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The Mysteries of the GI Tract:
Demystifying Chronic Diarrhea in Dogs
Stanley L. Marks, BVSc, PhD, DACVIM (Internal Medicine, Oncology), DACVN
Vomiting Cat Cases:
You Can Figure Them Out
Debra L. Zoran, DVM, PhD, DACVIM
Nutrition for Senior Dogs:
New Tricks for Feeding Old Dogs
Julie A Churchill, DVM, PhD, DACVN
Pet Food Myth Busters: Answering Common
Questions Owners Ask About Pet Food
Lisa M. Freeman, DVM, PhD, DACVN
Sponsored by:
2015 NAVC/WVC Symposia Proceedings
The Mysteries of the GI Tract:
Demystifying Chronic
Diarrhea in Dogs
Stanley L. Marks,
(Internal Medicine,
Oncology), DACVN
Professor of Small
Animal Medicine
University of California, Davis
School of Veterinary Medicine
Davis, California
iarrhea is generally regarded as the most consistent clinical sign of intestinal disease in dogs and cats and is one
of the most frustrating disorders for many veterinarians to
diagnose and manage. Incomplete resolution of the problem
can result in frustration and dissatisfaction for the owner and potential suffering for the animal. Antibiotics are commonly administered injudiciously to diarrheic animals, with resolution of clinical
signs often wrongly attributed to eradication of a putative infectious pathogen.
Chronic diarrhea is persistent or relapsing over a period of 3 to 4 weeks or longer. In contrast to acute diarrhea that is often self-limiting and does not typically require a comprehensive workup, chronic cases warrant a step-by-step approach to obtain a diagnosis and
formulate an optimal therapeutic plan. The exception to this rule is in dogs with acute hemorrhagic diarrhea syndrome that can be associated with a number of infectious and non-
The Mysteries of the GI Tract: Demystifying Chronic Diarrhea in Dogs
infectious causes and typically lasts less than
1 week.
The history and physical examination are
paramount for determining whether the diarrhea is caused by primary disease of the
gastrointestinal (GI) tract or is secondary to
extraintestinal diseases such as pancreatic insufficiency or Addison’s disease (Table 1).
The need for performing fecal screening for
putative enteropathogens, resting cortisol
for Addison’s disease, tests for pancreatitis
[canine pancreas specific lipase (Spec cPL,
IDEXX Laboratories) and ultrasound], or
abdominal radiographs for GI foreign bodies should be based upon the patient’s signalment, history (including vaccination
history), and physical examination findings.
The categorization of diarrhea into small
bowel or large bowel in origin is helpful for
prioritizing certain differentials (Table 1)
and for determining which segment of
bowel to biopsy if indicated. Caution is warranted in this over-simplistic anatomic differentiation of the affected segment of bowel
because animals manifesting clinical signs of
colitis often have concurrent disease in the
small bowel and vice versa. In addition,
most veterinary gastroenterologists prefer to
biopsy the small and large intestine when
feasible to maximize diagnostic yield of the
procedure. Failure to consider the role of the
diet or dietary supplements in precipitating
or alleviating the GI disorder can result in
delayed diagnosis or improper dietary recommendations. The history should also
focus on the duration of the diarrhea, the appearance of the feces (color, volume, mucus,
presence of fresh blood), worming and vaccination history, defecation frequency, aggravating or alleviating factors, and defecation
Fecal Examination for Parasites
The diagnosis of GI parasites in dogs and
cats is an integral component of small ani-
mal practice. The following guidelines can
help veterinarians maximize the diagnostic
yield of fecal examinations for parasites.
1. Fresh fecal specimens should be refrigerated to facilitate preservation of eggs,
oocysts, and cysts if immediate fecal flotation cannot be performed following collection.
2. Centrifugation fecal flotation is vastly
superior to standing (gravitational) flotation.1,2 The type of flotation solution and
its specific gravity does affect the diagnostic yield. Aqueous zinc sulfate
(ZnSO4) with a specific gravity of 1.18 to
Common Differentials for Chronic Diarrhea in Dogs
Inflammatory bowel disease
Infiltrative neoplasia: lymphoma, mast cell tumor,
Endoparasites: helminths, Giardia, Cystoisospora,
Food-responsive enteropathy
Bacterial, viral, and fungal enteropathogens:
Campylobacter, Salmonella, Histoplasma spp, Pythium
Intestinal obstruction secondary to strictures,
Primary GI Disorders
Extragastrointestinal Disorders
Addison’s disease
Exocrine pancreatic insufficiency
Pancreatic neoplasia
Liver failure: uncommon cause of diarrhea
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
Diagnostic Approach to Dogs with Chronic Enteropathies
• Detailed and accurate, including comprehensive dietary history
Physical examination
Minimum database
• Serum biochemistry panel
• Urinalysis
• Fecal centrifugation flotation and direct wet-prep
Additional fecal tests that may be warranted
• Fecal Giardia ELISA or IFA test for Giardia and Cryptosporidium:
Fecal ELISA for Giardia should be used only as a screening test to
diagnose infection before initiating anthelmintic therapy
• Fecal enteric panel (culture and toxin assays) or fecal PCR
panel: Reserve for animals developing diarrhea after boarding
or show attendance, cats and dogs with acute onset of bloody
diarrhea in association with evidence of sepsis or diarrhea,
outbreaks occurring in more than one pet in a household, and
zoonotic concerns (Campylobacter, Salmonella) in diarrheic
pets in contact with immunocompromised humans
• Abdominal radiography: Relatively low-yield procedure in
animals with chronic diarrhea but is indicated in animals
with suspected partial obstructions from foreign body/
intussusception/mass or gas distention/torsion of the GI tract
Dietary trial
• Elimination diet or hydrolyzed diet: Selected based on the
animal’s dietary history; recommend dietary trial to help rule out
food-responsive enteropathy before procuring intestinal biopsies
in stable animals (no evidence of hypoalbuminemia,
hypocobalaminemia, fever, melena)
• High-fiber diet: Can be tried in animals with colitis if there is no
response to an elimination diet trial; response should be
recognized within 7 to 10 days of initiating the trial diet
Antibiotic trial
• Antibiotic-responsive diarrhea (ARD) affects large and giant
breed dogs predominantly and is associated with signs of
enteritis or colitis
• Tylosin (5–10 mg/kg q24h PO) is the drug of choice for dogs with
suspected ARD and is administered prior to procurement of
intestinal biopsies in dogs failing to show an adequate response
to dietary therapy
Empirical deworming with broad-spectrum anthelmintic
Tests of assimilation
• Serum cobalamin and folate: Assessment of absorption in the
ileum and jejunum, respectively
• Trypsin-like immunoreactivity (cTLI): Diagnosis of exocrine
pancreatic insufficiency
• Abdominal ultrasonography: Evaluation of the pancreas;
intestinal wall thickening, layering of the wall, echogenicity of
layers; mesenteric lymph nodes; liver; spleen; kidneys; presence
of peritoneal fluid
Miscellaneous tests or procedures
• Spec cPL: Pancreatitis
• Thyroxine (T4) in dogs with polyphagia, weight loss and diarrhea
and no evidence of exocrine pancreatic insufficiency or chronic
• Rectal scraping: pythiosis, histoplasmosis, protothecosis, and
eosinophilic colitis or proctitis
GI biopsies
• Endoscopy: Recommended to procure ileal biopsies particularly
when serum cobalamin concentration is abnormally decreased
• Full-thickness biopsy specimens: Laparotomy versus laparoscopy
1.2 has been widely recommended because it will float cysts, oocysts, and most
helminth eggs with a minimum of distortion and fecal debris. Other acceptable
solutions include Sheather’s sugar and
sodium nitrate.
3. Giardia and Cryptosporidium immunoassays increase the diagnostic yield of
the fecal exam when performed in parallel
with centrifugation flotation. Enzymelinked immunosorbent assays (ELISAs)
detect Giardia cyst-wall protein 1 (GCWP
1) and are generally easy to perform and interpret. The SNAP Giardia Test (IDEXX
Laboratories) is a rapid in-house enzyme
immunoassay that can be performed on
fresh or previously frozen feces or samples
stored at 2°C to 7°C for up to 7 days.3
ELISAs should not be used to assess response to therapy in animals that have completed a recent course of anthelmintics
because animals can remain positive for Giardia spp on the SNAP ELISA for several
weeks following successful eradication of the
parasite. A second type of immunoassay
called direct immunofluorescence (DIF)4
has the added benefit of detecting both
Giardia and Cryptosporidium in feces, but
The Mysteries of the GI Tract: Demystifying Chronic Diarrhea in Dogs
mans. Dogs have mainly assemblages C
and D; cats have assemblages A1 and F;
humans have assemblages A2 and B. Assemblages can be determined via PCR5 to
determine the likelihood of zoonotic
transmission from animals to humans, although the risk for transmission of Giardia spp to humans is generally very low.
Figure 1. Positive direct-immunofluorescence (DIF)
assay showing the smaller round apple-green fluorescent oocysts of Cryptosporidium and the
larger oval-shaped cysts of Giardia in a puppy
with diarrhea. Magnification 400X
Figure 2. Abundant hairpin-shaped gram-positive endospores consistent with Clostridium perfringens in a healthy nondiarrheic puppy that
presented for routine vaccination. Magnification 400X
requires a fluorescent microscope. A positive result is indicated by apple green fluorescence of the cyst (Giardia) or oocyst
(Cryptosporidium) (Figure 1). Morphologic identification is necessary for this
4. Polymerase chain reaction (PCR)-based
tests for Giardia and Cryptosporidium
spp are commercially available although
the author recommends fecal flotation
and DIF or ELISA testing for the routine
diagnosis of both organisms. An exception
is the use of PCR for determining Giardia
“assemblages” to assess the infectivity potential of the isolate for animals and hu-
Fecal Examination for Bacteria
1. PCR and bacterial culture/toxin
imunoassays are low-yield diagnostic
procedures in animals with diarrhea if the
tests are performed injudiciously.6 If bacterial enteritis or enterocolitis is suspected, the feces should be cultured or
PCR should be performed for specific enteropathogens, such as Salmonella spp or
Campylobacter jejuni. Fecal PCR is superior to culture for the diagnosis of
Campylobacter spp, and facilitates the
rapid diagnosis of multiple species of
2. Fecal cytology on stained fecal smears is
commonly performed to identify the underlying cause of diarrhea by looking for
spiral-shaped bacteria (Campylobacter-like
organisms), white blood cells, and fecal endospores associated with Clostridium perfringens. Unfortunately, the detection of
increased fecal endospores is of no clinical
diagnostic utility8,9 (Figure 2) and the
overall value of stained fecal smears is extremely limited. Detection of spiral-shaped
organisms resembling Campylobacter spp
is insufficient when used alone to diagnosis Campylobacter-associated diarrhea.
Veterinarians should be cognizant of the fact
that most bacterial enteropathogens are associated with self-limiting diarrhea, and injudicious administration of antimicrobials could
be more harmful than beneficial. Supportive
therapy and appropriate hygiene control
should be considered in all cats with suspected
or confirmed bacteria-associated diarrhea. An-
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
Most bacterial
are associated
with self-limiting
diarrhea. …
should be
administered only
to animals
systemic signs of
timicrobials should be administered only to animals manifesting systemic signs of illness.
of serum
and folate
insight into
the functional
integrity of the
ileum and
Interpretation of Hematology &
Serum Biochemistry Panels
The complete blood count (CBC) may reveal
peripheral eosinophilia secondary to endoparasitism, eosinophilic inflammatory bowel disease (IBD), Addison’s, abdominal mast cell
neoplasia, or lymphoma (paraneoplastic phenomenon). Anemia may result from enteric
blood loss or from depressed erythropoiesis
caused by systemic disease or chronic inflammation.
The serum biochemistry panel can provide
additional information pertaining to the likely
cause of diarrhea and help rule out extra-GI
causes of diarrhea (renal disease, hepatic insufficiency). Protein-losing enteropathies represent a syndrome of intestinal disorders
(severe IBD, lymphoma, intestinal ulceration)
that typically manifest with abnormal loss of
serum proteins across an inflamed or abnormally permeable intestinal mucosal barrier.
Hypocholesterolemia can be seen secondary
to malabsorption. A discordant BUN:creatinine ratio results from dehydration (prerenal
azotemia), GI bleeding, high-protein meal,
and cachexia. Elevated liver enzymes should
be interpreted cautiously in dogs with intestinal disease or pancreatitis because drainage
of bacteria or endotoxin via the portal circulation can precipitate a “reactive hepatopathy.”
Tests of Intestinal Function
Measurement of serum cobalamin and folate concentrations provides insight into the
functional integrity of the ileum and jejunum, respectively. Low serum cobalamin
has been described in dogs in association
with a variety of GI diseases, including IBD,
intestinal lymphoma, and lymphangiectasia.
Mucosal repair is impeded when cobalamin
is deficient and its absorption impaired.
Dogs that are deficient in cobalamin are typically administered cyanocobalamin subcu-
taneously (SC) on a weekly basis at 250 to
1500 µg/dose (depending on the animal’s
weight) SC for 6 weeks, followed by dosing
every 2 to 3 weeks for the indefinite future.
Abdominal Imaging
Survey abdominal radiography is a relatively
low-yield procedure in most dogs with
chronic diarrhea but is indicated in animals
suspected of having partial obstructions
caused by foreign bodies, intussusceptions,
or masses, or in those with gas distention or
displacement of the stomach or bowel. Abdominal ultrasonography is complementary
to survey abdominal radiography; it is more
sensitive for detection of abdominal masses,
intestinal mural thickening, intussusceptions, “tiger-stripe” lines in the mucosa (Figure 3), and mesenteric lymphadenopathy.10
In addition, ultrasound-guided percutaneous
biopsy or aspiration of masses is an effective
diagnostic procedure. Contrast radiography
and fluoroscopy are occasionally indicated for
identifying partial obstructions and intestinal
motility disorders, respectively.
Endoscopy & Biopsy
Pitfalls & Recommendations
Endoscopy is a valuable procedure for diag-
Figure 3. Ultrasound image of a segment of duodenum from a 4-year-old castrated male toy
poodle with severe intestinal lymphangiectasia.
Note the hyperechoic lines (“tiger-stripes”) extending from the lumen of the duodenum to the
submucosal layer. This finding is highly supportive of intestinal lymphangiectasia in dogs.
The Mysteries of the GI Tract: Demystifying Chronic Diarrhea in Dogs
Figure 4. Endoscopic view of the duodenum of
a 5-year-old castrated male Rottweiler with
histopathologically confirmed IBD. The mucosa
is erythematous and granular in appearance.
nosis of intestinal mucosal disorders associated with morphologic changes, but it does
not differentiate intestinal motility disorders, secretory diarrheas, or brush-border
enzyme defects. In addition, lesions of the
intestinal submucosa and muscularis propria
layers of bowel can easily be missed, and endoscopy is limited by the working length of
the scope, precluding examination of the jejunum. With the support of the World Small
Animal Veterinary Association, the Gastrointestinal Standardization Group has proposed
a standardized histologic evaluation system
that can be applied to all companion animal
gastroenterologic disorders to minimize interobserver observation among pathologists.11
Food-Responsive Enteropathy
Food-responsive enteropathy is a common
cause of chronic diarrhea in dogs and the
disorder is associated with a relatively high
response rate (45%–60%) to the feeding of
elimination diets containing novel, single
sources of protein (intact or hydrolyzed).1214
Most dogs with a food-responsive enteropathy show a relatively rapid resolution
of clinical signs within 3 to 4 days following
implementation of dietary therapy. In a re-
port of dogs with lymphocytic–plasmacytic
colitis, clinical signs resolved in all 13 cases
with introduction of an elimination diet,
and of 11 dogs rechallenged with their original diet, 9 relapsed.12 The theoretical basis
for protein hydrolysate diets is that reduction in immunogenic epitopes being presented to the mucosal immune system
during dysregulation will increase the potential for resolution. Thus, the argument
for the use of a hydrolysate diet is independent of whether a diet-specific immunologic response is suspected. Experience
with protein hydrolysate diets is increasing
and anecdotally they appear to be effective
adjuncts to pharmacologic therapy or even
as the sole therapy. Clinical resolution with
histologic improvement has been reported
in 4 of 6 dogs with refractory IBD when
treated with a hydrolyzed soy-protein diet
alone.13 In addition, feeding a hydrolyzed
diet to 18 dogs with chronic small bowel enteropathy was shown to be superior to feeding a highly digestible control diet for
long-term management.14 It is possible,
however, that nutritional factors other than
protein hydrolysis were responsible for the
improvement. These factors could include
dietary digestibility, correction of vitamin or
mineral deficiencies, reduced fat content,
lowered n-6:n-3 fatty acid ratio, and possible immunomodulatory effect of soy
isoflavones within the hydrolyzed diets.
Antibiotic-Responsive Diarrhea (ARD)
or Tylosin-Responsive Diarrhea
ARD is essentially a canine phenomenon
and is seen more commonly in large and
giant-breed dogs. German shepherd dogs
appear to be particularly predisposed to
ARD that is characterized by small bowel or
large bowel diarrhea in the absence of an underlying cause.15 These dogs do not appear
to have bacterial overgrowth (SIBO), but
rather a dysbiosis of their microbiota. ARD
is typically managed with tylosin at 5 to 10
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
The argument
for the use of a
hydrolysate diet
is independent
of whether a
response is
mg/kg every 24 hours for 3 to 4 weeks; however, many dogs may need to be treated for
4 weeks or longer. Many dogs with ARD
have failed to respond to metronidazole administration.
of probiotics to
dogs with IBD
represents a
novel alternative
modality that
warrants further
Inflammatory Bowel Disease
Diagnosis of IBD is based on compatible
clinical signs (chronic diarrhea, vomiting,
weight loss, with or without borborygmus
and flatulence) and exclusion of metabolic,
infectious, neoplastic, and obstructive disorders of the gut. Biopsies must show histologic evidence of moderate to marked
infiltration of the GI mucosa by inflammatory cells (predominantly lymphocytes and
plasma cells) and changes in mucosal architecture for a diagnosis of IBD to be rendered
(Figure 4). Management of canine IBD includes elimination or hypoallergenic diets,
antimicrobials (tylosin, metronidazole)
and/or immunomodulatory drugs (prednisolone, budesonide, chlorambucil), and
cyanocobalamin supplementation.
Administration of probiotics to dogs with
IBD represents a novel alternative therapeutic modality that warrants further investigation. Probiotics have also been utilized to
facilitate eradication of intestinal parasites.
A recent study documented the ability of the
probiotic organism Enterococcus faecium
SF68 (FortiFlora, Nestlé Purina) to antagonize Giardia intestinalis infection in mice.16
Oral feeding of E faecium strain SF68 starting 7 days before inoculation with Giardia
trophozoites significantly increased the production of specific anti-Giardia intestinal
IgA and blood IgG and increased CD4(+)
T cells, with associated diminution in the
number of active trophozoites in the small
intestine and decreased shedding of fecal
Giardia antigens (GSA65 protein). Probiotic administration of VSL #3 strain to dogs
with IBD has also been associated with clinical improvement and enhancement of regulatory T-cell markers [FoxP3+ cells and
transforming growth factor-β (TGF-β)+
cells] compared with a placebo-control
Intestinal Lymphangiectasia
Protein-losing enteropathy (PLE) is a syndrome caused by a variety of gastrointestinal diseases causing the enteric loss of
albumin and globulin. Intestinal inflammation, infiltration, ulceration, blood loss, and
primary or secondary lymphangiectasia
(Figure 5) are well-documented causes of
PLE. If left untreated, the final outcome of
PLE is panhypoproteinemia with decreased
intravascular oncotic pressure and the development of abdominal and pleural effusion (Figure 6), peripheral edema, and
Figure 5. Segment of jejunum from a Yorkshire
terrier showing marked erythema, lipogranulomas, and dilated lacteals visible on the serosal
surface of the bowel during an exploratory laparotomy.
Figure 6. A 3-year-old spayed female golden retriever with severe cachexia and abdominal distention secondary to ascites associated with
intestinal lymphangiectasia.
The Mysteries of the GI Tract: Demystifying Chronic Diarrhea in Dogs
death. An important sequel to PLE includes
thromboembolic disease secondary to the
loss of antithrombin. The signalment of the
animal is important as certain breeds such
as the Yorkshire terrier, soft-coated Wheaten
terrier, Norwegian lundehund, and Basenji
are predisposed to PLE. Additional abnormalities found on the serum biochemistry
profile in association with PLE include
hypocholesterolemia (secondary to malabsorption) and hypocalcemia. The multifactorial causes include hypoalbuminemia
(affects total calcium), decreased absorption
of vitamin D, and malabsorption of magnesium. Measurement of total and ionized
serum magnesium is recommended in animals with GI disease and hypocalcemia.
Moderate dietary fat restriction is one of
the most important aspects in the management of dogs with intestinal lymphangiectasia. Diets that are highly digestible and
contain less than 25% fat calories are most
commonly recommended. The author recommends the feeding of a premium commercial-based diet if possible; however, there
are a small number of dogs with severe lymphangiectasia that will need further fat restriction than that provided in commercial
diets, and home-cooked diets are warranted.
These home-cooked diets should be made
up by a veterinary nutritionist to ensure that
the diets are complete and balanced. Dogs
with concurrent IBD and lymphangiectasia
are more challenging to manage from a dietary perspective because these animals need
a novel, select protein source or hydrolyzed
diet that is also moderately fat restricted,
such as Purina Veterinary Diets HA Hypoallergenic Canine Formula (Nestlé Purina).
The current vegetarian formulation of HA
contains a soy-protein hydrolysate and contains 24% fat calories, representing a viable
dietary option for dogs with lymphangiectasia with or without concurrent IBD.
1. Comparison of common fecal flotation techniques
for the recovery of parasite eggs and oocysts. Dryden MW, Payne PA, Ridley R, et al. Vet Ther 6:15-28,
2. Accurate diagnosis of Giardia spp. and proper examination procedures. Dryden MW, Payne PA, Smith
V. Vet Ther 7:4-14, 2006.
3. Prevalence of Giardia in symptomatic dogs and cats
throughout the United States as determined by the
IDEXX SNAP Giardia test. Carlin EP, Bowman DD,
Scarlett JM, et al. Vet Ther 3:199-206, 2006.
4. Evaluation of immunofluorescence microscopy and
enzyme-linked immunosorbent assay in detection of
Cryptosporidium and Giardia infections in asymptomatic dogs. Rimhanen-Finne R, Enemark HL,
Kolehmainen J, et al. Vet Parasitol 145:345-348, 2007.
5. Comparisons of mammalian Giardia duodenalis assemblages based on the β-giardin, glutamate dehydrogenase and triose phosphate isomerase genes.
Scorza AV, Ballweber LR, Tangtrongsup S, et al. Vet
Parasitol 189:182-188, 2012.
6. Enteropathogenic bacteria in dogs and cats: Diagnosis, epidemiology, treatment, and control. Marks
SL, Rankin SC, Byrne BA, Weese JS. J Vet Intern Med
25:1195-1208, 2011.
7. Prevalence of selected bacterial and parasitic agents
in feces from diarrheic and healthy control cats from
Northern California. Queen EV, Marks SL, Farver TB.
J Vet Intern Med 26:54-60, 2012.
8. Genotypic and phenotypic characterization of
Clostridium perfringens and Clostridium difficile in
diarrheic and healthy dogs. Marks SL, Kather EJ,
Kass PH, Melli AC. J Vet Intern Med 16:533-540, 2002.
9. Evaluation of methods to diagnose Clostridium perfringens-associated diarrhea in dogs. Marks SL, Melli
AC, Kass PH, et al. JAVMA 214:357-360, 1999.
10. Ultrasonographic evaluation of gastrointestinal diseases in small animals. Penninck DG, Nyland TG,
Kerr LY, et al. Vet Radiol 31:134-141, 1990.
11. Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats.
Willard MD, Jergens AE, Duncan RB, et al. JAVMA
220:1177-1182, 2002.
12. Nutritional management of idiopathic chronic colitis in the dog. Nelson RW, Stookey LJ, Kazacos E. J Vet
Intern Med 2:133-137, 1988.
13. Dietary trial using a commercial hypoallergenic diet
containing hydrolyzed protein for dogs with inflammatory bowel disease. Marks SL, Laflamme D,
McCandlish AP. Vet Ther 3:109-118, 2002.
14. A randomized, open-label, positively-controlled
field trial of a hydrolyzed protein diet in dogs with
chronic small bowel enteropathy. Mandigers PJ, Biourge V, van den Ingh TS, et al. J Vet Intern Med
24:1350-1357, 2010.
15. Tylosin-responsive chronic diarrhea in dogs. Westermarck E, Skrzypczak T, Harmoinen J, et al. J Vet Intern Med 19:177-186, 2005.
16. Enterococcus faecium SF68 enhances the immune response to Giardia intestinalis in mice. Benjacoub J,
Pérez PF, Rochat F, et al. J Nutr 135(5):1171-1176, 2005.
17. Comparison of microbiological, histological, and
immunomodulatory parameters in response to treatment with either combination therapy with prednisone and metronidazole or probiotic VSL#3
strains in dogs with idiopathic inflammatory bowel
disease. Rossi G, Pengo G, Caldin M, et al. PLoS One
9:e94699, 2015.
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
dietary fat
restriction is
one of the
most important
aspects in the
of dogs with
Vomiting Cat Cases:
You Can Figure Them Out
Debra L. Zoran, DVM, PhD,
College of Veterinary
Texas A&M University
College Station, Texas
omiting, one of the most common reasons for cats to be
presented for evaluation, is often considered to be “normal.” There is some truth to the idea that cats vomit more
readily from eating too much or too fast; eating foods that are unusual, especially food that contains toxins; or grooming (vomiting
hair). However, such vomiting should not be routine. If it is, there is
often an underlying cause that needs to be addressed. Adult and
senior cats have different causes of vomiting than kittens do, but
there are similarities in the approach to diagnosis of vomiting in cats
of any age.
To simplify the process, it is sometimes helpful to separate the multitude of causes of vomiting into two more distinct groups: vomiting caused by diseases or disorders of the gastrointestinal (GI) tract itself or vomiting due to systemic or non-GI diseases and disorders
that trigger either peripheral or central neural pathways (Table 1). Vomiting caused by primary GI diseases includes such differentials as infectious, inflammatory, parasitic, anatomic
Vomiting Cat Cases: You Can Figure Them Out
(obstructive, trichobezoars), neoplastic (alimentary lymphoma), and drug-related or
food-related (hypersensitivity, intolerance disorders).1-3 Cats that are vomiting due to extraGI diseases may have a myriad of different
systemic problems, but endocrinopathies (eg,
hyperthyroidism), metabolic diseases (eg,
renal or liver failure), inflammatory diseases
of the liver or pancreas, cardiovascular diseases (eg, heartworm disease), central nervous system (CNS) disorders (eg, vestibular or
inflammatory CNS diseases), and neoplasia
(eg, mast cell tumors, other cancers affecting
visceral organs outside the GI tract) are the
most common.3-6
This wide spectrum of potential causes of
vomiting in cats increases the difficulty of
making a definitive diagnosis. Nevertheless,
it is important to carefully consider each of
the potential differentials to prevent the
problem from progressing to create further
problems. This article provides an overview
of the process of making a diagnosis of some
of the more common causes of vomiting in
cats and discusses the best approaches to
their treatment. Because it is an important
factor, the role of diet in both diagnosis and
treatment of vomiting is also discussed.
Primary Gastrointestinal Disease
The GI tract should always be carefully evaluated in a cat that is vomiting; however,
vomiting is not pathognomonic for gastric
or intestinal disease. Furthermore, while it
is rare for laboratory evaluation (ie, hemogram, serum biochemistry panel, urinalysis) to provide the definitive diagnosis for
primary GI disease, initial evaluation of the
vomiting cat should include a minimum
database of routine blood analysis and, if appropriate, thyroid testing, GI function testing, and viral serology––particularly in adult
or senior cats with chronic (>3 weeks) vomiting. It is important to note that these tests
may not reveal the primary problem but are
necessary to determine basic physiologic sta-
Approach to Diagnosis of Vomiting
Primary GI Causes
Extra-GI Causes
• Gastric parasitic or
infectious disease
• Gastric or intestinal
• Pancreatic disease (pancreatitis or exocrine
pancreatic insufficiency)
• Cholangitis or hepatic disease (hepatic lipidosis,
intrahepatic cholestasis, cholesterolemia, infection)
• Gastric ulcers or
• Gastric motility
• Gastric outflow
• Dietary hypersensitivity
(allergy or intolerance)
• Intestinal dysbiosis
• Mechanical or
obstructive disease
• Endocrinopathies (eg, hyperthyroidism,
diabetic ketoacidosis)
• Systemic infectious disease (eg, toxoplasmosis,
feline infectious peritonitis, fungal)
• Neoplasia (eg, lymphosarcoma, especially in
abdomen or brain, mast cell tumor)
• Heartworm/parasitic lung disease
• Acute or chronic renal disease
• Diseases of CNS, causing nausea
CNS = central nervous system, GI = gastrointestinal, IBD = inflammatory bowel disease
tus (ie, electrolyte, acid–base, fluid needs)
and rule out other systemic diseases.
GI function testing includes that of feline
pancreatic lipase immunoreactivity, feline
trypsin-like immunoreactivity, cobalamin,
and folate. These tests are important for assessing pancreatic function but also give an
indication of small intestinal health, as cobalamin and folate are important indicators of
intestinal dysbiosis or disease.
If primary GI disease is considered likely
based on physical examination, history, or
normal laboratory results, then imaging (eg,
radiographs, abdominal ultrasound) is indicated either to make a definitive diagnosis
or identify abnormalities that require further
diagnostic steps. Radiographs and abdominal ultrasound have different purposes based
on the likely differentials. If a foreign body
is suspected (eg, young cat/kitten), a radiograph is reasonable. On the other hand, if
diseases of the bowel wall or abdominal organs requiring ability to measure layers or
size are suspected (eg, inflammatory bowel
disease [adult cat]), then abdominal ultrasonography is the best approach.
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
If primary
GI disease is
likely, then
imaging is
either to make
a definitive
or identify
that require
In some cats, more invasive tests (eg, gastroduodenoscopy, exploratory laparotomy)
may be required to obtain biopsy material
or remove the problem (obstruction). The
decision to pursue endoscopy versus exploratory surgery depends on availability of
necessary equipment and expertise as well as
the likelihood that endoscopy can be a useful diagnostic or treatment tool (eg, an endoscope will not reach the mid or distal
The diagnosis
of both food
and intolerance
is based on
removing the
substance from
the diet.
Gastric Disease
Among gastric diseases to consider as causes
of vomiting are parasitic infestation (eg, with
Physaloptera or Ollanus spp), bacterial infections (eg, with Helicobacter spp), neoplastic
diseases (eg, lymphoma, adenocarcinoma,
leiomyosarcoma), inflammatory diseases (eg,
ulcers, inflammatory bowel disease [IBD]),
obstructive disorders (eg, hairballs, foreign
bodies, masses), and diet-related causes (ie, intolerance, hypersensitivity). Specific diagnosis
of individual causes may require additional
procedures (eg, histopathologic evidence of
spiral organisms deep in gastric glands associated with gastritis) to rule them in or out.
Small Intestinal Disease
Small intestinal disease in cats is a common
cause of vomiting associated with the prevalence of inflammatory disease; however, true
idiopathic IBD must be distinguished from
the simple presence of inflammatory infiltrates in the small bowel, as a variety of dietary, infectious, and parasitic agents can
cause either inflammation in the small bowel
or dysbiosis, the latter of which causes inflammation.
Dietary sensitivity and intolerance are also
important causes of vomiting in cats and
should trigger appropriate dietary trials to
rule them out. This process may be easier
said than done, as finding a commercially
available food without the offending substance (intolerance) or antigen (hypersensi-
tivity) and that the cat will readily consume
is a challenge. In most cases of small intestinal disease affecting the intestinal wall, with
the exception of adverse reactions to food,
obtaining a definitive diagnosis will require
biopsy––either via endoscopy or exploratory
Adverse Reactions/Sensitivity
to Food
Food intolerance, food allergy (hypersensitivity), food poisoning, food idiosyncrasy,
and pharmacologic reactions to foods all fall
under the category of adverse reactions to
food.7 Discussion here is limited to food intolerance and food hypersensitivity (allergy).
Food intolerance, a nonimmunologic, abnormal physiologic response to a food, nutrient, or food additive, is the most common
cause of food sensitivity in cats. Food allergy,
or hypersensitivity, is characterized by adverse reactions to a food or food additive
(typically protein) with a proven immunologic basis. Both allergy to and intolerance
of food can result in vomiting, diarrhea, or
a combination of signs, depending on the
effects: food allergy is more commonly associated with vomiting and dermatologic
signs, whereas intolerances of food can present with vomiting or diarrhea but do not
produce dermatologic signs.
Dietary Elimination Trial
The diagnosis of both food hypersensitivity
and intolerance is based on removing the offending substance from the diet. The major
difference between the diagnostic processes
of these two types of adverse food reactions
is the length of time on the diet that is required to achieve a response and the need to
identify a novel protein source. Cats with
food hypersensitivity require 8 to 12 weeks
on a novel antigen (eg, novel protein or hydrolyzed protein) elimination diet before an
improvement will be seen. Alternatively, in
cats with food intolerance, resolution of signs
Vomiting Cat Cases: You Can Figure Them Out
usually occurs within days (7–14 days is typical) of a diet change in which the offending
substance is removed, unless other factors influence the response.
A variety of commercially available and
homemade elimination formulations can be
used, as can those using hydrolyzed proteins.
Many different brands fall under the category
of “highly digestible,” "sensitive," and "novel,"
but the key is to remember that they are not all
alike. Thus, when one product from this category is not accepted by the cat, is ineffective, or
seems to make the problem worse, you cannot
assume that all products in this category will
fail. Highly digestible products from different
pet food manufacturers have a variety of formulations (Table 2), including different protein and carbohydrate sources, different levels
of fat, and various additives designed to promote intestinal health (eg, fructooligosaccharides, maltooligosaccharides, omega-3 fatty
acids, antioxidant vitamins, soluble fiber). The
same is true for hydrolyzed food products.
If one type of highly digestible food has
been fed for at least 2 weeks with minimal
response, it is entirely reasonable to try either
another comparable product from a different source or an entirely different dietary
strategy (eg, high protein/low carbohydrate,
novel antigen, hydrolyzed protein). Thus, a
dietary trial consisting of novel meat-source
proteins or hydrolyzed foods may not be adequate to remove the offending items from
the diet. For example, if the problem is being
created by presence or type of carbohydrate
in the food, feeding a formulation high in
protein (>40% metabolizable energy [ME])
and low in carbohydrates (<10% ME) that
is highly digestible (>85% digestibility of
protein) will resolve the problem.
In some cats, however, the only way to remove the source and confirm this problem is
by feeding a homemade food that consists of a
meat source (eg, cooked chicken thigh with
the fat included) and a vitamin/mineral supplement but no added carbohydrate or other
Dietary Protein Levels & Protein Sources in Selected
Highly Digestible Diets for Cats
Feline Food (dry)
Protein (% DM / Source)
Purina Veterinary Diets Feline Formula EN
56% / soy protein isolate
Hill’s Prescription Diet i/d Feline
40% / chicken meal
IAMS Veterinary Formula Intestinal
Plus Low-Residue
32% / chicken by product meal
Royal Canin Veterinary Diet Feline
Gastrointestinal High Energy HE
30% / chicken meal
DM = dry matter
ingredients. This diet eliminates carbohydrates
and all other commercial food additives and
can be fed for up to 2 to 3 weeks, but a complete and balanced food should be formulated
by a nutritionist if it must be fed longer.
The key feature that separates food intolerance from an allergy is that once the offending agent is removed from the diet, the
vomiting (or other GI signs) will resolve
quickly. Another key point is that in dietary
intolerance the offending substance may be
difficult to identify using typical commercial foods, thus a food trial using a homemade diet can be quite helpful.
The key point is that dietary management
is a process of trial and error. No single diet or
diet family will benefit all cats in all situations.
Inflammatory or ImmuneMediated Causes of Vomiting
IBD, a commonly diagnosed condition of
adult cats, is likely due to multiple causes but
ultimately culminates from a combination of
genetic susceptibility, intestinal microbial
dysbiosis, and persistent inflammation of the
gut wall, resulting in signs of vomiting, diarrhea, weight loss, or combinations of all
three.8 Idiopathic IBD is characterized by
persistent clinical signs of GI disease occurring with histologic evidence of mucosal inflammation and structural changes of the
villous epithelium without an identifiable or
correctable cause (eg, food).
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
A dietary trial
of novel
proteins or
foods may not
be adequate
to remove the
offending items
from the diet.
Studies of
probiotic therapy
in cats have
primarily focused
on the use of
Fortiflora (Purina)
in a shelter
among kittens or
young cats with
parasitic diseases
etc) or stressinduced
A number of possible causes of intestinal inflammation must be considered in the diagnostic process, and all should be investigated
thoroughly or therapeutic trials instituted
prior to settling on the diagnosis of idiopathic
IBD––a disease requiring long-term therapy
with immunosuppressive drugs. In particular,
appropriate food trials are an extremely important component of both diagnosis and
therapy of cats with suspected IBD (or GI disease in general). In addition, the diagnostic
plan for a cat with chronic vomiting should
include assessment of thyroid and feline
leukemia virus/feline immunodeficiency virus
(FeLV/FIV) status as well as intestinal vitamin
(cobalamin/folate) status.
Serum cobalamin levels in cats commonly
decrease with chronic pancreatitis or severe
bowel disease; in cats with hypocobalaminemia, inappetence or vomiting will not resolve
until replacement therapy has been instituted.9
Cobalamin therapy (250 g/cat SC weekly for
6 weeks, then once every other week) in some
cats may be lifelong, while in others once the
clinical disease resolves the supplementation
can be discontinued.
In addition, radiography and ultrasonography are important in detecting the presence of infiltrative diseases, such as feline
infectious peritonitis, granulomas, histoplasmosis, or lymphosarcoma. Ultrasonography
has been particularly helpful in identifying
intestinal wall layer changes and mesenteric
lymphadenopathy––two findings that support intestinal inflammation or disease but
do not differentiate type. Ultimately, intestinal biopsies, obtained either endoscopically
or at exploratory surgery, are essential for
both diagnosing IBD and ruling out other
specific causes of GI clinical signs.
Treating IBD
At this time, therapy of IBD in cats continues to include inflammatory suppression and
antibiotic therapy, and while evidence to support a specific role for probiotic therapy is
lacking, its use to help control dysbiosis or
IBD seems to have merit. The most effective
therapies for IBD include steroids (prednisolone or methylprednisolone, 1–2 mg/kg
q12h PO) or other drugs that interrupt the
proinflammatory pathways active in the gut.
In cats intolerant to steroids or those in which
steroids are no longer effective, immunosuppressive therapy may be necessary. Currently,
either chlorambucil or cyclosporine is most
frequently chosen.
Metronidazole (5–10 mg/kg q12h PO) or
tylosin (5–15 mg/kg q12h PO) has been effective for control of bacteria-associated disease
and continues to be recommended for initial
therapy of IBD. Whether this action can be
attributed to the antibiotic effects of these
drugs and their influence on the intestinal microflora or their immune-modulating activities is unknown. Nevertheless, such therapy is
often helpful. Caution is advised in using either drug on a continuous or long-term basis
but especially metronidazole due to its potential for genotoxicity. If needed, they should be
used intermittently, not continuously.
Studies of probiotic therapy in cats have
primarily focused on the use of Fortiflora
(Purina) in a shelter environment among kittens or young cats with parasitic diseases
(giardiasis, cryptosporidiosis, etc) or stressinduced diarrhea. Under these circumstances,
probiotic therapy resulted in a faster resolution of diarrhea and more rapid resolution of
infection. However, placebo-controlled clinical trials using probiotics in cats with IBD
are only in their early stages, so specific recommendations await their findings.
Finally, general agreement exists among
gastroenterologists that foods with fewer
carbohydrates (a source of intolerance and
maldigestion) and based on highly digestible
protein sources (primarily meat) are beneficial in cats with IBD, reducing the bacterial
changes that can occur when undigested
foods remain in the GI tract. These formulations may include so-called hypoallergenic
Vomiting Cat Cases: You Can Figure Them Out
diets but do not necessarily require hypoallergenicity. A
scoring system that can be
used in monitoring response
to treatment of IBD as well as
to assist in diagnosis in cats in
which IBD is suspected has
been published by Albert Jergens et al.8
Extraintestinal Causes
of Vomiting: Feline
Pancreatitis &
Management of Feline Vomiting
acute from chronic
(>3 wk)
Physical exam
Foreign body
Endoscopy or
Laboratory data
(CBC, serum biochemistry panel, UA
GI panel, FeLV/FIV, T4, HW, fecal, etc)
Nonspecific cause
(radiographs, US)
Specific cause
- Renal
- Infectious
- Liver
- Pancreas
- Endocrine
(DM, Addison's, thyroid disease)
- Cancer
- Heartworm
Foreign body
(biopsy) or
Specific & supportive therapy
Feline pancreatitis is difficult
Symptomatic/Supportive Therapy
Specific Therapy
to diagnose definitively anteIV fluids
Blood transfusion
DM = diabetes mellitus, FeLV = feline leukemia virus,
mortem, especially in its more
FIV = feline immunodeficiency virus, HW = heartworm,
T = thyroxine, UA = urinalysis, US = ultrasonography
common lymphoplasmacytic
Insulin or specific drugs
form, and is associated with
vomiting only occasionally or
intermittently.4,10 This difficulty is partly attributable to lack of both
of cats to hide overt signs and the apparent
specific clinical signs in cats and a highly
response of cats given pain relief medication.
sensitive test for diagnosis of the disease.
Thus, clinical signs may be quite variable,
The clinical signs of pancreatitis in cats can
and this must be taken into consideration
be quite different from those in dogs. Acute
with each patient.
necrotizing pancreatitis is frequently encounRoutine evaluation of vomiting cats with
tered in obese dogs fed a high-fat diet, while
suspected pancreatitis or other extra-GI causes
cats are more likely to be underweight and
of vomiting is similar to that mentioned above:
high-fat diets do not appear to be an impora minimum database, GI function testing, and
tant predisposing factor. Cats of all ages, sexes,
retroviral testing are always appropriate. Tests
and breeds are affected, although Siamese cats
for hyperthyroidism, liver function, or other
reportedly have the more acute, necrotizing
specific tests may be indicated in some cats.
form of pancreatitis more frequently.
Hematologic findings in cats with panThe most common form in cats, lymcreatitis are nonspecific but may include
phoplasmacytic pancreatitis, is more insidinonregenerative anemia, leukocytosis, or
ous, and the clinical signs are vague, with
leukopenia (less common). In a recent study,
the most common being lethargy (100% of
cats with pancreatitis consistently had elevated
cats in one study), anorexia, and dehydrawhite blood cells (20,300/L) and mild detion.11 Vomiting and anterior abdominal
creases in platelets (mean, 180,000/L). Neutrophils were not degenerate or toxic. Reported
pain, which are common clinical signs in
changes in the serum biochemistry profile indogs with acute pancreatitis, occur in only
clude elevated serum alanine aminotransferase
35% and 25% of cats, respectively. How(ALT), elevated serum alkaline phosphatase
ever, there is strong belief among feline prac(ALP), hyperbilirubinemia, hyper- or hypotitioners that pancreatic pain or discomfort
cholesterolemia, hyperglycemia, azotemia, and
may be underreported due to the tendency
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
In cats with
pancreatitis, it
is still necessary
to evaluate the
historical, physical
and laboratory
data as well
as imaging
along with the
fPLI results, when
making a
hypokalemia. Common abnormalities in cats
with severe pancreatitis were hyperglycemia
(180 mg/dL), hyperbilirubinemia (2.5 mg/dL),
hypocholesterolemia (130 mg/dL), and hypoalbuminemia (1.8 g/dL).
In cats with mild or lymphoplasmacytic
pancreatitis, liver enzyme elevations were
more common, with γ-glutamyl tranferase,
ALP, and ALT being moderately elevated.
Hypocalcemia is less commonly observed
but, when present, may be a poor prognostic sign seen in cats with severe pancreatitis
or multiple-organ dysfunction. Serum lipase
may be increased early in acute pancreatitis,
but in a recent study, amylase and lipase
were found to be of little diagnostic value in
distinguishing normal cats from those with
pancreatitis. There are no changes in the urinalysis consistently observed or specific for
pancreatitis in cats.
The feline trypsin-like immunoreactivity
(fTLI) test is the definitive test for diagnosis
of exocrine pancreatic insufficiency. While an
increase in fTLI can be found in cats with
pancreatitis, a normal value does not rule out
pancreatitis, as the leakage of enzymes tends
to decrease rapidly following an event and the
enzymes are inactivated and scavenged by the
body’s peptidases (eg, macroglobulin) within
12 to 24 hours following an acute insult. This
test is very useful in cats with chronic pancreatitis, however, as they may sustain a loss of
pancreatic function, indicated by a decreased
fTLI. In fact, in a recent unpublished study
by the author's group of 150 cats with exocrine pancreatic insufficiency tested at the
Texas A&M GI laboratory, the most common clinical sign was weight loss (85%) not
diarrhea (45%) or vomiting. Thus, measurement of fTLI is an important aspect of assessment in cats with chronic low-grade
inflammation of the pancreas that may not
have overt signs of inflammation or illness
but have lost significant pancreatic functional
The test of choice for pancreatic leakage
is the radioimmunoassay for feline pancreatic lipase (fPLI); this test has a sensitivity
and specificity of nearly 100% in cats with
severe pancreatitis (determined by pancreatic biopsy).12 However, the sensitivity in
moderate pancreatitis was found to be 80%
and as low as 65% in mild pancreatitis,
while the specificity in healthy cats was
75%. Thus, in cats with suspected chronic
pancreatitis, it is still necessary to evaluate
the combined historical, physical examination, and laboratory data as well as imaging
information, along with the fPLI results,
when making a diagnosis.
Imaging Studies
Imaging studies are frequently used to help
identify cats with acute pancreatitis, but in
those cats with the more common chronic
form, changes on ultrasound imaging can be
particularly subject to interpretation and operator expertise. The most common ultrasonographic findings are hypoechoic pancreas,
hyperechoic mesentery, mass effect, dilated
common bile duct, or normal appearance
throughout. In a recent study, mild pancreatitis was still shown to be difficult to diagnose via abdominal ultrasound imaging, but
ultrasound was 80% sensitive and 88% specific in cats with moderate to severe pancreatitis.13
The most reliable method for making an
accurate diagnosis of pancreatic disease remains direct visualization and histopathology. This approach can be expensive and can
increase the risk for complications (during
anesthesia/surgery). In cases with focal involvement, which is common with chronic
pancreatitis, lesions may be missed. In short,
pancreatitis remains a challenging diagnosis
and an even more challenging disease to
treat once the diagnosis has been confirmed.
Feline Liver Diseases (Cholangitis,
Idiopathic Hepatic Lipidosis)
Cats have four major types of liver disease:
Vomiting Cat Cases: You Can Figure Them Out
hepatic lipidosis, cholangiohepatitis complex, infectious hepatitis (eg, feline infectious
peritonitis, toxoplasmosis, fungal/parasitic
hepatitis), and neoplastic liver disease (eg,
lymphoma). As with most diseases of the
liver, histopathology is an important step in
determining treatment and prognosis. Nevertheless, once a diagnosis has been obtained,
the goal for treatment of cats with liver disease is to provide optimal nutritional and
pharmacologic support that maximizes liver
function; minimizes future liver or biliary
duct damage or scarring; controls concurrent
clinical signs, such as vomiting; and thus
promotes a high quality of life.
Inflammatory, infectious, or metabolic
liver disease can be present in cats with few
external clinical signs other than inappetence, vomiting, or lethargy or can cause severe illness resulting in development of
ascites, icterus, hepatoencephalopathy, coagulopathy, and loss of ability to metabolize
protein or carbohydrates appropriately.
Thus, there is no single set of clinical signs
or laboratory abnormalities that can define
all liver disease patients. Nevertheless, some
important clues can help guide the clinician
to making a definitive diagnosis.
The most common cause of severe liver disease or failure in the cat is idiopathic hepatic
lipidosis, but the most common cause of increased liver enzymes and chronic intermittent
clinical signs is cholangitis/cholangiohepatitis.
In several recent studies using biopsy results to
confirm diagnosis, cats with inflammation of
the peribiliary structures consistent with
cholangitis also had lymphoplasmacytic infiltrate in the pancreas (66%–75% in separate
studies).13,14 Thus, there is growing evidence
that these two diseases in cats may be linked:
when one occurs, the other follows. At this
time, there is no agreement about cause; however, there is some evidence that bacteria may
be an important culprit, as bacterial DNA was
found in at least 30% of livers with a neutrophilic inflammatory component.15 Con-
versely, in another article, no bacterial DNA
was found, but the majority of study cats had
the more chronic lymphocytic form of the disease.16 Whether this dichotomy represents two
separate diseases or different stages/phases of
the same disease (acute progressing to chronic)
is unknown, but it suggests that further work
to better control and define the origin of intestinal dysbiosis in cats is warranted.
Finally, a number of other important extraGI causes of vomiting also need to be considered, including chronic renal disease,
endocrinopathies (eg, hyperthyroidism, diabetic ketoacidosis), and other systemic diseases
(eg, heartworm disease). A complete discussion of each is not possible, but readers are reminded to consider these possibilities when
confronted with vomiting cats for which a definitive diagnosis has not been made.
Nonspecific Therapy of Vomiting
Several antiemetic agents are available for use
in cats (Table 3); some are more commonly
used in the hospital setting because they are
injectable and may require frequent administration. The newest antiemetic drug family, neurokinin (NK) inhibitors, represented
by maropitant, are clearly the most effective
in cats. In addition to the excellent antinausea effects of maropitant, it also appears to
be effective for controlling visceral pain,
which may be an essential aspect of therapy
in feline chronic pancreatitis and other visceral causes of vomiting. The feline dose is 1
to 2 mg/kg PO or SC q24h for 3 to 5 days,
but it may be given longer if needed.
The 5-HT3 antagonists are effective
antiemetic agents for cats as well at doses of
0.5 to 1.0 mg/kg of ondansetron, 0.1 to 0.5
mg/kg of granisetron, or 0.5 to 1.0 mg/kg of
dolasetron PO or IV q12–24h. In addition,
cats may be treated with chlorpromazine, an
α2-adrenergic antagonist, at 0.2–0.4 mg/kg
q8h SC or IM. Dopaminergic antagonists
such as metoclopramide are less effective
in the cat and, because they antagonize
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
In addition to
the excellent
effects of
maropitant, it
also appears
to be effective
for controlling
visceral pain,
which may be
an essential
aspect of
therapy in
feline chronic
and other
visceral causes
of vomiting.
Feline Doses for Antiemetic Drugs
Drug Class
Location of Action
α2-Adrenergic antagonists
Central (CRTZ/vomiting center)
0.1–0.5 mg/kg q8h SC
0.2–0.4 mg/kg q8h SC
D2 dopaminergic antagonists
Central (CRTZ) and peripheral
(GI smooth muscle)
0.2–0.4 mg/kg q6–8h SC
H1 histaminergic antagonists
Central (CRTZ)
0.2–0.4 mg/kg q8h SC
2–4 mg/kg q8–12h SC
2–4 mg/kg q8–12h SC
5-HT3 serotonergic antagonists
Central (CRTZ/vomiting center);
peripheral (vagal afferents)
0.5–1.0 mg/kg q12–24h PO, IV
0.1–0.5 mg/kg q12–24h PO, IV
0.5–1.0 mg/kg q12–24h PO, IV
5-HT4 serotonergic antagonists
Peripheral (myenteric neurons)
1.25–2.5 mg/cat q8–12h PO
NK1 neurokinin antagonists
Central (CRTZ/vomiting center)
1–2 mg/kg q24h PO, SC
CRTZ = chemoreceptor trigger zone
While nonspecific
therapy may be
indicated to
control vomiting,
finding the cause
is more important
than simply
controlling the
clinical sign.
dopamine, may potentially reduce pancreatic blood flow. (This effect has not been
proven in cats with pancreatitis.)
While such nonspecific therapy may be
indicated to control vomiting, finding the
cause is more important than simply controlling the clinical sign. Thus, antiemetic
therapy should be used judiciously in the
clinical setting and as an adjunct to therapy
for the primary problem.
1. Adverse reactions to foods: Allergies versus intolerance. Roudebush P. In Ettinger SJ, Feldman EC (eds):
Textbook of Veterinary Internal Medicine, ed 6––St
Louis, MO: Elsevier, 2005, p 153.
2. Feline intestinal lymphoma. Richter K. Vet Clin
North Am Small Anim Pract 33:1083-1098, 2003.
3. Acute and chronic vomiting. Simpson KW. In BSAVA
Manual of Canine and Feline Gastroenterology, ed 2––
Gloucester, UK: British Small Animal Veterinary Association, 2005, pp 73-78.
4. Pancreatitis in cats: Diagnosis and management of a
challenging disease. Zoran DL. JAAHA 42:1-9, 2006.
5. Medical management of hyperthyroidism. Trepanier
LA. Vet Clin North Am Small Anim Pract 37:775-788,
6. Vomiting. Washabau RJ. In Canine and Feline Gastroenterology, 1st ed—St. Louis, MO: Elsevier, 2013, pp
7. Adverse food reactions. Cave N. In Canine and Feline
Gastroenterology, 1st ed—St Louis, MO: Elsevier, 2013,
pp 398-407.
8. Clinical staging of inflammatory bowel disease. Jergens AE, Crandall JM. In August JR (ed): Consultations
in Feline Internal Medicine, vol 5––St Louis, MO: Elsevier, 2006, p 127.
9. Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease.
Simpson KW, Fyfe J, Cornetta A, et al. J Vet Intern Med
15:26-32, 2001.
10. Prevalence and histopathologic characteristics of
pancreatitis in cats. DeCock HE, Forman MA, Farver
TB, Marks SL. Vet Pathol 44:39-49, 2007.
11. Evaluation of feline pancreatic lipase immunoreactivity and helical computed tomography versus conventional testing for the diagnosis of feline
pancreatitis. Forman MA, Marks SL, DeCock HE, et
al. J Vet Intern Med 18:807-810, 2004.
12. Ultrasonography of the normal feline pancreas and
associated anatomic landmarks: A prospective study
of 20 cats. Etue SM, Penninck DG, Labato M, et al.
Vet Radiol Ultrasound 42:330-336, 2001.
13. Clinical features of inflammatory liver disease in
cats: 41 cases (1983-1993). Gagne JM, Armstrong PJ,
Weiss DJ, et al. JAVMA 214:513-516, 1999.
14. Feline cholangitis: A necropsy study of 44 cats
(1986-2008). Clark JE, Haddad JL, Brown DC, et al.
J Feline Med Surg 13:570-575, 2011.
15. Culture independent detection of bacteria in feline
inflammatory liver disease. Twedt DC, Janeczko SD,
et al. J Vet Intern Med 23:729, 2009.
16. Histopathologic features, immunophenotyping,
clonality, and eubacterial fluorescence in situ hybridization in cats with lymphocytic cholangitis/
cholangiohepatitis. Warren A, Center S, McDonough
S, et al. Vet Pathol 48:627-641, 2011.
Suggested Reading
Clinical differentiation of acute necrotizing from chronic
nonsuppurative pancreatitis in cats. Ferreri J, Hardam
E, Kimmel SE, et al. JAVMA 223:469-474, 2003.
Vomiting Cat Cases: You Can Figure Them Out
Nutrition for Senior Dogs: New
Tricks for Feeding Old Dogs
Julie A. Churchill,
College of Veterinary
University of Minnesota
St. Paul, Minnesota
enior dogs commonly present to veterinarians for primary care
and represent approximately one third of the pet dog population.1 Life spans are increasing and thus both the percentage
and the age of elder dogs may be increasing.2 Pet owners perceive
that most pets, including senior dogs, are healthy and do not require
a therapeutic food,3 but they are still left with hundreds of pet foods
from which to choose. Advice and information recommending the
best food is available almost anywhere—from trainers to pet food retailers, from magazines, internet sources, and social media. It is important to remember, however, that there is no established AAFCO
nutrient profile for a “senior” life stage; thus the nutrient content of
products marketed for senior pets varies widely. This makes it even
more critical for the veterinary health care team to play an active
role in providing credible nutritional advice, especially for senior dogs
that have unique nutritional concerns.
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
changes that
occur in middleaged and senior
dogs make them
less tolerant of
deficiencies or
The point at which a dog progresses from
adult to a senior or geriatric life stage is variable
and subjective. Life expectancies vary widely
among dogs depending on breed and body
size. Aging changes can also be variable, including loss of senses (hearing or vision), reduced energy requirements and lean body
mass, as well as a decline in various organ functions. The American Animal Hospital Association (AAHA) Senior Care Guidelines suggest
that, with the exception of large-breed dogs,
most dog breeds reach middle age by 7 to 8
years of age and should be considered seniors
when they reach the last 25% of the predicted
life span for their breed.4 Despite this arbitrary
categorization, physiologic changes that occur
in middle-aged and senior dogs make them
less tolerant of nutritional deficiencies or excesses. Middle-aged dogs are “at risk” or more
vulnerable to age-related health problems.
Middle age may bring an increasing incidence
of chronic diseases, many of which can be influenced by nutritional management.5 A vital
component of preventive medical care thus
Initial Screen: Assessing for Nutritional Risk Factors
History of:
Treats/snacks/human foods >10%
Inadequate information/inappropriate feeding/food
Unconventional diets
Previous/ongoing medical problems
GI signs
Life stage needs
Time of spay/neuter
Any abnormal BCS (≠5/9)
Any MCS <3
Unintentional weight loss OR gain
New medical condition
Poor skin/hair coat
Dental disease
Adapted from Table 2, AAHA Nutrition Assessment Guidelines
BCS = body condition score
MCS = muscle condition score
Requires extended
evaluation if (✔)
should include a “senior” screen or health risk
assessment for early detection of health problems and adjustments to care to prevent or
slow onset of age-related diseases. Every senior
health screen should include a thorough nutritional assessment followed by an individualized nutritional recommendation.
Before any diet changes are recommended,
a nutritional evaluation should be performed. Each nutritional assessment and
recommendation should include three components: the patient, the diet, and feeding
management factors.6 An accurate diet history is invaluable when assessing the nutritional health of the patient and will be vital
to formulating an individualized diet plan.
Understanding the nutritional changes that
occur with aging and identifying any
changes in the individual patient can help
the clinician better match the appropriate
food with the patient’s unique needs. The
patient, the food, and the pet owner’s feeding practices are interrelated and require reassessment. Health and nutritional status are
not static, especially in senior pets, but
rather a dynamic process worthy of continued reevaluation and treatment modifications to match changing needs of the pet.
Patient Assessment
An initial assessment of the patient can be
done quickly and utilizes information collected as part of a health assessment: a complete medical and diet history and a
thorough physical examination and appropriate lab work (eg, complete blood count,
serum biochemical profile, urinalysis). The
nutritional screening process (Table 1) can
quickly identify patients with “nutritional”
risks. Healthy seniors (those without identified risks) that are eating a nutritionally balanced diet, have a healthy body weight,
good body and muscle condition scores
(BCS, MCS), and are free of significant
Nutrition for Senior Dogs: New Tricks for Feeding Old Dogs
physical or laboratory abnormalities need no
further evaluation at this time. A pet-specific nutrition assessment and recommendation for healthy seniors can be done
quickly. Nutritional recommendations
should include the specific name of food
that matches the pet’s current nutritional
needs, the amount and frequency for feeding, and a monitoring plan. In many of
these patients, the feeding recommendation
involves little or potentially no change, but
should include a verification and validation
for the owner that the current food and
feeding plan meets the pet’s needs, and a
documentation of the current feeding plan
in the medical record.
If nutritional risk factors or age-related problems are identified, an extended evaluation
and management plan is indicated (Table 2).
This in-depth evaluation should address some
common age-related conditions that may be
influenced by nutritional management:
• Weight management: achieve
or maintain a healthy body weight
• Osteoarthritis
• Cognitive dysfunction
Diet Assessment
A complete diet history is important for evaluating the pet’s current nutritional status. Ideally, the animal’s exact diet (brand and
amounts eaten) should be obtained as well as
all snacks, treats, and nutritional supplements
by type and amount. The drug/supplement
history should include questions about the use
of food to administer medication, as it may
comprise a significant portion of the dog’s intake. Diet history information combined with
the patient assessment provides information
about the patient’s daily caloric requirements
and specific nutrient intake, which should be
compared with the patient’s individual needs.
For example, an overweight pet with a robust
appetite should not be fed a calorie-dense
Extended Screening: Assessing Senior Dogs
for Nutritionally Relevant Age-Related Factors
Abnormal body condition
• Is this pet overweight or underweight?
• Is the pet eating appropriate amounts of a balanced diet?
• Assess appetite and intake
• Assess ability to eat: prehension, mastication, swallowing for those
underweight and/or with poor intake
• Assess sensory input: smell, vision, palatability of food. Consider
palatability enhancer if necessary
Mobility and access to food and water
• Is the pet able to walk? Access to food provided? Able to stand to eat?
• Other pets or physical limitations impairing access?
Mobility and exercise
• Is the pet’s MCS normal (3/3)?
• Presence of osteoarthritis, lameness, pain? These play a role in
maintenance of comfort, fitness, and healthy BCS
• Activity minimizes sarcopenia
• Exercise and activity provide mental stimulation and environmental enrichment
Cognitive function assessment
• Disorientation/confusion: becomes lost or confused, fails to recognize
familiar people?
• Changed interactions with family members? Isolates or seeks
attention less often?
• Change in sleep/activity cycles? Wanders or paces, sleeps more in day,
less at night?
• Loss of house training (nonmedical reasons)
BCS = body condition score
MCS = muscle condition score
product. Reducing the amount of a high-calorie product could lead to deficiencies of other
essential nutrients and increase hunger or undesirable food-seeking behaviors.
Feeding Management Assessment
Feeding practices and preferences influence
a pet’s intake. Determine whether other pets
present competition or limit access to food.
Determine whether food is accurately measured, how much / how often food is offered,
and how much is eaten. Determine if there
have been recent changes to the feeding plan
and why, as well how the pet accepted those
changes. This information will allow the veterinary team to determine the nutritional
adequacy of the current diet, as well as help
identify factors that could contribute to potential success or problems with adherence
to a new recommendation.
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
If no adjustments
are made to the
pet’s energy
intake to account
for the reduction
in LBM, activity,
and MER, then
the senior pet will
gain weight and
the risk for obesity
will increase.
Reassessment and
Modification of Treatment Plan
Nutritional assessment of senior pets is an
ongoing process. Dogs experience a variable
and wide variety of metabolic changes as
they age. It is important to communicate
and engage pet owners to create the expectation of continued reassessment and treatment modifications that accommodate the
specific changes observed in each individual
dog rather than adopting a “senior” protocol. A vigilant monitoring plan allows early
detection of problems if they arise and a better opportunity to intervene or modify the
pet’s individualized nutritional plan to improve its health. Partner with clients to help
ensure success and maintain adherence to
the feeding and monitoring goals.
Aging results in changes to both structure and
function of the gastrointestinal (GI) tract;
however, no studies report clinically relevant
differences in nutrient absorption between
young adult and geriatric dogs.7 Maintenance
energy requirement (MER) is defined as the
energy required to keep an animal in a “maintenance state,” or maintaining a normal activity. MER varies depending on factors such as
breed, health, neuter status, and age. As dogs
age, MER decreases ~25%, with the greatest
decrease at middle age (7 years).8 Loss of lean
body mass (LBM) appears to be the primary
factor influencing the reduction in energy requirements.9 Lean body mass accounts for
about 96% of an animal’s basal energy expenditure.10 Aging dogs are less active, which also
contributes to reduced LBM and MER. If no
adjustments are made to the pet’s energy intake to account for the reduction in LBM, activity, and MER, then the senior pet will gain
weight and the risk for obesity will increase.
Body condition score should be closely monitored in older dogs to prevent obesity because
unhealthy weight gain exacerbates many agerelated conditions. A higher protein to calorie
ratio diet would be beneficial to promote ideal
weight maintenance in senior pets identified
at risk for obesity.11 Results from Purina’s lifetime study revealed lower disease incidence,
later onset of disease, and increased life span in
calorically restricted dogs. Dogs fed a 25% reduction compared with controls lived an average of 13.0 years compared with 11.2 years.12
Maintaining energy balance and avoiding unhealthy weight gain is one of the most important goals for senior dogs.
Elder humans exhibit decreased thirst and
drinking when challenged by fluid deprivation.
Although not confirmed in dogs, a similar response is expected.5 Thus water intake should
be monitored or ensured when elder dogs are
exercising or exposed to hot environments.
Senior dogs may also be at risk for dehydration
if they have subclinical renal insufficiency.
When a senior pet’s appetite is good but water
intake is suspect, add water to the food to ensure adequate intake and hydration.
Protein requirements increase with age due
to increased protein turnover and reduced
protein synthesis.13,14 Healthy senior dogs do
not benefit from protein restriction15 and
may be harmed by limiting dietary protein.16 Protein restriction of seniors could be
more detrimental than protein deficiency in
younger animals.17 As a general guideline for
estimating minimum daily protein needs,
provide 2.55 g protein per kg body weight
(BW) or ~1 g protein per lb BW.13,17-19 This
level of protein intake should minimize risk
for protein deficiency. Senior dogs, however,
may need up to 50% more than this.13
Older dogs also require fewer calories, or less
food, than younger dogs. Diets for older
dogs should not only contain fewer calories
but more protein or a higher protein:calorie
Nutrition for Senior Dogs: New Tricks for Feeding Old Dogs
ratio to meet age-related nutritional needs.
Based on the diet history, assure the dog is
meeting minimum daily protein needs (~1 g
protein/lb BW minimum). Food with 25% of
calories from quality protein should meet the
needs of most healthy aged dogs and minimize
loss of LBM. Assess MCS to monitor LBM.
Although the most common age-related conditions are best managed with a multimodal
approach combining nutritional strategies,
exercise or environmental enrichment, and
possible medical management, this discussion
focuses on nutritional management.
Hyperadiposity, the most prevalent form of
malnutrition, contributes to many of the
diseases linked with obesity.21-23 Still, pets
that are overweight go unrecognized or may
not have this health concern addressed.
Based on the canine life span study,12 which
demonstrated many negative health consequences of being overweight, weight management should remain a top priority for
senior pets. Yet it remains one of the most
significant health problems among middleaged and elder dogs. Monitor the pet’s diet,
BW, BCS, and MCS at each visit. Once excess weight is diagnosed, action should be
taken to achieve healthy BW and BCS. Creating a negative energy balance promotes
weight loss. This is best achieved by feeding
low-calorie foods with increased protein
content and increased nutrient:calorie ratio to
assure adequate intake of essential nutrients.
Degenerative Joint Disease
Osteoarthritis (OA) affects as many as 20%
of dogs and obesity is recognized as a primary risk factor.24 Nutritional strategies for
OA include the following:
• Weight and Muscle Management Loss
of excess body weight/fat can improve clinical signs of lameness in arthritic dogs.25
Strategies to maintain healthy body weight,
BCS, and LBM and prevent sarcopenia
should be prioritized for senior dogs. This
can be achieved by selecting a complete
and balanced diet that meets protein and
other nutrient needs while providing the
amount of calories to prevent excess body
fat gain. The goal is to delay onset / prevent progression of OA.
• Long Chain Omega-3 Fatty Acids (n-3)
show the greatest evidence for synovial antiinflammatory effects26,27 compared with
other nutraceuticals. Marine oils (eicosapentaenoic acid [EPA] > docosahexaenoic acid
[DHA])28 are preferred with more effective
antiinflammatory effects compared with
shorter-chain flax or other plant-source n-3
oils. There is no standard accepted dose.
Cognitive Dysfunction
As many as 20% to 68% of middle-aged to
elderly dogs experience cognitive dysfunction or behavioral changes, which can manifest in varying degrees of mental decline29
(see Table 2). Nutraceuticals may have potential use both in prevention and treatment, but are best when combined with
environmental enrichment.30-32
• Antioxidants The brain is especially susceptible to free radical damage and cognitive
dysfunction. Multiple studies have shown
improved clinical signs of age-related cognitive changes in dogs fed antioxidant-enriched
diets or supplements.30-32
• Medium Chain Triglycerides (MCTs)
Supplementation with MCTs has been
shown to improve cognitive performance
and preserve brain structure of elder dogs.
MCTs provide an alternative cerebral energy
source by way of ketones without restricting
dietary carbohydrate or proteins.34,35
• Supplements versus Enriched Diets One
caveat for using nutraceutical supplementa-
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
As many as 20%
to 68% of middleaged to elderly
dogs experience
dysfunction or
changes, which
can manifest in
varying degrees
of mental
tion is that that these supplements have not
been adequately assessed for efficacy, optimal
doses, or nutrient interactions. When considering a diet containing the supplement or
prescribing a supplement, assess the nutrient
composition of the “base diet.” Confirm that
the base diet meets the macronutrient needs
of the patient and that it will provide an adequate dose of the intended supplement as
fed. If not, it would be prudent to select a
more appropriate diet and give the intended
dose of supplement.
When considering
a diet containing
the supplement
or prescribing
a supplement,
assess the nutrient
composition of
the “base diet.”
1. Banfield Pet Hospital State of Pet Health Report (2013).
Accessed September 1, 2014 from
2. Total pet ownership and pet population. US Pet Ownership & Demographics Sourcebook. Schamburg, IL: American
Veterinary Medical Association. AVMA Membership &
Field Services, 2012, pp 1-49.
3. Pet feeding practices among dog and cat owners in the
United States and Australia. Laflamme DP, Abood SK,
Fascetti AJ, et al. JAVMA 232:687-694, 2008.
4. AAHA Senior Care Guidelines for Dogs and Cats. Epstein M, Kuehn NF, Landsberg G, et al. JAAHA 41:81-91,
5. Age-related changes in nutrient utilization by companion animals. Fahey GC, Barry KA, Swanson KS. Annu Rev
Nutr 28:425-445, 2008.
6. AAHA Nutritional Assessment Guidelines for Dogs and
Cats. Baldwin K, Bartges J, Buffington T, et al. JAAHA
46:285-296, 2010.
7. Nutrition of aging dogs. Larsen JA, Farcas A. Vet Clin
Small Anim Pract 44:741-759, 2014.
8. Effect of age on maintenance energy requirements and
apparent digestibility of canine diets. Laflamme DP, Martineau B, Jones W, et al. Compend Contin Educ Pract Vet
22(suppl 9A);113, 2000.
9. Factors influencing lean body mass in aging dogs. Kealy
RD. Compend Contin Educ Pract Vet 21:34-37, 1998.
10. The inter-organ flux of substrates in fed and fasted man,
as indicated by arterio-venous balance studies. Elia M.
Nutr Res Rev 4:3-31, 1991.
11. AAHA Weight Management Guidelines for Dogs and
Cats. Brooks D, Churchill J, Fein K, et al. JAAHA 50:1-10,
12. Effects of diet restriction on life span and age-related
changes in dogs. Kealy RD, Lawler DF, Ballam JM, et al.
JAVMA 220:1315-1320, 2002.
13. Determination of optimal dietary protein requirements
of young and old dogs. Wannemacher RW Jr, McCoy JR.
J Nutr 88:66-74, 1966.
14. Age-related changes in protein synthesis. Richardson A,
Birchenall-Sparks MC. Rev Biol Res Aging 1:255-273,1983.
15. The influence of dietary protein, lipid, phosphorus and
sodium on renal structure and function in geriatric dogs.
Churchill J, PhD thesis. Department of Veterinary Clinical
Sciences, College of Veterinary Medicine, University of
Minnesota, St Paul, MN, 2001.
16. Effect of moderate protein deficiency on immune function. McMurray DN. Compend Contin Educ Pract Vet
21:21-24, 1999.
17. Nutrition for aging cats and dogs and the importance of
body condition. Laflamme DP. Vet Clin North Am Small
Anim Pract 35:713-742, 2005.
18. Survey of opinions about nutritional requirements of
senior dogs and analysis of nutrient profiles of commercially available diets for senior dogs. Hutchinson D,
Freeman L, Schreiner K, et al. Intern J Appl Res Vet Med
9(1):68-70, 2011.
19. Nutrient Requirements of Dogs and Cats. National Research Council. The National Academies Press. Washington, DC, 2006, p 119.
20. Beneficial effects of dietary mineral restriction in
dogs with marked reduction of functional renal mass.
Brown SA, Crowell WA, Barsanti JA, et al. J Am Soc
Nephrol 1:1169-1179, 1991.
21. The effects of obesity-associated insulin resistance on
mRNA expression of peroxisome proliferator-activated
receptor-γ target genes, in dogs. Gayet C, Leray V, Saito
M, et al. Br J Nutr 98:497-503, 2007.
22. Comparison of adipokine concentrations and markers
of inflammation in obese versus lean dogs. Eirmann LA,
Freeman LM, Laflamme DP, et al. Intern J Appl Res Vet Med
7:196-205, 2009.
23. Improvement in insulin resistance and reduction in
plasma inflammatory adipokines after weight loss in
obese dogs. German AJ, Hervera M, Hunter L, et al. Dom
Anim Endocrinol 37:214-226, 2009.
24. Osteoarthritis and body weight. Foye PM, Stitik TP, Chen
B, et al. Nutr Res 20:899-903, 2000.
25. Effect of weight reduction on clinical signs of lameness
in dogs with hip osteoarthritis. Impellizeri JA, Tetrick MA,
Muir P. JAVMA 216:1089-1091, 2000.
26. Effects of different n6:n3 fatty acid ratio diets on canine
stifle osteoarthritis. Bartges JW, Budsberg SC, Pazak HE.
Orthopedic Research Society 47th Annual Meeting, 2001.
27. Effects of feeding a high omega-3 fatty acids diet in dogs
with naturally occurring osteoarthritis. Moreau M,
Troncy E, Del Castillo JR, et al. J Anim Physiol Anim Nutr
(Berl) 97:830-837, 2012.
28. Dietary eicosapentaenoic acid and docosahexaenoic acid
equally incorporate as decosahexaenoic acid but differ
in inflammatory effects. Sierra S, Lara-Villoslada F, Comalada M, et al. Nutrition 24:245-254, 2008.
29. Prevalence and risk factors for behavioural changes associated with age-related cognitive impairment in geriatric dogs. Zakona G, Garcia-Belenguer S, Chacon G, et al.
J Small Anim Pract 50:87-91, 2009.
30. BDNF increases with behavioral enrichment and an antioxidant diet in aged dog. Fahnestock M, Marchese M,
Head E, et al. Neurobiol Aging 33(3):546-554, 2012.
31. Synergistic effects of long-term antioxidant diet and behavioral enrichment on beta-amyloid load and nonamyloidogenic processing in aged canines. Pop V, Head
E, Hill MA, et al. J Neurosci 30:9831-9839, 2010.
32. Nutritional management of brain aging in dogs. Roudebush P, Zicker SC, Cotman CW, et al. JAVMA 227:722728, 2005.
33. Enhancing brain functions in senior dogs: A new nutritional approach. Pan Y. Topics in Comp Anim Med
26:1,10-16, 2011.
34. Dietary enrichment with medium chain triglycerides
(AC-1203) elevates polyunsaturated fatty acids in the
parietal cortex of aged dogs: Implications for treating
age-related cognitive decline. Taha AY, Henderson ST,
Burnham WM. Neurochem Res 34:1619-1625, 2009.
35. Dietary supplementation with medium-chain TAG has
long-lasting cognition-enhancing effects in aged dogs.
Pan Y, Larson B, Araujo JA, et al. Br J Nutr 103:1746-1754,
Nutrition for Senior Dogs: New Tricks for Feeding Old Dogs
Pet Food Myth Busters:
Answering Common
Questions Owners Ask
About Pet Food
Lisa M. Freeman,
Cummings School of
Veterinary Medicine
Tufts University
North Grafton, Massachusetts
any owners make decisions about pet foods based not
on fact, but on the many current myths and misconceptions that prevail. The first step to dispelling pet food myths
is to be aware of what your patients are eating.
A complete diet history for every patient at every visit is important for a number of reasons.
Knowing what a patient is eating can help to diagnose health concerns—for example, if owners are feeding an unbalanced homemade or vegetarian diet; foods with potential hazards, such
as raw meat diets (or other raw products, such as rawhides, bully sticks, or freeze-dried treats);
commercial diets that are not nutritionally complete and balanced; or diets manufactured by
companies with questionable nutritional and quality control protocols. The diet history also
can help to determine whether the current diet is optimized for maintaining health or, in the
case of animals with medical conditions, for helping to manage disease.
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
Providing reliable
nutrition resources
and helping
understand how
to make more
decisions about
what they read or
hear can help to
ensure their pets
are receiving
optimal nutrition.
In addition to collecting information on the
animal’s current diet, which includes the pet
food, treats, table food, rawhides, dental products, dietary supplements, and foods used to
administer medications, it also is important to
make a specific recommendation about the animal’s diet. This may be as simple as saying,
“You’re feeding an excellent diet to Fluffy and
are keeping her in perfect body condition.
Keep up the good work!” Supporting sound
nutrition decisions can help to reinforce these
behaviors and makes it less likely that the
owner will seek out nutritional information
from other less reliable sources. Conversely, if
the owner is feeding a diet that is not optimal,
make a specific recommendation for a more
appropriate diet (or treats, supplements, etc)
and explain why you’re making this recommendation. Providing reliable nutrition resources and helping owners understand how
to make more objective decisions about what
they read or hear can help to ensure their pets
are receiving optimal nutrition. In addition, it
is important for the veterinary healthcare team
to be prepared with answers to common questions and to be able to debunk myths. Some of
the common questions owners ask are below.a
What is the best food to feed my pet?
Despite all the marketing claims to the contrary, there is no best diet for all pets. Every
pet is unique, so the goal is to find the best
food for the individual pet. Expense doesn’t
necessarily equate with quality. Some inexpensive foods have years of rigorous scientific testing behind them and some very
expensive foods lack vital nutrients or are
based on unsound science. Larger companies generally have more stringent quality
control protocols, employ expert nutritionists and food scientists, and strive to increase
collective nutrition knowledge through re-
search. Smaller manufacturers may have less
control over ingredient or final product
quality, perform less laboratory testing, and
are less likely to employ full- or part-time
veterinary nutritionists.
Is the ingredient list a good way to
determine the quality of a pet food?
Although ingredient lists are commonly
used by lay people to determine the quality
of pet foods, this approach has many pitfalls
and can be subject to intentional manipulation by the food manufacturer. Ingredients
are listed on labels in order of weight, including water, so ingredients with high
water content (like fresh meats and vegetables) are listed before similar amounts of dry
ingredients, even though they may contribute fewer nutrients overall.
Pets require nutrients, not ingredients. A
food full of great-sounding ingredients can
be less nutritious than one containing less
appealing (to people) ingredients. Some
manufacturers may add ingredients to products solely for marketing purposes, to increase the appeal of the food to consumers.
These ingredients may have unproven benefits, be present in miniscule amounts, and
provide nothing to the food but added expense. More ingredients also mean increased
quality control measures (and more time
and expense) are necessary to ensure that the
finished product adheres to the desired nutrient formulation.
Modified from Tufts University’s Cummings School of Veterinary Medicine Nutrition website:
Pet Food Myth Busters
My friend says that grains
are bad for dogs. Is this correct?
Whole grains, rather than being fillers, contribute valuable nutrients including protein,
vitamins, minerals, essential fatty acids, and
fiber to foods while helping to keep the fat
and calories lower than if animal products
were used in their place. Even refined grains
such as white rice can have beneficial health
implications depending on the type of food
and the pet. Dogs and cats can efficiently digest and use nutrients from grains. Allergies
to grains (and even to animal proteins such
as chicken, beef, and dairy) are actually very
uncommon in dogs and cats.
It is becoming more common in the saturated pet food market for manufacturers to
perpetuate myths to sell products and increase market share. Grain-free foods are
often an example of this strategy. Many such
products merely substitute highly refined
starches such as those from potatoes or tapioca in place of grains. These ingredients
often provide fewer nutrients and less fiber
than whole grains while costing more.
I read online that by-products can
include hair, hooves, and floor
sweepings. Is this true?
By-products are commonly vilified, often by
pet food manufacturers that are trying to carve
out market share for themselves. By-products
(mainly organ meats and entrails) often provide more nutrients than muscle meats on a
per-weight basis and are important components and even delicacies of human diets in
other countries. The term by-product indicates
that the ingredient is a leftover from animal carcasses once the desirable (for Americans) muscle meat has been removed. The Association of
American Feed Control Officials (AAFCO)
definitions of mammalian by-products specifically exclude hair, hooves, horn, hide trimmings, manure, and intestinal contents as well
as anything that is not specifically part of the
carcass (eg, floor sweepings). As with all ingre-
dients, the quality of by-products can vary, so it
is important to select manufacturers that have
stringent internal quality control standards.
I’ve heard that raw diets prevent
and/or solve a lot of health problems
in pets. Is this true?
Despite anecdotal reports from pet owners and
even some veterinarians, there is currently no
evidence that raw foods offer any benefits over
cooked ones. There is substantial evidence,
however, that raw foods may be associated
with nutritional deficiencies, bacterial and parasitic infections, and other health concerns in
pets. These foods also pose potential risk to
people—especially those that are immunocompromised, such as young children, the elderly, and patients receiving immune-modifying
drugs or who have cancer.
Pets that eat contaminated raw foods have
been demonstrated to shed viable pathologic
organisms in their feces, and it is likely that
areas that they frequent also are contaminated.
As numerous recalls and some pathogen surveys in the last few years have proven, all raw
meat, regardless of source, should be considered to be contaminated until proven otherwise.
In addition to food safety concerns, nearly
all home-prepared raw diets and many commercially available raw products are deficient
in essential nutrients. It is also common for
commercial raw products to be very high in
fat, which may not be tolerated by some animals. Check the list of recommended websites
at the end of this article for information about
raw meat diets.
There is
evidence that
raw foods may
be associated
with nutritional
bacterial and
infections, and
other health
concerns in pets.
These foods also
pose potential risk
to people.
Are home-cooked foods healthier for
my pet than commercial products?
High-quality commercial pet foods have
been tested over decades to provide adequate
nutrition for the dog or cat. With the exception of some pets with multiple or severe
health concerns, there is a commercial food
that is appropriate for every pet, and nutri-
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
is important to reduce calories after surgery to
reduce the risk for obesity.
With the
exception of
some pets with
multiple or
severe health
concerns, there
is a commercial
food that is
appropriate for
every pet, and
diseases are
rare in pets
that are fed
good quality
tional deficiency diseases are rare in pets that
are fed good quality commercial products.
While home-cooked foods allow more control of ingredients and customization to the
specific pet, most home-cooked food recipes
are not formulated by a qualified veterinary
nutritionist and are vague and deficient in
multiple essential nutrients, making them
much less nutritious than commercial foods.
Even when the recipe is nutritionally balanced, there is no evidence that the average
animal receives better nutrition from a homecooked food than a commercial food. For the
vast majority of pet owners, commercial pet
foods offer the best nutrition with the most
convenience and affordability.
What is the best diet for a growing
puppy or kitten?
Growing kittens should be fed a kitten food
or an “all life stages” formula until 1 year of
age. Growing small- and medium-breed
puppies need a puppy or “all life stages” formula until 1 year of age. Large- and giantbreed puppies (adult size >50 lb) need a
food specifically designed for large-breed
puppies until 12 to 18 months of age. It is
ideal if the product has passed AAFCO feeding trials rather than merely being “formulated
to meet” the nutrient profiles for growth.
Throughout growth, it is important to keep a
puppy or kitten lean to reduce risks for health
problems and to optimize its life span. Spaying
or neutering reduces calorie requirements, so it
An owner’s decision about what to feed his
or her pet has become a more complicated
question than it once was. There is no single
“best” food for all pets because optimal
diet(s) depends on many factors, such as life
stage, body condition, exercise (or lack
thereof ), environment, and health status.
Often owners base their decisions on marketing messages rather than objective nutritional data. Although there are limitations,
the information provided on a pet food label
can provide helpful guidance for making objective selections of appropriate foods. The
two most useful pieces of information on a
pet food label are the nutritional adequacy
statement and the manufacturer.
Nutritional Adequacy
The AAFCO adequacy statement must be
included on all pet food labels in the United
States. This statement confirms three important facts:
1. Whether the diet is complete and balanced. All over-the-counter foods should
be complete and balanced. If the statement reads “for intermittent or supplemental use only,” it is not complete and
balanced. The product may be acceptable
as a veterinary therapeutic food to be used
for a specific purpose––eg, in a case of severe kidney disease––but should be avoided
for everyday feeding.
2. If the food is complete and balanced, for
which life stage is it intended? AAFCO provides nutrient profiles and feeding trial requirements for growth, reproduction, and
adult maintenance but not for senior/geriatric status. A food that is formulated to
meet the AAFCO profiles for all life
Pet Food Myth Busters
stages must meet the minimum nutrient
levels for both growth and adult maintenance.
3. How did the company determine that the
food is complete and balanced? Labels
may include one of two statements regarding nutritional adequacy:
• “[Product name] is formulated to meet
the nutritional levels established by the
AAFCO Dog (Cat) Food Nutrient Profiles for [life stage(s)].” This determination is based either on the recipe or on
analytic testing of the finished product
(preferably the latter).
• “Animal feeding tests using AAFCO
procedures substantiate [product name]
provides complete and balanced nutrition for [life stage(s)].” Feeding trial
evaluation of food is the basis of this
statement. While feeding trials help to
test for the food’s nutritional adequacy,
they do not guarantee that the food provides adequate nutrition under all conditions.
In addition, I recommend that foods also be
selected based on the important criteria
below to help to ensure that the food is
made by a reputable and knowledgeable
company with strict quality control measures:
The manufacturer’s name and contact information should be provided. The manufacturer should then be contacted for
answers to the following questions:
1. If the product is tested using AAFCO nutrient profiles rather than feeding trials,
does it do so by formulation or by analysis of the finished product? The latter is
2. Do they employ a full-time qualified nutritionist? What is this nutritionist’s name
and qualifications? Appropriate qualifications are either a PhD in animal nutrition
or board certification by the American
College of Veterinary Nutrition or the
European College of Veterinary Comparative Nutrition. Who formulates their
foods and what are his/her credentials?
3. Where are their ingredients produced and
their food manufactured?
4. What specific quality control measures do
they use to assure the consistency and
quality of ingredients and the end product? Examples include certification of a
manufacturer’s procedures (eg, by Hazard Analysis and Critical Control Points,
Global Food Safety Initiative, or American Feeding Industry Association); testing ingredients and end products for
nutrient content, pathogens, and aflatoxins; materials risk assessments; and supplier audits.
5. Can they (and will they) provide information on levels for any requested nutrient (protein, phosphorus, sodium, etc)
for the dog or cat food in question? An
average/typical analysis is preferable as a
guaranteed analysis provides only the
minimums or maximums and not an
exact number. These values should ideally
be given on an energy basis (ie, grams per
100 or 1,000 kilocalories) rather than on
an “as fed” or “dry matter” basis. The latter two do not account for the variable
energy density of different foods.
6. What is the caloric value per gram, can,
or cup of the food?
7. What kind of product research has been
conducted? Are the results published in
peer-reviewed journals?
If a manufacturer
cannot/will not
provide any of
this information,
one should be
cautious about
using that brand.
If a manufacturer cannot/will not provide
any of this information, one should be cautious about using that brand.
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
Nutrition Guidelines
• World Small Animal Veterinary Association
Nutritional Assessment Guidelines
• American Animal Hospital Association
Nutritional Assessment Guidelines
Tools for the Veterinary Health Care Team
• World Small Animal Veterinary Association
Nutrition Toolkit
• Pet Nutrition Alliance
Pet Nutrition – General Information
for Pet Owners
• National Research Council
downloadable booklets: Your Dog’s
Nutritional Needs and Your Cat’s
Nutritional Needs
• World Small Animal Veterinary Association
Nutrition Toolkit (The Savvy Dog Owner’s
Guide to Nutrition on the Internet, The
Savvy Cat Owner’s Guide to Nutrition on
the Internet, and Selecting the Best Food
for Your Pet)
Pet Nutrition – General Information
for Veterinarians (Nutrition Myths)
• Cummings School of Veterinary Medicine
at Tufts University Nutrition Service
Frequently Asked Questions
• Nestlé Purina Nutrition Myths
• P&G Deciphering Fact from Fiction
(co-written by Dr. Freeman)
Commercial Pet Food
• Association of American Feed Control
Officials: Information on regulations,
labeling, and other important facts about
pet food
• FAQs about pet foods
• Federal Drug Administration (FDA) Pet
Food site: Information, links, food safety
issues, recalls, pet food labels, reporting
• Pet Food Institute: Information on
ingredient definitions, nutrition myths,
labeling regulations
Home-Cooked Pet Food
• Cummings School of Veterinary Medicine
at Tufts University Nutrition Service
Frequently Asked Questions
• American College of Veterinary Nutrition:
Listing of board-certified veterinary
nutritionists who will formulate nutritionally
balanced homemade food recipes for
veterinarians and/or pet owners
• BalanceIT: Commercial website that
offers semi-customized balanced homecooked food recipes for pet owners with
healthy pets. Veterinarians can customize
preformulated recipes for animals with
medical conditions.
Dietary Supplements
• Consumerlab: Site (with a small
subscription fee for use) that
independently evaluates dietary
supplements (primarily for human
supplements but some pet supplements
are included)
• Food and Drug Administration (FDA):
Regulatory and safety issues of dietary
supplements, adverse event reporting
• Mayo Clinic Drugs and Supplements
Information: Fact sheets on human
supplements and herbs
• National Institutes of Health (NIH) Office of
Dietary Supplements: Evaluating
supplements, fact sheets, safety notices,
internet health info
• United States Department of Agriculture
(USDA) Food and Nutrition Information
Center: General supplement and nutrition
information, links to a variety of dietary
supplement websites
• United States Pharmacopeia Dietary
Supplement Verification Program:
Independent testing of dietary
supplements (human supplements only)
Raw Meat Diets
• Cummings School of Veterinary Medicine
at Tufts University Raw Diet Fact Sheet
• Freeman et al. Current knowledge about
the risks and benefits of raw meat–based
diets for dogs and cats. JAVMA 2013; 243:
1549-1558 (free access).
• Ohio State Indoor Pet Initiative: Nutrition
and other tips for optimizing the indoor
pet’s environment
• USDA Nutrient Database: Full nutrient
profiles on thousands of human foods
Pet Food Myth Busters
Critical Updates on Canine & Feline Health • 2015 NAVC/WVC Proceedings
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