Caderno de Anotações - Palestra Doença Intestinal Inflamatória em gatos. Profª Me. Monica Campello Daiha.

1. DOENÇA INTESTINAL INFLAMATÓRIA
Profª. Me. Mônica Daiha

2. Doença Inflamatória
Intestinal Crônica
Convivendo com o inimigo...
Msc. Monica Campello Daiha
Intituto Qualittas de Pós Graduação
!Definição:
!
!
Síndrome caracterizada pela resposta exacerbada
e descontrolada do trato digestório
a uma estimulação antigênica
!
em consequência à exposição
!
excessiva a antígenos.
Doença Inflamatória Intestinal Crônica

3. Doença Inflamatória Intestinal Crônica
!Ponto Importante:
!
!
Esta síndrome é responsável
!
por, no mínimo,
!
50% dos sintomas digestivos
!
observados em felinos.
7/13/2016 15 chistosas expresiones de gato que delatan perfectamente lo que están pensando | Upsocl
http://www.upsocl.com/verde/15-chistosas-expresiones-de-gato-que-delatan-perfectamente-lo-que-estan-pensando/ 2/13
Fuente
2. “Te arrepentirás de haberme puesto este ridículo jersey”
Fuente
ESCUCHÓ A UNA MUJER HABLANDO
DESCARADAMENTE SOBRE SU INFIDELIDAD.
ENTONCES PUBLICÓ ESTO EN FACEBOOK
PROBAMOS LOS EXTRAÑOS ATUENDOS DE
MANIQUÍES DE GRANDES TIENDAS. LO QUE
DESCUBRIMOS NOS DECEPCIONÓ
Fisiopatogenia
Resposta imune aos antígenos
ê
Influxo de células inflamatórias:
!
processo inflamatório na mucosa
ê
perda da integridade da mucosa:
ê
alteração de permeabilidade:
!
microorganismos da microbiota entérica e os antígenos
adentram na lâmina própria

4. Fatores Patogênicos
!Dieta
!
!Intolerância alimentar
!
!Hipersensibilidade alimentar
!
!
!Parasitos
!
!Infecções bacterianas
!
!Neoplasia
!
!
Fatores Patogênicos
6
JFMS CLINICAL PRACTICE 445
C L I N I C A L R E V I E W
Journal of Feline Medicine and Surgery (2012) 14, 445–458
Albert E Jergens
FELINE IDIOPATHIC INFLAMMATORY
BOWEL DISEASE
What we know and
what remains to be unraveled
Practical relevance: Feline idiopathic
inflammatory bowel disease (IBD)
denotes one form of chronic enteropathy
that is immunologically mediated and
characterized by persistent or recurrent
gastrointestinal (GI) signs and histologic
inflammation. Signs of vomiting, diarrhea and
weight loss generally predominate, and mucosal
inflammation may occur in any portion of the GI
tract (especially the small intestine). Affected cats
may also have concurrent inflammation in other
organs, such as the pancreas and liver, which may
impact clinical disease severity.
Clinical challenges: The exact etiologies of this
heterogeneous group of disorders have yet to be
determined, though results from basic science and
clinical studies suggest that interplay between
genetic factors and enteric bacteria is crucial for
disease development. The diagnosis is one of
exclusion and requires intestinal mucosal biopsy
to characterize the type and severity of the
inflammatory infiltrate, and to differentiate IBD from
other disorders, including alimentary lymphoma.
Controversy exists concerning the relative
diagnostic accuracy of endoscopic versus
full-thickness specimens for the diagnosis of IBD
and its differentiation from alimentary lymphoma.
Audience: This article is intended to provide
veterinary practitioners with a comprehensive
clinical update on idiopathic IBD in cats. It reviews
the current evidence-based data, the diagnostic
approach, the evolving histologic criteria, and
treatment options and outcome for feline patients
with this syndrome.
Current understanding of etiology
and pathogenesis
While the exact cause of inflammatory bowel disease (IBD) remains
unknown, current hypotheses suggest that feline IBD, similar to IBD
in humans and dogs, involves complex interactions between
environmental factors (ie, intestinal microbial imbalances, dietary
components) and the mucosal immune system, resulting in chronic
inflammation in susceptible cats (Figure 1).1
Genetic defects in the recognition of commensal versus pathogenic
bacteria by the innate immune system play a pivotal role in disease
pathogenesis in humans
and dogs with IBD.
Mutations in innate
immune receptors of
humans (NOD2/CARD 15)
and dogs (TLR4, TLR5)
have now been linked to
IBD susceptibility; and in
the presence of an enteric
microbiota may lead to
upregulated proinflamma-
tory cytokine production
(eg, IL-17, TNF-α) and
reduced bacterial clearance,
thereby promoting chronic intestinal inflammation.1–3
Whether
or not similar pathomechanisms come into play in the development
of idiopathic feline IBD has not been fully determined. However,
antigens derived from commensal bacteria are likely to be important
in driving disease pathogenesis, as increased populations of
mucosa-associated bacteria (ie, Enterobacteriaceae) have been linked to
clinical signs, cytokine mRNA and histopathologic lesions in cats
with IBD.4
Other studies have reported increased lamina propria myeloid/
histiocyte antigen-positive macrophages, upregulated epithelial major
histocompatibility complex (MHC) class II molecule expression,
and increased antibody reactivity to components of the commensal
DOI: 10.1177/1098612X12451548
© ISFM and AAFP 2012
Certain breed predispositions
(Siamese and other Asian
breeds) for IBD are recognized,
but any breed may be affected
and causal genetic defects have
not been identified to date.
Albert E Jergens
DVM PhD DACVIM
Department of Veterinary Clinical Sciences,
College of Veterinary Medicine,
Iowa State University,
Ames, IA 50011, USA
Email: ajergens@iastate.edu
at AMERICAN COLL VET DERMATOLOGY on June 27, 2016jfm.sagepub.comDownloaded from
!Defeitos genéticos:
!
flora comensal x flora patogênica x hospedeiro
!
humanos e cães: mutação receptores imunes
!
microbiota entérica: citocinas proinflamatórias
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Como estudar e lembrar tudo na hora da prova?
29 set, 2014 Estratégia de Estudo Martha Vergine
A pergunta título desse post é uma das mais pesquisadas pelos estudantes.
São muitos os anos que passamos nos bancos escolares e parece que por mais que o
tempo passe continuamos a sofrer quando o momento da prova chega.
Claro que o mau aluno, aquele que quase nem aparece nas aulas e, se aparece, está
apenas de corpo presente porém sua alma, isto é, concentração, está beeeeem
ausente, não tem mesmo como gostar do momento da prova, até porque só por um
milagre seria possível ele se lembrar da matéria e conseguir dar qualquer boa
resposta.
Sei que essa situação é extremada, pois a maioria dos alunos comparecem às aulas,
tentam prestar atenção e em casa ainda dão uma estudada. Entretanto, é só chegar
o momento da prova e parece que num passe de mágica esquecem toda a matéria.
Para esses também é um sofrimento responder as questões.
Sendo assim, o que fazer?
Sendo bom ou mau aluno parece que não faz diferença na hora da prova, pois esse
momento é bem difícil para ambos, então qual a saída?
Ah! Arrisco uma solução.
A solução para qualquer aluno é um CAT ! Isso mesmo um gatinho…
O CAT é uma acrônimo que irá te ajudar a lembrar da TRÍADE DO ESTUDANTE
PROFISSIONAL.
Gato??? Estudante pro ssional???
Nossa! Quanta novidade em um post só…
Calma que vou explicar.
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C L I N I C A L R E V I E W
Journal of Feline Medicine and Surgery (2012) 14, 445–458
Albert E Jergens
FELINE IDIOPATHIC INFLAMMATORY
BOWEL DISEASE
What we know and
what remains to be unraveled
Practical relevance: Feline idiopathic
inflammatory bowel disease (IBD)
denotes one form of chronic enteropathy
that is immunologically mediated and
characterized by persistent or recurrent
gastrointestinal (GI) signs and histologic
inflammation. Signs of vomiting, diarrhea and
weight loss generally predominate, and mucosal
inflammation may occur in any portion of the GI
tract (especially the small intestine). Affected cats
may also have concurrent inflammation in other
organs, such as the pancreas and liver, which may
impact clinical disease severity.
Clinical challenges: The exact etiologies of this
heterogeneous group of disorders have yet to be
determined, though results from basic science and
clinical studies suggest that interplay between
genetic factors and enteric bacteria is crucial for
disease development. The diagnosis is one of
exclusion and requires intestinal mucosal biopsy
to characterize the type and severity of the
inflammatory infiltrate, and to differentiate IBD from
other disorders, including alimentary lymphoma.
Controversy exists concerning the relative
diagnostic accuracy of endoscopic versus
full-thickness specimens for the diagnosis of IBD
and its differentiation from alimentary lymphoma.
Audience: This article is intended to provide
veterinary practitioners with a comprehensive
clinical update on idiopathic IBD in cats. It reviews
the current evidence-based data, the diagnostic
approach, the evolving histologic criteria, and
Current understanding of etiology
and pathogenesis
While the exact cause of inflammatory bowel disease (IBD) remains
unknown, current hypotheses suggest that feline IBD, similar to IBD
in humans and dogs, involves complex interactions between
environmental factors (ie, intestinal microbial imbalances, dietary
components) and the mucosal immune system, resulting in chronic
inflammation in susceptible cats (Figure 1).1
Genetic defects in the recognition of commensal versus pathogenic
bacteria by the innate immune system play a pivotal role in disease
pathogenesis in humans
and dogs with IBD.
Mutations in innate
immune receptors of
humans (NOD2/CARD 15)
and dogs (TLR4, TLR5)
have now been linked to
IBD susceptibility; and in
the presence of an enteric
microbiota may lead to
upregulated proinflamma-
tory cytokine production
(eg, IL-17, TNF-α) and
reduced bacterial clearance,
thereby promoting chronic intestinal inflammation.1–3
Whether
or not similar pathomechanisms come into play in the development
of idiopathic feline IBD has not been fully determined. However,
antigens derived from commensal bacteria are likely to be important
in driving disease pathogenesis, as increased populations of
mucosa-associated bacteria (ie, Enterobacteriaceae) have been linked to
clinical signs, cytokine mRNA and histopathologic lesions in cats
Certain breed predispositions
(Siamese and other Asian
breeds) for IBD are recognized,
but any breed may be affected
and causal genetic defects have
not been identified to date.

5. Principais variáveis da doença inflamatória
!
• Sistema imune da mucosa
(mediador e perpetuador dos danos teciduais)
!
• Suscetibilidade genética
!
• Microbiota entérica:
• Gato: 1.000.000.000/ml ☹
• Cão: 100.000/ml☺
Fisiopatogenia
Histórico
!Emagrecimento progressivo
!
!Letargia / Depressão
!
!Polifagia
!
!Hiporexia ou Anorexia
!
!Vômito
!
!Diarréia x Constipação
!
!
HISTÓRICO
Emagrecimento progressivo
Letargia / Depressão
Alterações no apetite:
- hiporexia ou anorexia
- polifagia: fase compensada

6. Diagnóstico Diferencial
Vômito Crônico:
!
!
45% doença inflamatória intestinal
!
18% pancreatite
!
5% malignidade gastrointestinal
!
3% outras causas
Mimetismo Clínico
!Sem alteração
!
!Caquexia
!
!Desidratação
!
!Mucosas Hipocoradas
!
!Linfadenopatia mesentérica
!
!Meteorismo

7. DIAGNÓSTICO
446 JFMS CLINICAL PRACTICE
(eg, use of prebiotics or probiotics) for cats.
This will require additional clinical trials (and
more research funding) to elucidate which
therapies are most efficacious in the preven-
tion and treatment of chronic IBD.
Figure 1 Chronic intestinal inflammation in feline IBD involves a complex interplay
between the mucosal immune system and the enteric microbiota in a genetically
susceptible host. Potential genetic factors affecting barrier function or innate and
adaptive immunity may predispose susceptible cats to gastrointestinal (GI) signs, aberrant
host responses and microbial imbalances (dysbiosis). Environmental factors (dietary
constituents, exposure to enteropathogens, NSAID or antibiotic administration, etc) likely
govern inflammation onset or reactivation (disease flares)
Integrate environment, history and physical examination
✜ At-risk breed (?), indoor/outdoor, diet, clinical signs, localizing findings
Investigate for parasites and enteric pathogens
✜ Fecal analysis (nematodes, protozoa), fecal culture, PCR (Tritrichomonas foetus)
Perform clinicopathologic testing
✜ Detect non-GI disease: CBC, biochemistry profile, urinalysis, fPLI, ± fTLI, bile acids,
total T4
, FeLV, FIV
✜ Detect/characterize GI disease: Hyperproteinemia, hypoalbuminemia (rare), low folate
or cobalmin, increased ALT/ALP, fPLI, low phosphorus
Perform advanced diagnostics
✜ Detect non-GI disease: Radiography, ultrasonography of intestines, liver, pancreas,
mesenteric lymph nodes, masses, effusions; FNA cytology ± biopsy
✜ Detect/characterize GI disease: Radiography, ultrasonography to detect intestinal
thickening, loss of layering, focal masses, hypoechoic appearance (pancreatitis),
hyperechoic appearance (hepatopathy), mesenteric lymphadenopathy;
intestinal biopsy via endoscopy, laparoscopy or laparotomy (include ileum);
± biopsy of liver, pancreas, lymph nodes
The clinician should first integrate patient history with findings made from the physical examination
and initial diagnostic testing to confirm or refute the presence of primary GI disease. Diagnostic
imaging and intestinal mucosal biopsy are then performed to characterize the nature and extent of
mucosal disease.
Modified from references 7 and 26
A diagnosis of
IBD is one of
exclusion and
requires careful
elimination of
IBD mimics.
D i a g n o s t i c a p p ro a c h t o f e l i n e I B D
at AMERICAN COLL VET DERMATOLOGY on June 27, 2016jfm.sagepub.comDownloaded from
JFMS CLINICAL PRACTICE 445
C L I N I C A L R E V I E W
Journal of Feline Medicine and Surgery (2012) 14, 445–458
Albert E Jergens
FELINE IDIOPATHIC INFLAMMATORY
BOWEL DISEASE
What we know and
what remains to be unraveled
Practical relevance: Feline idiopathic
inflammatory bowel disease (IBD)
denotes one form of chronic enteropathy
that is immunologically mediated and
characterized by persistent or recurrent
gastrointestinal (GI) signs and histologic
inflammation. Signs of vomiting, diarrhea and
weight loss generally predominate, and mucosal
inflammation may occur in any portion of the GI
tract (especially the small intestine). Affected cats
may also have concurrent inflammation in other
organs, such as the pancreas and liver, which may
impact clinical disease severity.
Clinical challenges: The exact etiologies of this
heterogeneous group of disorders have yet to be
determined, though results from basic science and
clinical studies suggest that interplay between
genetic factors and enteric bacteria is crucial for
disease development. The diagnosis is one of
exclusion and requires intestinal mucosal biopsy
to characterize the type and severity of the
inflammatory infiltrate, and to differentiate IBD from
other disorders, including alimentary lymphoma.
Controversy exists concerning the relative
diagnostic accuracy of endoscopic versus
full-thickness specimens for the diagnosis of IBD
and its differentiation from alimentary lymphoma.
Audience: This article is intended to provide
veterinary practitioners with a comprehensive
clinical update on idiopathic IBD in cats. It reviews
the current evidence-based data, the diagnostic
approach, the evolving histologic criteria, and
treatment options and outcome for feline patients
with this syndrome.
Current understanding of etiology
and pathogenesis
While the exact cause of inflammatory bowel disease (IBD) remains
unknown, current hypotheses suggest that feline IBD, similar to IBD
in humans and dogs, involves complex interactions between
environmental factors (ie, intestinal microbial imbalances, dietary
components) and the mucosal immune system, resulting in chronic
inflammation in susceptible cats (Figure 1).1
Genetic defects in the recognition of commensal versus pathogenic
bacteria by the innate immune system play a pivotal role in disease
pathogenesis in humans
and dogs with IBD.
Mutations in innate
immune receptors of
humans (NOD2/CARD 15)
and dogs (TLR4, TLR5)
have now been linked to
IBD susceptibility; and in
the presence of an enteric
microbiota may lead to
upregulated proinflamma-
tory cytokine production
(eg, IL-17, TNF-α) and
reduced bacterial clearance,
thereby promoting chronic intestinal inflammation.1–3
Whether
or not similar pathomechanisms come into play in the development
of idiopathic feline IBD has not been fully determined. However,
antigens derived from commensal bacteria are likely to be important
in driving disease pathogenesis, as increased populations of
mucosa-associated bacteria (ie, Enterobacteriaceae) have been linked to
clinical signs, cytokine mRNA and histopathologic lesions in cats
with IBD.4
Other studies have reported increased lamina propria myeloid/
histiocyte antigen-positive macrophages, upregulated epithelial major
histocompatibility complex (MHC) class II molecule expression,
and increased antibody reactivity to components of the commensal
DOI: 10.1177/1098612X12451548
© ISFM and AAFP 2012
Certain breed predispositions
(Siamese and other Asian
breeds) for IBD are recognized,
but any breed may be affected
and causal genetic defects have
not been identified to date.
Albert E Jergens
DVM PhD DACVIM
Department of Veterinary Clinical Sciences,
College of Veterinary Medicine,
Iowa State University,
Ames, IA 50011, USA
Email: ajergens@iastate.edu
at AMERICAN COLL VET DERMATOLOGY on June 27, 2016jfm.sagepub.comDownloaded from
Alterações Laboratoriais
!Anemia normocítica normocrômica
!
!Leucocitose neutrofílica sem desvio
!
!Hipoalbuminemia
!
!Sorologia FIV/FeLV
!
!Parasitológico
!

8. Exames por Imagem
!Ultrassonografia Abdominal
!
!Alteração da ecogenicidade
!
!Espessamento da parede
!
!Perda da definição das camadas da parede intestinal
!
!Aumento de volume dos linfonodos mesentéricos
!
M.V. Juliana Derenne
Diagnóstico
!Ponto Importante:
!
!
Doença Inflamatória Intestinal?
!
x
!
NEOPLASIA???
7/13/2016 gato+pensando.jpg (395×500)
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7/13/2016 15 chistosas expresiones de gato que delatan perfectamente lo que están pensando | Upsocl
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Fuente
6. Esperemos que ese perro disfrute de sus últimos minutos de
vida
SAPATILHA SUEDE
CRYSTAL PEARL
BLUSA ESTAMPA
SAMARKAND
OXFORD
PLATAFORMA
PALHA
Fuente
7. El famoso “grumpy cat” o gato gruñón

9. 186 JFMS CLINICAL PRACTICE
R E V I E W / Feline AL: classification, clinical signs and non-invasive diagnostics
neutrophilic leukocytosis is usually present,
which may be accompanied by a regenerative
left shift.31–33
A peripheral lymphocytosis
(with LGL morphology) was documented
in over 80% of cats with LGLL in two
studies.31,35
However, in two other studies
D i a g n o s t i c i n v e s t i g a t i o n
Tests to rule out other primary and secondary
gastrointestinal diseases in older cats with chronic
weight loss, vomiting and/or diarrhoea
Blood and urine tests
✜ Complete blood count
✜ Serum biochemical profile
✜ Serum total T4
✜ Serum cobalamin and folate
✜ FIV and FeLV serology
✜ Feline pancreatic lipase (Spec fPL;
Idexx Laboratories)
✜ Urinalysis
Therapeutic trials
✜ Fenbendazole (50 mg/kg PO q24h for 5 days)
Diagnostic imaging
✜ Abdominal ultrasonography
✜ Thoracic radiography
Dietary elimination trials
To investigate possible adverse food reactions:
✜ Single novel protein + carbohydrate
✜ Hydrolysed protein diet
Faecal tests
If small bowel diarrhoea is predominant:
✜ Faecal flotation assays
✜ Faecal immunoassays/direct fluorescent antigen tests/
PCR assays for detection of:
– Giardia species
– Cryptosporidium species
– Campylobacter species
– Enteropathogenic bacterial toxins
If mixed/large bowel diarrhoea is predominant:
✜ Faecal smears/culture/PCR assays for detection of
Tritrichomonas fetus
If there is bloody diarrhoea, especially in cats with fever
and an inflammatory leukogram:
✜ Faecal culture for enteropathogenic bacteria (Salmonella
species, Clostridium species, Campylobacter species)
lymphocytosis was uncommon in cats with
LGLL, although peripheral lymphoblasts
were present in 15% of cats.32,33
Since LGLs
can be identified with routine haematological
stains, peripheral blood smears should be
examined thoroughly in the assessment of
all cats where AL is suspected.
✜ Serum albumin The most common
serum biochemical abnormality in AL is
hypoalbuminaemia. In intestinal disease,
hypoalbuminaemia occurs when loss of
albumin into the lumen through a
compromised intestinal wall exceeds the
capacity of the liver to synthesise albumin.
Hypoalbuminaemia is less common in cats
with LGAL than in other forms of AL,
probably because the integrity of the
intestinal wall can be maintained until late in
the disease process.3,19,23,32,33,63
Elevations in
bilirubin or liver enzymes, or azotaemia, may
occur in cats with AL with hepatic or renal
involvement.23,24,32,60,63
✜ Serum cobalamin Up to 80% of cats with
LGAL are hypocobalaminaemic.25
This
finding is not unexpected since cobalamin is
absorbed from the ileum, and the ileum and
jejunum are the most common locations for
LGAL.22,23,27
Utilisation of cobalamin by
proliferating intestinal microflora in the
proximal intestine can further reduce
available cobalamin.64
✜ Serum folate Folate levels may be low,
normal or high in cats with LGAL.24,25
Folate
deconjugase, a brush border enzyme, and a
carrier protein required for folate absorption
are located only in proximal intestinal
enterocytes. Hence, low serum folate levels
occur with proximal intestinal disease due to
reduced mucosal absorption. High serum
folate levels can occur due to proliferation of
intestinal microflora that synthesise folate.64
Serum folate levels were low in 4% and high
in 37% of cats with LGAL in one report.25
The frequency of perturbations in serum
folate and cobalamin with other forms of AL
has not been evaluated.
Abdominal ultrasonography
Abdominal ultrasonography facilitates evalua-
tion of the gastrointestinal tract by assessment
of wall thickness, layering, motility and lumi-
nal content. Normal intestinal wall appears as a
five-layered image, with alternating hyper- and
hypoechoic layers corresponding to the lumi-
nal surface, mucosa, submucosa, muscularis
and serosa. Normal ultrasonographic intestinal
wall thicknesses are: duodenum and jejunum
≤2.8 mm, ileum ≤3.2 mm and colon ≤1.7 mm.65
Mesenteric lymph node diameter is generally
≤5 mm.66
Mural thickening can be further char-
acterised by symmetry, anatomical location and
whether it is focal, multifocal or diffuse.
by guest on April 15, 2012jfm.sagepub.comDownloaded from
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Journal of Feline Medicine and Surgery
http://jfm.sagepub.com/content/14/3/182
The online version of this article can be found at:
DOI: 10.1177/1098612X12439265
2012 14: 182Journal of Feline Medicine and Surgery
Vanessa Barrs and Julia Beatty
Feline alimentary lymphoma : 1. Classification, risk factors, clinical signs and non-invasive diagnostics
Published by:
International Society of Feline Medicine
American Association of Feline Practitioners
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186 JFMS CLINICAL PRACTICE
R E V I E W / Feline AL: classification, clinical signs and non-invasive diagnostics
neutrophilic leukocytosis is usually present,
which may be accompanied by a regenerative
left shift.31–33
A peripheral lymphocytosis
(with LGL morphology) was documented
in over 80% of cats with LGLL in two
studies.31,35
However, in two other studies
D i a g n o s t i c i n v e s t i g a t i o n
Tests to rule out other primary and secondary
gastrointestinal diseases in older cats with chronic
weight loss, vomiting and/or diarrhoea
Blood and urine tests
✜ Complete blood count
✜ Serum biochemical profile
✜ Serum total T4
✜ Serum cobalamin and folate
✜ FIV and FeLV serology
✜ Feline pancreatic lipase (Spec fPL;
Idexx Laboratories)
✜ Urinalysis
Therapeutic trials
✜ Fenbendazole (50 mg/kg PO q24h for 5 days)
Diagnostic imaging
✜ Abdominal ultrasonography
✜ Thoracic radiography
Dietary elimination trials
To investigate possible adverse food reactions:
✜ Single novel protein + carbohydrate
✜ Hydrolysed protein diet
Faecal tests
If small bowel diarrhoea is predominant:
✜ Faecal flotation assays
✜ Faecal immunoassays/direct fluorescent antigen tests/
PCR assays for detection of:
– Giardia species
– Cryptosporidium species
– Campylobacter species
– Enteropathogenic bacterial toxins
If mixed/large bowel diarrhoea is predominant:
✜ Faecal smears/culture/PCR assays for detection of
Tritrichomonas fetus
If there is bloody diarrhoea, especially in cats with fever
and an inflammatory leukogram:
✜ Faecal culture for enteropathogenic bacteria (Salmonella
species, Clostridium species, Campylobacter species)
lymphocytosis was uncommon in cats with
LGLL, although peripheral lymphoblasts
were present in 15% of cats.32,33
Since LGLs
can be identified with routine haematological
stains, peripheral blood smears should be
examined thoroughly in the assessment of
all cats where AL is suspected.
✜ Serum albumin The most common
serum biochemical abnormality in AL is
hypoalbuminaemia. In intestinal disease,
hypoalbuminaemia occurs when loss of
albumin into the lumen through a
compromised intestinal wall exceeds the
capacity of the liver to synthesise albumin.
Hypoalbuminaemia is less common in cats
with LGAL than in other forms of AL,
probably because the integrity of the
intestinal wall can be maintained until late in
the disease process.3,19,23,32,33,63
Elevations in
bilirubin or liver enzymes, or azotaemia, may
occur in cats with AL with hepatic or renal
involvement.23,24,32,60,63
✜ Serum cobalamin Up to 80% of cats with
LGAL are hypocobalaminaemic.25
This
finding is not unexpected since cobalamin is
absorbed from the ileum, and the ileum and
jejunum are the most common locations for
LGAL.22,23,27
Utilisation of cobalamin by
proliferating intestinal microflora in the
proximal intestine can further reduce
available cobalamin.64
✜ Serum folate Folate levels may be low,
normal or high in cats with LGAL.24,25
Folate
deconjugase, a brush border enzyme, and a
carrier protein required for folate absorption
are located only in proximal intestinal
enterocytes. Hence, low serum folate levels
occur with proximal intestinal disease due to
reduced mucosal absorption. High serum
folate levels can occur due to proliferation of
intestinal microflora that synthesise folate.64
Serum folate levels were low in 4% and high
in 37% of cats with LGAL in one report.25
The frequency of perturbations in serum
folate and cobalamin with other forms of AL
has not been evaluated.
Abdominal ultrasonography
Abdominal ultrasonography facilitates evalua-
tion of the gastrointestinal tract by assessment
of wall thickness, layering, motility and lumi-
nal content. Normal intestinal wall appears as a
five-layered image, with alternating hyper- and
hypoechoic layers corresponding to the lumi-
nal surface, mucosa, submucosa, muscularis
and serosa. Normal ultrasonographic intestinal
wall thicknesses are: duodenum and jejunum
≤2.8 mm, ileum ≤3.2 mm and colon ≤1.7 mm.65
Mesenteric lymph node diameter is generally
≤5 mm.66
Mural thickening can be further char-
acterised by symmetry, anatomical location and
whether it is focal, multifocal or diffuse.
by guest on April 15, 2012jfm.sagepub.comDownloaded from

11. AL PRACTICE
R E V I E W
Vanessa R Barrs
BVSc (Hons) MVetClinStud MANZCVSc (Small Animal)
FANZCVSc (Feline Med) GradCertEd (Higher Ed)*
Julia A Beatty
BSc (Hons) BVetMed PhD FANZCVSc (Feline Med)
GradCertEd (Higher Ed) MRCVS
Valentine Charlton Cat Centre,
Faculty of Veterinary Science,
University of Sydney,
Sydney NSW 2006, Australia
*Corresponding author.
Email: vanessa.barrs@sydney.edu.au
DOI: 10.1177/1098612X12439265
© ISFM and AAFP 2012
Vanessa Barrs and Julia Beatty
FELINE ALIMENTARY LYMPHOMA
1. Classification, risk factors,
clinical signs and non-invasive
diagnostics
entary
sts
iffer
osis is
riate
rentiation of low-grade
m lymphoplasmacytic
g, especially where
sies, which sample only
sa, are used. The major
te- and high-grade
other neoplastic
nal mass lesions.
nular lymphocyte
ce as it may be missed
predominantly middle-
sbred cats (median age
ence supporting this
V, derived from
spective case series,
m other species,
ation and the combined
e working in the field.
RT 2
art article, reviewing
mitations of various
eatment options and
ferent subtypes
phoma, appears
1 of this issue of
Surg and at
98612X12439266
Alimentary lymphoma – and its three clinical entities
Alimentary lymphoma (AL), the most common anatomical form of
lymphoma in cats, comprises a group of diseases centred on the gastro-
intestinal tract, with variable extraintestinal involvement. Three histo-
logical grades of AL are recognised: low (LGAL), intermediate (IGAL)
and high (HGAL). A separate histological subclassification of AL, large
granular lymphocyte lymphoma (LGLL), which can be of any grade,
is also described. Although these different subtypes of lymphoma
share features related to gastrointestinal dysfunction, such as weight
loss, vomiting and diarrhoea, there are major differences in clinical
presentation, techniques required for diagnosis, treatment and progno-
sis (Table 1). From a clinical perspective, LGAL and LGLL can be con-
sidered as separate entities and IGAL and HGAL can be considered
together as a third entity because, other than histological grade, the
clinical features of IGAL and HGAL are similar.1
Accurate diagnosis is
essential to differentiate these lymphomas from each other and from
other primary and secondary gastrointestinal diseases so that appro-
priate treatment can be initiated.
Classification and prevalence
Lymphoma is the most common intestinal neoplasm of cats, followed
by adenocarcinoma and then mast cell tumour. In a study of 1129 feline
intestinal neoplasms diagnosed histologically, 55% were lymphomas,
32% were adenocarcinomas and 4% were mast cell tumours.2
Feline
lymphoma can be classified by anatomical location, histological grade
and immunophenotype.
Anatomical classification
The traditional anatomical classification recognises mediastinal, multi-
centric, alimentary and extranodal forms. Of these, AL is the most com-
mon anatomical form identified.3–10
The declining influence of feline
leukaemia virus (FeLV) worldwide has resulted in an increase in the
relative prevalence of AL, since AL has the weakest association with
FeLV antigenaemia. Some studies suggest that the absolute incidence
by guest on April 15, 2012jfm.sagepub.comDownloaded from
182 JFMS CLINICAL PRACTICE
C L I N I C A L R E V I E W
Journal of Feline Medicine and Surgery (2012) 14, 182–190
Vanessa R Barrs
BVSc (Hons) MVetClinStud MANZCVSc (Small Animal)
FANZCVSc (Feline Med) GradCertEd (Higher Ed)*
Julia A Beatty
BSc (Hons) BVetMed PhD FANZCVSc (Feline Med)
GradCertEd (Higher Ed) MRCVS
Valentine Charlton Cat Centre,
Faculty of Veterinary Science,
University of Sydney,
Sydney NSW 2006, Australia
*Corresponding author.
Email: vanessa.barrs@sydney.edu.au
DOI: 10.1177/1098612X12439265
© ISFM and AAFP 2012
Vanessa Barrs and Julia Beatty
FELINE ALIMENTARY LYMPHOMA
1. Classification, risk factors,
clinical signs and non-invasive
diagnostics
Practical relevance Alimentary
lymphoma (AL) occurs
commonly in cats and exists
as distinct subtypes that differ
in their clinical course,
response to treatment and
prognosis. Accurate diagnosis is
important to guide appropriate
treatment.
Clinical challenges Differentiation of low-grade
alimentary lymphoma from lymphoplasmacytic
enteritis can be challenging, especially where
endoscopic intestinal biopsies, which sample only
the mucosa and submucosa, are used. The major
differentials for intermediate- and high-grade
alimentary lymphoma are other neoplastic
and non-neoplastic intestinal mass lesions.
The diagnosis of large granular lymphocyte
lymphoma requires vigilance as it may be missed
with routine diagnostics.
Patient group AL affects predominantly middle-
to old-aged domestic crossbred cats (median age
10–13 years).
Evidence base The evidence supporting this
review is grade II, III and IV, derived from
prospective studies, retrospective case series,
reviews, extrapolation from other species,
pathophysiological justification and the combined
clinical experience of those working in the field.
PART 2
Part 2 of this two-part article, reviewing
the benefits and limitations of various
biopsy techniques, treatment options and
prognosis for different subtypes
of alimentary lymphoma, appears
on pages 191–201 of this issue of
J Feline Med Surg and at
DOI: 10.1177/1098612X12439266
Alimentary lymphoma – and its three clinical entities
Alimentary lymphoma (AL), the most common anatomical form of
lymphoma in cats, comprises a group of diseases centred on the gastro-
intestinal tract, with variable extraintestinal involvement. Three histo-
logical grades of AL are recognised: low (LGAL), intermediate (IGAL)
and high (HGAL). A separate histological subclassification of AL, large
granular lymphocyte lymphoma (LGLL), which can be of any grade,
is also described. Although these different subtypes of lymphoma
share features related to gastrointestinal dysfunction, such as weight
loss, vomiting and diarrhoea, there are major differences in clinical
presentation, techniques required for diagnosis, treatment and progno-
sis (Table 1). From a clinical perspective, LGAL and LGLL can be con-
sidered as separate entities and IGAL and HGAL can be considered
together as a third entity because, other than histological grade, the
clinical features of IGAL and HGAL are similar.1
Accurate diagnosis is
essential to differentiate these lymphomas from each other and from
other primary and secondary gastrointestinal diseases so that appro-
priate treatment can be initiated.
Classification and prevalence
Lymphoma is the most common intestinal neoplasm of cats, followed
by adenocarcinoma and then mast cell tumour. In a study of 1129 feline
intestinal neoplasms diagnosed histologically, 55% were lymphomas,
32% were adenocarcinomas and 4% were mast cell tumours.2
Feline
lymphoma can be classified by anatomical location, histological grade
and immunophenotype.
Anatomical classification
The traditional anatomical classification recognises mediastinal, multi-
centric, alimentary and extranodal forms. Of these, AL is the most com-
mon anatomical form identified.3–10
The declining influence of feline
leukaemia virus (FeLV) worldwide has resulted in an increase in the
relative prevalence of AL, since AL has the weakest association with
FeLV antigenaemia. Some studies suggest that the absolute incidence
by guest on April 15, 2012jfm.sagepub.comDownloaded from
of AL has been established in humans.
In genetically predisposed individuals,
enteropathy-associated T cell lymphoma
(EATCL) can arise from clonal transformation
of intestinal IELs after chronic antigenic
stimulation.54,55
EATCL is the most common
neoplastic complication of coeliac disease.
Several lines of evidence support the
proposition that intestinal inflammation is
a risk factor for the development of T cell
lymphoma (of any histological grade) and
LGLL in cats. In two studies, 60% of cats
with intestinal T cell lymphoma and 33%
of cats with LGLL had chronic clinical
illnesses suggestive of pre-existing
inflammatory disease.31,56
Concurrent lymphoplasmacytic
enteritis (LPE) has been identified
in other regions of the alimentary
tract in up to 41% of cats
with LGAL of T cell
immunophenotype,22–24
and
apparent histological progression of
LPE to AL has been documented in
individual cases.57,58
Differential diagnosis
The presenting signs of AL are common to
many primary and secondary gastrointestinal
diseases. LPE is a major differential diagnosis
for LGAL in particular. A comparison between
cats with LPE and LGAL found no correlation
between clinical findings and the final diagno-
sis.61
In cats with intestinal mural mass
lesions, epithelial and mast cell neoplasia are
major differentials. Diagnostic tests recom-
mended to rule out other primary and second-
ary gastrointestinal diseases are listed in the
box on page 186.
Non-invasive diagnostics
Routine laboratory testing
✜ Haematology The most common
haematological abnormalities in cats with
AL are anaemia, due to chronic disease
and/or gastrointestinal blood loss, and
neutrophilia.3,24,25,31,32,63
While routine
haematology is of low diagnostic yield for
LGAL and I/HGAL, careful evaluation of a
peripheral blood film is an essential step for
the diagnosis of LGLL. In LGLL, marked
R E V I E W / Feline AL: classification, clinical signs and non-invasive diagnostics
LGAL
The most common clinical signs of LGAL are weight loss (Figure 1;
≥80%), vomiting (≥70%), diarrhoea (≥60%) and partial or com-
plete anorexia (≥50%). The appetite may be normal or, occasion-
ally, polyphagia is
noted. Less fre-
quently reported
signs include lethar-
gy and polydip-
sia.19,23–25,61
In the
majority of cases,
clinical signs are
chronic (present for
>1 month).23,24,61
Abdominal palpation
is often abnormal
(Figure 2); diffusely
thickened intestinal
loops are detected in
a third to more than
half of affected cats.
An abdominal mass
is palpable in
20–30% of cases, attributable to mesenteric lymph node
enlargement or, rarely, to a focal intestinal mass.19,23,24
I/HGAL and LGLL
Clinical signs in cats with I/HGAL and LGLL are similar to those
for LGAL but tend to be more acute and/or severe. A major
clinical difference, compared with LGAL, is the presence of a
palpable abdominal mass at diagnosis in the majority of cases
of I/HGAL and LGLL. The mass comprises focal intestinal thick-
ening and/or extraintestinal lesions, such as mesenteric lymph-
adenomegaly, hepatomegaly or renomegaly. Intussusception,
intestinal obstruction and intestinal perforation are more com-
mon in cases of I/HGAL than in LGAL.3,12,19,31,32,35,62
Figure 1 Weight loss
is present in 80% or
more of cats with
low-grade alimentary
lymphoma (LGAL)
Figure 2 Abdominal palpation can be normal in cats with LGAL,
but common abnormalities include diffusely thickened intestinal loops
or a palpably enlarged mesenteric lymph node
H i s t o r y a n d c l i n i c a l s i g n s
Abdominal palpation can be normal
in cats with LGAL . . . By contrast an
abdominal mass is palpable in most cats
with I/HGAL and LGLL.
Signalment
All forms of AL typically affect middle- to
old-aged domestic crossbred cats with a
median age at diagnosis of 10–13 years.
A slight male predisposition (1.5:1 male
to female ratio) for HGAL identified
in some reports, has not been
identified for LGAL or
LGLL.4–7,12,13,15,16,19,23–26,32,59,60
cells, necrosis, oedema and/or haemorrhage
(Figure 3).3,67,68
Transmural intestinal
thickening in I/HGAL is usually symmetrical
or concentric, in contrast to intestinal mast cell
tumours and adenocarcinomas where
intestinal wall thickening is often asymmetrical
or eccentric.69,70
Ultrasonographically, evidence
of extraintestinal involvement is common in
I/HGAL.3,12
JFMS CLINICAL PRACTICE 187
R E V I E W / Feline AL: classification, clinical signs and non-invasive diagnostics
Figure 4 (a) Mild diffuse
small intestinal wall
thickening (wall thickness
3.4 mm) in a cat with LGAL;
(b and c) severe small
intestinal wall thickening
in a cat with LGAL (wall
thickness 4.9 mm in b, and
4 mm in c). Note that the
alternating hyperechoic and
hypoechoic appearance of
intestinal layers seen in
healthy cats is preserved in
cats with LGAL
c
✜ I/HGAL The ultrasonographic features
of I/HGAL include transmural intestinal
thickening with disruption of normal wall
layering, reduced wall echogenicity,
localised hypomotility and abdominal
lymphadenomegaly. Loss of intestinal wall
layering occurs due to infiltration of the
intestinal wall with neoplastic or inflammatory
a
b
Figure 3 (a) Ultrasonographic
and (b) gross appearance
of a focal jejunal mass due
to high-grade alimentary
lymphoma (HGAL). The
intestinal wall is thickened
(1 cm) and has lost its normal
alternating hyperechoic and
hypoechoic wall layering
pattern. The symmetrical
concentrically thickened
intestinal wall is visualised in
(c) and vascularity identified
using power Doppler.
Extraintestinal involvement,
such as concurrent renal (d)
and hepatic (e) masses,
is common in HGAL.
Images (a), (c), (d) and (e)
courtesy of Karon Hoffman,
University Veterinary Teaching
Hospital, Sydney
a b c
d e
Transmural intestinal thickening in I/HGAL
is usually symmetrical or concentric.
by guest on April 15, 2012jfm.sagepub.comDownloaded from
Feline AL: classification, clinical signs and non-invasive diagnostics
g
s received no specific grant from any funding agency
c, commercial or not-for-profit sectors for the prepara-
review article.
of interest
s declare that there is no conflict of interest.
ces
, Jacobs RM, Norris A, Couto CG, Morrison WB, et al.
tologic classification of 602 cases of feline lympho-
ative disease using the National Cancer Institute
g formulation. J Vet Diagn Invest 2000; 12: 295–306.
K, Villamil JA, Selting KA, Tyler J and Henry CJ.
trends in feline intestinal neoplasia: an epidemio-
udy of 1129 cases in the Veterinary Medical Database
64 to 2004. J Am Anim Hosp Assoc 2011; 47: 28–36.
y OM, Moore AS, Cotter SM, Engler SJ, Brown D and
k DG. Alimentary lymphoma in cats: 28 cases
n LGAL, intestinal wall thickness
or increased, with preservation of
ng (Figure 4). In one study of cats
L and diffuse small intestinal
, mean wall thickness was 4.3 mm
5 mm, range 3.4–5.0 mm).23
c lymph node enlargement was also
n another report, 81% of cats with
evidence of intestinal thickening
inal ultrasonography.26
Importantly,
nographic features of LGAL do
guish it from LPE or other
hies.61,71
Thickening of the
s propria layer, which was found
ficantly associated with LGAL
PE or normal small intestine,
in the ranking of differentials.72
be emphasised that the finding of
estinal wall thickness and normal
c lymph nodes on abdominal
graphy does not rule out a
of LGAL; in patients with
clinical signs, intestinal biopsy
d. Less common findings on
graphic examination of cats with
ude a focal intestinal mass or
ption.23,24
Diffuse infiltration of the
be present histologically but is not
ntifiable ultrasonographically.23
The ultrasonographic features of
ats have not been described in
appear similar to I/HGAL.32
KEY POINTS
The finding of normal intestinal wall thickness and
normal mesenteric lymph nodes on ultrasonography
does not rule out a diagnosis of LGAL.
4 Gabor LJ, Malik R and Canfield PJ. Clinical and anatomical
features of lymphosarcoma in 118 cats. Aust Vet J 1998; 76:
725–732.
5 Vail DM, Moore AS, Ogilvie GK and Volk LM. Feline
lymphoma (145 cases): proliferation indices, cluster of dif-
ferentiation 3 immunoreactivity, and their association with
prognosis in 90 cats. J Vet Intern Med 1998; 12: 349–354.
6 Louwerens M, London CA, Pedersen NC and Lyons LA.
Feline lymphoma in the post-feline leukemia virus era. J Vet
Intern Med 2005; 19: 329–335.
7 Milner RJ, Peyton J, Cooke K, Fox LE, Gallagher A, Gordon P,
et al. Response rates and survival times for cats with lym-
phoma treated with the University of Wisconsin–Madison
chemotherapy protocol: 38 cases (1996–2003). J Am Vet Med
Assoc 2005; 227: 1118–1122.
8 Stutzer B, Lutz H, Majzoub M, Hermans W, Hirschberger J,
Sauter-Louis C, et al. Incidence of persistent viraemia and
latent feline leukemia virus infection in cats with lym-
phoma. J Feline Med Surg 2011; 13: 81–87.
9 Vezzali E, Parodi AL, Marcato PS and Bettini G.
Histopathologic classification of 171 cases of canine and
feline non-Hodgkin lymphoma according to the WHO.
✜ I/HGAL typically presents acutely and can often be diagnosed by
aspirate cytology of a mural intestinal mass or mesenteric lymph node.
✜ The clinical course of LGAL is chronic and LPE is a major
differential. Definitive diagnosis may not be possible on
histological evaluation of intestinal biopsy specimens alone.
Immunohistochemistry and clonality testing, in addition to routine
histopathology, can assist in differentiating LGAL from
inflammatory disease.
✜ LGLL is the least common subtype and runs an acute clinical
course. An index of suspicion is required to diagnose LGLL.
Cytological evaluation of peripheral blood films and fine-needle
aspirate biopsies is useful for diagnosis. For histological diagnosis,
Giemsa-stained plastic-embedded biopsy specimens are
necessary for reliable detection of granules within neoplastic
lymphocytes. Alternatively, immunohistochemistry can be
performed to detect the cytotoxic granule protein, granzyme B.
✜ Where the REAL/WHO histological classification scheme
is used for diagnosis of AL, clinicians should additionally
request that pathologists include the histological
grade of the lymphoma to help guide therapeutic
decisions.
JFMS CLINICAL PRACTICE 185
hed in humans.
sed individuals,
d T cell lymphoma
m clonal transformation
chronic antigenic
L is the most common
n of coeliac disease.
ce support the
nal inflammation is
velopment of T cell
ological grade) and
udies, 60% of cats
mphoma and 33%
chronic clinical
pre-existing
1,56
smacytic
n identified
alimentary
ts
4
and
rogression of
cumented in
Differential diagnosis
The presenting signs of AL are common to
many primary and secondary gastrointestinal
diseases. LPE is a major differential diagnosis
for LGAL in particular. A comparison between
cats with LPE and LGAL found no correlation
between clinical findings and the final diagno-
sis.61
In cats with intestinal mural mass
lesions, epithelial and mast cell neoplasia are
major differentials. Diagnostic tests recom-
mended to rule out other primary and second-
ary gastrointestinal diseases are listed in the
box on page 186.
Non-invasive diagnostics
Routine laboratory testing
✜ Haematology The most common
haematological abnormalities in cats with
AL are anaemia, due to chronic disease
and/or gastrointestinal blood loss, and
neutrophilia.3,24,25,31,32,63
While routine
haematology is of low diagnostic yield for
LGAL and I/HGAL, careful evaluation of a
peripheral blood film is an essential step for
the diagnosis of LGLL. In LGLL, marked
R E V I E W / Feline AL: classification, clinical signs and non-invasive diagnostics
al signs of LGAL are weight loss (Figure 1;
), diarrhoea (≥60%) and partial or com-
The appetite may be normal or, occasion-
tributable to mesenteric lymph node
o a focal intestinal mass.19,23,24
th I/HGAL and LGLL are similar to those
be more acute and/or severe. A major
pared with LGAL, is the presence of a
ss at diagnosis in the majority of cases
of I/HGAL and LGLL. The mass comprises focal intestinal thick-
ening and/or extraintestinal lesions, such as mesenteric lymph-
adenomegaly, hepatomegaly or renomegaly. Intussusception,
intestinal obstruction and intestinal perforation are more com-
mon in cases of I/HGAL than in LGAL.3,12,19,31,32,35,62
Figure 1 Weight loss
is present in 80% or
more of cats with
low-grade alimentary
lymphoma (LGAL)
Figure 2 Abdominal palpation can be normal in cats with LGAL,
but common abnormalities include diffusely thickened intestinal loops
or a palpably enlarged mesenteric lymph node
c l i n i c a l s i g n s
Abdominal palpation can be normal
in cats with LGAL . . . By contrast an
abdominal mass is palpable in most cats
with I/HGAL and LGLL.
Signalment
All forms of AL typically affect middle- to
old-aged domestic crossbred cats with a
median age at diagnosis of 10–13 years.
A slight male predisposition (1.5:1 male
to female ratio) for HGAL identified
in some reports, has not been
identified for LGAL or
LGLL.4–7,12,13,15,16,19,23–26,32,59,60
by guest on April 15, 2012jfm.sagepub.comDownloaded from
192 JFMS CLINICAL PRACTICE
histological demonstration of disruption of
normal lymph node architecture by the neo-
plastic infiltrate.
This contrasts with the diagnosis of
I/HGAL and LGLL, which can often be made
on the basis of aspiration cytology of focal
intestinal wall masses, enlarged mesenteric
R E V I E W / Feline AL: biopsy techniques, treatment options and prognosis
Figure 2 (a) Ileocaecocolic
high-grade alimentary
lymphoma (HGAL) and (b) a
cut surface from the same
specimen. Diagnosis of
HGAL can often be based
on cytology of ultrasound-
guided fine-needle aspirates
from a focal intestinal mass
or an enlarged mesenteric
lymph node. (c) Diff Quik
cytology of a concurrent
abdominal effusion, showing
neoplastic round cells and a
mitotic figure. Image (c)
courtesy of Dr Patricia Martin,
Veterinary Pathology
Diagnostic Services,
University of Sydneya
a
b c
Figure 3 (a) Diff Quik
stained smear of a fine-
needle aspirate biopsy from
an enlarged mesenteric
lymph node (b) and intestinal
mass (c) in a cat with large
granular lymphocyte
lymphoma (LGLL). In (a)
neoplastic round cells have
a basophilic cytoplasm
and contain large purple
intracytoplasmic granules
(arrows). Image (a) courtesy
of Dr Patricia Martin, Veterinary
Pathology Diagnostic Services,
University of Sydney
b
c
lymph nodes or extraintestinal mass lesions
(Figure 2).2–6
This is because of the characteris-
tic morphology of the neoplastic infiltrate
(large lymphoblastic cells or large granular
lymphocytes [LGLs]), which facilitates differ-
entiation from the background population of
lymphocytes. Also, modified Wright-Giemsa
stains (eg, Diff Quik; Dade Shearing) used for
cytological specimens are more sensitive for
detecting LGLs than haematoxylin and eosin
(HE) stains used for histological specimens.
On cytology, LGLs are identified as large
mononuclear cells with moderate amounts
of deeply basophilic cytoplasm containing
multiple blue or purple granules (Figure 3).5,7
On HE sections, LGLL may be erroneously
reported as I/HGAL. Reliable identification of
cytoplasmic granules in fixed tissues requires
evaluation of Giemsa-stained, plastic-embed-
ded tissue or immunohistochemistry to detect
the cytotoxic granule protein, granzyme B.8,9
Diagnostic considerations
for LGAL
Intestinal biopsy procurement
Histological evaluation of intestinal biopsies
is required for diagnosis of LGAL and for
other forms of AL where cytological evalua-
tion is not definitive (Figures 4 and 5). LGAL
is typically a diffuse or multifocal disease
affecting more than one region of the gastro-
intestinal tract. There is jejunal and ileal
involvement in over 90% of cases, duodenal
involvement in over 70% and gastric involve-
ment in 7–40% of cases.1,10,11
The distribution
of gastrointestinal involvement in lympho-
plasmacytic enteritis (LPE) is similar to LGAL
except that gastric involvement is more
common in LPE.11
by guest on April 15, 2012jfm.sagepub.comDownloaded from

12. 21
Low-grade alimentary lymphoma: clinicopathological
findings and response to treatment in 17 cases
Amy E Lingard BVSc (Hons), MACVSc (Feline Medicine)
1,a
, Katherine Briscoe BVSc (Hons), MACVSc
(Feline Medicine)
1
, Julia A Beatty BSc (Hons), BVetMed, PhD, FACVSc (Feline Medicine), MRCVS
1
, Antony S
Moore BVSc, MVSc, DACVIM (Oncology)
2
, Ann M Crowley BVSc (Hons), MACVSc, Diplomate American
College of Veterinary Pathologists
3
, Mark Krockenberger BSc (Vet), BVSc, PhD, MACVSc (Pathobiology),
MASM
4
, Richard K Churcher BVSc, FACVSc (Canine Medicine)
5
, Paul J Canfield DVSc, PhD,
GradCertEdStud, FRCPath (Veterinary Pathology), FACVSc (Clinical Pathology), MRCVS
4
, Vanessa R Barrs BVSc
(Hons), MVetClinStud, FACVSc (Feline Medicine), GradCertEd
1
*
1
Valentine Charlton Cat Centre,
Faculty of Veterinary Science, The
University of Sydney, NSW 2006,
Australia
2
Veterinary Oncology Consultants,
379 Lake Innes Drive, Wauchope
NSW 2446, Australia
3
Anapath, PO Box 504, Newport
NSW 2106, Australia
4
Veterinary Pathology Diagnostic
Services, Faculty of Veterinary
Science, The University of Sydney,
NSW 2006, Australia
5
North Shore Veterinary Specialist
Centre, 64 Atchison Street, Crows
Nest NSW 2065, Australia
Low-grade alimentary lymphoma (LGAL) was diagnosed by histological and
immunohistochemical evaluation of full-thickness biopsies from multiple
regions of the gastrointestinal tract collected during exploratory laparotomy in
17 cats. The most common clinical signs were weight loss (n ¼ 17) and vomiting
and/or diarrhoea (n ¼ 15). Clinical signs were chronic in 11 cases. Abdominal
palpation was abnormal in 12 cats, including diffuse intestinal thickening (n ¼ 8),
an abdominal mass due to mesenteric lymph node enlargement (n ¼ 5) and
a focal mural intestinal mass (n ¼ 1). The most common ultrasonographic finding
was normal or increased intestinal wall thickness with preservation of layering.
Ultrasound-guided fine-needle aspirates of mesenteric lymph nodes (n ¼ 9) were
incorrectly identified as benign lymphoid hyperplasia in eight cats, in which the
histological diagnosis from biopsies was lymphoma. There was neoplastic
infiltration of more than one anatomic region of the gastrointestinal tract in
16/17 cats. The jejunum (15/15 cats) and ileum (13/14 cats), followed by the
duodenum (10/12 cats), were the most frequently affected sites. Twelve cats
were treated with oral prednisolone and high-dose pulse chlorambucil, two with
a modified MadisoneWisconsin multiagent protocol and three with
a combination of both protocols. Thirteen of the 17 cats (76%) had complete
clinical remission with a median remission time of 18.9 months. Cats that
achieved complete remission had significantly longer median survival times
(19.3 months) than cats that did not achieve complete remission (n ¼ 4)
(4.1 months; P ¼ 0.019). The prognosis for cats with LGAL treated with oral
prednisolone in combination with high-dose pulse chlorambucil is good to
excellent.
Date accepted: 15 May 2009 Ó 2009 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.
A
limentary lymphoma is the most common
anatomic form of lymphoma in the cat.1e3
It is characterised by infiltration of the gas-
trointestinal tract with neoplastic lymphocytes, with
or without mesenteric lymph node involvement.4e6
Feline alimentary lymphoma can be histologically
classified by the National Cancer Institute Working
Formulation (NCIWF) as high-grade, intermediate-
grade or low-grade with the latter being common in
the diffuse form.7e11
A less commonly described
form of alimentary lymphoma is large granular lym-
phocytic lymphoma.12,13
Low-grade alimentary lymphoma (LGAL) was first
described as a clinical entity in cats in a retrospective
study of 29 cases.10
The diagnosis was based on histol-
ogy of haematoxylin and eosin (HE)-stained sections
from gastroduodenal endoscopic biopsies (EB).10
Cats with LGAL were reported to have a more favour-
able outcome when treated with oral prednisolone
and high-dose pulse chlorambucil compared to cats
*Corresponding author. E-mail: vbarrs@vetsci.usyd.edu.au
a
Present address: The Cat Clinic, 1 Miller Street, Prahran VIC
3181, Australia.
ARTICLE IN PRESS
Journal of Feline Medicine and Surgery (2009) --, --e--
doi:10.1016/j.jfms.2009.05.021
1098-612X/09/------+-- $36.00/0 Ó 2009 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Amy E Lingard et al., Low-grade alimentary lymphoma: clinicopathological findings and re-
sponse to treatment in 17 cases, J Feline Med Surg (2009), doi:10.1016/j.jfms.2009.05.021
Perda de peso: 17 gatos
Vômito e;ou Diarréia: 15 gatos
Palpação anormal: 12 gatos
Espessamento parede intestinal: 8 gatos
Massa abdominal + Aumento linfonodo: 5 gatos
Massa focal: 1 gato
J Am Vet Med Assoc. 2013 Nov 15;243(10):1455-61. doi: 10.2460/javma.
243.10.1455.
!
Diagnosis of chronic small bowel disease in cats: 100 cases
(2008-2012).
!
Norsworthy GD1, Scot Estep J, Kiupel M, Olson JC, Gassler LN.
!
OBJECTIVE: To determine whether a diagnosis of chronic small bowel disease could be
established in a subset of cats that had clinical signs of chronic vomiting, chronic small
bowel diarrhea, weight loss, or a combination of these, combined with
ultrasonographically determined thickening of the small bowel.
!
PROCEDURES: Medical records of cats with clinical signs of chronic vomiting, chronic small
bowel diarrhea, weight loss, or a combination of these, combined with
ultrasonographically determined small bowel thickening, that underwent laparotomy and
multiple small bowel biopsies between 2008 and 2012 were examined. Biopsy specimens
were submitted for histologic evaluation, immunohistochemical evaluation, and, when
findings were ambiguous, PCR assay for antigen receptor rearrangement.
!
RESULTS: Chronic small bowel disease was diagnosed in 99 of the 100 cats. The
most common diagnoses were chronic enteritis and intestinal lymphoma.

13. Diagnóstico
!Biópsia endoscópica:
amostras pequenas (máx. 2,8mm)
!
!Biópsia cirúrgica:
mucosa, submucosa e muscular
!
!
!
!
JFMS CLINICAL PRACTICE 451
– so-called ‘lymphoplasmacytic enteritis’ (LPE)
– is the most frequently reported form of feline
IBD.10,35,36
However, the appropriateness and
clinical relevance of the term lymphocytic/
plasmacytic enteritis is a contentious issue. For
example, LPE may also be associated with
intestinal parasites, dietary sensitivity and
feline hyperthyroidism.8
Moreover, cats with
and without signs of intestinal disease have
similar numbers of lymphocytes and plasma
cells in tissues.5
In hyperthyroid cats with LPE,
successful treatment (via I131
) of the hyper-
thyroidism has resulted in remission of
clinical signs but follow-up biopsies were
not performed to assess for eradication of
mucosal inflammation (author’s unpublished
observations).
Recent studies indicate that changes in
mucosal architecture, such as villous morphol-
ogy and fibrosis, are related to the presence and
severity of GI disease. These studies have used
quantitative observer-independent variables
(eg, proinflammatory cytokines, mucosal bacte-
ria) to identify histopathological correlates of
disease. In cats with signs of GI disease, villus
atrophy and fusion correlated with severity of
clinical signs and degree of proinflammatory
cytokine upregulation in the duodenal mucosa.
In a separate investigation, histopathologic
inflammation was correlated with clinical
signs, endoscopic lesions (ie, mucosal friability,
granularity and/or erosions), and clinicopatho-
logic abnormalities (ie, increased total protein
concentration, elevated ALT/ALP activities,
hypophosphatemia, hypocobalaminemia,
and/or increased fPLI) in cats with IBD.26
Surgical versus endoscopically obtained
biopsies
Biopsies for histopathologic diagnosis of IBD
are obligatory and they may be obtained
endoscopically (mucosal sample) or by
laparoscopy or exploratory laparotomy (full-
thickness sample). Controversy exists con-
cerning the relative diagnostic accuracy of
endoscopic versus full-thickness specimens
for the diagnosis of IBD and alimentary lym-
phoma. Making a correct diagnosis is further
complicated by the fact that these disorders
share a variety of overlapping features (eg,
clinical signs, physical examination findings,
abdominal ultrasonographic abnormalities
and histopathologic lesions) and that chronic
mucosal inflammation (eg, gastric Helicobacter
heilmannii infection) may progress to lym-
phoma in some instances.40
Endoscopic biopsy specimens of the stom-
ach and duodenum were considered inade-
quate compared with full-thickness biopsies
for differentiating IBD from lymphoma in one
study.14
However, duodenal (endoscopic)
assessment was limited to only 50% of the cats
and mucosal biopsy was performed blindly
(with only three specimens obtained per cat) in
8/22 (36%) of the cats. Because none of the cats
in this study had endoscopic biopsy of the
ileum performed, malignant infiltrates in this
organ could only be confirmed in full-
thickness specimens obtained by laparotomy.
In another study, the likelihood for diagnosis
of alimentary lymphoma was greatest in cats
undergoing multi-organ biopsy from all seg-
ments of the intestine and the mesenteric
diagnostic criteria vary and there is considerable controversy as
to the magnitude of the normal eosinophilic population in small
and large intestine and what is considered excessive. A diagno-
sis of EE is strengthened by the observation of eosinophils in the
submucosa and the presence of infiltrates in the mesenteric
lymph nodes.38
Clinical signs include small or large bowel diar-
rhea, vomiting, anorexia and weight loss. Physical examination
may detect palpably thickened intestinal loops (presumably due
to the submusosal eosinophilic infiltrates) but these may also be
a feature of non-EE intestinal infiltrative diseases. Peripheral
lymphadenopathy and hepatosplenomegaly are also reported in
lesions. Suppurative colitis may occur in young cats but is an
uncommon IBD variant.39
Clinical signs include large bowel
diarrhea, hematochezia, or tenesmus of variable severity.
Histopathologic lesions include dense infiltrates of neutrophils
accompanied by lesser numbers of lymphocytes and plasma
cells. The cause is unknown but this disorder may be associated
with enteropathogenic bacteria, including Clostridium species
and Campylobacter jejuni. Neutrophilic forms of IBD are rare and
the suspicion for a primary bacterial etiopathogenesis is based
on the abundant and complex intestinal microbiota present in the
colon.
Biopsies for
histopathologic
diagnosis of
IBD are
obligatory . . .
The ileum
seems to be a
consistently
affected organ
and should
always be
biopsied when
lymphoma or
IBD is
suspected.
at AMERICAN COLL VET DERMATOLOGY on June 27, 2016jfm.sagepub.comDownloaded from
JFMS CLINICAL PRACTICE 445
C L I N I C A L R E V I E W
Journal of Feline Medicine and Surgery (2012) 14, 445–458
Albert E Jergens
FELINE IDIOPATHIC INFLAMMATORY
BOWEL DISEASE
What we know and
what remains to be unraveled
Practical relevance: Feline idiopathic
inflammatory bowel disease (IBD)
denotes one form of chronic enteropathy
that is immunologically mediated and
characterized by persistent or recurrent
gastrointestinal (GI) signs and histologic
inflammation. Signs of vomiting, diarrhea and
weight loss generally predominate, and mucosal
inflammation may occur in any portion of the GI
tract (especially the small intestine). Affected cats
may also have concurrent inflammation in other
organs, such as the pancreas and liver, which may
impact clinical disease severity.
Clinical challenges: The exact etiologies of this
heterogeneous group of disorders have yet to be
determined, though results from basic science and
clinical studies suggest that interplay between
genetic factors and enteric bacteria is crucial for
disease development. The diagnosis is one of
exclusion and requires intestinal mucosal biopsy
to characterize the type and severity of the
inflammatory infiltrate, and to differentiate IBD from
other disorders, including alimentary lymphoma.
Controversy exists concerning the relative
diagnostic accuracy of endoscopic versus
full-thickness specimens for the diagnosis of IBD
and its differentiation from alimentary lymphoma.
Audience: This article is intended to provide
veterinary practitioners with a comprehensive
clinical update on idiopathic IBD in cats. It reviews
the current evidence-based data, the diagnostic
approach, the evolving histologic criteria, and
treatment options and outcome for feline patients
with this syndrome.
Current understanding of etiology
and pathogenesis
While the exact cause of inflammatory bowel disease (IBD) remains
unknown, current hypotheses suggest that feline IBD, similar to IBD
in humans and dogs, involves complex interactions between
environmental factors (ie, intestinal microbial imbalances, dietary
components) and the mucosal immune system, resulting in chronic
inflammation in susceptible cats (Figure 1).1
Genetic defects in the recognition of commensal versus pathogenic
bacteria by the innate immune system play a pivotal role in disease
pathogenesis in humans
and dogs with IBD.
Mutations in innate
immune receptors of
humans (NOD2/CARD 15)
and dogs (TLR4, TLR5)
have now been linked to
IBD susceptibility; and in
the presence of an enteric
microbiota may lead to
upregulated proinflamma-
tory cytokine production
(eg, IL-17, TNF-α) and
reduced bacterial clearance,
thereby promoting chronic intestinal inflammation.1–3
Whether
or not similar pathomechanisms come into play in the development
of idiopathic feline IBD has not been fully determined. However,
antigens derived from commensal bacteria are likely to be important
in driving disease pathogenesis, as increased populations of
mucosa-associated bacteria (ie, Enterobacteriaceae) have been linked to
clinical signs, cytokine mRNA and histopathologic lesions in cats
with IBD.4
Other studies have reported increased lamina propria myeloid/
histiocyte antigen-positive macrophages, upregulated epithelial major
histocompatibility complex (MHC) class II molecule expression,
and increased antibody reactivity to components of the commensal
DOI: 10.1177/1098612X12451548
© ISFM and AAFP 2012
Certain breed predispositions
(Siamese and other Asian
breeds) for IBD are recognized,
but any breed may be affected
and causal genetic defects have
not been identified to date.
Albert E Jergens
DVM PhD DACVIM
Department of Veterinary Clinical Sciences,
College of Veterinary Medicine,
Iowa State University,
Ames, IA 50011, USA
Email: ajergens@iastate.edu
at AMERICAN COLL VET DERMATOLOGY on June 27, 2016jfm.sagepub.comDownloaded from
TRATAMENTO

14. Tratamento
!Mudança da Dieta & Terapia Farmacológica
!
!Controle dietético
!
!Antibioticoterapia
!
!Corticoterapia
!
!Imunossupressores
!
Tratamento
!Dieta
!
!Restrição de gordura
!
!Proteína inexperiente
!
!Proteína ultra-hidrolisada
!
!

15. Tratamento
!Prednisolona (Prelone®3mg/ml-humano)
dose: 2mg/kg PO q.24hd
redução dose 25% q.30dias
duração do tto: 3 a 6 meses!!!
!
!Metronidazol (Flagyl®250mg-humano)
dose: 15mg/kg PO q.24h por 14 dias
redução dose 25% mais 14 dias
!
!Clorambucil (Leukeran®-humano)
dose: 2mg/gato PO q.72h por 21 dias
!
!Ciclosporina (Genuxal®-humano)
dose: 5mg/gato/PO/por 21dias
JFMS CLINICAL PRACTICE 445
C L I N I C A L R E V I E W
Journal of Feline Medicine and Surgery (2012) 14, 445–458
Albert E Jergens
FELINE IDIOPATHIC INFLAMMATORY
BOWEL DISEASE
What we know and
what remains to be unraveled
Practical relevance: Feline idiopathic
inflammatory bowel disease (IBD)
denotes one form of chronic enteropathy
that is immunologically mediated and
characterized by persistent or recurrent
gastrointestinal (GI) signs and histologic
inflammation. Signs of vomiting, diarrhea and
weight loss generally predominate, and mucosal
inflammation may occur in any portion of the GI
tract (especially the small intestine). Affected cats
may also have concurrent inflammation in other
organs, such as the pancreas and liver, which may
impact clinical disease severity.
Clinical challenges: The exact etiologies of this
heterogeneous group of disorders have yet to be
determined, though results from basic science and
clinical studies suggest that interplay between
genetic factors and enteric bacteria is crucial for
disease development. The diagnosis is one of
exclusion and requires intestinal mucosal biopsy
to characterize the type and severity of the
inflammatory infiltrate, and to differentiate IBD from
other disorders, including alimentary lymphoma.
Controversy exists concerning the relative
diagnostic accuracy of endoscopic versus
full-thickness specimens for the diagnosis of IBD
and its differentiation from alimentary lymphoma.
Audience: This article is intended to provide
veterinary practitioners with a comprehensive
clinical update on idiopathic IBD in cats. It reviews
the current evidence-based data, the diagnostic
approach, the evolving histologic criteria, and
treatment options and outcome for feline patients
with this syndrome.
Current understanding of etiology
and pathogenesis
While the exact cause of inflammatory bowel disease (IBD) remains
unknown, current hypotheses suggest that feline IBD, similar to IBD
in humans and dogs, involves complex interactions between
environmental factors (ie, intestinal microbial imbalances, dietary
components) and the mucosal immune system, resulting in chronic
inflammation in susceptible cats (Figure 1).1
Genetic defects in the recognition of commensal versus pathogenic
bacteria by the innate immune system play a pivotal role in disease
pathogenesis in humans
and dogs with IBD.
Mutations in innate
immune receptors of
humans (NOD2/CARD 15)
and dogs (TLR4, TLR5)
have now been linked to
IBD susceptibility; and in
the presence of an enteric
microbiota may lead to
upregulated proinflamma-
tory cytokine production
(eg, IL-17, TNF-α) and
reduced bacterial clearance,
thereby promoting chronic intestinal inflammation.1–3
Whether
or not similar pathomechanisms come into play in the development
of idiopathic feline IBD has not been fully determined. However,
antigens derived from commensal bacteria are likely to be important
in driving disease pathogenesis, as increased populations of
mucosa-associated bacteria (ie, Enterobacteriaceae) have been linked to
clinical signs, cytokine mRNA and histopathologic lesions in cats
with IBD.4
Other studies have reported increased lamina propria myeloid/
histiocyte antigen-positive macrophages, upregulated epithelial major
histocompatibility complex (MHC) class II molecule expression,
and increased antibody reactivity to components of the commensal
DOI: 10.1177/1098612X12451548
© ISFM and AAFP 2012
Certain breed predispositions
(Siamese and other Asian
breeds) for IBD are recognized,
but any breed may be affected
and causal genetic defects have
not been identified to date.
Albert E Jergens
DVM PhD DACVIM
Department of Veterinary Clinical Sciences,
College of Veterinary Medicine,
Iowa State University,
Ames, IA 50011, USA
Email: ajergens@iastate.edu
at AMERICAN COLL VET DERMATOLOGY on June 27, 2016jfm.sagepub.comDownloaded from
e o gordo? idoso? renal? cardiopata?
!Budesonida
!
!corticóide de ação local
!
!redução dos efeitos sistêmicos
!
!dose: 1mg/gato/dia (manipular)
!
!
!

16. Suplementos
!Cobalamina (vitamina B12-hidrossolúvel)
!
!deficiência B12:
!
!mudança da permeabilidade da mucosa
!
!redução absorção de nutrientes
!anemia em humanos
!
!dose: 250mcg/gato/semana/6sem
!
!
!
Suplementos
!FIBRAS SOLÚVEIS (Colite)
!
!Psylium
!
!substrato para simbiose colonica
!
!PROBIÓTICOS
!
!corrigir desequilíbrio e reduzir inflamação
!
!
!

17. Prognóstico
☺ Favorável ☺
!
☹ Exceto com linfoma intestinal
!
!
!
DODÓI
Obrigada! 32