In another study, Anderson and Johnson showed by electron microscopy that Propyl gallate leptospires belonging to saprophytic Phenelzine sulfate salt strain Patoc I and nonvirulent serovar Canicola retained their shape but lost their outer sheath after incubation with complement and immune serum. In contrast, leptospires of the virulent serovar Canicola were not affected at all by complement and antibodies. Incubation with either THP-1 cells or PBMC did not result in killing of any of the viable leptospiral strains. Indeed, previous studies reported similar findings, suggesting that phagocytosis or the release of bactericidal mediators are not major processes involved in the killing of leptospires. An important conclusion on this observation is that caution is needed by interpretation of results obtained with stripped models for exploring cytokine responses upon leptospiral infection. Additionally, the data presented herein emphasize the importance to use viable low passage isolates to study the host response to Leptospira infection. In conclusion, our results show that the innate human host response to leptospiraemia involve, but may not be limited to the action of TLR2, TLR4 and TLR5. Further research is needed on the mechanism of interactions of these TLRs to unravel their involvement during human leptospirosis. Friedreich ataxia is a fatal, autosomal recessive neurodegenerative disorder caused by homozygous GAA repeat expansion within intron 1 of the FXN gene. This mutation induces heterochromatin formation, likely due to abnormal non-B DNA or DNANRNA hybrid triplex structures, leading to FXN gene silencing and thus reduced expression of the essential mitochondrial protein, frataxin. Frataxin insufficiency culminates in mitochondrial iron accumulation and reduced activity of iron-sulfur cluster enzymes, including mitochondrial respiratory chain complexes and aconitase, leading to increased susceptibility to oxidative stress and resultant cell degeneration. The primary sites of FRDA pathology are the large sensory neurons of the dorsal root ganglia and the dentate nucleus of the cerebellum. However, there are also non-neuronal tissue dysfunctions including diabetes and cardiomyopathy, followed by death commonly in early adulthood.