murine model was used to verify the viability and pathogenicity of coccoid Helicobacter pylori
. For this purpose, 27 BALB/c mice were inoculated intragastrically
with 1 ml broth culture (108
organisms/ml) of a coccoid H. pylori clinical
isolate. The animals were divided into two groups. Nine were infected on a one-time
basis (GA1) and 18 were infected on two consecutive days (GA2). Other 27 mice
were inoculated with Brucella broth and divided in the same way; they composed
the control group. Mice were killed at 2, 3, 7, 14 and 21 days post inoculation
(pi). Fragments of stomach and duodenum were collected, fixed with 12% formalin
and stained by hematoxilin-eosin and Giemsa for histopathological examination.
Until the 14th day, only reinfected mice had mild-to-moderate inflammatory infiltrate
in the stomach. The infiltration was predominantly lymphomonocytic, although plasma
cells and eosinophils could be seen. However, at 21st day, severe eosinophilic
infiltration was present in the lamina propria and submucosa of gastric corpus.
In subgroup GA1, animals presented lymphomonocytic infiltration in the stomach
from 14th day pi. Our results showed that coccoid H. pylori was able to induce
an acute inflammatory response in stomach of reinfected mice since the initial
periods of infection.