic of intestinal lymphoma.

iagnosis of &5& is similar to diagnosis of 23&. ogs

with &5& may have eosinophilia and/or concurrent eosinophilic

respiratory or cutaneous dietary allergies with pruritus.5erman 7hepherd dogs seem to be overrepresented.iagnosis of feline &5& centers on finding intestinal eosinophilic

infiltrates however, splenic, hepatic, lymph node,

and bone marrow infiltrates and peripheral eosinophilia are

common.

Treatment!anine 23& treatment begins with elimination diets and

antibiotics in case what appears to be % is actually dietary

intolerance or A+&. ;ther therapy depends on the severity

of the 23&. 7omewhat more severe disease warrants

metronida:ole with or without high-dose corticosteroidtherapy (e.g., prednisolone, . mg/kg/day or budesonide in

steroid-intolerant patients). *ore severe disease, especially if

associated with hypoalbuminemia, usually reuires immunosuppressives

(e.g., a:athioprine or cyclosporine). !yclosporine

seems to be reasonably effective and works fasterthan a:athioprine administered every other day however, it

is also more epensive. &lemental diets, although epensive,

can be invaluable in severely emaciated or severely hypoproteinemic patients with severe inflammation as a way to feed

the patient and the intestinal mucosa without causing more

mucosal irritation. Failure of a dog to respond to 9appropriate9

therapy can be the result of inadeuate therapy, owner

noncompliance, or misdiagnosis (i.e., diagnosing 23& whenthe problem is lymphoma).

Feline 23& treatment is somewhat similar to that for

canine 23&. 6ighly digestible elimination diets may be curative

if what was thought to be % is actually food intolerance,

and therapeutic diets should always be used i f the catwill eat them. 6igh doses of corticosteroids are typically

administered early in cats because of their beneficial effects

and the cat's relative resistance to iatrogenic hyperadreno

corticism. 3rednisolone is preferred to prednisone in the cat,and methylprednisolone is typically more effective than

prednisolone. udesonide is primarily indicated in cats that

cannot tolerate the systemic effects of steroids (e.g., thosewith diabetes mellitus). 2ow-dose metronida:ole (


3/7

!hapter "#). 3arenteral administration of cobalamin to cats

with severely decreased serum concentrations may aid or be

necessary for remission of diarrhea. %f the cat responds to

this therapy, the elimination diet should be continued while

the medications are gradually tapered one at a time.!anine &5& treatment should focus on a strict hypoal

lergenic diet (e.g., fish and potato, turkey and potato). 3artiallyhydroly:ed diets may also be helpful, but they are not

a panacea for all 5% dietary allergies/intolerances. %t is importantto determine what the dog was fed previously when

selecting the dietary therapy. %f signs do not resolve with

dietary therapy, the addition of corticosteroid therapy isusually curative. Animals usually respond better to elimination

diets than to corticosteroids. 7ometimes, an animal i n i tially

responds to dietary management but relapses while still

eating this diet because it becomes allergic to one of the

ingredients. $his situation necessitates administration ofanother elimination diet. %n some animals that are very

prone to developing such intolerances, switching back and

forth from one elimination diet to another at -week intervals

helps to prevent this relapse from happening. (7ee

!hapter "# for more information on these therapies.)Feline &5& associated with hypereosinophilic syndrome

usually reuires high-dose corticosteroid therapy (i.e., prednisolone,

. to 0.0 mg/kg/day) response is often poor. !ats

with eosinophilic enteritis not caused by 6&7 often respondfavorably to elimination diets plus corticosteroid therapy.%f the dog or cat responds clinically, then the therapy

should be continued without change for another to weeks

to ensure that the clinical improvement is the result of the

therapy and not an unrelated transient improvement. ;nce

the clinician is convinced that the prescribed therapy isresponsible for the improvement seen, the animal should be

slowly weaned from the drugs, starting with those that have

the greatest potential for adverse effects. %f antiinflammatory

or immunosuppressive therapy was initially reuired, the

clinician should attempt to maintain the pet on every-otherdaycorticosteroid and a:athioprine therapy. %f that regimen

is successful, then the lowest effective dose of each should be

slowly determined. ;nly one change should be made at a

time, and the dose should not be decreased more freuently

than once every to " weeks, if possible. %f a homemade dietwas used initially, the clinician should seek to transition the

patient to a complete, balanced commercial elimination diet.

ietary and antibiotic therapy are usually the last to be

altered. $here is no obvious benefit to rebiopsying patients

that are clinically improving.

Prognosis$he prognosis for dogs and cats with 23& is often good, if

therapy is begun before the patient is emaciated. 7evere

hypoalbuminemia and a very poor body condition arethought to be suggestive that the patient may have more

difficulty responding. A markedly low serum cobalamin concentration

in the dog might be a poor prognostic sign, but

that is uncertain. *any animals will need to be on a special

diet for the rest of their lives. *any with moderate to severedisease will need prolonged medical therapy, which should

be tapered cautiously. %atrogenic !ushing's syndrome should

be avoided. 7everely affected animals may initially benefitfrom enteral or parenteral nutritional therapy. Although the

relationship is unclear, 23& has been suggested to be a potentiallyprelymphomatous lesion (see p. 0# for immunopro

liferative enteropathy in asen4is) however, this is uncertain.

%f a dog or cat with a prior diagnosis of 2 3& is later diagnosed

as having lymphoma, it may be 4ust as likely that either theinitial diagnosis of % was wrong (i.e., the patient had

lymphoma) or that the lymphoma developed independently

of the %.

LARGE INTESTINAL INFLAMMATORY


4/7

BOWEL DISEASE

Clinical Features%n the author's practice, Clostridium colitis, parasites, dietaryintolerance, and fiber-responsive diarrhea are responsible

for most cases referred and previously diagnosed as having

9intractable9 large bowel 9%.9 !anine lymphocyticplasmacytic

colitis (23!) typically causes large bowel diarrhea

(i.e., soft stools with or without blood or mucus no

appreciable weight loss). %n general, affected dogs are fundamentallyhealthy ecept for soft stools. %n cats hematoche:ia

is the most common clinical sign, and diarrhea is the second

most common sign. Feline 2 3 ! may occur by itself or concurrently

with 23&, whereas canine large bowel % seemsto be infreuently associated with small bowel %.

Diagnosisiagnosis (i.e., ecluding other causes and finding mucosal

histologic changes) is similar to that for small bowel %. %n

particular, Tritrichomonas can cause substantial mononuclearinfiltrates into feline colonic mucosa.

Treatment7teroids, metronida:ole, sulfasala:ine (A:ulfidine), mesalamine, or olsala:ine may be used in dogs with moderate to

severe 23!. !orticosteroids and/or metronida:ole may be

effective by themselves and/or allow lower doses of sulfasala:ine

to be successful. 6ypoallergenic and fiber-enriched dietsare often very helpful. %t is critical to eliminate colonic fungalinfections before begining immunosuppressive therapy.

6igh-fiber and hypoallergenic diets are also often beneficial

in cats in fact, most 9intractable9 feline 2 3 ! cases seen

in the author's practice are ultimately determined to be related

to diet. *ost cats with 23! respond well to prednisoloneand/or metronida:ole, and sulfasala:ine is rarely needed.

Prognosis$he prognosis for patients with colonic % tends to be

better than for small bowel %.

GRANULOMATOUS ENTERITIS/

GASTRITIS

!anine granulomatous enteritis/gastritis is uncommon, and

it can be diagnosed only histopathologically. $he clinicianshould search diligently for an etiology (e.g., fungal). !linical

signs are similar to those of other forms of %. Althoughcompared to !rohn's disease in people, the two are dissimilar.

%f the disease is locali:ed, surgical resection should be

considered i f the clinician is sure that there is not a systemiccause (e.g., fungal). %f it is diffuse, corticosteroids, metronida:ole,

antibiotics, a:athioprine, and dietary therapy should

be considered. $oo few cases have been described and treated

to allow generali:ations. $he prognosis is poor.

Feline granulomatous enteritis is a rare type of % thatcauses weight loss, protein-losing enteropathy, and perhaps

diarrhea it also reuires histopathologic confirmation. Affected

cats seem to respond to high-dose corticosteroid therapy, but

attempts to reduce the dose of glucocorticoids may cause

recurrence of clinical signs. $he prognosis is guarded.

IMMUNOPROLIFERATIVE ENTEROPATHY

IN BASENJIS

Etiology%mmunoproliferative enteropathy in asen4is is an intense

lymphocytic-plasmacytic small intestinal infiltrate often

associated with villous clubbing, m i l d lacteal dilation, gastric

rugal hypertrophy, lymphocytic gastritis, and/or gastricmucosal atrophy. %t probably has a genetic basis or predisposition,

and intestinal bacteria may play an important role.

Clinical Features$he disease tends to be a severe form of 23& that waes and

wanes, particularly as the animal is stressed (e.g., traveling,disease). ?eight loss, small intestinal diarrhea, vomiting,


5/7

and/or anoreia are commonly seen. *ost affected asen4is

start showing clinical signs by " to years of age.

Diagnosis*arked hypoalbuminemia and hyperglobulinemia are

common, especially in advanced cases. $he early stages ofthe disease resemble many other intestinal disorders. %n

advanced cases the clinical signs are so suggestive that a

presumptive diagnosis is often made without biopsy.

6owever, because other diseases (e.g., lymphoma, histoplasmosis)may mimic immunoproliferative enteropathy,alimentary tract biopsy is needed before aggressive immunosuppressive

therapy is begun.

Treatment$herapy may include highly digestible, elimination, or elementaldiets antibiotics for A+& (see p. =1) high-dose

corticosteroids metronida:ole and a:athioprine. +esponse

to therapy is variable, and affected dogs that respond are at

risk for relapse, especially if stressed.

Although a genetic basis is suspected, not enough isknown to be able to confidently recommend a breeding

program. 3erforming biopsy of the intestines of asymptomatic

dogs to identify animals in which the disease will develop

is dubious because clinically normal asen4is may have

lesions similar to those of dogs with diarrhea and weight loss,

although the changes tend to be milder.Prognosis*any affected animals die to " years after diagnosis. $he

prognosis is poor for recovery, but some dogs can be maintained

for prolonged periods of time with careful monitoringand care. %n a few dogs lymphoma later develops.

ENTEROPATHY IN CHINESE SHAR-PEIS

Etiology!hinese 7har-3eis have a poorly characteri:ed enteropathy

that may be uniue to them or may be a severe form of

%. !hinese 7har-3eis have immune system abnormalities

that may predispose them to eaggerated inflammatory

reactions.

Clinical Featuresiarrhea and/or weight loss (i.e., small intestinal dysfunction)

are the main clinical signs.

Diagnosis7mall intestinal biopsy is necessary for diagnosis. &osinophilic

and lymphocytic-plasmacytic intestinal infiltrates are

typically found. 7erum cobalamin concentrations are often

uite low.

Treatment$he animal is treated for % (i.e., elimination diets and

immunosuppressive drugs) and A+&.

PrognosisAffected !hinese 7har-3eis have a guarded prognosis.

PROTEIN-LOSING ENTEROPATHY

CAUSES OF PROTEIN-LOSING

ENTEROPATHY

Any intestinal disease that produces sufficient inflammation,infiltration, congestion, or bleeding can produce a proteinlosing

enteropathy (32& or gastropathy if it affects thestomach see o @-


6/7

caused by 23& or lymphoma. $herapy should be directed at

managing the underlying cause.

INTESTINAL LYMPHANGIECTASIA

Etiology%ntestinal lymphangiectasia (%2) is a disorder of the intestinal

lymphatic system of dogs. 2ymphatic obstruction causes

dilation and rupture of intestinal lacteals with subseuent

leakage of lymphatic contents (i.e., protein, lymphocytes,

and chylomicrons) into the intestinal submucosa, laminapropria, and lumen. Although these proteins may be digested

and resorbed, ecessive loss eceeds the intestine's ability to

resorb them, thus resulting in hypoalbuminemia. 2eakage of

lymphatic fat into the intestinal wall may cause granulomaformation, which eacerbates lymphatic obstruction. 8ot

reported in cats, the condition has many potential causes in

dogs (e.g., lymphatic obstruction, pericarditis, infiltrative

mesenteric lymph node disease, infiltrative intestinal mucosal

disease, congenital malformations). *ost cases of symptomatic%2 are idiopathic.

Clinical Featuresorkshire $erriers, 7oft !oated ?heaten $erriers, and

2undehunds appear to be at higher risk than other breeds.

7oft !oated ?heaten $erriers also have an unusually highincidence of protein-losing nephropathy. $he first sign of

disease caused by %2 may be transudative ascites. iarrhea isinconsistent and may occur early or late i n the course of the

disease, if at all. %ntestinal lipogranulomas (i.e., white nodules

in the intestinal serosa or mesentery) are sometimes foundat surgery. $hey are probably secondary to %2 (i.e., fat leaking

out of dilated lymphatic vessels), but they might worsen

eisting %2 by further obstructing lymphatics.

Diagnosis!linical pathologic evaluation is not diagnostic, but hypoalbuminemia

and hypocholesterolemia are epected. Although

panhypoproteinemia is classically attributed to 32&, animals

that were initially hyperglobulinemic may lose most of their

serum proteins and still have normal serum globulin concentrations.2ymphopenia is common but inconsistent.

iagnosis reuires intestinal histopathology. Feeding the

animal fat the night before the biopsy seems to make lesions

more obvious, and classic mucosal lesions may be seen endo

scopically (Fig. ""-@). &ndoscopic biopsies are often diagnos-

FIG 33-8Endoscopic image of the duodenum of a dog with lymphangiectasiaThe large white !dots! are dilated lacteals in thetips of the "illi

tic if done appropriately, but surgical biopsies are sometimes

reuired. %f full-thickness surgical biopsies are performed,

serosal patch grafting and nonabsorbable suture material

may decrease the risk of dehiscence. %2 may be locali:ed toone area of the intestines (e.g., ileum).

Treatment$he underlying cause of %2 is rarely determined, necessitating

reliance on symptomatic therapy. A n ultra-low-fat diet

essentially devoid of long-chain fatty acids helps to preventfurther intestinal lacteal engorgement and subseuent

protein loss. 3rednisolone (


7/7

therapy.

PROTEIN-LOSING ENTEROPATHY IN

SOFT-COATED WHEATEN TERRIERS

Etiology7oft !oated ?heaten $erriers (7!?$s) have a predisposition

to 32& and protein-losing nephropathy. $he cause uncertain, although food hypersensitivity has been reported

to be present in some affected dogs.

Clinical Features%ndividual dogs may have 32& or protein-losing nephropathy(or both). $ypical clinical signs may include vomiting,

diarrhea, weight loss, and ascites. Affected dogs are often

middle aged when diagnosed.

Diagnosis3anhypoproteinemia and hypocholesterolemia are common,

as with any 32&. 6istopathology of intestinal mucosa

may reveal lymphangiectasia, lymphangitis, or supposedly

%.

Treatment#Prognosis$reatment is typically as for lymphangiectasia and/or %.

$he prognosis appears guarded to poor for clinically i ll

animals, with most dying within a year of diagnosis.

FUNCTIONAL INTESTINAL DISEASE

IRRITABLE BOWEL SYNDROME

Etiology%rritable bowel syndrome (%7) i n people is characteri:ed bydiarrhea, constipation, and/or cramping (usually of the large

intestines) in which an organic lesion cannot be identified.

%t is an idiopathic large bowel disease in which all known

causes of diarrhea have been eliminated and a 9functional9

disorder is presumed. %7 in dogs is different and primarilyinvolves an idiopathic, chronic large bowel diarrhea in which

parasitic, dietary, bacterial, and inflammatory causes have

been eliminated. $here are probably various causes of this

syndrome in dogs.

Clinical Features!hronic large bowel diarrhea is the principal sign. Fecal

mucus is common, blood in the feces is infreuent, and

weight loss is very rare. 7ome dogs with %7 are small breeds

that are heavily imprinted on a single family member. !linical

signs may develop following separation of the dog fromthe favored person. ;ther dogs with %7 are nervous and

high-strung (e.g., police or guard dogs, especially 5erman

7hepherd ogs). 7ome dogs have no apparent initiating

cause.

Diagnosisiagnosis consists of eliminating known causes by physical

eamination, clinical pathologic data, fecal analysis, colonoscopy/

biopsy, and appropriately performed therapeutic trials.

Treatment$reatment with fiber-supplemented diets (i.e., B1C to >C

fiber on a dry matter basis) is often helpful (see p. ">@). *any

animals must receive fiber chronically to prevent relapse.

Anticholinergics occasionally are useful (e.g., propantheline,

#.= mg/kg or dicyclomine, #.

Documents

Dieta la animale