What Is CPE in Medical Terms?

The acronym CPE in a medical context most commonly refers to Carbapenemase-Producing Enterobacteriaceae. This collection of bacteria represents a significant and escalating public health threat. CPE is a type of multidrug-resistant organism, often called a “superbug,” that possesses a mechanism rendering many powerful antibiotics ineffective. Its increasing prevalence complicates patient care in healthcare settings worldwide.

Defining Carbapenemase-Producing Enterobacteriaceae

The name Carbapenemase-Producing Enterobacteriaceae refers to a family of Gram-negative bacteria. Enterobacteriaceae commonly reside in the human gut as normal flora, including species like Escherichia coli and Klebsiella pneumoniae. These bacteria cause infections when they move outside the gut into areas like the bloodstream, urinary tract, or lungs.

Carbapenems are broad-spectrum beta-lactam antibiotics historically reserved as a last-line treatment for severe, drug-resistant infections. Their unique structure allows them to overcome many common bacterial resistance mechanisms. The problem arises when these bacteria acquire a gene enabling them to produce an enzyme called a carbapenemase.

Carbapenemase disables the antibiotic by hydrolyzing the beta-lactam ring structure common to carbapenems, penicillins, and cephalosporins. This action makes the drug useless against the infection. The genes encoding these enzymes are often carried on mobile genetic elements called plasmids, allowing the resistance mechanism to be easily transferred between different bacterial species. The resulting CPE bacteria are resistant to virtually all beta-lactam drugs, severely restricting treatment options.

How CPE Spreads and Who Is At Risk

CPE bacteria primarily spread through direct or indirect contact, making them a significant concern within healthcare environments. Transmission often occurs via healthcare workers’ hands or contaminated medical equipment and surfaces. The fecal-oral route is prevalent because the bacteria colonize the gastrointestinal tract, allowing them to be shed in stool.

A person can be colonized with CPE, meaning the bacteria are present in the gut without causing an active infection. Colonized individuals can still transmit the bacteria to others, and colonization is a necessary precursor to developing an infection. The presence of CPE in the environment, such as sink drains or improperly cleaned surfaces, also contributes to spread within hospital settings.

Certain patient populations face a higher risk of colonization and subsequent infection. Individuals with prolonged hospital stays, especially in intensive care units, are particularly susceptible. The presence of invasive medical devices, such as catheters or breathing tubes, increases risk by providing a pathway for bacteria to enter the body. Major risk factors also include recent international travel for medical procedures. Previous hospitalization in a facility with a high CPE prevalence is another risk factor.

Clinical Diagnosis and Treatment Challenges

Identifying a CPE infection begins with collecting clinical samples from the infected site, such as blood, urine, or wound fluid, which are then cultured in a laboratory. Since CPE colonization is often asymptomatic, screening is a routine practice for high-risk patients upon hospital admission, typically involving a rectal swab. Once cultured, technicians must confirm carbapenem resistance and the presence of the carbapenemase enzyme.

Phenotypic tests, like the modified carbapenem inactivation method, detect the enzyme’s activity. Molecular tests, such as Polymerase Chain Reaction (PCR), rapidly identify specific resistance genes like KPC, NDM, or OXA-48. Prompt identification of the specific carbapenemase type is important because it dictates which remaining antibiotics might be effective. A delay in diagnosis contributes significantly to the high mortality rates associated with these infections.

The treatment of active CPE infections presents an extreme challenge due to limited therapeutic options. Clinicians often rely on older antibiotics, such as polymyxins (like colistin) or tigecycline, which were historically avoided due to toxicity or limited efficacy. Polymyxins carry a significant risk of kidney damage and neurotoxicity. Tigecycline may not achieve sufficient concentrations to treat severe systemic infections.

Fortunately, newer antibiotic-beta-lactamase inhibitor combinations offer hope against specific types of CPE. Drugs like ceftazidime-avibactam, meropenem-vaborbactam, and imipenem-cilastatin-relebactam are active against certain carbapenemases, particularly KPC. Cefiderocol, a unique siderophore cephalosporin, is another effective option against difficult-to-treat strains. Treatment regimens often involve a combination of two or three agents. Even with optimal treatment, the mortality rate for serious CPE bloodstream infections can be as high as 50%.

Preventing the Spread of CPE

Containing CPE spread relies heavily on consistent infection control practices within healthcare facilities. The most effective measure is strict adherence to hand hygiene protocols by all staff, patients, and visitors, using soap and water or an alcohol-based hand rub. This practice is important after contact with a patient, their environment, or using the toilet.

Patients identified as colonized or infected with CPE are typically placed under contact isolation precautions, often requiring a single room. Staff entering these rooms must consistently wear personal protective equipment, including gloves and gowns, to prevent bacterial transfer. Enhanced cleaning and disinfection of the patient’s environment and shared medical equipment are necessary to eliminate bacteria from surfaces and reservoirs.

Controlling antibiotic use, known as antimicrobial stewardship, is a powerful preventative strategy. Minimizing the unnecessary or prolonged use of broad-spectrum antibiotics, including carbapenems, reduces the selective pressure that drives resistance development. Combining meticulous hygiene, isolation, environmental control, and judicious antibiotic use helps slow the spread of this dangerous organism.