Thirteen patients with leptospirosis were identified, as confirmed by laboratory analysis during the last 5 years in our laboratory, who came from urban areas of Tokyo, Japan. All of the patients came into contact with rats before the onset of illness. Seventeen per cent of Norway rats captured in the inner cities of Tokyo carried leptospires in their kidneys. Most of these rat isolates were Leptospira interrogans serovar Copenhageni/Icterohaemorrhagiae. Antibodies against these serovars and their DNA were detected in the patients. This suggests that rats are important reservoirs of leptospirosis, and that rat-borne leptospires occur in urban areas of Tokyo.

Maternally inherited female-biased sex ratios have been documented in many invertebrate species. One cause of such biased sex ratios is male killing, i.e. only males die. In most species, male killing occurs during embryonic stages (early male killing) and is associated with cytoplasmic bacteria, including Wolbachia, Spiroplasma, Rickettsia, Flavobacteria and gamma proteobacteria. However, the oriental tea tortrix, Homona magnanima, is one of the few species in which male death occurs in the larval or pupal stage, and is thus an example of late male killing. We partially purified the agent causing late male killing in H. magnanima and showed that it consists of two RNA sequences. This represents an entirely novel agent causing late male killing.

The late male-killing phenomenon was reported in the oriental tea tortrix, Homona magnanima, but its gross pathology and histopathology have not been elucidated. The present study investigated pathological changes in larvae of a late male-killing strain of H. magnanima (LMK). Most male LMK larvae died during the last instar or pupal stage, and dead male larvae showed characteristic signs and symptoms of male killing. The body color of male LMK larvae started to change 4 d after molting into the fifth instar and became increasingly opaque white. Male LMK larvae weighed significantly less than normal-strain (NSR) males. Midgut epithelial cells of male LMK larvae developed normally and microvilli were observed on the luminal side 3 d after the final molt. Regenerative cells of male LMK larvae were observed on the basement membrane but these cells did not develop to pupal midgut cells. From 7 d after the final molt, midgut cells of male LMK larvae were discharged into the lumen as granules and regenerative cells elongated from the basement membrane. All midgut cells of male LMK larvae dropped into the lumen just before death and no cells were observed on the basement membrane. The fat body of male LMK larvae contained large fat granules in the cytoplasm but became a tumor-like cell mass that finally fused with epidermal cells. These changes were specific to LMK males; no differences in the developmental pattern or morphology were observed between female LMK and NSR larvae. From these results, it is suggested that the degradation of midgut epithelial cells may be the main reason for late male killing.