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

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Chapter | 14 Gastrointestinal Function
(1997) . Although Gram-negative bacilli such as Escherichia
coli, Klebsiella, Proteus, and Pseudomonas spp. are known
to be potent ammonia producers, reports pertaining to the
role of specific organisms in affected horses has been limited
to Clostridium sordelli (Desrochers et al., 2003 ).
Urea toxicity and ammonia intoxication, as well as
ingestion of high protein feeds, were ruled out as causes of
hyperammonemia in horses described by Peek et al. (1997) .
Horses would have to ingest a large amount of urea to
become toxic for a couple of reasons: (1) most of the urea is
absorbed in the small intestine before reaching the caecum,
which is the predominant site of urease activity; (2) urease
activity in the horse’s caecum is much less than that in the
cow’s rumen. Although horses are much more susceptible
to ammonia salts than urea, none of the horses were on pastures
that had been fertilized with ammonia salts.
M . Clostridial-Associated Diseases in
Horses and Cows
Clostridium difficile has been reported in several sources as
a cause of colitis in horses and various small bowel disorders
in horses, foals, and ponies. The potential role of this
organism in causing duodenitis-proximal jejunitis (DPJ)
in horses was proposed by Arroyo et al. (2006) . DPJ was
previously thought to be an idiopathic condition characterized
by inflammation and edema of the duodenum and
jejunum. Affected horses acutely developed signs of colic,
depression, ileus, fluid accumulation in the small intestine
and stomach, and endotoxemia. In the study reported by
Arroyo and his coinvestigator, toxigenic strains of C. difficile
were isolated from 10/10 horses with DPJ, and only
1 of 16 horses with other causes of nasogastric reflux.
C. perfrigens or Salmonella spp. were ruled out as causes
of DPF in affected horses.
Horses with proximal enteritis are predisposed to
hepatic injury ( Davis et al., 2003 ). When compared to
horses with small intestinal strangulation obstruction
(SISO), horses with proximal enteritis had significantly
higher serum gamma-glutamyltransferase (GGT), aspartate
aminotransferase, and alkaline phosphatase activities.
Horses with proximal enteritis were 12.1 times more
likely to have high GGT activities than were horses with
SISO. Suspected mechanisms for hepatic injury were
ascending infection from the common bile duct, absorption
of endotoxin or inflammatory mediators from the portal
circulation, or hepatic hypoxia resulting from systemic
inflammation and endotoxemic shock.
Hemorrhagic bowel syndrome (HBS) or jejunal hemorrhage
syndrome is an acute sporadic enteric disease recognized
most frequently in dairy cattle ( Berghaus et al.,
2005 ). Affected cows develop clinical signs consistent with
intestinal obstruction, which is attributed to segmental
necrohemorrhagic enteritis and large intraluminal blood
clots. Clostridium perfringens and Aspergillus fumigatus
have received the most attention as possible etiological
agents. The implementation of management practices
to achieve high mild production, as well as increased consumption
of high-energy rations, seems to be predisposing
a risk factor. The fatality risk is very high, and seldom does
medical and surgical intervention change the outcome.
IX . DISTURBANCES OF RUMEN
FUNCTION
The digestive process of ruminants differs from that of other
animals because rumen microbial digestion occurs before
other normal digestive processes. The short-chain fatty acids
(acetic, propionic, and butyric acids) are the primary end
products of rumen fermentation and are the chief sources of
energy available to ruminants from the diet. Cellulose, which
undergoes only limited digestion in most simple-stomached
animals, is readily digested because of the cellulitic bacteria
in the rumen. Ruminal bacteria can also use significant
quantities of nonprotein nitrogen (NPN) for protein synthesis,
and this bacterial protein subsequently can be utilized to
meet the protein requirements of the animal. Under experimental
conditions, ruminants may grow and reproduce while
receiving diets containing only NPN (e.g., urea) sources of
nitrogen. Bacterial production of vitamins can also meet
essentially all the requirements of ruminants.
Although nutritionally essential, bacterial fermentation
within the rumen presents certain unusual hazards for
ruminants. For example, when rapid changes in diet occur,
the products of fermentation can be released more rapidly
than they can be removed or utilized. Acute rumen tympany,
acute indigestion or D-lactic acidosis, and urea poisoning
are diseases that result from such abrupt changes in
diet ( Hungate, 1966, 1968 ).
A . Acute Rumen Indigestion (Rumen
Overload, Lactic Acidosis)
Acute rumen indigestion occurs in sheep or cattle consuming
high-roughage diets when they inadvertently
are allowed access to large amounts of readily fermentable
carbohydrate (e.g., grain or apples) ( Dunlop, 1972 ).
Streptococcus bovis is the rumen microorganism believed
to be chiefly responsible for rapid fermentation and for
production of large quantities of lactic acid ( Hungate et al.,
1952 ; Krogh, 1963a, 1963b ).
When lactic acid accumulates more rapidly than it
is absorbed, rumen pH falls and rumen atony develops.
Rumen bacteria produce a racemic mixture of lactic acid.
Some L-lactate is absorbed and metabolized by the liver and
other tissues, but D-lactate cannot be utilized and contributes
significantly to the acid load of the body. The excessive
lactic acid production results in metabolic acidosis