Can photocatalytic materials combat AMR

Can photocatalytic materials combat AMR

Spectrum Blue explores the historical resistance to innovation in medicine, drawing parallels with the current challenge of antimicrobial resistance and the potential of new technologies like photocatalytic materials to address it.

We like to think of innovation as inevitable. In reality, it is often resisted, especially when it asks us to act on what we cannot see.

The discovery of germ theory

In the 1840s, Ignaz Semmelweis was working in the maternity wards of the Vienna General Hospital, where two nearly identical clinics produced very different outcomes. In one, staffed by physicians and medical students, women frequently died from puerperal fever. In the other, run by midwives, mortality was significantly lower. The discrepancy was persistent and unexplained.

The turning point came after the death of Semmelweis’s colleague, Jakob Kolletschka, who developed a fatal infection following a scalpel injury during an autopsy. The symptoms closely resembled those of the women dying in the clinic. Semmelweis drew a connection that others had not: material from cadavers, carried on the hands of physicians, was somehow causing disease. Without a framework like germ theory, he described these as ‘cadaverous particles.’

In 1847, he introduced a policy requiring handwashing with chlorinated lime before patient contact. The effect was immediate and dramatic. Mortality rates dropped from as high as 10-18% to around 1-2% (Semmelweis, 1861; Best and Neuhauser, 2004). Yet the response was negative. Many physicians rejected the findings, in part because they implied that doctors themselves were responsible for patient deaths. Others objected to the lack of a theoretical explanation. The data were empirical, but the mechanism remained invisible. Semmelweis faced increasing opposition, and his work was largely dismissed during his lifetime.

The discovery of penicillin

Several decades later, the invisible would return, this time in a laboratory in London. In 1928, Alexander Fleming noticed that a mould contaminating one of his bacterial culture plates had created a clear zone where bacteria could not grow. He identified the mould as Penicillium and recognised that it released a substance with antibacterial properties. However, Fleming was unable to stabilise or purify this substance for therapeutic use, and for years, the observation remained a scientific curiosity rather than a medical solution.

Alexander Fleming.
©shutterstock/Prachaya Roekdeethaweesab

It was not until the late 1930s that Howard Florey, Ernst Chain, and their team at Oxford revisited the problem. They developed methods to extract and concentrate penicillin, though yields were extremely low and the compound was unstable. Early experiments involved treating infected mice, demonstrating clear survival benefits (Chain et al., 1940). Human trials followed under constrained conditions, including attempts to recover and reuse penicillin from patients’ urine due to limited supply.

Unlike popular belief, the success of penicillin was not a single moment of discovery but a process of overcoming chemical, biological, and logistical barriers. Even then, scaling production required coordinated industrial efforts during World War II. What began as an observation in a petri dish became a cornerstone of modern medicine only through sustained effort against technical uncertainty and initial scepticism (Ligon, 2004).

Antimicrobial discoveries of the future

Today, we are again confronted with the limits of what we can see and control. Antimicrobial resistance is rising across bacterial pathogens, with global estimates attributing millions of deaths annually to resistant infections (Murray et al., 2022). At the same time, fungal pathogens such as Candida auris have emerged in healthcare settings, combining environmental persistence with resistance to multiple antifungal drugs (CDC, 2023). These organisms are not new, but their impact is increasing under current clinical and ecological conditions.

The pressure to respond is increasing, but the direction of that response is not obvious. Much of modern medicine operates downstream of the problem, responding after infection occurs and relying on the assumption that treatment can outpace microbial adaptation.

An alternative is to shift the point of intervention earlier, to the interface between microorganisms and their environment.

Photocatalytic materials represent one such approach. These systems, often based on semiconductors such as titanium dioxide, generate reactive oxygen species when exposed to light. These species interact directly with microorganisms at surfaces, disrupting membranes, proteins, and genetic material (Fujishima et al., 2008). The mechanism is non-specific, acting through oxidative stress rather than targeted biochemical pathways.

The limitation has traditionally been the need for ultraviolet activation, which restricts practical use. More recent developments, including work patented by Spectrum Blue, focus on modifying photocatalytic materials to function under visible light through doping strategies and pigment-based systems (Chen et al., 2010). This enables antimicrobial activity under ambient conditions, without requiring controlled irradiation.

This changes the role of photocatalytic materials in infection control. Surfaces can actively reduce microbial load continuously, without relying on discrete cleaning events or repeated chemical treatments.

At the same time, this approach does not fit easily within existing evaluation frameworks. Current systems are designed to measure acute interventions such as disinfectants or antibiotics, not continuous, low-level antimicrobial activity embedded in materials.

As in the time of Semmelweis and the early development of penicillin, the challenge is not only technical. It is conceptual. It requires accepting that controlling microorganisms may depend as much on redesigning environments as on developing new treatments.

References

  • Longo LD. Die Aetiologie, der Bergriff und die Prophylaxis des Kindbettfiebers [The etiology, concept and prevention of childbed fever. 1861]. Am J Obstet Gynecol. 1995 Jan;172(1 Pt 1):236-7. German. PMID: 7847547.
  • Best M, Neuhauser D. Ignaz Semmelweis and the birth of infection control. Qual Saf Health Care. 2004 Jun;13(3):233-4. doi: 10.1136/qhc.13.3.233. PMID: 15175497; PMCID: PMC1743827.
  • Chain E, Florey HW, Gardner AD, Heatley NG, Jennings MA, Orr-Ewing J, Sanders AG. THE CLASSIC: penicillin as a chemotherapeutic agent. 1940. Clin Orthop Relat Res. 2005 Oct;439:23-6. doi: 10.1097/01.blo.0000183429.83168.07. PMID: 16205132.
  • Ligon BL. Penicillin: its discovery and early development. Semin Pediatr Infect Dis. 2004 Jan;15(1):52-7. doi: 10.1053/j.spid.2004.02.001. PMID: 15175995.
  • Antimicrobial Resistance Collaborators. Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis. Lancet. 2022 Feb 12;399(10325):629-655. doi: 10.1016/S0140-6736(21)02724-0. Epub 2022 Jan 19. Erratum in: Lancet. 2022 Oct 1;400(10358):1102. doi: 10.1016/S0140-6736(21)02653-2. PMID: 35065702; PMCID: PMC8841637.
  • Centers for Disease Control and Prevention. (2026, February 25). Clinical overview of Candida auris. National Center for Emerging and Zoonotic Infectious Diseases. Retrieved April 17, 2026, from
    https://www.cdc.gov/candida-auris/hcp/clinical-overview/index.html
  • Fujishima, Akira & Zhang, Xintong & Tryk, Donald. (2008). TiO2 Photocatalysis and Related Surface Phenomena. Surface Science Reports. 63. 515-582. 10.1016/j.surfrep.2008.10.001.


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