Bullous pemphigoid in an infant using complementary medicine.

Bullous pemphigoid (BP) is an acquired immunobullous disorder rarely seen in childhood. We report the case of an infant with BP successfully treated with oral corticosteroids. The onset of BP was associated with use of complementary medications and we speculate that these may have been triggering factors.

Duration of anti-adhesive and bactericidal activities of milk from vaccinated sows on Escherichia coli O149 in the digestive tract of piglets during the nursing period.

Piglets were exposed orogastrically to Escherichia coli to enable study of the duration of anti-adhesive and bactericidal activities of milk of sows vaccinated with a K88 enriched E coli vaccine. There was a marked increase in the number of the challenge strain in the digestive tract of weaned piglets of all ages (between 888 and 2144 per cent). In contrast, there was a decrease in their number (75 per cent) in the day-old colostrum-fed piglets. When the piglets were two weeks old milk was still capable of reducing the rate of proliferation of the pathogen but at five weeks it proliferated at equal rates in the digestive tract of both suckling and weaned litter-mates. The rate of adhesion of the K88 positive E coli to the small intestine of colostrum deprived piglets was high (5 x 108/g). Rate of adhesion fell gradually in weaned piglets from 5.4 x 107/g at two weeks to 2.0 x 106/g at four to five weeks of age. In contrast, resistance of the small intestine of suckling pigs to adhesion by K88-positive E coli remained relatively stable through the five week period of nursing bacterial counts ranging from 5 x 104/g to 3 x 104/g of tissue.

The effect of colostrum or past colibacillosis on the adhesion of Escherichia coli to the small intestine of the pig.

Nursing litters of vaccinated (K88 antigen) and non-vaccinated gilts as well as weaned piglets, which had recovered from natural colibacillosis, were exposed to Escherichia coli O149: K91(B), K88ac(L) orogastrically and 3-4 h after exposure a proportion of each group was killed for adhesion studies; others were kept for clinical observations. From killed piglets duodenal contents were collected and after washing of the duodenum by standardised techniques it was homogenised. Viable counts of E coli O149 in these specimens were carried out and compared. Colicounts in the duodenal contents and in the homogenate of washed duodenum of naturally infected piglets were also compared. There was less than tenfold difference in counts of K88-positive E coli between duodenal contents and washed duodenum of piglets which were (A) naturally infected, (B) colostrum deprived and experimentally infected, or (C) were from colostrum fed groups where those litter mates which were kept for clinical observation died of colibacillosis. There was 10(3)-10(5)-fold difference in E coli O149 counts between comparable specimens from piglets which (a) recently recovered from K88-positive E coli infection at the time of oral challenge or (b) were from colostrum fed groups where those litter mates which were kept for clinical observation survived oral challenge. It is concluded that adhesion of K88-positive E coli to the epithelium of the anterior small intestine of the pig is a feature of natural as well as experimental colibacillosis. Such adhesion may be prevented by (i) earlier natural infection of K88-positive E coli or (ii) by the ingestion of colostrum of K88 antigen vaccinated dams.