Small Animal Clinical Nutrition
Small Animal Clinical Nutrition
Small Animal Clinical Nutrition
Chapter
Introduction to Feeding
Normal Cats
P. Jane Armstrong
Kathy L. Gross
Iveta Becvarova
Jacques Debraekeleer
INTRODUCTION
Cats were probably domesticated between 1600 and 1500 BC.
Early Egyptians considered cats sacred and valued them for
their natural hunting and predatory behavior, which helped
control rodent populations. Little consideration for the nutritional needs of cats was required during the early days of
domestication. As domestic cats evolved from mouse catcher to
household companion, the need to understand their unique
nutritional requirements also increased. Today, it is well accepted that proper nutrition and care throughout life maximizes
health, longevity and quality of life. Providing proper guidance
about the nutritional management of cats requires an understanding of: 1) the basic principles of nutrition (Chapters 5 and
6), 2) the foods and nutrients commonly fed to cats, 3) how to
assess nutrient availability and quality of various foodstuffs and
foods, 4) foods and feeding practices that may positively or negatively affect health and 5) the unique nutritional needs of cats
throughout the lifecycle.
Demographics
Cats are the most popular pets in the United States, totaling
approximately 77 million (APPMA, 2003). More than onethird of the households in the U.S. own cats with an average of
2.1 cats per cat-owning household. In 1996, the ratio of male to
female cats was roughly equal and nearly 80% of pet cats in the
U.S. were neutered (Table 19-1) (Lund et al, 1999). Table 19-2
lists the 10 countries with the largest pet cat populations.
Mixed-breed cats, domestic shorthairs and longhairs, make up
an estimated 95% of the worlds domestic cat population. They
result from random rather than selective breeding. Domestic
shorthair and longhair cats display a wide variety of sizes, and
coat colors, patterns and lengths. Although most cats in the U.S.
are non-pedigreed, the Cat Fanciers Association registered 41
different breeds in 2005. The four most common breeds were
Persians, Maine coons, Siamese and Abyssinians (CFA, 2005).
Compared with dogs, cats make up a smaller proportion of
the pets seen by veterinarians, but that proportion is increasing.
Now, nearly 68% of cat owners in the U.S. regularly use veterinary services. In 2001, cats visited veterinary clinics once per
year compared with 0.79 visits per year in 1987 (Center for
Information Management, 2002). In 2001, cat owners spent
$6.3 billion toward the health and well being of their cats. Cat
food sales followed the upward trend in cat ownership and
health care with almost $4.3 billion of sales in the U.S. in 1997
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CATS AS CARNIVORES
Taxonomically, cats and dogs are members of the order
Carnivora and are therefore classified as carnivores (Table 124). From a dietary perspective, however, dogs are omnivores
(Chapter 12) and domestic cats and other members of the
superfamily Feloidea are strict or true carnivores, along with
raptors, mosquitoes and some coldwater fish. This basic difference is supported by specific behavioral, anatomic, physiologic
and metabolic adaptations of cats to a strictly carnivorous diet.
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Limbs
The retractable claws of cats are a unique adaptation to hunting. The sharp tips of the claws with hook-like curves and needle features are ideal for capturing and securing prey, yet they
are easily retracted so they do not make noise when cats stalk
prey. In contrast, the claws of dogs play only a secondary role in
capturing prey.
Oral Cavity
Cats and dogs have the same number of incisor, canine and carnassial teeth (i.e., the enlarged upper premolar and lower molar
teeth specialized for shearing flesh); however, cats have fewer
premolar and molar teeth, and they do not possess fissured
crowns, which are a hallmark of omnivorous animals (Figure
19-2). The jaws of cats have limited lateromedial and craniocaudal movement, thereby limiting grinding ability. The scissors-like action of the carnassial teeth is ideal for delivering the
cervical bite used to transect the spinal cord and immobilize or
kill prey. Cats lack salivary amylase used to initiate digestion of
dietary starches. This adaptation reflects the nutritional composition of the typical prey (i.e., low starch content).
Stomach
Because cats evolved to eat small frequent meals, the stomach is
less important as a storage reservoir compared with the stomach
of dogs. Thus, the stomach of domestic cats is simpler than that
of dogs (i.e., relatively smaller with a smaller glandular fundus).
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ANOREXIA
Although a few days of inappetence is not particularly detrimental to an
otherwise healthy cat, prolonged inadequate calorie intake results in
malnutrition, reduced immune function and increased risk for hepatic
lipidosis. Anorexia may be caused by stress, unacceptable foods or
concurrent disease. Most commonly, cats presented to veterinarians for
anorexia have a concurrent disease. Cats may endure prolonged starvation rather than eat an unpalatable food. Therefore, advising owners
that a cat will eat when it gets hungry enough can have deadly
results. Anorexia of more than three days duration, even in an otherwise healthy-appearing cat, warrants investigation by a veterinarian.
A thorough history is useful for differentiating potential causes of
anorexia. To determine if inadequate food acceptance is the cause,
offer a small selection of highly palatable foods along with the typical
food. Because improperly stored foods may develop off flavors, bacterial contamination or fungal growth, confirm that the product is fresh
and wholesome. Environmental or emotional factors reported to result
in stress-mediated anorexia include hospitalization, boarding, travel,
introduction of new people or pets to the household, loss of a companion, overcrowding, high temperatures and excessive handling. Stressmediated anorexia is usually diagnosed from the history and by ruling
out other diseases. Providing a quiet secluded area will often allow a
cat to relax sufficiently enough to begin eating. Often, increasing the
foods palatability will improve food intake. Warming food, changing the
food form, adding water or choosing foods high in animal protein and
fat can enhance food palatability. If cats are highly stressed or appropriate feeding sites are unavailable, mild tranquilizers or appetite stimulants (e.g., mirtazapine, oxazepam or cyproheptadine) may be beneficial (Chapter 25). Force feeding may be accepted by some cats but
others find the process so stressful that any benefit is far outweighed
by the additional stress.
FIXED-FOOD PREFERENCES
The food type fed by the owner during a kittens first six months influences the pattern of food preferences throughout life. Although uncommon, kittens exposed to a very limited number of foods may develop a
food fixation, refusing to eat anything but a single food. Adult cats fed
highly palatable, single-item foods have been reported to develop fixedfood preferences as well.
Cats with food fixations can be particularly troublesome if dietary
modifications are necessary. Cats with strong food preferences should
be transitioned to the new food over a prolonged period. Convert to the
desired food by replacing 10 to 20% of the old food with an equal
al bacterial overgrowth in dogs (NRC, 2006). Although the
reason for this finding is unclear, their relatively short small
intestine and carnivorous physiology have been suggested as
possibilities. Increased numbers of small intestinal bacteria
might enhance protein and fat digestion (Zoran, 2002).
Certain amino acid transporters in the small intestines of cats
are highly adaptable, particularly the transporter responsible for
arginine uptake. This finding underscores the importance of
the amount of protein and specific amino acids in foods for
cats. Unlike omnivores, cats are unable to synthesize significant
quantities of ornithine or citrulline within the intestine. Both
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amount of the new food on Day 1, then gradually increase the ratio of
new to old over the next 14 days. A more gradual transition may be
required if food intake drops below 70% of maintenance levels. Cats
should be monitored to ensure they are not selecting the preferred food
from the food dish and that food intake remains adequate. Feeding kittens and cats a variety of foods (both different forms of food and different brands) and not feeding single-item foods can avoid food fixations.
This approach is strongly recommended as disease management later
in life often requires a dietary change.
LEARNED TASTE AVERSIONS
Cats may develop learned aversions to certain foods when feeding is
paired with a negative GI experience. The negative experience can be
physical, emotional or physiologic. Typically, aversions occur when cats
consume a food immediately before an episode of nausea or vomiting.
Foods that were readily consumed before the negative incident will be
avoided subsequently. Clinically, aversions may develop when GI upset
is induced by various diseases, drugs or treatment protocols. Foods
with high salience (i.e., strong odors or high protein levels) are more
likely to become aversive and should not be fed within 24 hours of
anticipated GI upsets. Aversions have been documented to last up to
40 days in cats. Learned aversions are considered an adaptive
response. By avoiding foods that previously caused gastric distress,
cats will avoid eating foods likely to be spoiled or tainted. From a clinical perspective, consideration of food aversions often equates to delaying introduction of a therapeutic food, such as a diet for chronic kidney
disease, until the cats GI signs have been controlled with other medical management.
POLYPHAGIA
Various diseases, drugs and psychological stresses can mediate excessive food consumption. Rarely, polyphagia (hyperphagia) may occur
with diseases involving the central nervous system, particularly with
lesions of the ventromedial hypothalamus. Presence of weight loss or
gain is of key diagnostic importance. Polyphagia with weight loss is
almost always associated with an underlying disease process or simple underfeeding. Caloric intake should always be calculated because
underfeeding can result in a ravenous appetite that may be misinterpreted as abnormal. Nutritional management of polyphagia requires an
accurate diagnosis because treatment is aimed at the primary disease.
The Bibliography for Box 19-1 can be found at www.markmorris.org.
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Ratio
4:1
6:1
10:1
14:1
Protein Metabolism
Protein metabolism is unique in cats and is manifested by an
unusually high maintenance requirement for protein as compared with canine requirements (Table 19-5) and a special need
for four amino acids: arginine, taurine, methionine and cystine.
The protein requirement for growth in kittens is only 50%
higher than that of puppies, whereas the protein requirement
for feline maintenance is twice that of adult dogs. The higher
protein requirement of cats is not due to an exceptionally high
requirement for any specific amino acid (Table 19-6); instead,
it is caused by a high activity of hepatic enzymes (i.e., transaminases and deaminases) that remove amino groups from amino
acids so the resulting ketoacids can be used for energy or glucose production. Unlike omnivores and herbivores, cats have a
limited ability to decrease the activity of these enzymes when
fed low-protein foods. The cats strict adherence to a diet of
animal tissue likely resulted in a lack of evolutionary pressure to
accommodate lower protein food sources. Hepatic enzyme systems are constantly active; therefore, a fixed amount of dietary
protein is always catabolized for energy (MacDonald et al,
1984). The gluconeogenic enzymes in feline liver appear to be
continuously active, unlike the situation in most other species,
including dogs (MacDonald et al, 1984). In addition, an alternate hepatic gluconeogenic pathway common in flesh-eating
animals is active in cats (Beliveau and Freedland, 1982). This
pathway uses serine as a glucose precursor. Serine is a nonessential amino acid found in large amounts in muscle, milk and egg.
ARGININE
Arginine deficiency in cats causes one of the most dramatic
responses of any nutrient deficiency. Cats cannot synthesize
sufficient ornithine or citrulline for conversion to arginine,
which is needed for the urea cycle. After a cat eats a meal, the
highly active protein catabolic enzymes in its liver produce
ammonia, which is absorbed from the colon.
Without arginine, the urea cycle cannot convert ammonia to
urea and ammonia toxicity occurs (MacDonald et al, 1984).
Eating a single meal devoid of arginine may result in hyperammonemia in less than one hour. Affected cats exhibit severe signs
of ammonia toxicity (i.e., vocalization, emesis, ptyalism, hyper-
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Nutrients
Recommended
allowance for
kittens**
% DM
22.5
-
Recommended
allowance for
puppies**
% DM
17.5
-
Crude protein
EAA
Amino acids
Arginine***
0.96
0.66
Histidine
0.33
0.25
Isoleucine
0.54
0.50
Leucine
1.28
0.82
Lysine
0.85
0.70
Methionine (met + cys)
0.44 (0.88)
0.26 (0.53)
Phenylalanine (phe + tyr)
0.5 (1.91)
0.50 (1.00)
Threonine
0.65
0.63
Tryptophan
0.16
0.18
Valine
0.64
0.56
Taurine (extruded)
0.1
Taurine (canned)
0.17
the amino acid felinine. Felinine is a branched-chain, sulfurcontaining -amino acid found in the urine of domestic cats.
Its biologic function has not been fully elucidated. The most
widely accepted possible role for felinine, or its breakdown
product in urine, is as a pheromone, which is of importance in
territorial marking. Sexually immature kittens have been
reported not to excrete felinine and adult males excrete more
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or both, with only about 40% of taurine-deficient cats exhibiting clinical signs.a,b
Clinical signs of FCRD are inapparent until significant visual
impairment has occurred. Then, owners may notice their cat bumping into objects or miscalculating jumps. Early disease may be
detected during ophthalmic examination. Changes in retinal function
can be demonstrated by electroretinograms before retinal lesions
appear. The development of FCRD apparently requires three or more
months of taurine depletion. Initially, lesions appear as dark granular focal defects in the area centralis, slightly temporal to the optic
disk. As degeneration progresses, the lesion becomes hyperreflective and extends in a band across the tapetum. Complete blindness
ensues with full degeneration of the retina and attenuation of retinal
vessels. Structural changes within the retina are permanent.
Therefore, a diagnosis of FCRD does not reflect the current taurine
status of a cat, but indicates a period of prolonged taurine deficiency has occurred.
Cats with DCM may be clinically normal or present acutely with
signs of heart failure. Clinical signs may include lethargy, anorexia
and dyspnea. Physical findings may include pleural effusion, pulmonary edema, gallop heart rhythms, systolic murmurs and ventricular dysrhythmias. Cats in severe heart failure are hypothermic, have
pale mucous membranes, poor pulse quality and are often too weak
to stand. Only about one-third of cats with DCM have concurrent
FCRD. DCM is confirmed by echocardiography. Findings most often
include dilatation of the left atrium and ventricle and decreased left
ventricle contractility.
REPRODUCTION AND FETAL DEVELOPMENT
Reproduction and fetal development are severely impaired in taurine-deficient queens. Conception and implantation appear normal;
however, fetal death is frequently observed near 25 days of gestation, followed by abortion or resorption. In a group of taurine-deficient queens, only 38% of 33 matings resulted in term deliveries,
with an average of 2.1 live births.
Developmental abnormalities reported to occur in kittens born to
taurine-deficient queens include poor survival, cerebellar dysgenesis, abnormal hind-limb development and thoracic kyphosis, which
appears as a dorsoventral flattening of the thoracic cavity. Severe
hydrocephalus and anencephaly may be present in aborted fetuses.
Surviving kittens are often small and weak. Growth is depressed up
to 40% in the immediate postnatal period.
DIAGNOSIS
The diagnosis of taurine deficiency is based on clinical signs and low
plasma and whole blood taurine concentrations. Care must be used
when evaluating plasma taurine concentrations because levels may
be altered by sample handling errors and feeding. Fasting may
reduce plasma taurine concentrations, whereas poor handling may
allow taurine contamination from platelets and white blood cells.
Although plasma taurine concentrations reflect the labile taurine
pool, whole blood taurine concentrations better reflect tissue taurine
status. Normal plasma taurine levels in cats may vary up to fivefold
(50 to 250 nmol/ml). Plasma taurine values less than 40 nmol/ml
may suggest taurine deficiency. Cats with clinical signs of deficien-
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Fat Metabolism
Cats have the ability to digest and use high levels of dietary fat
(as is present in animal tissue). Like other true carnivores, cats
have a special need for arachidonic acid (AA) (20:4n6) because
they have a limited ability to synthesize it from linoleic acid
(18:2n6), unlike dogs and other omnivores (MacDonald et al,
1984, 1984a). An exogenous source of AA is especially important for more demanding lifestages, such as gestation, lactation
and growth. The basis for this additional requirement is the low
hepatic delta-6 desaturase activity in cats (Sinclair et al, 1979).
Delta-6 desaturase is the rate-limiting factor in the conversion
of linoleic acid to -linolenic acid, which is further elongated
and desaturated to form AA. AA is abundant in animal tissues,
particularly in organ meats and neural tissues, but absent in
plants. Thus, the dietary requirement for AA has little consequence if cats consume animal tissues (MacDonald et al, 1984).
Vitamin Metabolism
The vitamin needs of cats differ from those of dogs in several
ways. Cats do not convert sufficient amounts of tryptophan to
niacin (DaSilva et al, 1952). An animal tissue-based diet is well
supplied with niacin from NAD and NADP (nicotinamideadenine dinucleotide phosphate) coenzymes; therefore, cats
dont need to produce niacin from tryptophan. Although cats
possess all the enzymes needed for niacin synthesis, the high
activity of enzymes in the catabolic pathway (picolinic carboxylase) far exceeds the rate of niacin synthesis (Morris and
Rogers, 1983). As a result, the niacin requirement of cats is 2.4
times higher than that of dogs (NRC, 2006).
The prosthetic group of all transaminases is pyridoxine (vitamin B6) (Stryer, 1975). Cats have high transaminase activities,
consistent with consuming a diet from which considerable
energy is derived from dietary protein. Therefore, it is logical to
expect that their pyridoxine turnover and requirement would be
higher than that of omnivores. The pyridoxine requirement of
cats is estimated to be 1.7 times higher than that of dogs
(NRC, 2006).
Vitamin A occurs naturally only in animal tissue. Plants synthesize vitamin A precursors (e.g., -carotene). Omnivorous
and herbivorous animals can convert -carotene to vitamin A;
cats cannot because they lack intestinal dioxygenase that cleaves
-carotene to retinol. In addition, cats have insufficient 7-dehydrocholesterol in the skin to meet the metabolic need for vitamin D photosynthesis; therefore, they require a dietary source
of vitamin D (How et al, 1994, 1994a; Morris, 1996). Vitamin
D is relatively abundant in animal liver; therefore, the need for
dermal production is minimal and alternate pathways rapidly
metabolize 7-dehydrocholesterol. Vitamin D is fairly ubiquitous in animal fats and primary vitamin D deficiency has been
identified only in cats fed experimental diets.
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Water
Water needs of cats also differ from those of dogs, not because
of feline feeding behaviors (i.e., carnivorous vs. omnivorous) but
because of their ancestors adaptation to environmental
extremes. Domestic cats are thought to have descended from
the African wildcat (Felis silvestris libyca), a desert dweller.
Several unique features of water balance in cats may be
explained by adaptation to a dry environment. Cats are able to
survive on less water than dogs and may fail to increase water
intake at minor levels of dehydration, up to 4% of body weight
(Anderson, 1982). Cats compensate for reduced water intake,
in part, by forming highly concentrated urine. Unfortunately,
this strong concentrating ability coupled with a weak thirst
drive may result in highly saturated urine, increasing the risk of
crystalluria or urolithiasis, both components of the feline lower
urinary tract disease complex.
Cats consume 1.5 to 2 ml of water/g of dry matter (DM).
This 2:1 ratio of water to DM is similar to that of typical prey.
This ratio represents approximately 0.5 ml water/kcal ME
intake. Practical recommendations for water provision are somewhat higher at 1 ml water/kcal ME. Water ingested from moist
LIFESTAGE NUTRITION
Lifestage nutrition is the practice of feeding foods designed to
meet an animals optimal nutritional needs at a specific age or
physiologic state (e.g., maintenance, reproduction or growth).
The concept of lifestage nutrition recognizes that feeding either
below or above an optimal nutrient level can negatively affect
biologic performance and health (Figure 5-2). This concept
differs markedly from feeding a single product for all lifestages
(i.e., all-purpose foods), whereby nutrients are added at levels to
meet the highest potential need (i.e., usually growth and reproduction). For maximum benefit, risk assessment and preventive
plans should begin well before the onset of disease. The value
of lifestage nutrition is greater if risk factor management is also
incorporated into the feeding practice. A narrower range of
nutrient recommendations often emerges when age and physiologic needs are reviewed in conjunction with reducing nutritional risk factors for disease.
Calcium
Breeders sometimes provide supplemental calcium during pregnancy, lactation or growth. Additional calcium is rarely necessary, except
for cats fed a homemade food or queens with eclampsia, and may
lead to nutritional excess or nutrient imbalances in cats fed complete
and balanced commercial cat foods.
Chromium
Chromium has been called a glucose tolerance factor for its role in
normal glucose homeostasis and insulin action in experimental animals. Chromium supplementation promotes lean tissue accretion in
growing livestock. Thus, health food stores now stock chromium as
an anti-diabetic nutrient and fat-burner for people. Little information exists about the effect of chromium supplementation in cats.
Some caution may be warranted given excess chromium has been
associated with chromosomal damage.
Brewers Yeast/Thiamin
Brewers yeast and thiamin have been promoted as coat conditioners
and flea preventives for dogs and cats. Although brewers yeast is a
good source of B vitamins, particularly thiamin, research has not
proven its efficacy as a flea repellent.
RAW MEATS
Breeders and owners commonly feed raw meats to cats. Raw muscle and organ meats are highly palatable, digestible and generally
nutritious when supplemented with appropriate vitamins and minerals. Cooking destroys some nutrients and increases the availability of
others. A benefit to feeding raw meat to cats has not been documented, and the disadvantages far outweigh any advantages. Raw meat,
even when flash frozen, may contain harmful bacteria (e.g.,
Salmonella spp. and Escherichia coli) and parasites (e.g., Toxoplasma
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ACKNOWLEDGMENT
The authors and editors acknowledge the contributions of Dr.
Claudia A. Kirk in the previous edition of Small Animal
Clinical Nutrition.
REFERENCES
The references for Chapter 19 can be found at
www.markmorris.org.
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Minerals
Providing adequate calcium is a concern in any homemade food.
A variety of calcium supplements are available from health food
stores and pharmacies. Many plant ingredients contain components (e.g., fibers or phytates) that severely compromise the
availability of certain trace elements. The availability of iron, zinc
and copper is of particular concern in high-phytate and high-fiber
foods (Chapter 5). These minerals should be provided as a highly available source.
Fat
Of the nutrients required by cats, arachidonic acid is the one not
commercially available. To provide arachidonate directly, cats
must be given animal fat or tissue as a nutritional source.
However, cats can convert -linolenic acid (18:3n6) to arachidonic acid (20:4n6) via delta 5-desaturase. -linolenic acid is available from plant oils (e.g., borage and evening primrose oils).
Prolonged feeding and reproductive trials using -linolenic acid
have not been reported; thus, the suitability of these oils as longterm arachidonic acid supplements is unknown. Because cats
fed foods high in polyunsaturated fatty acids may develop steatitis, cats fed vegetarian foods with large quantities of plant oils
should be protected with added vitamin E.
DOG FOOD
Most dog foods are not nutritionally adequate for the maintenance, growth and reproduction of cats. Nutrients most likely to
be deficient are protein, taurine, niacin, vitamin B6, methionine
and choline. Clinical signs of deficiency depend on which nutrients are deficient and to what degree.
FOOD TOXINS
Food toxicities are relatively infrequent in cats. Most notable is
hemolytic anemia caused by onion toxicity. Certain disulfides
found in onions promote oxidative damage to cat hemoglobin,
resulting in Heinz body production and red cell removal. The toxic
compound appears to be highly stable, because it remains active
in cooked onion-based broth and onion powder. Hemolytic anemia has been described in a cat fed commercial baby food containing onion powder. Onion toxicity was not proved but the anemia resolved with a diet change. Subsequent studies have
demonstrated toxic effects at levels of 2.5% dry matter.
Therefore, it is prudent to avoid feeding food or seasonings containing onion powder or onions. Chapter 11 provides more information about foodborne toxins.
Theobromine
Theobromine is a toxic methylxanthine found in chocolate. The
clinical signs of toxicity include vomiting, diarrhea, vascular collapse and death. The oral LD50 of theobromine is 200 mg/kg
body weight. Approximately 40 to 50 g of cocoa would need to
be consumed to provide this dose of theobromine, which is
undoubtedly why clinical reports of chocolate toxicoses in cats
are rare.
Histamine
Histamine is a primary amine arising from the decarboxylation of
histidine. Histamine toxicosis has been reported to occur in cats
after ingestion of certain species of spoiled fish. Affected cats
developed salivation, vomiting and diarrhea about 30 minutes
after eating uncooked anchovies. Myosis, lacrimation, tachypnea
and tachycardia were evident upon physical examination. A survey detailing the histamine content of North American cat foods
found foods were well below the 500 mg/g (wet/weight) level
considered hazardous in people. Thus, histamine toxicosis is
most likely to occur in cats fed improperly handled fish that has
undergone spoilage.
ENDNOTE
a. Kirk CA. Unpublished data. 1992.
The Bibliography for Box 19-3 can be found at
www.markmorris.org.