Effects of Mycobacterium bovis BCG, bacterial lipopolysaccharide and hydrocortisone on the development of immunity to Plasmodium berghei.

M y c o b a c t e r i u m b o v i s ( B C G ) s ignif icant ly e n h a n c e d the d e v e l o p m e n t o f im­ muni ty b y CFW, C57BL/6 , C 5 7 B L / 1 0 S c N and B A L B / c ( N u + ) m i c e t o the e r y t h r o c y t i c s tages o f P. berghei. M i c e t reated wi th B C G requ i r ed f e w e r c y c l e s o f in fec t ion and Pansidar ( p y r i m e t h a m i n e + su l f adox ine ) c u r e in o r d e r to d e v e l o p s o l i d immun i ty than unt rea ted , i m m u n i z e d m i c e . H o w e v e r , t hose , m i c e t reated wi th B C G at 30 days b e f o r e the ini t ia t ion o f i m m u n i z a t i o n s h o w e d an ear l iear l o s s o f i m m u n i t y to P. be rghe i than those m i c e w h i c h r e c e i v e d B C G at 14 d a y s o r n o B C G . Thus , B C G e n h a n c e d the hos t i m m u n e r e s p o n s e t o P. berghei dur ing an initial infec t ion , b u t s h o r t e n e d the length o f i m m u n i t y s o that mice w e r e m o r e suscep t ib le to P. berghei dur ing subsequen t in fec t ions . T r e a t m e n t o f CFW, B A L R / c and C57BL/6 m i c e w i t h bacter ia l l i p o p o l y s a c c h a r i d e o r h y d r o c o r t i s o n e aceta te ( H D C ) c a u s e d the a n i m a l s t o requi re m o r e c y c l e s o f i n f ec t i ons and d rug c u r e in o r d e r t o attain i m m u n i t y than c o n t r o l s . T r e a t m e n t o f i m m u n i z e d C57BTV lOScN m i c e w i t h h y d r o c o r t i s o n e c o m p l e t e l y a b o l i s h e d thei r abi l i ty t o surv ive a P. berghei infec t ion .