Human–Microbe Symbiosis & the Microbiome

Symbiotic Relationships Between Humans & Microbes

Symbiosis describes any close association between two living organisms and, in microbiology, explains how microbes live on, in, or at the expense of us. Three distinct relationship‐types exist.

Mutualism

In mutualism both partners benefit. A textbook human example is the gut commensal E.\;coli. Certain strains colonise the intestinal epithelium, clinging to the microvilli with fimbriae (hair-like pili) while bathing in a nutrient stream of partially digested food. As a biochemical “side hustle” they synthesise vitamin K, which our bloodstream absorbs. Vitamin K catalyses maturation of clotting factors (prothrombin et al.), turning immature proteins into active ones able to form fibrin clots. Without adequate vitamin K a human bleeds excessively. Newborns lack an established coliform population and do not yet ingest leafy greens, so they receive prophylactic intramuscular vitamin K injections.

Commensalism

Commensalism denotes a relationship where one organism benefits and the other is neither harmed nor helped (and may be unaware of the guest). Barnacles hitchhiking on humpback whales illustrate this perfectly: the crustaceans gain food, shelter, and transport while the whale remains indifferent. Large portions of our normal flora fit this model; they obtain nutrients and a niche, whereas we generally never notice them. From a diagnostic standpoint, distinguishing harmless commensals from pathogenic invaders on culture plates demands deep knowledge of “what normally lives where.”

Parasitism

Parasitism occurs when one organism benefits and the host is harmed. The scabies mite (illustrated by the lecturer’s plush toy) burrows into skin, consumes blood, lays eggs, causes pruritic tunnels, and may provoke anaemia. Viruses—e.g.
SARS-CoV-2 (the COVID-19 agent)—are obligate intracellular parasites because they require host cells to replicate. Parasites are therefore not counted within the normal flora.

Opportunistic Shift

Some microbes toggle between categories depending on location. Staphylococcus aureus is a benign skin commensal but, when introduced into deeper tissue via a cut, behaves as an opportunistic pathogen, creating abscesses.

The Human Microbiome: Size, Diversity & Significance

Humans harbour more microbial cells than human cells—roughly 1.3:1, translating to 10^{13}\text{–}10^{14} bacterial cells across >10 000 species. Although hard to catalogue completely, the microbiome:

1. Protects us from infection by out-competing pathogens.
2. Aids digestion & metabolism (fermentation, vitamin synthesis, bile-acid modification).
3. Educates/modulates the immune system, preventing inappropriate auto-reactivity.

Viruses and multicellular parasites can persist silently in healthy people but are traditionally excluded from “normal flora.” Yeasts/fungi (e.g. Candida spp.) are included provided they remain numerically minor.

Acquisition & Evolution of the Microbiome

• In utero: Modern evidence shows a low-level maternal trans-placental seeding of amniotic fluid with bacteria.

• Birth: Delivery method matters. Vaginal birth exposes the neonate to maternal vaginal/rectal flora; caesarean infants encounter more skin/environmental microbes.

• Early life: Feeding mode (breast vs. formula), home environment, geographic region, and the universal toddler habit of mouthing objects diversify the flora and train immunity. By toddlerhood a child carries a largely stable, personal microbial fingerprint.

• Throughout life: Diet, antibiotics, disease, travel, and lifestyle (e.g.
vaping) continually remodel the community, making “one healthy microbiome” definition impossible.

Regional Microbiomes & Their Niches

Different body sites impose unique pH, oxygen tension, temperature, and nutrient profiles, selecting for distinct bacterial consortia.

• Skin: Dominated by Staphylococcus spp., Corynebacterium, Cutibacterium; they metabolise sweat components, generating odour and producing antimicrobial fatty acids.
• Oropharynx / Mouth: Shares traits with the gut (continuous external tube). Houses streptococci, Neisseria, anaerobes, and low levels of Candida; disruption yields dental caries or thrush.
• Respiratory tract: Fewer bacteria than mouth; mucociliary clearance defences keep counts low.
• Gut (small + large intestine): The densest microbial habitat. Anaerobes such as Bacteroides, Clostridium, Lactobacillus, Bifidobacterium, and coliforms abound.
• Vagina: Acidic pH sustains Lactobacillus dominance; loss allows fungal overgrowth or gram-negative shift.
• “Sacred houses” analogy: Trouble arises when residents migrate—e.g.
coliforms entering the urinary tract.

Spotlight on Nasal (“Snot”) Microbiome

Adults secrete >100\,\text{mL} of mucus daily; children often more owing to naïve immune exposure. Color/consistency offers diagnostic clues:

• Clear/runny – irritants (pollen, cold air).
• White – early viral response (leucocyte influx).
• Yellow-green/thick – late viral stage or bacterial sinusitis (dead neutrophils).
• Bloody – mechanical trauma.

Research links nasal microbial composition to sex, age, geography, diet, and vaping. Experimental “snot transplants” are under investigation to alleviate chronic rhinitis or hay fever, suggesting nasal mucus may become a personalised-medicine biomarker.

Quantitative Snapshot of Faecal Flora

Approximate bacterial counts per gram of faeces:

• Coliforms (e.g. E. coli): 10^{7}\text{–}10^{8}
• Lactobacillus spp.: 10^{7}\text{–}10^{9}
• Bifidobacterium spp.: 10^{8}\text{–}10^{11}
• Clostridium spp. (including C. difficile): 10^{6}\text{–}10^{8}

Many commercial probiotics spotlight Lactobacillus and Bifidobacterium. Practical challenges exist: orally ingested bacteria must survive the stomach’s low pH (≈ pH\,2) before reaching the intestines, raising questions about efficacy.

Functional Benefits of a Healthy Gut Community

1. Immune Stimulation “Gym Effect”: Continuous low-level microbial antigen exposure keeps lymphocytes fit, preventing misguided auto-immunity.
2. Colonisation Resistance: Healthy flora secrete antimicrobial compounds and compete for binding sites & nutrients, blocking pathogen settlement.
3. Metabolic Support: Fermentation of indigestible polysaccharides, vitamin synthesis (K, B$_{12}$, folate), and modulation of bile acids.

Antibiotic courses can create a “red-zone” dysbiosis: benign flora die, epithelial barriers weaken, pathogens invade, evoke cytokine storms, and perpetuate inflammation.

Diseases from Microbiome Overgrowth or Misplacement

• Dental caries: Streptococcus mutans metabolises dietary sugars to acid, demineralising enamel → cavities. Brushing mechanically disrupts the biofilm.

• Urinary tract infections (UTI): Perineal coliforms (usually E. coli) ascend the short female urethra, inflaming bladder/renal tract.

• Endocarditis post-dentistry: Oral streptococci enter bloodstream during dental work, seed damaged heart valves.

• Skin abscesses: S. aureus penetrates micro-trauma → boils filled with pus; presents hot, red, painful.

• Human bite / “clenched-fist” injury: Oral anaerobes and aerobes inoculate knuckle lacerations when one punches another’s teeth. Infection progresses rapidly within <12 h, requiring surgical drainage plus antibiotics.

• Oral thrush (candidiasis): Overgrowth of Candida when bacterial competitors are suppressed (antibiotics, steroid inhalers, altered pH).

• Vaginal candidiasis or bacterial vaginosis: Loss of lactobacilli raises pH, enabling Candida or gram-negative bacteria.

Case Study: Clostridium difficile–Associated Disease (CDAD)

C. difficile normally sits quiescent in gut flora. Broad-spectrum antibiotics may eliminate competitors, leaving C. difficile dominant. Toxigenic strains produce exotoxins → pseudomembranous colitis characterised by yellow plaques (fibrin + neutrophils + mucin) lining the colon, severe diarrhoea, cramps, fever.

Spores are alcohol-resistant and survive routine cleaning, facilitating nosocomial outbreaks. Recurrent cases respond poorly to antibiotics but remarkably to faecal microbiota transplant (FMT): donor stool, screened for pathogens, is infused via colonoscope, re-seeding a healthy consortium that out-competes C. difficile and restores balance—often within days.

Ethical, Philosophical & Practical Considerations

• Personalised medicine: Microbiome profiling (gut, nasal, skin) may guide diet, probiotic, or transplant therapies but raises privacy and regulatory questions.
• Antibiotic stewardship: Minimising unnecessary prescriptions preserves microbiome integrity and prevents opportunistic disease.
• Hygiene hypothesis: Controlled microbial exposure in childhood arguably lowers asthma and allergy prevalence, challenging over-sanitised lifestyles.
• Probiotic marketing: Scientific evidence is mixed; survivability through the gastric barrier, strain specificity, and dose remain debated.

Key Numerical & Statistical References

• Microbe:human cell ratio ≈ 1.3:1.
• Total microbial load ≈ 10^{13}\text{–}10^{14} cells.
• >10\,000 microbial species described in humans.
• Adults secrete >100\,\text{mL} nasal mucus daily.
• Post-antibiotic C. difficile infection risk rises sharply with each extra day of broad-spectrum therapy (epidemiological data referenced anecdotally by lecturer).

Consolidated Take-Home Messages

1. Humans are supra-organisms: microbial cells outnumber human cells and deliver indispensable functions.
2. Symbiotic relationships range across a spectrum—mutualistic, commensal, parasitic—with some microbes shifting category when displaced.
3. Microbiome composition is body-site-specific, individualised, shaped from before birth through environment, diet, and antibiotics.
4. Healthy flora promote immunity, competitive exclusion, and metabolism; dysbiosis enables infections such as UTIs, thrush, skin abscesses, endocarditis, or CDAD.
5. Treatments now extend beyond killing pathogens to re-installing communities (e.g. nasal or faecal transplants), heralding a microbiome-centred era of medicine.