F Rosa Rubicondior: Malevolent Designer News - How Creationists' Favourite Sadist Kills Its Victims With Plague

Thursday 15 December 2022

Malevolent Designer News - How Creationists' Favourite Sadist Kills Its Victims With Plague

Oropsylla montana (a ground squirrel flea) infected and blocked with Yersinia pestis
Creationism's divine malevolence is now using the microorganism, Yersinia pestis, with which it killed 30%-60% of European humans and 75-200 million humans worldwide between 1346 and 1353, to have periodic bouts of killing rodents such as rats, mice, gerbils, squirrels, marmots and prairie dogs.
Having created these rodents, according to Creationists, it then designed Yersinia pestis to kill them, using different species of flea as vectors to make sure the plague spreads quickly and widely.

Now scientists have worked out why it changes periodically from an enzootic to an epizootic disease. It's all down to what happens in the gut of infected fleas which spread the disease. They have published their findings today in the open access journal, PLOS Pathogens.

According to information provided ahead of publication:
Scientists have long been puzzled how the bubonic plague bacteria, Yersinia pestis, can cause both stable, enzootic disease among rodents, as well as sudden, lethal epizootic outbreaks that decimate the same rodent populations. A new study concludes that the difference might relate to the fleas that carry Y. pestis between animals. Fleas with only early-phase infection are insufficient to drive an epizootic among most wild rodents, and favor a more stable enzootic state, according to the research published this week in PLOS Pathogens by Joseph Hinnebusch of the National Institute of Allergy and Infections Diseases Rocky Mountain Laboratories, U.S., and colleagues.

Plague primarily afflicts rodents, including rats, mice, gerbils, squirrels, marmots and prairie dogs. The bacteria circulate within these host populations through several flea vector species. Fleas can transmit Y. pestis in different stages following an infectious blood meal; transmission can occur the very next time they feed, a phenomenon referred to as early-phase transmission. Later, “blockage-dependent transmission” occurs after Y. pestis forms a bacterial biofilm in the fleas’ digestive systems, blocking the flow of an incoming meal and causing blood to recoil back into the bite site after mixing with the biofilm.

Our models suggest that exposure of most wild rodents to sublethal, immunizing doses of Y. pestis transmitted during the early phase may ameliorate rapid epizootic spread by reducing the number of susceptible individuals in the population. In many situations early-phase transmission may be more important in maintaining the enzootic state than in driving an epizootic.

The authors
In the new study, researchers for the first time empirically evaluated the relative efficiency of the different phases of transmission by individual fleas. Cohorts of a ground squirrel flea, Oropsylla montana, were infected by feeding on mouse or rat blood infected with Y. pestis. Transmission efficiency of individual O. montana fleas was then measured over a four-week period and the researchers created models to show how this efficiency would translate to the spread of Y. pestis through a rodent population.

The results indicated that blockage-dependent transmission is much more efficient than early-phase transmission, in terms of the probability of transmission, the number of bacteria transmitted, and the capability of driving an epizootic outbreak. Early-phase transmission, the models showed, could drive an epizootic only in naïve, very susceptible host populations and when the flea burden is high. Moreover, the low dose of bacteria typically transmitted in early-phase transmission may “immunize” many individuals, acting to promote an enzootic state.
In the abstract and authors' summary in PLOS Pathogens, the authors say:

Yersinia pestis, the bacterial agent of plague, is enzootic in many parts of the world within wild rodent populations and is transmitted by different flea vectors. The ecology of plague is complex, with rodent hosts exhibiting varying susceptibilities to overt disease and their fleas exhibiting varying levels of vector competence. A long-standing question in plague ecology concerns the conditions that lead to occasional epizootics among susceptible rodents. Many factors are involved, but a major one is the transmission efficiency of the flea vector. In this study, using Oropsylla montana (a ground squirrel flea that is a major plague vector in the western United States), we comparatively quantified the efficiency of the two basic modes of flea-borne transmission. Transmission efficiency by the early-phase mechanism was strongly affected by the host blood source. Subsequent biofilm-dependent transmission by blocked fleas was less influenced by host blood and was more efficient. Mathematical modeling predicted that early-phase transmission could drive an epizootic only among highly susceptible rodents with certain blood characteristics, but that transmission by blocked O. montana could do so in more resistant hosts irrespective of their blood characteristics. The models further suggested that for most wild rodents, exposure to sublethal doses of Y. pestis transmitted during the early phase may restrain rapid epizootic spread by increasing the number of immune, resistant individuals in the population.

Author summary

The ecology of bubonic plague is complex but depends largely on flea-borne transmission. Certain susceptible rodents experience periodic epizootics that can decimate local populations, but the conditions that lead to these episodes are not fully understood. Fleas can transmit Yersinia pestis, the bacterial agent of plague, during two different phases: an early phase within the first few days after their infectious blood meal and again sometime later after the development of a Y. pestis biofilm in the flea foregut. The relative contribution of these two transmission modes to plague ecology has not been systematically examined. Our results indicate that in most ecological contexts early-phase transmission is too inefficient to drive an epizootic, but instead acts to reduce the number of susceptible individuals in a population, thereby favoring a more stable enzootic state.

Ingenious, or what?

Having realised that rodent populations could build up a level of resistance to plague because it had designed an immune system to do so, Creationism's putative designer came up with a method to get around this resistance periodically and, in the words of the authors of this study, "decimate local populations" of rodents. It did this by designing Y. pestis to form a biofilm (i.e. a sheet of bacteria, organised like a simple multicellular organism), to block the digestive tract of the flea vector, forcing it to inject a lethal dose of bacteria into the victim when it next takes a blood meal. Such a simple solution to a problem caused by the efficient functioning of the rodents' immune systems which it designed to protect them from the pathogens it designed to make them sick.

And a typically obsessive, complex process for producing more Y. pestis bacteria, apparently for no other purpose than to make rodents, and occasionally still, humans, sick.

For reason which no Creationists has yet admitted to, they would prefer you had this view of their putative creator god rather than that you understood how the natural process of evolution by natural selection is perfectly capable of explaining how these parasite-host relationships arise without intelligent intervention and with the indifference to any suffering of a mindless natural process.

Thank you for sharing!

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