Did God Create Flesh-Eating Bacteria? A Creation Model for the Origin of Human Disease

Did God Create Flesh-Eating Bacteria? A Creation Model for the Origin of Human Disease

“How are flesh-eating bacteria consistent with an all-powerful, all-loving God?” This question was posed to me on a recent episode (January 19, 2010) of our I Didn’t Know That! podcast.

It’s a provocative, yet sensible, question. Necrotizing fasciitis (or flesh-eating disease) is a bacterial infection of the deepest layers of the skin and subcutaneous tissues. The infection consists of either several microbial species (Type I) or a single species (Type II). A number of different bacteria cause this gruesome disease including: Streptococcus pyogenes, Staphylococcus aureus, Vibrio vulnificus, and Clostridium perfringens.

Despite the name, flesh-eating microbes don’t really eat flesh. Instead, they destroy tissue near the site of infection by releasing toxins. This tissue destruction yields the repulsive, superficial appearance of the skin and muscle being consumed by the bacteria.

Did God create bacteria to infect humans and cause diseases like necrotizing fasciitis? Are these microbes part of God’s good creation? Such queries highlight the need to augment our creation model to formally include an explanation for the origin of human diseases.

Foundational Tenets

Two ideas form the basis for the model.

Microorganisms can be understood as part of God’s good design. Although people commonly think of microbes in a negative light, they actually play a key role in ecosystems and in maintaining human health. As a case in point, viruses function critically in cycling nutrients in the oceans. These microbes infect and destroy other microorganisms, resulting in the release of nutrients into the ecosystem.1 Viruses are also useful in biomedical applications like gene therapy.2 The properties that make viruses infectious are the same characteristics that make them suitable for gene therapy. In this sense, viruses could be understood as part of God’s providential care for humanity.

Microbial parasites play an essential part in maintaining ecosystem stability by controlling population numbers.3

Bacteria have performed vital tasks throughout Earth’s history, transforming the atmosphere and oceans to make advanced life possible. Bacterial action has also created metal deposits that now serve as key resources in paving the way for advanced human civilization and technology.

Additionally, bacteria help maintain human health. Scientists now possess the tools to characterize (identify) the microbial flora associated with the human body. Over 100 trillion bacterial cells occupy the exterior and interior surfaces of humans. (For reference there are about 10 trillion cells that comprise the human body.) Estimates indicate that over a thousand bacterial species exist in the human gut, a few hundred in the mouth, and around one hundred species on the human skin. (Interestingly, there are only about one hundred pathogenic species of bacteria.) In fact over 99% of the genes associated with the human organism come from surface bacteria.4 (For a detailed discussion on recent work cataloguing the genes associated with the microbiome of the human gut listen to the March 5, 2010 episode of our podcast Science News Flash.)

The human microbial flora plays a critical role in human health. For example, a recent study demonstrated that bacteria on the skin surface prevent excessive inflammation when injury occurs.5 Bacteria in the gut help harvest energy from food), and changes in the gut flora are associated with obesity.6

Researchers also think that lack of exposure to bacteria during the early years of life is responsible for the increase in autoimmune disorders, such as asthma, and may lead to increased risk of cardiovascular disease in later life.7 (This idea is referred to as the hygiene hypothesis.)

Microorganisms can evolve. At RTB, we are skeptical of the evolutionary paradigm. From our perspective, the origin and history of life cannot be explained apart from the direct involvement of a Creator. But that doesn’t mean we necessarily reject all forms of biological evolution. It is clear that species can vary (or adapt) over time, and evidence exists that one species can give rise to a closely related sister species. There is also an abundance of evidence that microorganisms (like viruses, bacteria, and single-celled eukaryotes) evolve. It is not surprising that single-celled microbes and viruses can evolve, given their extremely large population sizes and capacity to take up large pieces of DNA from their surroundings and incorporate these biomolecular fragments into their genomes.

Creation Model for the Origin of Human Disease

While RTB scholars would maintain that God created microbes for a variety of reasons, (including parasites that infect animals and other life-forms to control their populations), he did not create corresponding human pathogens when he made human beings. We would assert, however, that he did create beneficial microbes that would form mutualistic symbiotic associations with humans by populating their exterior and interior surfaces.

But because microorganisms can evolve, our model predicts that a small fraction of the human microbiome became pathogenic over time as a consequence of mutations occurring within the context of the large population sizes. Once pathogens emerged, they could transfer their toxin-producing genes to other microbes through horizontal (or lateral) gene transfer, creating new disease-causing strains. A recent example of this process explains the emergence of the deadlyE. coli strain, O157:H7. Most strains of E. coli (found in the human gut) are harmless. The O157:H7 strain appears to have originated when toxin-encoding genes were transferred to a benign strain of E. coli from the microbe Shigella, a human pathogen.

Microbes that infect other animals would be another source of human pathogens. Again, mutations would allow these microbes to jump from the animal host to humans. Host-hopping occurs quite frequently with viruses and explains, for example, the genesis of HIV, which appears to have originated from SIV, a virus that infects chimpanzees, and SARS, which may have hopped from an avian host to humans. (Incidentally, host-jumping can work the other direction as well. Researchers recently observed that a strain of Staphylococcus aureus in poultry originated from a human host.8

Successful tracing of the origin of human parasites and their spread around the world using genetic diversity patterns in human pathogens, such as Helicobacter pylori (the bacterium that causes ulcers and stomach cancer), provides further support for the RTB model. Interestingly, the timing and location of many pathogens’ origin closely coincides with the timing and location for humanity’s origin . And the pattern of human pathogens’ spread around the world follows the migration routes that humans took as they populated the planet.

So, within the framework of the RTB model, how can the origin of flesh-eating microbes specifically be explained? One possibility is that bacterial strains that cause necrotizing fasciitis in animals host-jumped to humans. Another possible explanation is that non-flesh-eating strains were associated with humans all along, but recently evolved tissue-destructive capabilities. In light of the second option, scientists from The Methodist Hospital Research Institute in Houston discovered that a single mutation decreases the virulence of a necrotizing strain of Streptococcus.9 This single change leads to a sequence of biochemical changes that reduces the amount of an enzyme, called a protease, secreted by the bacterium into the host’s tissue. This is a good thing, because proteases are enzymes that digest proteins and would degrade muscle and connective tissues. This result suggests that the reverse could have happened. Any change that initiates or increases protease secretion into the extracellular environment could cause necrosis, transforming a relatively benign microbe into a frightening killer strain.

The RTB creation model readily accounts for the origin of human diseases and at the same time allows us to view viruses, bacteria, and other human pathogens as part of God’s good creation. The capacity of microbes to evolve after they were created brought about human infectious diseases. From this perspective, the existence of flesh-eating bacteria is fully compatible with an all-powerful Creator who loves and cares for His creation.

  1. Steven W. Wilhelm and Curtis A. Suttle, “Viruses and Nutrient Cycles in the Sea,” BioScience 49 (January 20, 1999): 781–88.
  2. Nathalie Cartier et al., “Hematopoietic Stem Cell Gene Therapy with a Lentiviral Vector in X-Linked Adrenoleukodystrophy,” Science 326 (November 6, 2009): 818–23.
  3. Peter J. Hudson, Andrew P. Dobson, and Kevin D. Lafferty, “Is a Healthy Ecosystem One That Is Rich in Parasites?” Trends in Ecology and Evolution 21 (July 1, 2006): 381–85.
  4. Junjie Qin et al., “A Human Gut Microbial Gene Catalogue Established by Metagenomic Sequencing,” Nature 464 (March 4, 2010): 59–67.
  5. Yuping Lai et al., “Commensal Bacteria Regulate Toll-Like Receptor 3-Dependent Inflammation after Skin Injury,” Nature Medicine 15 (November 22, 2009): 1377–82.
  6. Peter J. Turnbaugh et al., “An Obesity-Associated Gut Microbiome with Increased Capacity for Energy Harvest,” Nature 444 (December 21, 2006): 1027–31; Ruth E. Ley et al., “Microbial Ecology: Human Gut Microbes Associated with Obesity,” Nature 444 ( December 21, 2006): 1022–23.
  7. Francisco Guarner et al., “Mechanisms of Disease: The Hygiene Hypothesis Revisited,” Nature Reviews Gastroenterology & Hepatology 3 (May 2006): 275–84; Thomas W. McDade et al., “Early Origins of Inflammation: Microbial Exposure in Infancy Predict Lower Levels of C-Reactive Protein in Adulthood,” Proceedings of the Royal Society B: Biological Sciences 277 (April 7, 2010): 1129–37.
  8. Bethan V. Lowder et al., “Recent Human-to-Poultry Host Jump, Adaptation, and Pandemic Spread of Staphylococcus aureus,” Proceedings of the National Academy of Sciences, USA 106 (November 17, 2009): 19545–50.
  9. Randall J. Olsen et al., “Decreased Necrotizing Fasciitis Capacity Caused by a Single Nucleotide Mutation that Alters a Multiple Gene Virulence Axis,” Proceedings of the National Academy of Sciences, USA 107 (January 12, 2010): 888–93.