Before the advent of antibiotics, we lived with Staphylococcus aureus strains on our skin that existed in a complex mixture of commensal and virulent strategies, but antibiotics suddenly applied very strong selective pressure against any vaguely virulent strategy. Thus, following the model, the observed sudden decrease in both virulence and transmissibility of virulent strains makes a lot of sense. However, the sudden increase in both virulence and transmissibility of virulent strains that we’ve seen in multi-drug resistant (MRSA) strains also makes sense. Indeed, if you look back far enough in the literature all of the crazy new and terrible virulence factors we are now seeing in MRSA strains all existed before the 1930s. For example, while the pyomyositis and necrotizing pneumonia we are now seeing is commonly associated with poverty, tropical climates and HIV, ie: things which didn’t get much attention prior to 1935, it was described. (At lest with this source you’ll need to wade your way past the kinds of phrases that start with “Africans are not different from any other humans, however, …” to page 1214) Until recently it would not be terribly remarkable, being easily addressed with a simple round of I.V. antibiotics. I just found a reference in my Robbins Basic Pathology (8th ed.) which confirms that Staphylococcus aureus, as well as Klebsiella pneumoniae and Streptococcus pyogenes, has been implicated in causing necrotizing pneumonia since the turn of the century. Additionally, the PVL toxin which that first paper describes as now being found in pneumonia was initially discovered by Van deVelde in 1894 and was named after Sir Philip Noel Panton and Francis Valentine when they associated it with soft tissue infections in 1932. All of this makes logical sense anyhow, the mechanisms of antibiotic resistance are not associated with pathogenesis.
JC de Roode, AJ Yates, & S Altizer. Published 2002 in Proc. R. Soc. Lond. B doi:10.1098/rspb.2002.1976
We used the nuclear polyhedrosis virus of the gypsy moth, Lymantria dispar, to investigate whether the timing of transmission influences the evolution of virulence. In theory, early transmission should favour rapid replication and increase virulence, while late transmission should favour slower replication and reduce virulence. We tested this prediction by subjecting one set of 10 virus lineages to early transmission (Early viruses) and another set to late transmission (Late viruses). Each lineage of virus underwent nine cycles of transmission. Virulence assays on these lineages indicated that viruses transmitted early were significantly more lethal than those transmitted late. Increased exploitation of the host appears to come at a cost, however. While Early viruses initially produced more progeny, Late viruses were ultimately more productive over the entire duration of the infection. These results illustrate fitness trade-offs associated with the evolution of virulence and indicate that milder viruses can obtain a numerical advantage when mild and harmful strains tend to infect separate hosts.
Virulence-transmission trade-offs and population divergence in virulence in a naturally occurring butterfly parasite (PDF).
VS Cooper, MH Reiskind, et al. Published 2002 in PNAS doi:10.1073/pnas.0710909105
Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions—such as vaccines—may alter virulence evolution, yet empirical support is critically lacking. We studied a protozoan parasite of monarch butterflies and found that higher levels of within-host replication resulted in both higher virulence and greater transmission, thus lending support to the idea that selection for parasite transmission can favor parasite genotypes that cause substantial harm. Parasite fitness was maximized at an intermediate level of parasite replication, beyond which the cost of increased host mortality outweighed the benefit of increased transmission. A separate experiment confirmed genetic relationships between parasite replication and virulence, and showed that parasite genotypes from two monarch populations caused different virulence. These results show that selection on parasite transmission can explain why parasites harm their hosts, and suggest that constraints imposed by host ecology can lead to population divergence in parasite virulence.