01 January 2016 0 10K Report

We would like to make a vaccine to protect animal hosts against an entire bacterial species as this is economically favourable.

When can this type of approach work?  Only when the bacterial group have adopted a "burn down the house to keep warm" mode of existence meaning that that are near obligately pathogenic and burn through the animal host like a fire.

Classic vaccinology techniques tend to protect animal hosts from bacterial isolates/species that have adopted a "burn down the house to keep warm" mode of existence (obligately pathogenic).  This is true because the very nature of their existence tends to make them relatively clonal.  These organisms burn through their host like a fire with little time for genetic change, and a nuanced proteome. Also, bacterial vaccine targets may be openly displayed and virulence genes relatively unregulated.

Classic vaccinology fails miserably in protecting animal hosts from bacterial isolates/species that establish a stable relationship with the host and are triggered to cause disease by host trauma and other factors (trigger pathogens).  The reason that classic vaccinology fails is because these types of bacteria have a very low level of clonality and every isolate recovered from a host may be relatively unique. This uniqueness precludes a single vaccine from being universally effective at the "species" level.

Obligately pathogenic bacteria need to find a host and find a hold at very low numbers, then compete with what microflora already there and then express a proteome that may cause disease, all a relatively low biomass. Trigger pathogens are the exact opposite. These bacteria tend to coexist long term with the host in huge numbers, and with their "virulence" genes are tightly regulated in the off position.  All these bacteria need to do it turn one or 2 genes on to dehabilitate or kill the host, and there really is no defense against this.  This is rare because bacteria need us more than we need them, and only occurs under specific conditions such as impending host death or presence of a competitor. The better the tuning of the bacteria to the host, the lesser the chance of inappropriate triggering in the bacteria to the disease causing state.

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