Lancaster farming. (Lancaster, Pa., etc.) 1955-current, March 11, 2000, Image 36

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    A36-Lancaster Farming, Saturday, March 11, 2000
Crohn’s-Johne’s Connection: Scientists Look Into Controversy , Herd Control Options
(Continued from Page A 1)
21st Century Conference at the
Grantville Holiday Inn.
What science has found is
that a predisposition to acquir
ing Crohn’s is inherited in 15-30
percent of the cases, according
to the professor who studies dis
ease in the human gastrointesti
nal (GI) tract. The disease is
similar in humans in that it at
tacks the small Intestine, accord
ing to Bayless, but can attack
any part of the intestinal tract.
Johne’s, on one hand, is an ill
ness that infects primaiily
young cattle. Clinical symptoms
include diarrhea, loss of diet, re
duction in the amount of milk in
dairy animals, a general
“gaunt” appearance of cattle,
and other problems.
Crohn’s, on the other hand,
also affects young people the
average age of human onset of
the disease is 27 years old, with
similar symptoms.
Crohn’s is more frequent in
people of European descent,
more common in whites, and is
more common in Ashkenazi
Jews. It is more common in
urban and developed countries
but remarkably is less common
in those with poor sanitation as
a child. There is increased sever
ity in smokers. But there is no
evidence it can be passed from
human to human (including pa
tient spouses, physicians treat
ing CD, veterinarians treating
Johne’s, and farm workers or
families working with herds in
fected with Johne’s).
About 400,000 people in the
U.S. have Crohn’s disease.
About bO percent have surgery
to get a specific diagnosis.
“Is (mycobacterium paratu
berculosis what causes
Johne’s) a human pathogen?
Can it cause human disease?”
said Bayless.
Bay less noted that there is no
proof that the same bacterium
causes Crohn’s disease. Science
cannot identify the antigen and
there is no immune response.
To treat Crohn’s, various an
tibiotics are used. Bayless pro
vided a picture of a girl who had
Crohn’s onset at 10 years of age.
She looked gaunt and had leg
lesions.
Even former President
Dwight D. Eisenhower was a
victim of Crohn’s. And he was a
Pennsylvania farmer.
“Are farmers at risk of
Crohn’s disease?” Bayless said.
Bayless noted the evidence is in
conclusive. Sweden, which has
no Johne’s disease, has a high
incidence of Crohn’s.
The cause could be related to
perhaps a bacteria, a virus, di
etary, genetics, or some kind of
combination of the above with a
total immune system failure.
More work is under way.
Though samples of human
and cattle intestine match for re
sponse to Johne’s and Crohn’s
infections, that could be simply
because the intestinal tract has a
limited response to any type of
infection.
The Crohn’s and Colitis
Foundation of America spends
$4 million annually to research
the disease. They can be con
tacted at their Website,
www.ccfa.org.
Bayless pointed to a recent
workshop sponsored by the Na
tional Institute of Health on
Dec. 14, 1998 to see if a connec
tion between the two diseases
could be made. These were the
conclusions from the workshop
summary available on the Web
site www.niaid.nih.gov/dmid
/crohns.html:
• There is insufficient evi
dence to prove or disprove that
Mycobacterium avium subspe
cies paratuberculosis (MAP) is a
human pathogen or that it is the
cause of Crohn’s disease. Con
siderable controversy continues
to exist in the scientific commu
nity on this point.
• The difficulty in detecting
and growing the organism, or
being able to demonstrate a con
sistent immune response to it in
Crohn’s disease (CD) patients,
continues to frustrate research-
• Newer methodologies in
cluding the detection of micro
bial DNA sequences and
functional genomics are avail
able and should be applied in the
search for a microbial etiology of
Crohn’s disease. A wide net
should be cast. Characterization
of microbial “communities” as
sociated with this disease should
be sought. Comparison with the
completed genome sequences of
the related species M. tubercu
losis, M. leprae, and M. avium
may provide clues to the genetic
basis of the pathogenesis of
MAP.
• Good animal models for
CD do not exist and should be
sought. The development of ad
ditional genetically engineered
mouse strains or primate models
may be worthwhile, since cur
rent models do not develop
much of the pathology associ
ated with CD. Large animals,
including sheep and cattle that
get Johne’s disease from MAP
should be treated with vigorous
antimicrobial, anti
inflammatory, and immunosup
pressive treatment (typical of
what is used in humans) in con
junction with molecular charac
terization of associated
microbial populations and
strains.
• If MAP is proven to be a
human pathogen, there is the
potential for an enormous
impact on human health due to
the prevalence of this organism
on the farm and in water. Fur
ther study of MAP as a food
and/or waterborne pathogen
should be conducted. Viable
MAP should be sought in com
mercial milk and other dairy
products as well as in meat.
Conclusive studies of the effec
tiveness of pasteurization using
commercial equipment and pro
cess rather than laboratory
simulations should be per
formed. In order to conduct the
above, standard methods for the
concentration, detection, and in
vitro culture of Map should be
developed and used by partici
pating researchers. Federal
agencies with regulatory author
ity over the food supply should
consider conducting such re
search in cooperation with rele
vant food production industries
and academic researchers.
Dr. Robert Whitlock, profes
sor of the school of veterinary
medicine at the University of
Pennsylvania New Bolton
Center, spoke about Johne’s dis
ease in cattle and how important
control efforts are.
When asked about the possi
ble connections of drinking raw,
unpasteurized milk, Whitlock
noted that he drank it as a child
himself. But for those who drink
it, the risk of ingesting Johne’s is
Day two of the conference featured speakers, from left, Theodore Bayless, professor
of medicine, head of gastroenterology, Johns Hopkins University; Ron Schultz, profes
sor and chair of pathobiological sciences, School of Veterinary Medicine, University of
Wisconsin; Robert Whitlock, professor, School of Veterinary Medicine, University of
Pennsylvania New Bolton Center; and Dave Galligan, section chief of animal health,
economics, and nutrition, School of Veterinary Medicine at University of Pennsylvania
New Bolton Center.
Speakers at the Pennsylvania Agriculture in the 21st Century included, from left, Ken
neth Bailey, associate professor of ag economics, Penn State; Dave Galligan, section
chief of animal health, economics, and nutrition, School of Veterinary Medicine at Uni
versity of Pennsylvania’s New Bolton Center; Steve Watrin, director of dairy business
services, Land O’Lakes, St. Paul, Minn.; Dave Pyburn, director of veterinary medicine,
National Pork Producers Council; Julie Funk, extension food safety specialist, North Ca
rolina Extension Service; Eugene Gantz, president, Agßisk Strategies Inc., Millersburg;
Dan Ferber, free-lance science journalist, Urbana, III.; Ron Schultz, professor and chair
of pathobiological sciences, School of Veterinary Medicine, University of Wisconsin;
Ron Roberts, Sterling, Scotland; and Don Bell, poultry specialist, University of Califor
nia.
“very, very, very small.’’
Also, the bacterium will not
survive the pilot commercial
pasteurization methods with
their short-term, high tempera
tures, Whitlock noted.
However, dairy producers
must learn to focus more on
eradication programs, including
culling the older, higher
shedding animals first and cre
ating a program that is
economically viable to protect
the more valuable young stock.
Johne’s is a chronic bacterial
infection that begins in the
young calf and can take a long
time as long as 10 years to
be clinically evident. But most
animals on the farm that have it
“don’t show any clinical signs,”
Whitlock said.
Usually if the herd animal
identified at the top is shedding
and has clinic signs, there could
be 15-20 animals infected that
aren’t showing any clinical
signs. They look “perfectly
normal,” he said.
Also, cows in the summertime
cooling off in a farm stream or
pond can infect other cows read
ily.
Other animals, including
dairy goats and deer are even
more susceptible to it. Whitlock
tion between the two diseases
could be made. These were the
conclusions from the workshop
summary available on the Web
site www.niaid.nih.gov/dmid
/crohns.html:
• There is insufficient evi
dence to prove or disprove that
Mycobacterium avium subspe
cies paratuberculosis (MAP) is a
human pathogen or that it is the
cause of Crohn’s disease. Con
siderable controversy continues
to exist in the scientific commu
nity on this point.
• The difficulty in detecting
and growing the organism, or
being able to demonstrate a con
sistent immune response to it in
Crohn’s disease (CD) patients,
continues to frustrate research-
• Newer methodologies in
cluding the detection of micro
bial DNA sequences and
functional genomics are avail
able and should be applied in the
search for a microbial etiology of
Crohn’s disease. A wide net
should be cast. Characterization
of microbial “communities” as
sociated with this disease should
be sought. Comparison with the
completed genome sequences of
the related species M. tubercu
losis, M. leprae, and M. avium
may provide clues to the genetic
basis of the pathogenesis of
MAP.
• Good animal models for
CD do not exist and should be
sought. The development of ad
ditional genetically engineered
mouse strains or primate models
may be worthwhile, since cur
rent models do not develop
much of the pathology associ
ated with CD. Large animals,
including sheep and cattle that
get Johne’s disease from MAP
should be treated with vigorous
antimicrobial, anti
inflammatory, and immunosup
pressive treatment (typical of
what is used in humans) in con
junction with molecular charac
terization of associated
microbial populations and
strains.
• If MAP is proven to be a
human pathogen, there is the
(Turn to Page A 37)