Agent genetically altered

Bammert GF et al. Genome-wide expression patterns in Saccharomyces cerevisiae comparison of drug treatments and genetic alterations affecting biosynthesis of ergosterol. Antimicrob Agents Che-mother 2000 44 1255-1265. 

Loss of tumor suppressor gene is the most common genetic alteration found in human cancers. Deletion of one or both alleles of p53 (p53 knockout mice) increases the incidence of neoplasia and decreases latency of tumor development. When p53 knockout mice are exposed to genotoxic agents, they rapidly develop neoplasms in a range of tissues. Sensitive targets in p53 mice are often comparable to those in normal mice and hence, their utility as a model. 

The possibility of genetically altered agents, which introduces the potential for many more scenarios, suggests that model-based approaches to identify and track biological attacks for estimating who might be exposed will be prudent for some years. 

Secondary resistance—Develops upon exposure to an antifungal agent and can be either reversible, due to transient adaptation, or acquired as a result of one or more genetic alterations. 

A wide variety of species have been treated with both case-associated and reconstituted oils, with only a few reports that some of the classical symptoms have been observed in mice (eosinophilia and elevated IgE) and rats (lung oedema, respiratory difficulties, splenomegaly). Possible explanations for the generally negative results in animal models are that toxic oil syndrome may be a uniquely human disease, animals may have a lower sensitivity to toxic oils, the dose used may not have been adequate, and multiple agents, genetic factors, and biochemical alterations may be involved in disease development. 

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