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 BRIEF COMMUNICATION
Dietary factors do not influence the clinical expression of
swine dysentery
Roy N. Kirkwood, DVM, PhD; Suxi X. Huang, PhD; Margaret McFall;
Frank X. Aherne, PhD
Kirkwood RN, Huang SX, McFall M, et al. Dietary factors do
not influence the clinical expression of swine dysentery. Swine
Health Prod. 2000;8(2):73-76. This article is also available
in PDF format.
RNK: Royal Veterinary College, Hawkshead Lane, North Mymms,
Herts, United Kingdom AL9 7TA; SXH, MM, FXA: Alberta Agriculture
Food and Rural Development, Canada
Summary
Three experiments were performed to determine the effect of
manipulating the amount of fermentable substrates entering the
large intestine on the incidence of swine dysentery after experimental
infection with 1.8 x 1010 Brachyspira hyodysenteriae
per day for 3 consecutive days. In Experiment One, diets were
formulated to contain a high proportion of fermentable fiber (30%
wheat shorts and 15% raw potato starch), or a high proportion
of nonfermentable fiber (15% ground oat hulls), or a low proportion
of fiber (corn-soybean meal diet). In Experiment Two, diets were
formulated either with highly digestible parboiled rice and animal
protein, which would provide little substrate for fermentation
in the large intestine, or 25% beet pulp to provide a high content
of fermentable fiber. A commercial barley-wheat soybean meal grower
diet was used as the control. In Experiment Three, the experimental
diet was formulated with highly digestible cooked rice and animal
protein and the control diet was a commercial barley-wheat soybean
meal grower diet. In all experiments, the diets failed to provide
satisfactory protection against experimental infection with
B. hyodysenteriae.
 Keywords: swine,
Brachyspira hyodysenteriae, diet, fermentable fiber
Received: August 18, 1999
Accepted: December 13, 1999
Swine dysentery is a
mucohemorrhagic colitis characterized bywasting and diarrheic
feces that contain mucus, blood, and necrotic material.1
The etiology is the spirochete Brachyspira hyodysenteriae.
The disease causes economic loss due to pig mortality and severe
depression in growth rates.1 It is widely believed
that the clinical expression of swine dysentery might be influenced
by diet. Prohaszka, et al, observed that feeding a diet high in
cellulose/hemicellulose prevented the clinical signs associated
with infection with B. hyodysenteriae.2 They
suggested that by supplying more fermentable substrate to the
colon, the diet increases volatile fatty acid (VFA) production,
reducing colonic pH and creating an unfavorable environment for
the spirochetes. In support of this hypothesis, anecdotal evidence
indicates that control of spirochetal diarrhea (not swine dysentery)
may be achieved by switching from a pelleted to a meal diet. This
would increase the amount of resistant starch entering the cecum
and colon, thereby increasing fermentation and VFA production.
In contrast to the above, it was recently reported that highly
fermentable diets allowed swine dysentery to develop, but that
highly digestible diets were protective.3,4 These investigators
have suggested that highly digestible diets limit the amount of
substrate entering the cecum and colon and so reduce microbial
fermentation and VFA production. Presumably, either limiting substrate
or increasing colonic pH produces a protective effect. Further
studies are clearly needed to clarify these contradictory results
and to determine whether susceptibility to swine dysentery can
be controlled nutritionally by feeding diets that lead to high
or low fermentation in the large intestine.
Materials and methods
For Experiments One and Two, 24 barrows were obtained from
the University of Alberta swine herd that were clinically free
of swine dysentery and without clinical evidence of spirochetal
colitis. For Experiment Three, 20 barrows were obtained from a
commercial herd, also free of clinical swine dysentery and spirochetal
colitis. Although no bacterial isolation was attempted to verify
that the herds were free of B. hyodystenteriae and B.
pilosicoli, there had never been a case of swine dysentery
over the entire history of either herd used in these three experiments.
All experimental pigs were housed in groups of four in a temperature-controlled
animal room (20-22 degrees C, 68-72 degrees F) and were fed ad
libitum either a commercial grower diet or an experimental diet.
Daily feed intakes were not calculated due to the nature of the
experimental diets, which allowed considerable spillage onto the
floor. Water was freely accessible from a low-pressure drinking
nipple.
Inoculant
The spirochete suspensions were prepared by inoculating blood
agar plates with the bacteria and then incubating the plates anaerobically
for 48 hours. The bacteria were harvested from six plates and
mixed in 21 mL sterile phosphate-buffered saline. One mL of the
suspension was used for a viability count. There were approximately
3 x 108 CFU per mL of suspension.
Experiment One
Twelve pigs from the University of Alberta herd were assigned
to one of three diets (Table 1):
- 2918 kcal per kg DE with a high proportion of fermentable
fiber (30% wheat shorts and 15% raw potato starch; 10.7% neutral
detergent fiber) in an attempt to simulate the high-fiber diet
that Prohaszka and Lukacs2 found to be protective
against swine dysentery (n = 4);
- 3048 kcal per kg DE with a high proportion of nonfermentable
fiber (15% ground oat hulls; 19.1% neutral detergent fiber) to
serve as a control high fiber diet (n = 4); or
- 3579 kcal per kg DE with a low proportion of fiber (corn/heat-treated,
solvent extracted, dehulled soybean meal diet; 7.3% neutral detergent
fiber) (n = 4).
The diets for Experiment One were isonitrogenous (16.5%-17%
crude protein) and were formulated with locally available ingredients.
After an 8-day adaptation period, pigs were fasted for 18 hours
(Figure 1). Then, on each of 3 consecutive
days, each pig was intragastrically inoculated via a stomach tube
with 60 mL of the B. hyodysenteriae (B204) suspension (1.8
x 1010 spirochetes per day).
Pigs were euthanized at study day 16 and sections of distal
ileum, cecum, proximal colon, middle colon, and distal colon were
collected for reculture of spirochetes. No statistical analysis
was performed on data.
Experiment Two
Rather than use conventional locally available ingredients,
the experimental diets for Experiment Two were formulated to resemble
as closely as possible those that have been previously reported
to be protective against swine dysentery, and were compared to
a commercial barley/soybean meal grower diet. Twelve pigs were
assigned by weight to one of three diet treatments (Table 1):
- a low fiber-high digestibility diet, including 78% parboiled
rice that provided 17.8% crude protein, 3435 kcal per kg DE,
and 9.7% neutral detergent fiber (n = 4);
- a high fermentable fiber diet, including 25% beet pulp that
provided 17.7% crude protein, 3036 kcal per kg DE, and 18.3%
neutral detergent fiber (n = 4); or
- a control diet, which was a commercial barley/soybean meal
grower diet, and provided 19.6% crude protein, 3402 kcal/kg DE,
and 10.1% neutral detergent fiber (n = 4).
After an 8-day adaptation period, pigs were fasted for 18 hours
(Figure 1). Then, on each of 3 consecutive
days, each pig was intragastrically inoculated with 60 mL of the
B. hyodysenteriae (B204) suspension (1.8 x 1010
spirochetes per day). Pigs were euthanized at study day 16 and
sections of distal ileum, cecum, proximal colon, middle colon,
and distal colon were collected for reculture of spirochetes.
No statistical analysis was performed on data.
Experiment Three
Twenty pigs were assigned to one of two isonitrogenous diets
(18.8%-19.6% crude protein; Table 1):
- a highly digestible experimental diet, formulated with 73.8%
rice cooked in an oven until very soft, that supplied 3159 kcal
per kg DE in order to closely approximate the protective diet
described by Pluske, et al. (n = 10);4 or
- a commercial barley/soybean meal grower diet (n = 10).
After a 21-day adaptation period followed by an 12- to 14-hour
fast, four pigs from each dietary treatment were euthanized and
the contents of the cecum, proximal colon, and distal colon were
collected (Figure 1). The pH of these
samples was determined within 5 minutes of death using a portable
pH meter (Horiba Ltd.; Irvine, California). Where necessary, colonic
content was liquefied in distilled water prior to insertion of
the pH probe. Data for dietary effects on colonic pH were compared
by a repeated-measures ANOVA using Number Cruncher Statistical
System (Kaysville, UT).
The remaining pigs were intragastrically inoculated with 60
mL of the B. hyodysenteriae (B204) suspension (1.8 x 1010
spirochetes per day) on each of 3 consecutive days. Pigs were
euthanized at study day 33 and sections of distal ileum, cecum,
proximal colon, middle colon, and distal colon were collected
for reculture of spirochetes.
Results
The average initial bodyweight of the pigs in all experiments
was 20 kg (44 lb) (range 18-22 kg, 39.6-48.4 lb).
Experiment One
All pigs developed a mucohemorrhagic diarrhea within 16 days
of inoculation. In this experiment, none of the diets provided
protection to the pigs against dysentery.
Experiment Two
All pigs, except for one fed the parboiled rice diet, developed
a mucohemorrhagic diarrhea within 15 days of inoculation. In this
experiment, none of the diets provided protection to the pigs
against swine dysentery.
Experiment Three
At the end of the 21-day adaptation period, the pH of colonic
content (cecum and proximal and distal colon) was higher in the
pigs fed cooked rice than in those fed the commercial grower diet
(P<.02; Figure 2). All pigs
except for two that received the commercial grower diet developed
a mucohemorrhagic diarrhea within 7 days of inoculation. In this
experiment, neither diet provided adequate protection to the pigs
against swine dysentery.
Discussion
In the present study, the high fermentable-fiber diets did
not reduce the incidence or severity of swine dysentery compared
to control diets. The inconsistency of our results with those
of Prohaszka and Lukacs2 might be due to differences
in the experimental design: their experiment was performed under
noncontrolled field conditions on farms where a field strain of
B. hyodysenteriae was endemic. In our experimental model,
the pigs were fasted for 12-18 hours before inoculation on each
of 3 consecutive days with a laboratory strain of B. hyodysenteriae.
Under the conditions of the experimental model, when the bacteria
entered the large intestine and proliferated, there may have been
limited fermentable substrates available.
The results of Experiments Two and Three contrast with reports
from Australia3,4 since no protective effect was observed
from feeding diets formulated with either parboiled or cooked
rice. The reason that we failed to obtain any dietary protection
against swine dysentery is not known. The cecal and colonic pH
in our cooked rice-fed pigs were similar to those observed by
the Australian investigators, suggesting that the colonic response
to the diets were not different. However, the pH values that result
from fermentation of substances entering the large intestine may
not be a precise measure of the relative favorability of the environment
to spirochetes. Indeed, 95% of strains of B. hyodysenteriae
can utilize most monosaccharides and produce acids with a pH of
6 and below.5
It is known that B. hyodysenteriae requires the presence
of other bacteria before it can colonize the colonic mucosa.6
It is possible that the resident flora in our pigs differed from
that in the Australian pigs and so interacted differently with
B. hyodysenteriae, resulting in a different clinical outcome.
Finally, we used a different strain of B. hyodysenteriae
than did the Australian workers and our strain may respond differently
to enteric environmental changes associated with the feeding of
cooked rice.
In spite of previous work2-4 and our observations,
it is still unclear as to whether highly digestible or highly
fermentable diets can protect pigs from infection by B. hyodysenteriae.
Other experimental infection models need to be evaluated to eliminate
the effect of feed withdrawal on the normal digestive and fermentation
process in the intestine of pigs.
Acknowledgements
We are very grateful to Shirley Rawluk, Carol Goertz, Arlene
Otto, Louise Hawker, and Vicki Maitland for technical support
and Dr. Artur Cegielski and graduate students for assistance in
the management of this study. The B. hyodysenteriae was
generously provided by Dr. K.R. Mittal, University of Montreal,
St. Hyacinthe, Quebec. This study was made possible by the financial
support of the Alberta Pork Producers Development Corporation
and the Alberta Agricultural Research Institute.
References
1. Taylor DJ. Pig Diseases (6th ed).
The Burlington Press: Cambridge, UK.
2. Prohaszka L, Lukacs K. Influence of the diet in the
antibacterial effect of volatile fatty acids and on the development
of swine dysentery. Zbl Vet Med B. 1984;31:779-785.
3. Siba PM, Pethick DW, Hampson DJ. Pigs experimentally infected
with Serpulina hyodysenteriae can be protected from developing
swine dysentery by feeding them a highly digestible diet. Epidemiol
Infect. 1996;116:207-216.
4. Pluske JR, Siba PM, Pethick DW, Durmic Z, Mullan BP, Hampson
DJ. The incidence of swine dysentery in pigs can be reduced by
feeding diets that limit the amount of fermentable substrate entering
the large intestine. J Nutr. 1996;126:2920-2933.
5. Smibert RM. Anaerobic Spirochetes. In: Balows A, Hausler
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Matthews PJ. Swine dysentery: studies of gnotobiotic pigs inoculated
with Treponema hyodysenteriae, Bacteriodes vulgatus
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