The primary aim of the work reported in this
thesis was to transmit intestinal adenomatosis to
experimental piglets, thus enabling a study of the
role of Campylobacter sputorum subspecies mucosalis
(mucosalis) in the pathogenesis of the disease.
Field cases of porcine intestinal adenomatosis
(PIA) were studied, initially to provide experience
for the author in the techniques used, and later to
obtain infective mucosa and strains of mucosalis
with which to orally dose experimental piglets.
Naturally-farrowed, cross-suckled piglets were
exposed to adenomatous mucosa and cultures of
mucosalis. Mucosalis was not isolated from the
enteric mucosa at necropsy and no lesions of
adenomatosis were found, hence alternative approaches
to the problem were tried.
Naturally-farrowed, colostrum-deprived piglets
were exposed to adenomatous mucosa, but did not
survive for long enough to assess whether adenomatous
change would have occurred. The absence of maternallyacquired
immunity did not appear to enhance greatly
the establishment of mucosalis in the gut.
Gnotobiotic piglets were exposed to cultures of
mucosalis alone or in combination with rotavirus.
Mucosalis established and persisted in the lumen
of the gut in both groups but lesions of adenomatosis
did not develop.
Weaned pigs, exposed to either dual mucosalis
and rotavirus, or dual mucosalis and enterotoxigenic
Esch erichia coli infections, did not develop
adenomatosis and mucosalis was not isolated from the
gut at necropsy.
Finally a series of experiments was carried out,
on both milk-fed and creep-fed piglets, to investigate
whether Cryptosporidia, protozoan parasites of the
surface of epithelial cells, could promote parasitism
of pig enterocytes by mucosalis. There was no
evidence that Cryptosporidia enhanced the establishment of mucosalis in the gut, and adenomatous change
was not observed.