A 4-month-old girl presented to our pediatric emergency department with septic shock requiring fluid resuscitation and vasoactive support. Laboratory findings suggested severe bacterial infection with a procalcitonin level of 249.5 ng/mL (reference < 0.05 ng/mL). Empirical antimicrobial treatment with piperacillin/tazobactam was instantly initiated.

The patient exhibited progressively enlarging ecchymoses consistent with purpura fulminans. Cefotaxime and vancomycin were therefore immediately added, given the suspicion of meningococcal sepsis. Markedly elevated D-dimers (>35 mg/L), thrombocytopenia (nadir 37 G/L) and severely reduced protein-C activity (14%) confirmed the presence of Disseminated Intravascular Coagulation (DIC), further supporting the suspected diagnosis. Following transfusions of platelets, fresh frozen plasma and protein-C concentrate, coagulation parameters eventually normalized.

At presentation, a peripheral blood smear was prepared for morphological evaluation of leukocytes and revealed the findings shown in Fig. 1. Intraleukocytic and peri-/intraerythrocytic cocci and diplococci were identified. Further microbiological PCR-diagnostics confirmed invasive Neisseria meningitidis (serogroup W). The patient recovered completely.

Fig. 1.

Peripheral blood smear of a 4-month-old girl (black arrow probably indicating the inactivated X-chromosome [“Barr body”]) with meningococcal sepsis. The exceedingly rare findings of intraleukocytic cocci and diplococci (black arrowhead) and peri-/intraerythrocytic diplococci (black asterisk) are depicted. Microbiological PCR-diagnostics confirmed invasive infection with Neisseria meningitidis serogroup W.

Intraleukocytic detection of meningococci in peripheral blood smears remains a rare finding.1 A direct correlation between clinical severity/bacterial load and the detectability of meningococci in peripheral blood smears has not been established yet.2 However, if present, this finding may precede definitive microbiological results by days.

Neisseria meningitis can bind to erythrocyte Complement Receptor 1 (CR1) on the surface of red blood cells, facilitating evasion of phagocytosis by leukocytes and favoring meningococcal survival within the bloodstream. Visualization of meningococci adjacent to or within erythrocytes is exceedingly rare.3 Mechanistically, CR1 acts as an inhibitor of the classical complement cascade by serving as a co-factor for factor I, which cleaves C3b and C4b into inactive forms, thus preventing formation of the membrane attack complex and subsequent bacterial lysis.4

In ambiguous cases, a cost-effective peripheral blood smear can complement clinical findings in septic shock and guide therapeutic decisions.