Acute vs. Chronic Bacterial Infections — Are We Asking the Right Questions?

Challenging Old infection Assumptions

For a long time, there has been a tendency to describe acute and chronic bacterial infections as two very distinct biological worlds. The traditional view goes something like this: acute infections are driven by free-floating, planktonic bacterial cells that multiply rapidly and overwhelm the host defenses by sheer growth rate. In contrast, chronic infections — such as those found in cystic fibrosis lungs, chronic wounds, or around implants — are dominated by bacteria organized in biofilms, living in dense communities enclosed in protective matrices, growing slowly, and showing remarkable tolerance to both antibiotics and immune responses.

This distinction has shaped decades of research, diagnostics, and therapeutic strategies. The story seemed neat — almost too neat. Acute equals planktonic, chronic equals biofilm. Fast versus slow. Vulnerable versus protected.

biology rarely fits neatly into our definitions 

Over the past several years, new evidence has started to challenge this simple dichotomy¹. For instance, if we look closely at acute infections such as community-acquired pneumonia, we often find that bacteria are not freely swimming in the infected tissue or sputum. Instead, they are aggregated — clustered together in structures that, under the microscope, look a lot like biofilms. These bacterial aggregates can exhibit higher metabolic activity than the bacteria found in long-term chronic infections, yet they are still far from behaving like planktonic cells growing exponentially in laboratory broth.

So what are we actually looking at?

If acute infections are also dominated by aggregates and biofilm-like structures, maybe the fundamental difference between acute and chronic infections is not about “biofilm versus planktonic” at all. Perhaps it’s more about metabolic state, environmental context, and host interaction than physical organization.

This perspective forces us to ask uncomfortable but necessary questions: Are we using the right model systems when we study infection biology? If we use liquid cultures to represent acute infections, are we truly mimicking the physiological state of the bacteria that cause them? And if chronic infections are defined by persistence rather than structure, does it even make sense to define biofilms as strictly surface-attached, matrix-enclosed entities?

Maybe the boundaries between acute and chronic infections — or between biofilm and planktonic lifestyles — are not as rigid as we once thought. Perhaps they are points on a continuum, where bacterial behavior shifts dynamically depending on nutrient availability, host responses, and time. To understand infection fundamentally, we may need to move beyond definitions and start asking what really drives bacterial survival and resilience inside the host.

References
1. Bacterial biofilms predominate in both acute and chronic human lung infections, Kolpen et al, Thorax. 2022 Oct;77(10):1015-1022.

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