An Atypical Presentation Of Atypical Pneumonia: Legionella Causing Guillain-Barre Syndrome

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Conference Proceeding

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Publication Title

J Gen Intern Med


Learning Objective #1: Recognize an atypical presentation of Legionella pneumonia Learning Objective #2: Identify the association between Guillain-Barre variants and infectious syndromes CASE: A 29 year-old-female with history of Systemic Lupus Erythema-tosus on plaquenil presented with two weeks of nausea, emesis, and cough. During that time she developed progressive numbness in bilateral lower extremities and began to experience falls at home. On presentation she was afebrile but hypoxic requiring intubation. She had no leukocyto-sis but did present with a moderate hyponatremia to 127. Chest X-ray showed patchy infiltrates and urine legionella antigen was positive. She was started on treatment with moxifloxacin. Her weakness progressed to involve all extremities and respiratory muscles with decreased reflexes. A lumbar puncture was unremarkable with WBC 0, RBC 3 and protein 45 mg/dL. Electromyography (EMG) on day nine of hospitalization showed severe sensorimotor axonal polyneuropathy. She was treated with five days of intravenous immunoglobulin (IVIg) and seven sessions of plas-mapheresis with limited improvement in weakness. The patient eventually required tracheostomy due to persistent weakness. We present an atypical case of legionella pneumonia causing Guillain-Barre Syndrome. IMPACT/DISCUSSION: Legionella is an important cause of community acquired pneumonia, often with severe symptoms and a mortality rate up to 10%. Patients with legionella pneumonia can present with extrapulmonary manifestations including emesis, diarrhea, chest pain, scant hemoptysis, and high fever. Mild neurologic symptoms including headache and encepha-lopathy are sometimes seen. There are few case reports of Guillain Barre variants associated with legionella pneumonia, though over two-thirds of patients with GBS have a proceeding respiratory or gastrointestinal illness. The weakness associated with GBS is typically progressive, symmetrical, and ascending-with maximal weakness occurring within two-four weeks from symptom onset. Though up to one-third of patients may require mechanical ventilation, nearly 80 percent make a near-complete recovery. Both IVIg and plasmapheresis have demonstrated in randomized controlled trials to shorten time to neurologic recovery in GBS, though the recovery phase can take several months and can require intensive rehabilitation. Conclusion: Though weakness in critically ill patients is often attributed to critical illness myopathy, careful attention should be paid to timing, intensity, and progression of neurologic symptoms. Guillain-Barre syndrome has a known association with infections therefore clinical suspicion should remain high in patients with the combination of infection and rapidly progressive weakness.





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