Meningococcal Sepsis with Disseminated Intravascular Coagulation
The most likely organism is Neisseria meningitidis (meningococcus), characterized by lipopolysaccharide (endotoxin) that induces disseminated intravascular coagulation, as evidenced by the thrombocytopenia (80,000/μl) and clinical presentation of septic shock in this young military recruit.
Clinical Reasoning for Meningococcal Disease
This 19-year-old military recruit living in barracks presents with the classic constellation of meningococcal disease:
Age and setting: Meningococcal infection predominantly affects adolescents and young adults, with military recruits in barracks representing a high-risk population due to close-quarter living conditions 1
Rash characteristics: The maculopapular rash can occur with meningococcal sepsis, though it may take other forms including purpuric or petechial patterns; when a rash is present in the context of meningitis, N. meningitidis is the causative organism in 92% of cases 1
Meningeal signs: The combination of severe headache, photophobia, stiff neck, and blurred vision indicates meningeal involvement, which occurs in approximately 60% of meningococcal disease presentations 1
Septic shock features: The hypotension (100/60 mm Hg), tachycardia (126/min), and high fever (40°C) indicate shock resulting from hypovolemia (capillary leak syndrome), myocardial dysfunction, and altered vasomotor tone characteristic of meningococcal sepsis 1
Laboratory Findings Supporting Meningococcemia
Gram-negative cocci in blood cultures: This definitively identifies N. meningitidis, a gram-negative diplococcus 2
Thrombocytopenia (80,000/μl): This indicates disseminated intravascular coagulation (DIC), a hallmark complication of meningococcal sepsis caused by the lipopolysaccharide endotoxin 2, 3
Leukocytosis with left shift: The WBC count of 26,000/μl with 25% band forms indicates severe bacterial infection, though this can vary in meningococcal disease 1
Why Lipopolysaccharide (LPS) is the Correct Answer
The lipopolysaccharide (oligosaccharide) component of the meningococcal outer membrane is the key virulence factor that induces DIC through the following mechanism:
LPS triggers massive cytokine release and activates the coagulation cascade 2
Platelets adhere to damaged vascular surfaces in meningococcemia, leading to consumption and thrombocytopenia 3
The capillary leak syndrome and vascular damage result from endotoxin-mediated injury 1
This explains the clinical triad of hypotension, thrombocytopenia, and multiorgan dysfunction seen in this patient 1, 2
Excluding Other Answer Choices
Poly-glutamic acid capsule: This describes Bacillus anthracis, not N. meningitidis; anthrax does not present with this clinical picture
Protein toxin from vaginal tampons: This describes toxic shock syndrome from Staphylococcus aureus, which would not grow as gram-negative cocci
Tropism for placental tissue with erythritol: This describes Brucella species, which cause undulant fever without this acute presentation
Toxins A and B in large bowel: This describes Clostridioides difficile, which causes antibiotic-associated colitis, not bacteremia with meningitis
Critical Management Implications
Immediate antibiotic therapy: This patient requires urgent ceftriaxone or cefotaxime without waiting for confirmatory testing, as meningococcal sepsis can progress from initial symptoms to death within 12-48 hours if untreated 2
Risk factors for fatal outcome: This patient exhibits multiple poor prognostic features including hypotension, shock, thrombocytopenia, and coagulopathy 1
Close contact prophylaxis: Military barracks contacts require prophylactic antibiotics to prevent secondary cases 2