Helicobacter pylori was first cultured in vitro in 1982. This bacterium is a spiral gram-negative rod which grows under microaerophilic conditions. The ecological niche is the mucosa of the human stomach which had been thought to be aseptic before the discovery of this bacterium. This organism causes a long-lasting infection throughout a person's life if there is no medical intervention. Numerous persons are infected with the organism around the world, and the rate of infection in Japan is nearly 50% of the population. However, the route of infection remains unclear because the organism has not been isolated from any environment other than several animals. H. pylori is now recognized as a causative agent of gastritis and peptic ulcers. Though gastritis, and especially chronic active gastritis, is observed at least histologically in all persons with H. pylori, peptic ulcers develop in only some infected persons. Specific factors in the host and/or the bacteria are needed for the development of peptic ulcer disease. Furthermore, H. pylori is considered to be related to the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma, especially those of low grade. Also, H. pylori infection is a major determinant for initiating the sequence of events leading to gastric cancer. In some patients with low-grade gastric MALT lymphoma, the eradication of H. pylori led to a regression of lesion. Gastric cancer has been induced in Mongolian gerbils with long-term H. pylori infection. The combinations of drugs, which consist of an antisecretory agent (acid-supressing agent) and antimicrobial agents, are used for the eradication of the organism. Eradication therapy is recommended at least for patients with peptic ulcers.

Epidemiological studies suggest that patients with multiple sclerosis (MS) are exposed to some infectious agent(s) before puberty. The presence of virus-induced demyelination in animal models indicates that demyelination can occur following the trigger of a virus infection. Data regarding the immunological abnormalities to measles virus (MV) and the presence of neurological complications induced by MV infection suggest that MV may be a causative agent of the demyelination observed in MS. Numerous virological studies (e.g., morphological observation, virus isolation, and the search for the MV gene) have been performed, though definite evidence identifying MV as the causative agent has not yet been obtained.

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown origin. It has been speculated that infectious agents are responsible for triggering RA. Persistent infection with human parvovirus B19 and its induction of immunopathology are hypothesized to explain the initiation and perpetuation of the disease process.

Several infectious childhood diseases can be prevented by vaccination. A survey of hospital admissions for such diseases was conducted in Aichi Prefecture over 5 years beginning in 1994. A questionnaire was sent annually to hospitals with 100 or more beds to obtain information on pediatric patients requiring hospitalization for 10 vaccine preventable diseases. Information was obtained on 3,953 patients. Most admissions were for measles (49%), followed by mumps, chickenpox, pertussis, rubella, and tuberculosis. Over half of the patients were under 3 years old, with 20% aged under 12 months, 25% aged from 12 months to 2 years, and 10% aged from 2 to 3 years. The average hospital stay was longest for tuberculosis and pertussis, and was around 1 week for the other diseases. Familial transmission was the most common source of infection identified. The only death was an unvaccinated patient with measles pneumonia. Sequelae were reported at the time of discharge in 15 patients (0.4%), and were permanent in some cases. Some 96% of the patients surveyed were unvaccinated against the disease causing hospitalization. The fact that there were 14 patients with sequelae and the one patient who died were unvaccinated, emphasizes the need to promote vaccination.

Parasitism by Plasmodium yoelii yoelii induced 18 polypeptides in the salivary glands of aging malaria vector Anopheles stephensi. A polypeptide of low molecular size (30 kDa) could generally be induced at all infected stages. On day 5 post blood feeding (PBF), no new polypeptide could be found in the salivary glands. Seven polypeptides of low molecular size and 3 of high molecular size could be induced on day 11 PBF, which inducibility coincided with the invasion of the salivary glands by the sporozoites. Quantitatively, soluble proteins decreased in the salivary glands by about one-third in females that had consumed infected or uninfected blood meal on day 9 (oocysts stage) as compared to nonfeeding females. However, on day 15, in the salivary glands invaded by sporozoites, the amount of proteins obtained from infected females was approximately 26% lower than that obtained from uninfected females. A similar reduction was also observed in aged (20 days PBF) salivary glands of infected mosquitoes. These proteins could confer parasite tolerance to the females and enhance parasite transmission potential.