Infectious Disease · Bacterial Infections
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Caused by Neisseria meningitidis, presenting with abrupt fever, myalgias, and a rapidly spreading petechial rash that coalesces into purpura fulminans.
Ceftriaxone is the first-line empiric antibiotic and must be given immediately without waiting for cultures.
Gold-standard diagnosis is blood and CSF culture, with Gram stain showing gram-negative intracellular diplococci.
Do not delay antibiotics to obtain a lumbar puncture in an unstable patient or one with signs of increased intracranial pressure.
Endotoxin-driven cytokine release causes disseminated intravascular coagulation (DIC) with thrombocytopenia, elevated PT/PTT, and elevated D-dimer.
Adrenal hemorrhage produces the classic Waterhouse-Friderichsen syndrome with acute adrenal insufficiency and refractory shock.
Close contacts need prophylaxis with rifampin, ceftriaxone, or ciprofloxacin; rifampin is contraindicated in pregnancy, so use ceftriaxone.
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A previously healthy 19-year-old college dormitory resident presents with 12 hours of high fever, severe myalgias, and headache. Over the past two hours a petechial rash has spread across his trunk and lower extremities, with several lesions coalescing into large purpuric patches. He is hypotensive and tachycardic. Labs show thrombocytopenia, prolonged PT and PTT, and elevated D-dimer.
Which of the following is the most appropriate immediate next step in management?
Immediate empiric IV ceftriaxone.
Abrupt fever with a rapidly progressive petechial-to-purpuric rash, shock, and DIC in a dormitory resident is meningococcemia, a medical emergency. Empiric IV ceftriaxone must be given immediately and should never be delayed for cultures or lumbar puncture in an unstable patient.
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Etiology / Epidemiology
Caused by Neisseria meningitidis, primarily affecting infants, adolescents, and young adults in crowded environments like dorms or barracks.
Clinical Manifestations
Abrupt onset of fever, myalgias, and a rapidly spreading petechial rash that coalesces into life-threatening purpura fulminans.
Diagnosis
Blood and CSF cultures are the gold standard, classically revealing gram-negative intracellular diplococci.
Treatment
Immediately administer intravenous Ceftriaxone; close contacts mandate prophylaxis with Rifampin, Ceftriaxone, or Ciprofloxacin.
Prognosis
Extremely high mortality without rapid intervention, with survivors often requiring limb amputations due to ischemic necrosis.
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Epidemiology & Etiology
Caused by Neisseria meningitidis, an encapsulated gram-negative diplococcus. Peak incidence occurs in infants <1 year and adolescents/young adults living in close quarters like college dormitories or military barracks. Transmission is via respiratory droplets, and complement deficiencies (C5-C9) or asplenia drastically increase susceptibility to severe, recurrent disease.
Pertinent Anatomy
The bacteria initially colonize the nasopharyngeal mucosa before invading the submucosa and entering the bloodstream. Dissemination targets the meninges, skin microvasculature, and the adrenal glands, leading to devastating systemic complications.
Pathophysiology
Following bloodstream invasion, the bacteria release massive quantities of lipooligosaccharide (LOS) endotoxin. This triggers an overwhelming systemic release of cytokines (TNF-alpha, IL-1), causing profound endothelial damage and capillary leak. The resulting endothelial injury initiates systemic microvascular thrombosis and disseminated intravascular coagulation (DIC). Microthrombi consume platelets and clotting factors, leading to simultaneous widespread hemorrhage and ischemic tissue necrosis.
Clinical Manifestations
Presents abruptly with high fever, severe myalgias, and a rapidly spreading petechial rash predominantly on the trunk and lower extremities. The rash quickly coalesces into purpura fulminans, presenting as large ecchymoses and ischemic necrosis of digits and limbs. Patients rapidly develop profound septic shock with hypotension and tachycardia. If the adrenal glands hemorrhage, the classic Waterhouse-Friderichsen syndrome ensues, characterized by acute adrenal insufficiency and refractory shock.
Diagnosis
The gold standard for definitive diagnosis is blood culture and cerebrospinal fluid (CSF) culture if signs of meningitis are present. Gram stain classically reveals gram-negative intracellular diplococci. Laboratory evaluation shows marked thrombocytopenia, elevated PT/PTT, and elevated D-dimer, confirming disseminated intravascular coagulation (DIC). Do not delay antibiotic therapy to obtain a lumbar puncture if the patient is unstable or showing signs of increased intracranial pressure.
Treatment
This is a medical emergency requiring immediate empiric intravenous antibiotics without waiting for culture results. Ceftriaxone is the first-line agent, often combined with Vancomycin empirically until sensitivities result. Aggressive fluid resuscitation and vasopressors are critical for managing septic shock. Post-exposure prophylaxis for close contacts is mandatory and consists of Rifampin, intramuscular Ceftriaxone, or oral Ciprofloxacin. Rifampin is contraindicated in pregnancy, making Ceftriaxone the preferred prophylactic choice for pregnant contacts.
Prognosis
Carries a mortality rate of 10-15% even with appropriate therapy, rising to >40% if meningococcal septic shock develops. Survivors frequently suffer severe permanent sequelae including limb amputations, extensive skin scarring requiring grafting, and sensorineural hearing loss.
Differential Diagnosis
Rocky Mountain Spotted Fever: Presents with a petechial rash that classically begins on the wrists and ankles before spreading centrally.
Toxic Shock Syndrome: Features a diffuse macular erythroderma (sunburn-like rash) followed by desquamation, rather than purpura.
Infective Endocarditis: Subacute presentation with Janeway lesions, Osler nodes, and a new heart murmur.
Henoch-Schönlein Purpura (IgA Vasculitis): Palpable purpura strictly on the lower extremities and buttocks, accompanied by abdominal pain and arthralgias.