Incorporating germination-induction into decontamination strategies for bacterial spores.

Bacterial spores resist environmental extremes and protect key spore macromolecules until more supportive conditions arise. Spores germinate upon sensing specific molecules, such as nutrients. Germination is regulated by specialized mechanisms or structural features of the spore that limit contact with germinants and enzymes that regulate germination. Importantly, germination renders spores more susceptible to inactivating processes such as heat, desiccation, and ultraviolet radiation, to which they are normally refractory. Thus, germination can be intentionally induced through a process called germination-induction and subsequent treatment of these germinated spores with common disinfectants or gentle heat will inactivate them. However, while the principle of germination-induction has been shown effective in the laboratory, this strategy has not yet been fully implemented in real-word scenarios. Here, we briefly review the mechanisms of bacterial spore germination and discuss the evolution of germination-induction as a decontamination strategy. Finally, we examine progress towards implementing germination-induction in three contexts: biodefense, hospital settings and food manufacture. SIGNIFICANCE AND IMPACT: This article reviews implementation of germination-induction as part of a decontamination strategy for the cleanup of bacterial spores. To our knowledge this is the first time that germination-induction studies have been reviewed in this context. This article will provide a resource which summarizes the mechanisms of germination in Clostridia and Bacillus species, challenges and successes in germination-induction, and potential areas where this strategy may be implemented.

Crescentic fibrillary glomerulonephritis associated with intermittent rifampin therapy for pulmonary tuberculosis.

This case study reveals an unusual finding of rapidly proliferative crescentic glomerulonephritis in a patient treated with rifampin who had no other identifiable causes for developing this disease. This patient underwent a 10-month regimen of rifampin and isoniazid for pulmonary tuberculosis and was discovered to have developed signs of severe renal failure five weeks after completion of therapy. Renal biopsy revealed severe glomerulonephritis with crescents, electron dense fibrillar deposits and moderate lymphocytic interstitial infiltrate. Other possible causes of rapidly progressive glomerulonephritis were investigated and ruled out. This report documents the unusual occurrence of rapidly progressive glomerulonephritis with crescents and fibrillar glomerulonephritis in a patient treated with rifampin.