Case Presentation: A previously healthy 56-year-old female with mitral valve prolapse presented to a Georgia hospital with several days of headache and chest pain. Six weeks prior to admission (PTA), she visited her family ranch in west Texas for three weeks. One week PTA, she developed fever, myalgias, fatigue, and pleuritic chest pain. Her chest x-ray was consistent with community acquired pneumonia and she was prescribed azithromycin and amoxicillin-clavulanate. Her symptoms persisted and she developed headache with photophobia and vomiting.
While in west Texas, she had cleaned rodent droppings from a house and skimmed pond scum. She had no direct contact with any animals, although cats, rabbits, deer, rodents, and cattle were on the ranch. A cow gave birth while she was there, but she was not present. She did endorse mosquito bites but no known tick exposure. She ate homemade goat cheese from a neighbor.

Physical exam was pertinent for temperature of 39° C. She had pain with neck flexion but no frank nuchal rigidity and no Kernig or Brudzinski signs. Lungs were clear bilaterally, without dullness or egophony. Abdomen was nontender with no organomegaly. Skin showed no rashes, bites or other lesions, and she had no joint effusions. Labs showed mildly elevated alkaline phosphatase to 1.6x normal, AST to 1.5x normal, and ALT to 1.8x normal, and chest x-ray demonstrated a left lower lobe opacity. Lumbar puncture was normal. An initial Coxiella burnetii IgG phase II titer of 1:64, rising over four-fold to 1:512 three weeks later, confirmed the diagnosis of acute Q fever. Symptoms improved upon initiation of doxycycline therapy.

Discussion: Q fever—a zoonotic disease caused by the intracellular bacterium C. burnetii—occurs annually in <3 per 10 million persons in the US. The acute clinical manifestations include a flu-like illness, pneumonia, and hepatitis. The major reservoirs of C. burnetii include arthropods, birds, and mammals; infected mammals shed the bacteria in their urine, feces, milk, vaginal mucus, and parturient fluids. C. burnetii is highly contagious, and inhalation of a single organism can cause infection. It is also robust and can persist as a spore. Humans are incidental hosts most commonly infected via inhalation of contaminated aerosols from mammalian byproducts—which can travel over 11 miles—as well as via direct contact with contaminated animals, placenta, wool, or fomites. C. burnetii infection has recently been associated with contact with ponds, environmental water sources (e.g. sewage treatment plants), and consumption of contaminated unpasteurized dairy products. Our patient had multiple potential sources of exposure, even without direct contact with livestock.

Conclusions: Although C. burnetii infection is typically associated with direct or close contact with livestock, clinicians should consider less common forms of inoculation such as distant spread of contaminated aerosols, contact with contaminated water sources, and ingestion of contaminated unpasteurized dairy products.