Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

VIII. Disturbances of Gastrointestinal Function
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increased fecal loss of α 1-proteinase inhibitor in dogs with
PLE is associated with a significant decrease in fecal proteolytic
activity and may result in a false-positive diagnosis
of exocrine pancreatic insufficiency.
The studies performed by Fetz et al. (2006b) proved
that cats with chronic gastrointestinal disease can be associated
with gastrointestinal protein loss. The upper limit
of the reference range for mean fecal α 1-PI concentrations
in healthy cats was 1.6 μ g/g; the concentrations in
eight of the nine study cats ranged from 2.2 to 180.77. Fetz
et al. (2006a) reported that increased fecal α 1-PI concentrations
in association with low serum albumin and total
protein levels are common findings in cats with inflammatory
bowel disease (IBD) and gastrointestinal neoplasia.
Furthermore, fecal α 1-PI concentrations tend to be higher
in cats with severe IBD or neoplasia when compared to
cats with mild to moderate IBD.
K . Ulcerative Colitis
Canine ulcerative colitis, including granulomatous colitis
of boxer dogs, has been reported ( Ewing and Gomez,
1973 ; Gomez et al., 1977 ; Kennedy and Cello, 1966 ;
Koch and Skelley, 1967 ; Russell et al., 1971 ; Sander and
Langham, 1968 ; Van Kruininger et al., 1965). In boxer
dogs, the disease is characterized by intractable diarrhea
that is often hemorrhagic. Histopathologically, there
is a granulomatous or histiocytic submucosal infiltrate
and the macrophages are laden with periodic-acid-Schiffpositive
material. Immunopathological studies describe
an increase in IgG3 and IgG4 plasma cells, PAS positive
macrophages and CD3-T cells, L1- and MHC11-positive
cells, with pathological lesions similar to human ulcerative
colitis ( German et al., 2003 ). Electron photomicrography
demonstrated bacteria in the macrophages ( Russell et al.,
1971 ), and, in some instances, these organisms resembled
Chlamydia. Mycoplasma has been cultured from the colon
and regional lymph nodes in four boxers, but attempts to
reproduce granulomatous colitis with Mycoplasma have
been unsuccessful. Until recently, this failure to identify or
isolate an infectious agent has led to the belief that granulomatous
colitis of boxers is an immune-mediated disease.
The development of culture-independent techniques
utilizing PCR probes has renewed suspicion that granulomatous
colitis in normal dogs is an infectious disease
( Simpson et al., 2006 ). Colonic biopsies from affected
dogs (13 boxers with colitis) and 38 control dogs were
examined by fluorescent in situ hybridization (FISH) with
a eubacterial 16s rRna probe. Culture, 16s rDNA sequencing,
and histochemistry were used to define invasive flora
and guide subsequent FISH. Intramucosal bacteria, predominantly
Gram-negative coccobacilli, were present in
the affected boxers, but none of the controls. Culture and
16s rDNA sequencing yielded mostly Enterobacteriaceae
and invasive bacteria hybridized with FISH probes to
E. coli. These findings complement the observation that
affected boxers often respond to enrofloxacin alone or in
combination with amoxicillin and metronidazole.
Cases of ulcerative colitis in dogs have also been attributed
to trichuriasis, balantidiasis, protothecosis, histoplasmosis,
eosinophilic ulcerative colitis, or neoplasia ( Lorenz,
1975 ). Severe ulcerative colitis has also been reported in
cats and in some the feline leukemia virus (FeLV) is demonstrated.
Feline panleukopenia can also cause colonic lesions.
Biochemical manifestations of ulcerative colitis depend
on the duration and severity of illness, the degree of colorectal
involvement, and the presence of systemic complications.
In severe cases of long duration with extensive colorectal
involvement, hypoalbuminemia and hypergammaglobulinemia
are often observed. Hypoalbuminemia is attributed
to increased loss of plasma through the denuded and
inflamed colorectal mucosa and hypergammaglobulinemia
is the response to continuing chronic inflammation.
L . Equine Hyperammonemia
Hyperammonemia and subsequent neurological signs
have been documented in horses with liver disease ( Divers
et al., 2006 ) , adult horses with gastrointestinal disease and
presumed bacterial overgrowth ( Desrochers et al., 2003 ;
Peek et al., 1997 ; Sharkey et al. , 2006 ), nursing foals with
portosystemic shunts ( Fortier et al., 1996 ), and weanling
Morgan foals with a genetic abnormality in hepatic ammonia
metabolism ( McCornico et al., 1997 ). The shunt foals
and Morgan weanlings are discussed elsewhere.
Pertinent to this chapter is the incidence of hyperammonemia
in horses with gastrointestinal dysfunction (i.e., colic
and diarrhea) that do not have hepatic disease. There is an
increased absorption of ammonia across inflamed intestinal
mucosa, or massive overproduction of ammonia within
the lumen of the gut, or a combination of both. Under normal
circumstances, ammonia is delivered to liver via portal
circulation and is metabolized by the Krebs-Hensleit
cycle to urea and glutamine. Systemic hyperammonemia
results when this cycle is overwhelmed. Ammonia readily
crosses the blood-brain barrier and, in high concentrations,
has a toxic effect on neuronal cell membranes. Resulting
encephalopathic signs may be reversible if the underlying
intestinal lesion or ammonia-producing bacteria are treated
in an appropriate manner.
A diagnosis of idiopathic hyperammonemia of intestinal
origin is based on the absence of infectious, toxic, or developmental
causes. In some of the reported cases, recent travel
or suspected changes in feeding or husbandry preceded the
acute onset of gastrointestinal signs. Increased blood ammonia
levels and subsequent encephalopathy developed within
a matter of hours. Hyperglycemia and metabolic acidemia
were also unique to the cases described by Peek et al.