Many people like to live in communities and cities. Bacteria, archaea, and fungi also like to live in communities which grow into biofilms.
Biofilms are organized colonies of microbes living inside a protective dome. You’ve seen biofilms if you’ve ever cleaned out the p-trap under the sink and extract gooey gobs of slimy gunk … aka biofilms. In the plumbing, the biofilm-domes protect the bacteria from various threats from what goes down the drain—soaps, alcohol, mouthwash, antibiotics (triclosan), etc.
Biofilms are survival mechanisms. Biofilm-building microbes surround their colonies with a polysaccharide shell that prevents the immune system from recognizing them1. The immune system seeks a protein on the pathogen cell wall, but the biofilm sugar does not have that protein.
For example, Protein NLRP7 serves as one of immune system’s macrophage scouts2. It identifies gram-positive pathogens such as staphococcus aureus, streptococcus, and listeria monocytogens via protein recognition.
Good & Bad Biofilms
In the human body, both probiotic and pathogenic species of archaea, bacteria, fungi make biofilms. This is important because most conversations about biofilms denigrate them as being bad. But good species make biofilms too.
Scientists used to think that infectious bacteria were planktonic meaning that they swam around freely like plankton in the ocean. Instead, most bacteria hide in biofilms that adhere to the tissue. As they become crowded or overpopulated, the biofilm releases bacteria to become planktonic colonizers and explorers.
Fly In The Ointment
Antibiotic therapy is based on killing planktonic bacteria. But now we know that 80% of human bacterial infections come from pathogenic biofilms adhering to the tissue3. Biofilms are found in many tissues, e.g. lungs, sinuses, vagina, prostate, intestines, ears (estuation) and more.
If a person has repeated infections (e.g. sinusitis, colitis, vaginitis, urethritis, prostatitis, bronchitis, otitis media), it’s a fair assumption that there are biofilms present. The challenge of pathogenic biofilms is that they are resistant to antibiotics, calling for stronger and stronger (and more dangerous) drugs.
The good news is that biofilms are less resistant to botanicals, and not resistant at all to bacteriophages—viruses that destroy only a particular species of bacteria, and no others.
Once inside the biofilm, microbes specialize in certain tasks. Just like in human cities, there’s structural maintainers, police, administrators, food-purveyors, and waste management. When a antibiotic molecule encounters a biofilm, specialized bacteria recognize it as toxic, sample it, die, and get pumped out of the biofilm. They teach the other bacteria via quorum sensing to mutate and thwart the antibiotic. This is the start of antibiotic resistance. Often, after the illness, the biofilms remain, and later, when the circumstances are right, there’s another infection.
With antibiotics, there’s the dangerous process of antibiotic resistance. In the futile arms race between microbes and poisoning them with antibiotics, the bacteria have the advantage because they quickly quorum sense, alter and share DNA, and mutate to safety.
Certainly antibiotics have saved millions of lives. But Nature teaches that there are better ways to control pathogenic species starting with a healthy terrain—a biodiverse, well-populated microbiome of probiotic species that directly control pathogenic biofilm production. A healthy terrain also involves avoiding toxins (pesticides/herbicides, chemicals), cellular nutrition, and use of culinary herbs and spices.
Biofilms Sequester Minerals
To build a biofilm, bacteria first adhere to a surface and secret the gummy sugars to make it stick. The polysaccharide “glue” also sequesters calcium, magnesium, iron, lead, mercury, whatever mineral-elements are available. Biofilms may also sequester a few bacteria from another species. Thus is possible for a probiotic biofilm to sequester a pathogenic species, keep it in check, and have it perform metabolic functions that support the biofilm.
Candida & Heavy Metals
In the 1980’s many people confronted Candida (yeast/fungus) as an enemy of health. One author wrote, “Candida is your friend.” His point was that candida biofilms sequestered heavy metals (such as iron, mercury, lead, cobalt, nickel, copper, arsenic, – any metal that is dense and toxic. So candida, while harming health, also prevented heavy metals such as mercury (amalgam dental fillings), or cadmium (gasoline) from getting into the bloodstream. Today, most natural health candida programs employ heavy metal detox support such as super-activated charcoal.
When people killed the unwanted candida, either by Rx drugs such as Nystatin™ or Fluconazole™, or by herbs such as pau d’arco and berberine-rich goldenseal, barberry, Oregon grape, and coptis, they could experience Jarisch-Herxheimer reactions. These reactions of feeling worse before feeling better were caused by the release of heavy metals from the dying candida biofilms, and from macrophages releasing cytokines as they cleaned up weakened and dying microbes.
SIBO / SIFO
Today, the natural health practitioner must address biofilms to help people get over microbial infections. SIBO (Small Intestinal Bacterial Overgrowth) and SIFO (Small Intestinal Fungal Overgrowth) are often associated with biofilms4. Thus a comprehensive program might include botanicals called biofilm disruptors such as goldenseal, oregano oil, black walnut, artemisia, echinacea, gentian, etc.).
Other biofilm disruptors include fibrinolytic, proteolytic enzymes5 (nattokinase, lumbrokinase, trypsin, chymotrypsin, serrapeptase), and N-acetyl cysteine6. Perhaps the most exciting research is supplemental bacteriophages which easily penetrate biofilms7. Bacteriophages don’t cause Herx reactions because they fragment the bacteria and do not elicit phagocyte cytokines.
As science learns more about the microbial kingdoms, biofilms, and the balance of nature, we learn new ways to work with the teeming throngs of beneficial microbes that serve human health.
- Barshak MB, Durand ML. The role of infection and antibiotics in chronic rhinosinusitis. Laryngoscope Investig Otolaryngol. 2017 Jan 23;2(1):36-42. doi: 10.1002/lio2.61. PMID: 28894821; PMCID: PMC5510277.
- Sonal Khare, Andrea Dorfleutner, Nicole B. Bryan, Chawon Yun, Alexander D. Radian, Lucia de Almeida, Yon Rojanasakul, Christian Stehlik, An NLRP7-Containing Inflammasome Mediates Recognition of Microbial Lipopeptides in Human Macrophages, Immunity,Volume 36, Issue 3,2012, Pages 464-476, ISSN 1074-7613, https://doi.org/10.1016/j.immuni.2012.02.001. https://www.sciencedirect.com/science/article/pii/S1074761312000490)
- Römling U, Balsalobre C. Biofilm infections, their resilience to therapy and innovative treatment strategies. J Intern Med. 2012 Dec;272(6):541-61. doi: 10.1111/joim.12004. Epub 2012 Oct 29. PMID: 23025745.
- von Rosenvinge EC, O’May GA, Macfarlane S, Macfarlane GT, Shirtliff ME. Microbial biofilms and gastrointestinal diseases. Pathog Dis. 2013;67(1):25-38. doi:10.1111/2049-632X.12020
- Hogan S, O’Gara JP, O’Neill E. Novel Treatment of Staphylococcus aureus Device-Related Infections Using Fibrinolytic Agents. Antimicrob Agents Chemother. 2018 Jan 25;62(2):e02008-17. doi: 10.1128/AAC.02008-17. PMID: 29203484; PMCID: PMC5786758.
- Domenech M, García E. N-Acetyl-l-Cysteine and Cysteamine as New Strategies against Mixed Biofilms of Nonencapsulated Streptococcus pneumoniae and Nontypeable Haemophilus influenzae. Antimicrob Agents Chemother. 2017 Jan 24;61(2):e01992-16. doi: 10.1128/AAC.01992-16. PMID: 27919900; PMCID: PMC5278723.
- Harper DR, Parracho HMRT, Walker J, et al. Bacteriophages and Biofilms. Antibiotics (Basel). 2014;3(3):270-284. Published 2014 Jun 25. doi:10.3390/antibiotics3030270