Interaction of group B streptococcal opacity variants with the host defense system.
Group B streptococci (GBS) demonstrate high-frequency phase variation of colony opacity. Colony opacity is a function of chain length, with opaque colonies consisting of GBS that form longer chains. Because opaque variants do not grow on standard streptococcal media, the role of opacity variation in GBS infection has not been studied. We have isolated stable variants from type III GBS that are either transparent (variants 1.2 and 1.3) or opaque (variants 1.1 and 1.5). In this study, we evaluated the interactions of these variants with different components of the host immune system both in vitro and in vivo. Opaque GBS were less immunogenic than transparent GBS. Opaque GBS were more susceptible to killing by polymorphonuclear neutrophils (PMNs) and could induce a chemiluminescent response of PMNs in the absence of antibody (Ab) or complement. Transparent GBS did not induce neutrophil chemiluminescence in the absence of Ab and complement. However, in the presence of Ab and complement, transparent GBS induced a stronger chemiluminescent response than did opaque GBS. Scanning electron micrographs of PMNs and GBS demonstrated differences in the attachment and engulfment of the different variants by the PMNs as well as different effects of the GBS on the PMNs themselves. Interactions with complement were affected by GBS opacity as well, with opaque variant 1.1 initiating complement activation in the absence of any Ab. The virulence of the GBS opacity variants was studied in vivo by inoculation of graded numbers of GBS into newborn mice. Transparent variants 1.2 and 1.3 were most virulent, with variant 1.1 intermediate and variant 1.5 minimally virulent. However, in mixed infections, variant 1.5 greatly enhanced the virulence of small numbers of transparent GBS. These results indicate that the opacity status of GBS can influence the interaction between the GBS and the host immune system.
Pincus
S H
SH
Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.
Cole
R L
RL
Kamanga-Sollo
E
E
Fischer
S H
SH
D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology*; D003167:Complement Activation; D007114:Immunization; D008163:Luminescent Measurements; D051379:Mice; D008807:Mice, Inbred BALB C; D008855:Microscopy, Electron, Scanning; D009504:Neutrophils / Q000276:immunology* / Q000648:ultrastructure; D013290:Streptococcal Infections / Q000382:microbiology; D013292:Streptococcus agalactiae / Q000276:immunology* / Q000472:pathogenicity / Q000648:ultrastructure; D014774:Virulence
D000907:Antibodies, Bacterial