When a patient presents with signs of infection, a timely diagnosis is essential. This is especially true for patients with severe infections such as LRTI, secondary bacterial infection associated with COVID-19, or sepsis.
It is common to encounter patients who present symptoms—such as cough, shortness of breath, and fever—that can be associated with several different diagnoses (e.g. a case of chronic obstructive pulmonary disease (COPD) exacerbation). One of your first questions will likely be, “Does my patient have a bacterial infection or is there a non-bacterial cause of the current exacerbation?” Followed by, “Does the patient need antibiotics?”
Whether in the emergency department (ED), intensive care unit (ICU) or another hospital ward, consider ordering a procalcitonin (PCT) test along with other diagnostic tests when a bacterial infection is possible.
PCT is a pro-hormone that is highly sensitive and specific for bacterial infection. PCT provides insights into the risk of a patient having a bacterial infection, as well as the severity of that infection. We’ve shared how PCT can help reduce antibiotic exposure and bolster antibiotic stewardship programs. Let’s dive deeper into the science of what PCT is and how it can aid in differentiation between viral and bacterial infections.
PCT is a protein consisting of 116 amino acids and can be detected in the blood in response to bacterial infection with systemic inflammatory reactions.
Procalcitonin is the precursor protein of the hormone Calcitonin.3 Both PCT and Calcitonin are distinct proteins.
Calcitonin is exclusively produced by C-cells of the thyroid gland in response to hormonal stimuli. It plays an important role in the pathway and regulation of calcium and phosphate in bone metabolism and is the main medullary thyroid carcinoma (MTC) tumor marker.4
In healthy individuals, the prohormone PCT is rapidly processed into the mature hormone calcitonin. Therefore, PCT values in non-infected individuals are very low: < 0.1 µg/L.4
In case of bacterial insult, PCT can be induced outside the thyroid gland, in the parenchymal tissue of many organs, and then released into circulation in large amounts4
At first, cytokine-stimulated adherent monocytes release PCT in low quantities (< 2h). While this synthesis is limited, it plays an important role in the initiation of PCT synthesis in storage tissues of humans.4
This PCT burst is initiated in all storage tissues (peak 12-24h). Parenchymal tissue is the most common type of tissue in humans. As a result, extreme concentrations of PCT can be generated (100,000-fold increase in contrast to physiological concentrations).4 The PCT burst continues as long as the stimulus for synthesis exists.4
Additional experiments clarified why PCT is only synthesized during bacterial but not in viral infections. Cells were incubated with IL-1β and INF-γ, inflammatory cytokines known to be released during bacterial and viral infection, respectively. Whereas IL-1ß stimulated the PCT synthesis, the addition of IFN-y blocked this effect.5
Baseline PCT testing, in conjunction with clinical signs and symptoms, may tell you if a bacterial infection is likely or not. Initiation of antibiotic treatment depends on the severity of the illness and the patient’s outcome risk. In high-risk patients with severe illness in the ICU, initiation of empiric antibiotic treatment is based on clinical judgment. In patients with mild illness outside the ICU in which bacterial infection is uncertain, baseline PCT can help clinicians decide whether to initiate antibiotics or consider an alternative diagnosis.2 (Keep in mind: It only takes approximately 20 minutes to get results.)
Serial PCT measurements can indicate whether the patient is responding to the antibiotics or you need to consider a course change. PCT levels should be trended every 24 to 48 hours to determine when the infection has resolved enough that antibiotics can be safely stopped. Discontinuing antibiotic treatment can be considered in clinically stable patients when the PCT level has dropped below the respective cut-offs for sepsis or LRTI, or when it has decreased by ≥ 80% of the peak value
PCT levels may not be elevated in patients infected by certain atypical pathogens, such as Chlamydophila pneumoniae and Mycoplasma pneumoniae.6