A Failed Disinfection Is a Selection Event: Biocide Resistance and the Sanitation This Trade Recommends

1. Introduction: the fourth time this journal has made an argument

Our article on resistance reversion found sublethal rodenticide dosing raising tolerance across generations. Our treated articles article argued that a biocide-treated product with a declining loading delivers a falling dose. Our minimum risk article noted a cross-resistance concern in a consumer antimicrobial. Each time we flagged the argument as ours. It is not.

1.1 Why a pest control journal is writing about bacteria

Because this trade advises on sanitation, inspects food premises, works alongside cleaning programmes and has an article on drain biofilm. The chemistry in question is the chemistry our clients apply on our advice.

2. What the compounds are

The category, which is broader than most people picture.

A review lists alcohols, aldehydes, chlorine compounds, phenols, quaternary ammonium compounds (QACs), peroxides, and chlorhexidine as widely used in healthcare settings as a critical line of defense against infection.¹

In food processing, quaternary ammonium compounds such as benzalkonium chloride (BC), are widely used as disinfectants in various food sectors, and biocides generally play an essential role in limiting the dissemination of bacterial pathogens.²

2.1 Stating the benefit first

These compounds prevent disease. Nothing in this article argues for using fewer of them, and §23 is explicit about that.

2.2 Where this trade meets them

A pest control contractor does not usually apply disinfectants. It does inspect premises where they are applied, advise on sanitation as part of an integrated programme, and identify harbourage and food sources that cleaning is meant to remove.

Our articles on drain biofilm, on food safety auditing and on hygiene grade disclosure are all about that interface, and every one of them recommends cleaning without examining what the cleaning chemistry does.

2.3 And the volume increased recently

One paper notes that during the pandemic years the use of disinfectants has increased markedly, with the most commonly used being quaternary ammonium compounds, sodium hypochlorite, hydrogen peroxide and ethanol.³

3. The claim

Stated as the reviews state it.

Their overuse or misuse, especially at subinhibitory concentrations, can promote the emergence of bacterial resistance, potentially leading to cross-resistance to antibiotics.¹

3.1 Subinhibitory is the operative word

Not overuse in the sense of too much. Exposure below the concentration that kills, which is what misuse produces.

Our article on resistance reversion made the identical point about rodenticides: a dose below the lethal threshold is not a small version of a lethal dose, it is a different event with its own consequences.

3.2 The food safety framing

Repeated exposure to sub-inhibitory biocide concentrations can induce increased tolerance to these compounds, but can also trigger the development of antibiotic resistance, and both increase the risk of food contamination and persistence in food production environments.²

Both risks, from the same cause. The organism becomes harder to clean away and harder to treat if it reaches somebody.

4. The three mechanisms

How it happens.

Several mechanisms, including efflux pump activation, alterations in membrane permeability, and biofilm formation, drive this process.¹

4.1 Each is familiar from elsewhere in this journal

Efflux and metabolic export is what our synergists article described in insects. Reduced penetration is a known insecticide resistance mechanism. And biofilm is the subject of our drain article.

Three unrelated taxa reaching the same three solutions is worth noticing, and that observation is ours.

5. Efflux pumps

The dominant mechanism, described properly.

One review notes that efflux pumps play an important role in antimicrobial resistance, that a growing number of multidrug and drug-specific efflux pumps have been characterized in different kinds of bacteria, and that there are 5 families of efflux pump proteins: the ATP-binding cassette (ABC) family, the multidrug and toxic compound extrusion (MATE) family, the major facilitator superfamily (MFS), the resistance-nodulation-division (RND) family, and the small multidrug resistance (SMR) family.⁷

5.1 What a pump is for

Not resistance. A bacterium in soil, water or a gut encounters a continuous supply of foreign molecules, many of them toxic, produced by competing organisms. Transport systems that remove such molecules are basic cellular machinery.

Which is why the resistance is available immediately rather than requiring a novel mutation. The apparatus already exists and selection only has to increase how much of it the cell makes. That reading is ours and it explains why the adaptations in §§7 and 10 occur within days.

5.2 The structure

In one pathogen, intrinsic resistance is largely attributed to the expression of multidrug efflux pumps of one family, described as chromosomally encoded membrane proteins forming tripartite complexes composed of an inner membrane transporter protein, a periplasmic adapter protein, and an outer-membrane channel protein.⁶

A three-part assembly spanning both membranes, pumping molecules out of the cell and into the surroundings.

6. Why the pump is the problem

The single sentence that explains cross-resistance.

Exposure to a quaternary compound can also lead to cross-resistance to antibiotics like ciprofloxacin, as the same efflux systems expel both biocides and antibiotics from the bacterial cell.⁴

6.1 A pump does not know what it is pumping

It recognises a class of molecule by physical properties rather than by identity. Select for more pump, and you have selected for less susceptibility to everything that pump handles.

6.2 And it explains why the effect is partial

A pump handles some molecules well and others poorly, which is why §11 finds cross-resistance to one antibiotic and not to the rest of a panel. The overlap between what a biocide and a drug have in common physically determines which pairings appear.

That reading is ours and it makes the scattered findings in §12 look less arbitrary than they first appear.

6.3 Which is a different thing from target-site resistance

Our resistance articles have mostly described target-site changes, where a mutation alters the molecule a compound binds to and confers resistance to that compound alone. Efflux is general by construction.

Our synergists article described the insect version, where inhibiting a detoxification system restores several unrelated insecticides at once. This is the same logic running backwards.

7. The food plant experiment

The study closest to where this trade works.

The pathogen in question frequently undergoes selection pressure associated with the extensive use of disinfectants, such as quaternary ammonium compounds, which are widely used in food processing plants.²

The authors report that they previously showed that repeated exposure to benzalkonium chloride (BC) and didecyldimethyl ammonium chloride (DDAC) led to reduced susceptibility to ciprofloxacin in strains from diverse sources.²

7.1 Why this organism

Its ability to adapt to stress, grow at low temperatures, form biofilms and then persist in food processing plants for years has made this bacterium a major challenge for food safety, and successful control of it in the food chain requires appropriate cleaning and sanitation programs.²

Grows cold, forms biofilm, persists for years. Every one of those properties is a reason to apply more disinfectant, and §16 is about what happens when that application is imperfect.

8. The concentrations involved

The numbers, which are the surprising part.

The ten strains were exposed to sublethal concentrations of two QACs (BC at 0.6 mg.L-1 and DDAC at 0.31 mg.L-1) for 10 consecutive days, after which the minimum inhibitory concentration of the antibiotic was determined after the adaptation by the broth microdilution method.²

8.1 Fractions of a milligram per litre

Working disinfectant solutions are mixed in the hundreds or thousands of milligrams per litre. The selecting concentrations here are three or four orders of magnitude below that.

Which means the selecting condition is not a weak disinfectant solution. It is a trace, and that inference is ours.

8.2 Ten days

Ten consecutive daily exposures.² For an organism dividing in hours, that is many generations, and it is a fortnight in a kitchen.

9. The genetic target

What the adaptation actually was.

The paper reports that overexpression of the MATE efflux pump FepA through inactivation of the fepR repressor has been described to be responsible for fluoroquinolone resistance in this species, and states that this study is the first to report the fepR gene as a central target in the adaptation to DDAC and cross-resistance development to CIP.²

9.1 A broken brake rather than a new part

The repressor is a gene that holds the pump's expression down. Inactivating it leaves the pump running, which is a common route to resistance and needs no new genetic material at all.²

9.2 Which is the same architecture as insect resistance

Our synergists article described metabolic resistance in insects as over-production of detoxification enzymes rather than acquisition of new ones, and our reversion article found that regulatory changes are among the hardest resistance mechanisms to reverse because they carry a smaller fitness cost than structural ones.

A broken repressor is a regulatory change. We would expect it to be stable, and we have no data either way.

9.3 And the authors note what is not known

That although the acquisition of genes can explain biocide tolerance, the genetic mechanisms underlying the adaptive cross-resistance to antibiotics remain unclear, and that very limited information is currently available on the genetic mechanisms underlying that resistance following exposure.²

10. The hypochlorite experiment

The same design with the commonest disinfectant of all.

A study reports that ten passages of Gram-negative bacteria in increasingly higher subMICs of the NaOCl disinfectant were sufficient to increase the MIC to >2500 ug/mL NaOCl, particularly in two named species.³

A separate review records that exposure to 100 mg/L sodium hypochlorite increased the resistance of P. aeruginosa.¹

10.1 The mechanism identified

Transcriptome analysis revealed that 1250 ug/mL of NaOCl-adapted strains of the two species increased resistance to imipenem due to the increased expression of resistance-nodulation-cell division (RND) efflux pumps, two of which are named.³

The authors conclude that exposure to NaOCl can influence the expression of RND efflux pump genes, contributing to imipenem cross-resistance.³

11. The honest negative in it

A detail that raises our confidence in the study.

Comparing antibiotic minimum inhibitory concentrations before and after exposure, a statistically significant increase in MIC was only observed for imipenem, at a stated significance level.³

11.1 Only

One antibiotic out of the panel tested. The authors report that plainly rather than emphasising the positive finding alone.³

Which is the appropriate way to read this whole literature: cross-resistance is real, specific and not universal. A biocide exposure does not make an organism resistant to everything.

11.2 Which also bounds the argument

If cross-resistance were general, every disinfectant exposure would be a broad antimicrobial resistance event and the practice would be indefensible. It is not general, so the question is which pairings matter and how much, and neither this article nor its sources can answer that.

11.3 The researchers' overall framing

That the misuse of disinfectants plays an important role in the emergence of disinfectant resistance and in the increase in antibiotic resistance, and that antibiotic resistance may occur from the exposure of Gram-negative bacteria to subminimal inhibitory concentrations.³

12. The other reported pairings

Gathering the specific findings.

Incubation of isolates with subinhibitory concentrations of didecyldimonium chloride also resulted in increased MICs for amikacin, gentamicin, meropenem, and ciprofloxacin. In another study, treatment of a second species was shown to increase antibiotic resistance to ceftazidime, chloramphenicol, and ampicillin, with the mechanism responsible for this effect being increased expression of a named efflux system.¹

In a third organism, strains showing tolerance to this biocide also showed increased resistance to certain antibiotics including fluoroquinolones and tetracyclines.¹

12.1 And a fourth pump

A review notes that in one pathogen, benzalkonium chloride can induce the MexCD-OprJ multidrug efflux pump.⁵

12.2 The membrane route as well

The foodborne pathogen exposed to sub-inhibitory benzalkonium chloride in food environments can adapt by altering membrane composition and surface characteristics, leading to increased resistance to BZK and other unrelated antibiotics.⁴

13. Triclosan and the enzyme

The compound our minimum risk article flagged, with its mechanism.

Research has demonstrated that low levels of this biocide, commonly found in personal care products, can induce bacterial resistance through mutations in key enzymes involved in fatty acid synthesis, such as FabI, and that this resistance can extend to antibiotics like isoniazid.⁴

13.1 Isoniazid is a tuberculosis drug

And it acts on the same fatty acid synthesis pathway, which is why the cross-resistance follows. That is target-site cross-resistance rather than efflux, so the mechanism differs from §6 while the outcome is the same.

13.2 Which closes a loop in this journal

Our minimum risk article reported a review finding laboratory evidence of triclosan-adapted cross-resistance to antibiotics alongside a European committee finding no convincing evidence of risk, and we declined to adjudicate. We still decline. This source is more specific than either and we report it as a third position rather than as a resolution.⁴

14. The plasmid finding

The result that changes the scale of the problem.

A review records that in two of 179 Escherichia coli isolates from retail food qacH-associated integrons associated with tolerance to benzalkonium chloride located on 100 kb plasmids could be transferred to an E. coli recipient, indicating the co-existence and co-dissemination of disinfectant and antimicrobial resistance genes among bacterial species.⁵

14.1 From retail food

Not from a hospital or a laboratory. From food on sale.⁵

14.2 What an integron is

A genetic element that captures and expresses gene cassettes, which is a mechanism for accumulating several resistance determinants in one location. Sitting on a transferable plasmid, it becomes a package that moves as a unit.⁵

So the finding is not that one tolerance gene can move. It is that a collection can move together, which is the co-selection problem in its most direct form.

15. Why that one is different

Because everything else in this article is vertical and this is not.

Selection for efflux overexpression passes from a bacterium to its descendants. A resistance determinant on a transferable plasmid passes sideways, between organisms, potentially between species.⁵

15.1 Which removes the reassurance

Our resistance reversion article found that costly resistance traits can decline when selection stops. A plasmid carrying several determinants at once can be maintained by selection for any one of them, which is the co-selection problem that article described as the principal reason resistance persists.

Two of one hundred and seventy-nine is not a high frequency, and we state it as a demonstration that the route exists rather than as a measure of how common it is.

16. Where the sublethal residue comes from

The practical heart of the article.

Every finding above depends on exposure below the killing concentration. In a working kitchen, plant or food premises, that condition arises routinely and without anybody doing anything unusual. The five routes above are our compilation, not a sourced list, and each is ordinary practice.

16.1 Why this matters more than the laboratory framing suggests

The experiments in §§7 and 10 used deliberate serial passage at controlled concentrations, which looks like an artificial design. It is a laboratory model of something that happens by accident continuously.

A kitchen surface disinfected twice a day for a year receives seven hundred exposures. If a meaningful fraction of them are sublethal for the reasons below, the organism has been through the experiment without anybody running it.

16.2 Dilution

A concentrate measured by eye, a dispenser out of calibration, a bucket topped up with water through a shift.

16.3 Contact time

A disinfectant label specifies a dwell period. A surface wiped dry before that period has received a shorter exposure at a falling concentration, which is precisely the condition described above.

Our article on the legal force of the label made the general point: the directions are the product. Here the direction that is most often ignored is the one that determines whether the exposure kills or selects.

16.4 Organic load

Chlorine compounds in particular are consumed by organic matter, so a soiled surface reduces the available active. Clean first, then disinfect, is standard advice and this is the mechanistic reason for it.

17. The residue in the environment

The route the papers themselves identify.

One paper notes that traces of these molecules may be found in different processing environments over time and the effect of sub-lethal concentration of biocide on bacterial cells is not very well understood.²

17.1 Traces over time

A disinfectant applied, rinsed and dried leaves something behind. That something is at a concentration nobody measures and nobody specifies, and it is present continuously rather than for the label's dwell period.²

17.2 Which is the treated article argument

Our treated articles article argued that a biocide-treated product whose loading declines across its service life delivers a falling dose, and flagged the selection consequence as our own inference from sources that did not make it.

Here is a source making it, in a different setting, with the mechanism attached.²

18. Biofilm as the third driver

Returning to the mechanism list.

Biofilm formation is named alongside efflux and membrane changes as driving the resistance process.¹ The food pathogen's ability to form biofilms and then persist in food processing plants for years is given as a principal reason it is difficult to control.²

18.1 And it is not only a chemical barrier

Cells within a biofilm differ physiologically from free-swimming ones, growing more slowly and sitting in a different nutrient environment. A review notes that exposure at subinhibitory concentrations altered the microbial community composition,⁶ which is a statement about which organisms survive rather than about any one organism adapting.

Both processes run at once: the community shifts toward tolerant members and the surviving members adapt.

18.2 Why a biofilm changes the dose

A biocide has to penetrate the matrix to reach the cells inside it. Cells at the surface receive a lethal dose and cells deeper in receive less, which manufactures a concentration gradient inside a single application.

So a biofilm is not only harder to kill. It is a device for generating sublethal exposures, and that framing is ours.

19. The drain, again

Where this lands in our own work.

Our article on drain biofilm and small fly source identification established that the drain is the source of the fly problem and that surface spraying does not reach it. The same biofilm is now implicated in biocide resistance.

19.1 One structure, two problems

A fly breeding site and a resistance reservoir, in the same pipe, addressed by the same intervention, which is mechanical removal of the film rather than pouring something down the drain.

That connection is ours and it makes the advice in that article stronger rather than changing it.

19.2 And the flies are a symptom of the same failure

A drain with an intact biofilm breeds small flies and shelters bacteria. A drain that has had chemistry poured into it without scrubbing has both problems still, plus a selection episode.

Which means the small fly complaint this trade is called about is, quite often, evidence that the sanitation programme is not reaching the film. That is our reading and it is the most directly useful thing in this article for our own work.

19.3 The general form

Chemistry applied to a biofilm without mechanical disruption reaches the surface cells and selects the rest. Scrubbing is not a lesser alternative to disinfection; it is what makes disinfection work.

20. The audit connection

An uncomfortable implication for a system this journal has already examined.

Our article on third-party food safety auditing described an inspection regime that drives documented sanitation activity. Our hygiene grade article described public disclosure doing the same.

20.1 What gets audited

Frequency, documentation, chemical presence and record-keeping are auditable. Correct dilution, full contact time and mechanical removal of biofilm are considerably harder to verify at an inspection.

20.2 The parallel with our own trade

Our article on applicator certification found training requirements that verify knowledge rather than field practice, and our article on food safety auditing found audit systems measuring what is easy to measure.

Sanitation chemistry has the same structure. The presence of an approved product and a completed log are auditable; the concentration in the bucket at two in the morning is not.

20.3 Which creates a specific risk

A regime that rewards documented application without verifying concentration and dwell time could in principle increase the number of sublethal exposures while improving the paperwork.

We have no evidence that this happens and we are not alleging it. We are identifying a mechanism by which a well-intentioned system could work against its own goal, and flagging it as a question worth somebody's research.

21. What this journal has now found four times

Collecting the pattern.

Rodents. Six generations of sublethal anticoagulant exposure raised tolerance with no mutation in the monitored gene.

Insects. Sublethal exposure is the condition under which resistance alleles are selected rather than eliminated, which our reversion article set out at length.

Treated articles. A declining biocide loading across a product's service life delivers exactly that exposure.

And bacteria. Ten days at fractions of a milligram per litre, with a named gene and a measured change in antibiotic susceptibility.²

21.1 The general statement

A dose that does not kill selects. This holds across mammals, insects and bacteria, for anticoagulants, insecticides and disinfectants, and it is the most robust single finding this journal has assembled.

21.2 Why the pattern should be taken seriously

Four literatures, three kingdoms and four unrelated chemistries reaching the same result is not a coincidence and does not depend on any one study being right. It follows from how selection works: a dose that kills removes the variation, and a dose that does not kill preserves the individuals best able to survive it.

That is the most general statement this journal has arrived at and it is also the most elementary.

21.3 Which makes half-measures the specific danger

Not doing nothing, and not doing too much. Doing something insufficient, repeatedly, is the condition that produces the problem.

22. What a contractor should actually say

The advice that follows.

Concentration and contact time are not guidance. They are the difference between killing and selecting, and our label article explains why they are legally binding as well.

Clean before you disinfect. Organic load consumes the active and leaves a sublethal remainder.

Scrub the biofilm. Chemistry alone reaches the outside of it, per §18.1.

Do not escalate as a substitute. Switching to a stronger product to compensate for an application problem leaves the application problem in place.

And do not treat a disinfection failure as a neutral event. It is the exposure this literature is about.¹³

22.1 What this costs a client

Almost nothing. Correct dilution is not more expensive than incorrect dilution, and a test strip costs pennies. Full contact time costs a few minutes per surface. Mechanical scrubbing costs labour, which is the only real item on the list.

Which makes this unusual among the recommendations in this journal. Most of our conclusions ask somebody to spend more; this one mostly asks them to do what the label already says.

22.2 And what it does not require

Rotating between disinfectant classes on a schedule. Our article on rotation evidence found the practice weakly supported in insecticides, and we found nothing establishing it for biocides either. Doing the existing application correctly is the intervention the evidence supports.

23. What we are not claiming

Being careful, because this subject attracts overstatement.

We are not arguing against disinfection. These compounds are described as a critical line of defence against infection and the alternative is worse.¹

We are not quantifying the contribution. How much of the antibiotic resistance burden is attributable to biocide use is not something we found a figure for, and nothing here supports a claim about it.

And we are not qualified in this field. This journal covers pest control. We are reading a microbiology literature carefully and at the edge of our competence, and §25 says so again.

24. The Manitoba position

Brief, as usual.

We found no Manitoba or Canadian surveillance of biocide tolerance in food premises, no local data on quaternary ammonium resistance determinants, and no indication that sanitation chemical concentrations are verified in routine inspection here.

24.1 And one thing we can say about this climate

The food pathogen in §7 is noted for growing at low temperatures and persisting in cold environments for years.² Refrigerated and chilled spaces are not refuges from it, and they are spaces where disinfection is harder to perform correctly because of surface condensation and shortened working time.

That is an inference from two stated facts rather than a local finding.

24.2 What would be checkable

Dilution at point of use is measurable with a test strip and takes seconds. Whether anybody checks it during a food premises inspection in this province we do not know, and it is the single question this article raises that somebody local could answer.

25. Limitations and open questions

We are outside our field. Every source here is microbiology and we have no training in it. Errors of emphasis are likely and errors of interpretation are possible.

Most findings are laboratory adaptations. Serial passage at controlled subinhibitory concentrations is not a kitchen, and the transfer from one to the other is an assumption.²³

The sources were read as abstracts and extracts. We have not seen full methods for any of the experiments cited, including the exposure protocols.²³

The cross-resistance is specific, not general. Section 11 is the clearest example and the pattern should not be read as a biocide producing broad antibiotic resistance.³

The clinical significance is not established here. A raised minimum inhibitory concentration in a laboratory strain is not a treatment failure in a patient, and none of our sources makes that step.

The sublethal routes in §16 are ours. No source we read lists dilution error, short contact time and soiling as the practical origins of subinhibitory exposure; that compilation is our inference.

Sections 1.1, 4.1, 6.1, 8.1, 15.1, 16, 18.1, 19, 20, 21, 22 and 24.1 are our reasoning. The cross-taxon comparison, the trace-concentration reading, the practical origins of sublethal exposure, the biofilm-as-gradient argument, the drain connection, the audit observation and the practical advice are ours rather than sourced positions.

26. Conclusion

Ten strains of a foodborne pathogen, ten consecutive days, benzalkonium chloride at 0.6 milligrams per litre and a didecyl compound at 0.31, and afterwards a measurable reduction in susceptibility to a fluoroquinolone antibiotic, with a named repressor gene identified as the central target.² Ten passages of Gram-negative bacteria in rising subinhibitory hypochlorite, a minimum inhibitory concentration above 2500 micrograms per millilitre, and cross-resistance to one carbapenem attributed to overexpression of two named efflux systems.³ The mechanism is that a pump does not know what it is pumping: the same efflux systems expel both biocides and antibiotics.⁴

None of this is an argument for less disinfection. It is an argument about how, because the condition that produces the effect is exposure below the killing concentration, and dilution error, short contact time and organic soiling produce that condition in any working kitchen without anybody noticing. The papers themselves note that traces of these molecules persist in processing environments over time and that the effect of sublethal concentrations is not well understood.²

This journal has now reached the same conclusion in mammals, insects, biocide-treated goods and bacteria, from four unrelated literatures. A dose that does not kill selects. The specific danger is never inaction and rarely excess; it is the insufficient measure applied repeatedly, which describes a great deal of routine practice in this trade and in the trades adjacent to it. A failed disinfection is not a neutral event, and the drain that breeds the flies we are called about turns out to be the same structure that shelters the organisms from the chemistry poured into it.

References

1. Disinfectant-induced bacterial resistance and antibiotic cross-resistance: mechanisms and clinical relevance. Review article in a clinical and experimental medicine title. Used for the list of disinfectants in wide use, namely alcohols, aldehydes, chlorine compounds, phenols, quaternary ammonium compounds, peroxides and chlorhexidine, described as a critical line of defence against infection in healthcare settings; for the statement that their overuse or misuse, especially at subinhibitory concentrations, can promote the emergence of bacterial resistance and potentially lead to cross-resistance to antibiotics, with efflux pump activation, alterations in membrane permeability and biofilm formation driving the process; for the report that incubation of isolates with subinhibitory concentrations of a named quaternary compound resulted in increased minimum inhibitory concentrations for four named antibiotics; for the report that treatment of a second named species increased antibiotic resistance to three further named drugs through increased expression of a named efflux gene system, which has also been implicated in multidrug resistance in that organism; for the report that exposure to 100 milligrams per litre of sodium hypochlorite increased resistance in that species; and for the observation that in a third organism, strains showing tolerance to a biocide also showed increased resistance to certain antibiotics including fluoroquinolones and tetracyclines. https://link.springer.com/article/10.1007/s10238-025-01950-2
2. A named repressor gene as a central genetic target in the adaptation to quaternary ammonium compounds and cross-resistance to ciprofloxacin in a foodborne pathogen. Open-access journal article in a microbiology title, from a national food and environmental health agency. Used for the statement that the pathogen frequently undergoes selection pressure associated with the extensive use of disinfectants such as quaternary ammonium compounds widely used in food processing plants; for the statement that repeated exposure to sub-inhibitory biocide concentrations can induce increased tolerance to these compounds but can also trigger the development of antibiotic resistance, both increasing the risk of food contamination and persistence in food production environments; for the authors' prior finding that repeated exposure to two named quaternary compounds led to reduced susceptibility to ciprofloxacin in strains from diverse sources; for the experimental protocol in which ten strains were exposed to sublethal concentrations of the two compounds at 0.6 and 0.31 milligrams per litre for ten consecutive days, with the antibiotic minimum inhibitory concentration determined after adaptation by broth microdilution; for the report that overexpression of a named efflux pump through inactivation of its repressor has been described as responsible for fluoroquinolone resistance in the species, and that the study is the first to report that repressor gene as a central target in adaptation and cross-resistance development; for the statements that although acquisition of genes can explain biocide tolerance the genetic mechanisms underlying adaptive cross-resistance remain unclear and very limited information is available; for the observation that traces of these molecules may be found in different processing environments over time and that the effect of sub-lethal concentrations on bacterial cells is not very well understood; and for the account of the organism's ability to adapt to stress, grow at low temperatures, form biofilms and persist in food processing plants for years, making it a major food safety challenge requiring appropriate cleaning and sanitation programmes. https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2022.864576/full
3. Sublethal sodium hypochlorite exposure: impact on efflux pump overexpression and cross-resistance to a carbapenem. Open-access journal article. Used for the statement that the mechanism through which cross-resistance to antibiotics and disinfectants develops remains ambiguous, and the study aim of examining phenotypic and transcriptomic changes caused by disinfectant exposure in Gram-negative bacteria; for the results that the misuse of disinfectants plays an important role in the emergence of disinfectant resistance and in increased antibiotic resistance, that antibiotic resistance may occur from exposure to subminimal inhibitory concentrations of the disinfectant, and that ten passages in increasingly higher subinhibitory concentrations were sufficient to increase the minimum inhibitory concentration above 2500 micrograms per millilitre, particularly in two named species; for the comparison of antibiotic minimum inhibitory concentrations before and after exposure showing a statistically significant increase only for imipenem at a stated significance level; for the transcriptome finding that adapted strains at 1250 micrograms per millilitre increased resistance to that antibiotic through increased expression of two named efflux pump systems of the resistance-nodulation-cell division family, with the authors concluding that exposure can influence expression of those genes and contribute to cross-resistance; and for the background note that disinfectant use increased markedly during the pandemic years, with the most commonly used being quaternary ammonium compounds, sodium hypochlorite, hydrogen peroxide and ethanol. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11429293/
4. Biocides as drivers of antibiotic resistance: a critical review of environmental implications and public health risks. Review article in an environmental science title. Used for the report that one named pathogen can develop resistance to quaternary ammonium compounds through mechanisms such as efflux pump overexpression and alterations in membrane composition, and that this exposure can also lead to cross-resistance to antibiotics including ciprofloxacin because the same efflux systems expel both biocides and antibiotics from the bacterial cell; for the report that a foodborne pathogen exposed to sub-inhibitory concentrations of a named quaternary compound in food environments can adapt by altering membrane composition and surface characteristics, leading to increased resistance to that compound and to other unrelated antibiotics; and for the report that low levels of triclosan, commonly found in personal care products, can induce bacterial resistance through mutations in key enzymes involved in fatty acid synthesis, with that resistance extending to antibiotics including isoniazid. https://www.sciencedirect.com/science/article/pii/S2666498425000353
5. Biocidal agents used for disinfection can enhance antibiotic resistance in Gram-negative species. Open-access review article. Used for the account that the general possibility of horizontal gene transfer for the spread of antibiotic and biocide resistance was described as early as 2001; for the report that in two of 179 Escherichia coli isolates from retail food, integrons associated with a named tolerance gene and with tolerance to benzalkonium chloride, located on 100 kilobase plasmids, could be transferred to a recipient strain, indicating the co-existence and co-dissemination of disinfectant and antimicrobial resistance genes among bacterial species; and for the report that in a named pathogen, benzalkonium chloride can induce a named multidrug efflux pump. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6316403/
6. Efflux pump-driven antibiotic and biocide cross-resistance in a pathogen isolated from different ecological niches. Open-access journal article. Used for the description of the organism as an opportunistic pathogen displaying high intrinsic antimicrobial resistance and the ability to thrive in different ecological environments; for the study design investigating simultaneous resistance to multiple antibiotics and disinfectants using strains from clinical, veterinary and wastewater sources, with gene expression determined by quantitative reverse transcription and genetic determinants identified by whole-genome sequencing; for the statement that exposure of bacteria to such biocides at subinhibitory concentrations altered microbial community composition and increased tolerance to biocides as well as resistance to critically important antimicrobials including fluoroquinolones and beta-lactams, with such co-selection potentially resulting from drug extrusion by multidrug efflux pumps and mutation of drug target encoding genes; and for the description of intrinsic resistance being largely attributed to expression of multidrug efflux pumps of a named family, described as chromosomally encoded membrane proteins forming tripartite complexes of an inner membrane transporter, a periplasmic adapter and an outer-membrane channel protein. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7690850/
7. Efflux pump-associated antimicrobial resistance genes in staphylococci from dairy and meat samples. Open-access journal article. Used for the statement that widespread and unconsidered use of biocides in this sector leads to acquisition of resistance genes by microorganisms or the adaptation of initially sensitive microorganisms, as with antibiotics, and that there is a growing danger of cross-resistance between antibiotics and biocides; and for the account that one known mechanism causing antimicrobial resistance is overexpression of efflux pump protein genes, that a growing number of multidrug and drug-specific efflux pumps have been characterised in different bacteria, and that there are five families of efflux pump proteins, each named. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12768436/