Antimicrobial resistance (AMR) occurs when germs like bacteria and viruses evolve to defeat the drugs designed to kill them. While drug-resistant tuberculosis is a well-known example, it is part of a much broader public health challenge. The ability of these organisms to survive treatment makes infections harder to manage and increases the risk of disease spread, severe illness, and death. This resistance develops naturally but is accelerated by the misuse and overuse of antimicrobial medicines.
Prominent Drug-Resistant Bacterial Infections
Methicillin-resistant Staphylococcus aureus (MRSA) is a well-known drug-resistant bacterium. It frequently causes skin infections but can also lead to more dangerous conditions in the bloodstream or lungs. MRSA is resistant to a class of penicillin-like antibiotics called beta-lactams, including methicillin and amoxicillin. Once confined mainly to healthcare facilities, MRSA strains are now found circulating within the community.
Carbapenem-resistant Enterobacteriaceae (CRE) are another category of resistant bacteria. This family includes Klebsiella pneumoniae and Escherichia coli (E. coli), which are common in the human gut but can cause serious infections elsewhere. CRE are resistant to nearly all available antibiotics, including carbapenems, which are drugs of last resort. Infections occur in patients in healthcare settings who have weakened immune systems or require medical devices like ventilators.
Drug resistance also extends to sexually transmitted infections, with Neisseria gonorrhoeae being a primary concern. The bacterium that causes gonorrhea has developed resistance to nearly every class of antibiotic used to treat it, including penicillins, tetracyclines, and fluoroquinolones. This has forced public health organizations to update treatment guidelines. The current recommended treatment in the U.S. is a single injection of ceftriaxone, highlighting the limited options remaining.
Emerging Fungal and Parasitic Resistance
Drug resistance is not confined to bacteria; fungi and parasites are also developing defenses. A prominent example is the parasite Plasmodium falciparum, which causes the most lethal form of malaria. Resistance to artemisinin-based combination therapies (ACTs), the most effective treatment, has emerged in several parts of the world. This resistance appears as a delay in clearing parasites from the bloodstream after treatment, threatening global control efforts.
In the fungal realm, Candida auris has surfaced as a global health threat. This fungus can cause severe, invasive infections of the bloodstream, heart, and brain, particularly in hospital patients with compromised immune systems. C. auris is often resistant to multiple classes of antifungal drugs at once, making infections difficult to treat. It also persists on surfaces in healthcare environments, allowing it to spread easily.
Resistance in these organisms complicates treatment. For malaria, partial resistance to artemisinin means partner drugs in ACTs must be highly effective, straining the limited options. The rise of C. auris has created a need for new antifungal medications and better infection control in healthcare facilities to prevent outbreaks.
Antiviral Drug Resistance
Viruses can also evolve and develop resistance to antiviral medications. This is a concern in managing chronic viral infections like Human Immunodeficiency Virus (HIV). Because HIV replicates rapidly with a high mutation rate, resistant strains emerge quickly if a single drug is used. To overcome this, HIV is managed with antiretroviral therapy (ART), a combination of drugs that attacks the virus at different stages of its life cycle.
Seasonal influenza is another virus where drug resistance complicates treatment. Antivirals like oseltamivir (Tamiflu) work by blocking a protein called neuraminidase, preventing the virus from spreading between cells. However, mutations in the gene coding for this protein can reduce the drug’s effectiveness. This resistance is a concern in immunocompromised patients, as prolonged infections provide more opportunities for the virus to mutate.
The potential for antiviral resistance requires continuous surveillance of circulating viruses. For influenza, this monitoring helps determine which drugs will be effective during a flu season. For HIV, resistance testing is a standard part of care to ensure a patient’s treatment regimen remains effective.
Common Pathways to Drug Resistance
Microbes become resistant through two primary evolutionary pathways. The first is genetic mutation. As microbes replicate, random errors can occur in their genetic code. A rare mutation may alter the drug’s target, such as a specific protein, preventing the drug from binding to it. This renders the drug ineffective and allows the mutant microbe to survive and multiply.
The second pathway, prevalent among bacteria, is horizontal gene transfer. This process allows bacteria to share genetic material, including resistance genes. One common method is conjugation, where two bacteria connect and one passes a small piece of DNA called a plasmid to the other. This is like one bacterium handing a cheat sheet to another, instantly providing the tools to survive an antibiotic attack.
The ability to share resistance genes allows resistance to spread rapidly through a bacterial population. A single bacterium with a resistance plasmid can share it with its neighbors, even those of different species. These mobile genetic elements often carry instructions for defeating multiple antibiotics at once, leading to multidrug-resistant organisms that are difficult to treat.