Rapidly progressive streptococcal toxic shock syndrome epidemic in Kraków, 2023

The postpandemic era has witnessed a rise in the incidence of various infectious diseases, including those caused by Streptococcus pyogenes. This increase is not attributable to a new strain or increased antibiotic resistance; instead, it is believed to be associated with 2 phenomena: “immune debt,” that is, inability of the unprepared immune system to fight pathogens due to limited social interactions and lack of immunization after the pandemic, and “immune theft,” which refers to direct weakening of the immune system after COVID-19.¹ It is known that the expression of group A streptococcus (GAS) virulence factors, which are capable of changing the disease type from noninvasive to invasive, is controlled epigenetically, but human triggers are unknown.² The enlarged human reservoir of S. pyogenes has contributed to a surge in cases of streptococcal toxic shock syndrome (STSS), a severe complication of invasive GAS infections. The National Institute of Public Health – National Institute of Hygiene reports from Poland have shown an increase in the incidence of all S. pyogenes infections, including STSS, since the beginning of 2023 (Figure 1A).³

In the current report, we describe 6 patients with STSS admitted to the intensive care unit of the 5th Military Hospital with Polyclinic in Kraków between January and April 2023, representing over 14% of all cases in Poland at that time. The patients, 3 women and 3 men, at a median age of 61 years (interquartile range, 38–65), were admitted in critical condition, obtaining a median of 12.5 points on the Sequential Organ Failure Assessment (SOFA) score at the time of admission. No prior direct contact between the patients had been registered. Septic shock was evident, as indicated by high lactate levels, with a median peak value above 14.8 mmol/l (reference range [RR] <⁠2 mmol/l). Median levels of procalcitonin and C-reactive protein were 102 ng/ml and 335.8 mg/l, respectively (RR <⁠0.1 ng/ml and <⁠5 mg/l, respectively).

Overall, 5 out of 6 patients experienced significant skin complications, including swelling (Figure 1B), skin necrosis, ulcers, blisters with serous content, and rash. It is possible that intense treatment with pressor amines was the reason for necrosis of the distal phalanges or the auricle (Figure 1C–1E), demanding surgical debridement.

The GAS cultures came from blood, pleural effusion (Figure 1F), bronchoalveolar lavage, and skin swabs. Antibiograms revealed sensitivity to all tested antibacterial agents, including clindamycin and linezolid, which are additionally capable of inhibiting streptococcal pyrogenic exotoxin A; therefore, antimicrobial therapy was mainly based on 1 of these 2 agents.⁴ The patients were also treated with steroids. Hypotension was managed with very high doses of norepinephrine and vasopressin, while some patients required additional medications, such as epinephrine or dobutamine (median dose, 1.15 µg/kg/min, 0.04 U/min, 0.175 µg/kg/min, and 13.5 µg/kg/min, respectively).

The fulminant course of STSS led to death of 5 out of 6 patients (83%) within a few days. The median length of stay in the ICU was 2 days, whereas 2 patients died on the first day—rapid disease progression and high mortality reverberate in the literature.⁵ The patient who survived had the lowest SOFA score on admission (9 points). She was treated in the ICU for 14 days, and stayed another 14 days in the internal medicine ward.

The increasing incidence of STSS in the postpandemic period necessitates an urgent focus on early diagnosis; therefore, we need to implement a new system for prompt recognition of S. pyogenes infections.