Page 690 - Problem-Based Feline Medicine

682 PART 9 CAT WITH SIGNS OF GASTROINTESTINAL TRACT DISEASE

2–6 h or as a constant rate infusion). Frequent moni- other instruments, or via contact with oral secretions
toring (q 1–2 h) of blood glucose concentrations is directly.
necessary so that when the blood glucose level drops
Infection with Helicobacter organisms results in
below 16.8 mmol/L SI (300 mg/dl), 5% dextrose is
increased infiltration of the mucosa with polymor-
added to the fluids.
phonuclear cells and mononuclear cells, and is clas-
In cats that are not severely acidotic, and are still eating sified as chronic gastritis.
and not vomiting, insulin treatment may be instituted
Persistent infection is associated with increased
with NPH insulin (0.25–0.5 U/kg, SQ q 12 h), or where
development of gastric lymphoid follicles, especially
available PZI or glargine, with monitoring of blood glu-
in the antrum, the location of heaviest concentration of
cose levels (q 2–3 h).
organisms in most cats.
Cats that have urinary tract or other infections
At this time, there does not appear to be a breed or sex
should be treated with appropriate antibiotics.
predilection for infection or development of signs.
Vomiting is controlled with metoclopramide
The classical sign is chronic vomiting due to gastri-
(0.1–0.2 mg/kg q 12 h) as needed.
tis, but the incidence and true importance of
Cats that are able to eat without vomiting should be fed Helicobacter spp. in gastritis in cats is not known.
a highly palatable diet (see page 238). High-protein,
reduced-carbohydrate diets are advantageous in both Clinical signs
thin and obese diabetic cats unless they have concurrent
renal disease and need to eat a lower-protein diet. Chronic vomiting, weight loss and in some cases, pica
are reported in clinically affected cats.
HELICOBACTER SPP.* However, these organisms will be present in clini-
cally healthy animals, so a direct cause-and-effect
Classical signs relationship cannot be established.
● The classical sign is vomiting.
Diagnosis
Pathogenesis The diagnosis is made by histologic examination of
gastric mucosal tissue (usually obtained via
Helicobacter organisms known to colonize the feline
endoscopy). Either a special silver stain or modified
stomach include: H. pylori, H. felis, and H. bizzoze-
Giemsa stain must be used to identify the organisms.
ronii. Other Helicobacter spp. that have been identified
in the small intestine and liver of cats include Culture and organism identification is also required
H. cinaedi and H. fennelliae. The significance of these to make a definitive diagnosis, since not all spiral
organisms and their ability to cause clinical disease is organisms are pathogens or Helicobacter spp. Helico-
unknown. bacter spp. require special media and handling for
successful culture in vitro.
H. felis is commonly found in the stomach of cats and
may not be a feline pathogen, but H. pylori, which Helicobacter spp. produce urease that can be used to
causes peptic disease in humans, is believed to also be provisionally diagnose their presence, by placing
associated with gastritis in cats, especially cats in biopsy samples in urea broth or by using the com-
colonies or catteries. H. bizzozeronii is the most com- mercially available test (CloTest). However, this test
mon gastric colonizer in cats, and has experimentally is neither sensitive nor specific for Helicobacter
produced chronic gastritis in kittens. infection.

Infection is primarily transmitted via the oral–oral Serologic assays used in humans are not reliable for
route. Organisms are present in vomitus, oral secre- testing in cats because of the cross-reactivity between
tions and saliva, and may be transmitted via improp- other spiral organisms (commonly present in normal
erly disinfected dental equipment, endoscopes and cats) and H. pylori (the suspected pathogen).