Rahul Tuli

  • Designation: University of California, Riverside School of Medicine
  • Country: USA
  • Title: To Clinda or Not To Clinda in Toxic Shock Syndrome


Rahul Tuli is a 3rd-year medical student at the University of California, Riverside School of Medicine, and graduated from the University of California, Irvine, with a bachelor’s degree in Human Biology. His interests include vascular surgery and academic research aimed at enhancing clinical outcomes During his Infectious Disease rotation, he became interested in the adjuvant use of Clindamycin in patients with toxin-mediated infections despite its conflicting evidence. As such, Rahul hopes that this research can further uncover insights on the use of unverified medical interventions that may inadvertently contravene the fundamental principle of medicine to “first, not harm.”


Toxic Shock Syndrome (TSS) is a rare but life-threatening condition characterized by the sudden onset of shock and multiorgan failure, often triggered by toxin-producing gram-positive cocci bacteria, particularly Staphylococcus aureus and Streptococcus pyogenes. The pathophysiology of TSS involves the production of superantigens that disrupt the conventional antigen presentation pathway of class II major histocompatibility complex molecules on antigen-presenting cells to T-cell antigen receptors, subsequently leading to a dysregulated hyperimmune response characterized by the excessive release of proinflammatory cytokines. This cytokine storm results in a cascade of symptoms, including fever, myalgias, rash, mucosal sequelae, end-organ dysfunction, and shock, ultimately contributing to high mortality rates.

Current treatment modalities for TSS primarily focus on administering beta-lactam antibiotics targeting the causative pathogens and supportive care such as fluid resuscitation. However, despite aggressive management, mortality rates for TSS remain surprisingly high, underscoring the need for further investigation into adjunctive therapies that may improve patient outcomes.

Clindamycin, a lincosamide antibiotic, has emerged as a potential adjunctive therapy for TSS due to its ability to inhibit bacterial protein synthesis, including the production of exotoxins by S. aureus and S. pyogenes. Additionally, Clindamycin has been shown to exhibit immunomodulatory effects, enhancing chemotaxis, phagocytic activity, and intracellular killing by macrophages and neutrophils, which may contribute to the clearance of bacterial toxins and infected cells. However, using Clindamycin in TSS remains controversial, with limited clinical evidence supporting its efficacy and safety.

To address this knowledge gap, we conducted a retrospective cohort study using unidentified patient data from the TriNetX platform, a comprehensive electronic health records (EHR) system. A total of 2,213 patients diagnosed with TSS were included in the study, with cohorts divided based on whether they received adjunctive Clindamycin therapy during their hospitalization. Propensity score matching was utilized to balance baseline characteristics between the cohorts, including age, sex, ethnicity, and comorbidities (heart failure, chronic kidney disease, diabetes mellitus, hypertension, liver failure, obesity, and chronic obstructive pulmonary disease). Following matching, each cohort had 450 patients with demographics that were not significantly different.

Our analysis revealed a significant difference in mortality rates between the Clindamycin and non-clindamycin groups (p =0.0198), with higher mortality observed in patients receiving Clindamycin therapy. Secondary outcomes, including rates of severe sepsis, severe sepsis with septic shock, neutropenia, monocytosis, acute kidney injury, and cellulitis, were also significantly elevated in the Clindamycin group, further highlighting potential concerns regarding the use of Clindamycin in TSS management. Furthermore, patients in the adjuvant Clindamycin group who had TSS in addition to the aforementioned secondary outcomes had a significantly decreased survival probability between 0-14 days after TSS diagnosis.

These findings suggest that while Clindamycin may possess antimicrobial activity against implicated pathogens, its potentiation of the immune system may exacerbate the hyperimmune response observed in TSS, leading to adverse outcomes. Future research should focus on elucidating the underlying mechanisms of Clindamycin's effects in TSS and exploring alternative treatment strategies, such as those that suppress the immune system (i.e. glucocorticoids, TNF-alpha inhibitors), that may improve patient outcomes. Additionally, efforts to address potential confounders and biases in retrospective studies are warranted to ensure the validity and reliability of our findings.

In conclusion, our study provides important insights into using adjunctive Clindamycin therapy in TSS management. It underscores the need for further research to optimize treatment strategies for this life-threatening condition. Furthermore, it exemplifies the need to scrutinize current guidelines further for treating toxin-mediated infections with pathophysiology similar to TSS.

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