Page 229 - Small Animal Clinical Nutrition 5th Edition

232 Small Animal Clinical Nutrition

results (Fenwick, 1996). ESCHERICHIA COLI
E. coli is a well-known pathogen of people. However, the
Salmonellae produce a heat-labile endotoxin, which is
VetBooks.ir responsible for their pathologic effects. Clinical syndromes can role of E. coli as a pathogen of dogs and cats has been unclear
be divided into gastroenteritis, bacteremia/toxemia and organ
(Burrows et al, 1995; Olson et al, 1985). E. coli, strain
localization. Infections can usually be treated successfully with a O157:H7 has been involved in a number of outbreaks of
combination of appropriate antibacterial drugs and supportive foodborne illnesses stemming from improperly cooked meat
treatment. Persistent carriers are common and can be a source of purchased from fast-food restaurants (Potter, 1992).The same
human exposure. Proper cooking of foods and boiling water will strain has been incriminated in an unusual clinical syndrome
kill vegetative bacterial cells and inactivate the endotoxin. in racing greyhounds termed “Alabama rot” or “Greenetrack
disease” (Fenwick et al, 1995).This disease is characterized by
CLOSTRIDIUM BOTULINUM erythema, ulceration of the extremities and renal glomerular
The heat-labile toxin of the gram-positive, anaerobic, spore- pathology (Fenwick, 1996; Fenwick et al, 1995; Hertzke et al,
forming bacterium C. botulinum causes botulism. These sapro- 1995). No particular treatment has proved effective, but many
phytic bacilli are commonly found in soil and as contaminants animals will recover with symptomatic treatment and good
in raw meat, carrion and vegetables. They are not considered nursing care.
dangerous to man or animals unless allowed to grow under
anaerobic conditions in uncooked meats, improperly canned BACILLUS CEREUS
foods and the carcasses of dead animals. Under anaerobic con- B. cereus causes vomiting and diarrhea in people, but it is not
ditions, C. botulinum produces the most potent biotoxin known thought to pose a significant danger for foodborne illness in
(Klassen and Eaton, 1993). This powerful exotoxin blocks the animals (Turnbull and Kramer, 1991). At room temperature, B.
release of the neurotransmitter acetylcholine. Dogs are less sus- cereus flourishes, producing a potent endotoxin. The organism
ceptible to the effects of the toxin than people, but naturally is a ubiquitous, spore-forming aerobic saprophyte found in soil,
occurring botulism has occurred in dogs (Green, 1995; grains, cereal products and other foods (van Netten and
Barsanti, 1984; Barsanti et al, 1978). Cats, previously thought Kramer, 1992). As an example, it is commonly found in
to be resistant to botulinum toxin, have also been found to be uncooked rice (Ensminger et al, 1995). B. cereus has been found
c
susceptible. Eight cats fed pelican carrion contracted the dis- as a common isolate in samples of dry pet food. It has also
ease, and four died during the course of the illness.Toxigenic C. been isolated from food packaging paper and materials
botulinum type C bacteria were found in the stomach of one cat (Vaisanen et al, 1992).
and in the pelican muscle (Elad et al, 2004). Clinical signs can The standard heat used to manufacture pet foods is not
occur as early as 12 hours or as late as five to six days after the likely to destroy the spores of this organism. However, the
exotoxin is ingested. The primary clinical sign is generalized number of organisms isolated from pet food samples (<10 5
paralysis that starts in the posterior limbs and progresses to cells/g of food) is unlikely to cause foodborne disease in pets
quadriplegia. unless the food is exposed to moisture and heat conditions
Primary care consists of supportive treatment. Spontaneous conducive to bacterial proliferation (van Netten and Kramer,
recovery will occur provided the dose of toxin ingested was 1992; Claus and Berkeley, 1986; Drobniewski, 1993).
insufficient to severely affect vital functions, such as respiration. Therefore, pet owners should be warned not to add water to
Prevention can be achieved by heating foods before consump- dry pet foods and leave them exposed to high ambient tem-
tion to either 80°C (176°F) for 30 minutes or 100°C (212°F) for peratures for prolonged periods.
10 minutes (Ensminger et al, 1995).These heating protocols are
sufficient to destroy the heat-labile toxin of C. botulinum;how- NEORICKETTSIA SPECIES
ever, any bacterial spores present will survive this procedure. In dogs, Neorickettsia helminthoeca and N. elokominica, cause a
serious systemic infection known as salmon poisoning
STAPHYLOCOCCUS AUREUS (Breitschwerdt, 1995; Gorham and Foreyt, 1984). The disease
The ubiquitous staphylococci are common inhabitants of the is transmitted by ingestion of raw salmon containing the vector,
skin and mucous membranes of man and other animals (Jawetz a fluke named Nanophyetus salmincola.The fluke matures in five
et al, 1980). S. aureus is the most common cause of foodborne to seven days and then attaches to the intestinal mucosa of the
illness in people. The typical GI signs result from a potent S. host animal.The rickettsiae leave the fluke, invade the intestin-
aureus enterotoxin. Although S. aureus organisms are easily al mucosa and enter the bloodstream to produce an acute sys-
killed by heat, their enterotoxin can withstand typical cooking temic infection.
temperatures and even the canning process (Tatini, 1976). Clinical signs include vomiting, hemorrhagic diarrhea, high
Ingestion of about 25 µg of enterotoxin will produce nausea and fever, dehydration and peripheral lymphadenopathy.
vomiting within two to four hours in people. Spontaneous Tetracycline therapy is the treatment of choice. Supportive
recovery occurs in 24 to 48 hours. Dogs and cats are reported treatment with parenteral fluids is also indicated. The
to be tolerant to staphylococcal enterotoxin and have remained anthelmintic preferred for elimination of the fluke is fenbenda-
asymptomatic after administration of oral doses as high as 100 zole. If timely treatment is not instituted, mortality can reach
µg/kg body weight (Freer and Arbuthnott, 1986). b 50 to 90% (Burrows et al, 1995).