ABSTRACT
Viral influenza is a seasonal infection associated with significant morbidity and mortality. Rapidly fatal hemorrhagic pneumonia has been described in previously healthy individuals with ß-hemolytic Streptococcus pneumoniae in a small series of patients, but it is not common in patients coinfected with influenza B and ß-hemolytic Streptococcus, particularly since influenza B is considered less pathogenic than influenza A. However, despite being uncommon, this coinfection seems to be associated with high morbidity and mortality, particularly in healthy individuals. We present a case of a 46-year-old previously healthy white woman presenting with 4 days of shortness of breath, sore throat, subjective fevers, and nonproductive cough with rapidly fatal hemorrhagic pneumonia confirmed to have Group A ß-hemolytic Streptococcus and influenza B coinfection. On admission, she had a temperature of 103° F, room air oxygen saturation of 95%, a positive nasal swab for influenza B, and negative rapid strep test. Initial chest radiograph showed increased bibasilar interstitial markings. She was admitted to a regular floor and started on oseltamivir. Preliminary throat culture was positive for Group A ß-hemolytic Streptococcus and penicillin V was started. Respiratory status deteriorated requiring intubation and transfer to Intensive Care Unit. Subsequently, copious bleeding was noted in her endotracheal tube. A bedside bronchoscopy with bronchoalveolar lavage revealed a hemorrhagic pneumonitis. Despite aggressive efforts, she developed shock, arrested, and died Western District Office of the Chief Medical Examiner, Roanoke, VA, USA postadmission. Blood cultures, bronchoalveolar lavage, and postmortem pulmonary tissue grew Group A ß-hemolytic Streptococcus, only resistant to erythromycin.
ABSTRACT
Eosinophilic lung diseases are a diverse group of pulmonary disorders with an extensive list of differential diagnoses. Multiple drugs particularly antibiotics can cause pulmonary eosinophilia with variable pulmonary manifestations. Cutaneous drug reactions are common. Diagnosis is usually made on clinical history and blood eosinophilia with an accumulation of eosinophils in alveolar spaces on histologic analysis. Imaging findings are nonspecific. Stopping the offending agent is often enough while a short course of corticosteroids can hasten recovery. We present a unique case of eosinophilic pneumonia due to meropenem that highlights the importance of keeping a low threshold of suspicion regarding the etiology of drug-induced lung diseases as the current list is not exhaustive, and new agents are being identified continuously. A 51-year-old African American woman presented with fever, dyspnea, and diffuse pustular rash. She had been treated with meropenem intravenously through a peripherally inserted central catheter for 6 weeks before presentation for Pseudomonas aeruginosa septic arthritis of the left knee. She had a temperature of 102.2 F and SpO2of 86% on room air. Chest roentgenogram had scattered infiltrates and chest tomography showed bilateral ground-glass opacities. Laboratory workup showed peripheral eosinophilia. Bronchoalveolar lavage revealed a white blood cell of 2230 with 89% eosinophils. Skin lesions' biopsies showed pustular dermatosis, compatible with acute drug-induced eosinophilic lung disease with skin involvement. As meropenem was the only medication she had been exposed to, it was stopped and systemic steroids were initiated with improvement in respiratory and clinical status and complete recovery on follow-up.