Limits of the Germ Theory of Disease, By Brian Simpson

The germ theory of disease, solidified in the late 19th century by pioneers like Louis Pasteur and Robert Koch, remains one of the most transformative ideas in medicine. It posits that specific microorganisms — bacteria, viruses, fungi, parasites — cause infectious diseases, and that these pathogens can transmit from person to person or via contaminated sources. This framework underpins antibiotics, vaccines, sanitation improvements, and much of modern epidemiology, allegedly dramatically reducing mortality from once-devastating illnesses like cholera, tuberculosis, and smallpox.

Yet, as a January 27, 2026, article in The Daily Sceptic by diagnostic pathologist Dr. Clare Craig highlights, germ theory isn't the complete picture — especially for understanding viral transmission and the rhythmic patterns of epidemics. Craig argues there are "gaping holes" in how we explain why and when viral illnesses spread in populations, even while affirming viruses exist, can be isolated, sequenced, and cause disease in controlled settings. Her piece revives discussion of host factors — echoing elements of terrain theory — without fully endorsing denialism. This tension reveals real limits in a purely pathogen-centric view.

Core Strengths of Germ Theory

Germ theory excels at explaining causation in many cases:

Direct evidence of transmission: Genetic sequencing traces identical or mutating viral strains through clusters (e.g., SARS-CoV-2 outbreaks). High-dose human challenge studies show illness from deliberate exposure.

Mechanistic clarity: Viruses are visualized via electron microscopy, their structures (like spike proteins) characterized, and replication cycles understood.

Public health wins: Hygiene, isolation, and vaccination campaigns align with germ-focused interventions, yielding measurable drops in incidence.

Key Limitations and Unsolved Mysteries

The article spotlights observations that a strict "virus jumps, infects, causes wave" model struggles to explain fully:

1.Inconsistent Infectivity in Controlled Exposures: High-dose challenge trials can induce illness, but normal or low-dose exposures often fail — even when viral material is present. This suggests dose alone doesn't dictate outcome; host factors mediate whether infection takes hold or remains subclinical.

2.Synchronised Waves Without Clear Lags: Seasonal respiratory viruses (influenza, RSV, coronaviruses) peak with remarkable regularity — often every ~13 weeks in patterns like early January, April, July, late October in the UK. Hospital-acquired cases rise simultaneously with community peaks, defying expected transmission delays. Lockdowns or mass vaccination altered wave steepness but not core timing.

3.Geographic and Environmental Oddities: Waves can "skip" regions (e.g., parts of Eastern Europe in spring 2020) or show hemispheric differences (opposite seasonal gene expression shifts in Europe vs. Australia). Wastewater surveillance reveals cyclical viral presence, yet illness correlates more with host susceptibility windows than raw viral load.

4.Isolated Settings Like Submarines: Crews on long patrols experience persistent respiratory illnesses despite no new external exposures or significant viral mutations. This implies circulating pathogens exploit periodic host vulnerability rather than requiring constant reintroduction.

5.Mutation and Interference Don't Fully Explain Timing: Viral evolution (e.g., Omicron's faster mutation rate) doesn't disrupt the underlying rhythm. Influenza mutates rapidly yet follows similar seasonal peaks. Co-circulating viruses don't strictly "interfere" to dictate waves; what's dominant seems tied to what the population inhales during susceptible periods.

These patterns suggest viruses are omnipresent in aerosols, sewage, and carriers year-round, but illness erupts when collective host susceptibility rises — due to seasonal immune shifts (e.g., 25% of genes altering expression with daylight/vitamin D cycles), environmental entrainment, or other synchronizing factors.

Terrain Theory Echoes: Host as the Deciding Factor

Antoine Béchamp's 19th-century "terrain theory" argued disease arises from the body's internal environment ("terrain") rather than invading germs alone — germs as scavengers of weakened tissue, not primary causes.

Modern evidence supports this nuance:

Pre-existing conditions, nutrition (e.g., vitamin A/D status), stress, and genetics heavily determine severity.

Twin studies and genetic research show inherited immunodeficiencies shape infection risks.

Evolutionary biology notes pathogens evolve virulence for transmission, but host immunity often limits spread.

Craig proposes viruses as "necessary but not sufficient": they must be present, but illness timing hinges on a "human immune clock" synced to environmental cues (light, temperature, perhaps geomagnetic or other subtle factors). This hybrid model — germ + terrain — better fits data than pathogen-only explanations.

Balancing the Debate

Critics of such views warn against overcorrecting toward denialism, which surged during COVID-19 via online groups rejecting viruses outright. Mainstream sources emphasise germ theory's empirical triumphs and terrain theory's historical obsolescence in pure form. Yet, thoughtful voices (including some in immunology) acknowledge germ theory's simplifications: it excels at "what" causes disease but underplays "why now" or "why this person."

Recognizing limits invites better prediction—tracking immune seasonality, testing astronauts/submariners for delayed susceptibility shifts, or studying travellers crossing hemispheres.

In essence, germ theory isn't wrong — it's incomplete. Viruses drive contagion, but the host's terrain gates when and how severely disease manifests. As Craig concludes, after 170 years, science should evolve: stop fixating solely on the germ and integrate the dynamic human ecosystem it encounters. This nuanced view could refine prevention, moving beyond endless pathogen chasing toward supporting resilience in an inevitably microbe-filled world.

https://dailysceptic.org/2026/01/27/the-unsolved-mystery-of-how-viruses-spread-and-why-germ-theory-isnt-the-whole-answer/