RT Book, Section A1 Cherry, Cara A1 Kersh, Gilbert J. A2 Boulton, Matthew L. A2 Wallace, Robert B. SR Print(0) ID 1182667428 T1 Q Fever T2 Maxcy-Rosenau-Last Public Health & Preventive Medicine, 16e YR 2022 FD 2022 PB McGraw Hill PP New York, NY SN 9781259644511 LK accessmedicine.mhmedical.com/content.aspx?aid=1182667428 RD 2024/04/19 AB Q fever in humans is caused by infection with the gram-negative bacterium Coxiella burnetii. The organism grows intracellularly in a parasitophorous vacuole at acidic pH (4.75).1C. burnetii is a member of the gammaproteobacteria and is classified in the order Legionellales, family Coxiellaceae. This bacterium infects a broad range of animal species, and is thought to be transmitted primarily by inhalation, but tick transmission could play a role in maintaining the bacteria in wildlife. Q fever is a zoonosis, and humans usually acquire the disease via inhalation of contaminated dust or dried material from animal waste, with a small number of organisms (<10) thought to be able to initiate an infection.2 Infected livestock, such as cattle, sheep, and goats are the primary reservoirs for human exposure. The organism can grow to very high densities in the placenta of infected livestock. Therefore, these animals shed the largest amounts of C. burnetii during parturition. The replicative form of C. burnetii has been described as the “large cell variant” (LCV), whereas nonreplicating C. burnetii will form a spore-like “small cell variant” (SCV).3 The SCV is resistant to heat and desiccation resulting in impressive stability in the environment.4 The environmental stability, transmission by inhalation, and low infectious dose have led to classification of C. burnetii as a potential bioweapon and inclusion on the list of select agents maintained by the U.S. Department of Health and Human Services.