Helicobacter pylori (H. pylori), a gram-negative microaerophilic bacterial 
pathogen that colonizes the stomachs of more than half of all humans, is linked 
to chronic gastritis, peptic ulcers and gastric cancer. Spiral-shaped H. pylori 
undergo morphologic conversion to a viable but not culturable coccoid form when 
they transit from the microaerobic stomach into the anaerobic intestinal tract. 
However, little is known about the morphological and pathogenic characteristics 
of H. pylori under prolonged anaerobic conditions. In this study, scanning 
electron microscopy was used to document anaerobiosis-induced morphological 
changes of H. pylori, from helical to coccoid to a newly defined fragmented 
form. Western blot analysis indicated that all three forms express certain 
pathogenic proteins, including the bacterial cytotoxin-associated gene A (CagA), 
components of the cag-Type IV secretion system (TFSS), the blood group 
antigen-binding adhesin BabA, and UreA (an apoenzyme of urease), almost equally. 
Similar urease activities were also detected in all three forms of H. pylori. 
However, in contrast to the helical form, bacterial motility and TFSS activity 
were found to have been abrogated in the anaerobiosis-induced coccoid and 
fragmented forms of H. pylori. Notably, it was demonstrated that some of the 
anaerobiosis-induced fragmented state cells could be converted to 
proliferation-competent helical bacteria in vitro. These results indicate that 
prolonged exposure to the anaerobic intestine may not eliminate the potential 
for H. pylori to revert to the helical pathogenic state.