From the point of view of a micro-organism, the human body is a prime piece of real estate. For those bacteria and fungi that can avoid or fight off the immune systems, a human provides a whole range of moist, nutrient-filled little spaces in which to live. Some of these micro-organisms are harmless, growing and thriving within their niche without harming or disrupting the body they live within. Others are harmful, actively attacking the surrounding human cells in order to uptake nutrients. Many are opportunistic, mostly harmless, but with the potential to become deadly if the immune system is compromised in any way.
What is fascinating, however, is that all these micro-organisms don't just live their separate lives, dodging the immune system and growing in isolation. Both bacteria and fungi that live on and in the human body communicate with each other; sometimes to compete and fight, sometimes to cooperate and work together.
Competition: Bacteria vs. Fungi
As with any other niche for life, there is plenty of competition for space and resources within the human host. The bacteria Pseudomonas aeruginosa and the yeast Candida albicans are both opportunistic pathogens and are often isolated together in infections. This is particularly true of hospital-acquired infections in patients with a compromised immune system. As the yeast cells are so much larger, the bacteria are able to colonise and grow on them, killing the yeast in the process. They can also affect the yeast in more subtle ways, for example by secreting molecules that prevent the yeast cells transforming into biofilms or hyphae (long strands used for spreading into new areas).
Other bacteria are also able to restrict the growth and colonisation of C. albicans by secreting small communication molecules. This is why certain C. albicans infections, such as thrush, are more likely to appear after a course of antibiotics. Without any bacteria to fight against them, or to take up space and nutrients, the yeast can just take over.
Co-operation: Fungi + bacteria
It makes sense that two organisms in the same niche should compete for space and resources. Far more interesting is the fact that sometimes fungi and bacteria will work together in order to colonise the human body. The bacteria Staphylococcus aureus doesn't usually form biofilms when grown on clean surfaces, but in the presence of C. albicans it forms large multi-bacterial colonies using the strands of yeast as a scaffold. The image below (from reference 2) shows the yeast strands (in blue) co-colonising with the bacteria (in green). By forming biofilms together the fungi and bacteria are both better protected from the human immune system as well as from antibiotics.
The bacteria E.coli is also able to work with the C. albicans, releasing signalling molecules that increase the virulence of the yeast and induce formation of the invasive hyphae. In return the yeast can also increase the virulence of bacteria species such as E. faecalis and S. marcescens - co-infection studies in mice showed increased virulence when both the bacteria and fungi were present, compared with each species alone. It was also found that when the bacteria and fungi were injected at different sites co-infection was present at the area of fungi infection, not at the area of bacterial infection.
All of these interactions, both co-operative and competitive, build up a picture of an entire world within the human body: a range of micro-organisms of different shapes and sizes working around and among the human cells to grow and flourish. Although they are all considered 'micro-organisms' bacteria and fungi are from different kingdoms of life which makes their communication through shared molecules, and co-operation within biofilms, all the more remarkable.
Reference 1: Mallick EM, Bennett RJ (2013) Sensing of the Microbial Neighborhood by Candida albicans. PLoS Pathog 9(10): e1003661. doi:10.1371/journal.ppat.1003661
Reference 2: Harriott MM, Noverr MC. Importance of Candida-bacterial polymicrobial biofilms in disease. Trends Microbiol. 2011 Nov;19(11):557-63. doi: 10.1016/j.tim.2011.07.004.
Credit for image 2: wikimedia commons