Moo Is the Clue

Meeting: Hospital Medicine 2012, April 1-4, San Diego, Calif.

Abstract number: 97989

Case Presentation:

A 39–year–old female presented to the hospital with 2 weeks of fevers, diffuse pain, headaches, neck stiffness, photophobia, nausea and vomiting. Her past medical history includes hypothyroidism, diverticulitis, GERD and gluten intolerance. She denied smoking, alcohol, illicit drug use, recent travel or pets at home, but did report drinking raw milk through a cow share program over the past 2 years. On exam, she was febrile to 39.1C with other vital signs stable. She was alert and oriented, pupils were equal and reactive to light but with photophobia. She had mild nuchal rigidity and marked allodynia of the scalp and bilateral lower extremities. Neurological exam was otherwise nonfocal. Lung and cardiac exam were normal. She had a leukocytosis of 12,000 with left shift but otherwise laboratory testing was normal. The patient was started on broad spectrum antimicrobials for empiric coverage of meningitis. MRI of the brain and spine showed abnormal leptomeningeal enhancement. A lumbar puncture was performed and the CSF showed a WBC count of 1280 (39% neutrophils, 49% lymphocytes), protein of 175, glucose of 48. Blood and CSF cultures were negative. Evaluation for HIV, herpes simplex, varicella zoster, enteroviruses, arbovirus, cryptococcus, lymphocytic choriomeningitis, Epstein–Barr, cytomegalovirus, brucella, lyme disease, fungal infections, tuberculosis and lymphoma were negative. Q fever serologies showed elevated phase II IgG (1:256) indicative of probable acute Q fever. Antimicrobials were changed to IV doxycycline and ciprofloxacin to complete a 3 week course. Due to evidence of elevated intracranial pressure with papilledema and elevated CSF opening pressures, treatment also included serial lumbar punctures. Her symptoms resolved over 8–10 weeks. Repeat Q–fever serologies at 1 and 3 months after hospitalization did not demonstrate evolution to chronic Q–fever.

Discussion:

Q fever is a zoonosis caused by Coxiella burnetii. While inhalation of contaminated aerosols is the primary route of infection, this case highlights ingestion of raw milk as another route of transmission. Although acute Q–fever is asymptomatic in 60% of cases, a mild flu–like illness is the most common presentation in symptomatic patients. Hospitalization occurs in 2% of infected individuals usually due to fever, pneumonia, and/or hepatitis. Meningoencephalitis is a rare presentation and occurs in only 1% of hospitalized patients. Doxycycline is the treatment of choice for acute Q fever but most patients with meningoencephalitis have full recovery regardless of treatment choice. This patient was the index case in a cluster of 5 confirmed or probable cases of Q fever associated with raw milk consumption.

Conclusions:

Acute Q fever has a wide spectrum of clinical manifestations. It is important for clinicians to maintain a high index of suspicion in hospitalized patients with a relevant exposure. While this case describes a rare manifestation, it serves to increase awareness of acute Q fever.

To cite this abstract:

Jiang M, Khateeb R, Gandhi T. Moo Is the Clue. Abstract published at Hospital Medicine 2012, April 1-4, San Diego, Calif. Abstract 97989. Journal of Hospital Medicine. 2012; 7 (suppl 2). https://www.shmabstracts.com/abstract/moo-is-the-clue/. Accessed November 14, 2019.

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