Over the years it has been important for humans to control the populations of harmful insects and insecticides have been used for this purpose in agricultural and horticultural sectors. Synthetic insecticides, owing to their various side effects, have been widely replaced by biological insecticides. In this review we attempt to describe three bacterial species that are known to produce insecticidal toxins of tremendous biotechnological, agricultural, and economic importance. Bacillus thuringiensis (BT) accounts for 90% of the bioinsecticide market and it produces insecticidal toxins referred to as delta endotoxins. The other two bacteria belong to the genera Photorhabdus and Xenorhabdus, which are symbiotically associated with entomopathogenic nematodes of the families Heterorhabditidae and Steinernematidae respectively. Whereas, Xenorhabdus and Photorhabdus exist in a mutualistic association with the entomopathogenic nematodes, BT act alone. BT formulations are widely used in the field against insects; however, over the years there has been a gradual development of insect resistance against BT toxins. No resistance against Xenorhabdus or Photorhabdus has been reported to date. More recently BT transgenic crops have been prepared; however, there are growing concerns about the safety of these genetically modified crops. Nematodal formulations are also used in the field to curb harmful insect populations. Resistance development to entomopathogenic nematodes is unlikely due to the physical macroscopic nature of infection. Xenorhabdus and Photorhabdus transgenes have not yet been prepared; but are predicted to be available in the near future. In this review we start with an overview of the synthetic insecticides and then discuss Bacillus thuringiensis, Xenorhabdus nematophilus, and Photorhabdus luminescens in greater detail.
Rifampicin-resistant mutants of a live vaccine strain (LVS) of Francisella tularensis were produced and screened for virulence in mice; 4 avirulent clones with intraperitoneal (ip) LD50s > 10(6) cfu, compared with 10(2) cfu for LVS, were characterized. Growth characteristics at 37 degrees C, surface envelope proteins, and lipopolysaccharide profiles of resistant mutants were identical to those of LVS. Polymerase activity of the mutants was more resistant than the enzyme from LVS to the inhibitory action of rifampicin. Growth rates for mutants and LVS were similar during the first 5 h at 42 degrees C, but viability of the mutants decreased to < 0.01% at 24 h. LVS and mutants differed in their ability to grow in vitro in host macrophages: LVS increased 580-fold over 72 h; mutants increased 33-fold. After ip inoculation of the organisms into mice, increasing numbers of LVS from peritoneal cells were isolated; mutants decreased over 4 days.
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