Q fever, a widespread zoonotic disease caused by Coxiella burnetiid, produces a complex and polymorphic disease in humans. As a zoonotic disease, control in animals will influence the level of disease seen in humans, thus resulting in interesting one health perspectives for disease control. Here the authors describe the clinical manifestations in animals and humans, as well as the current diagnostic methods available and the strategies for disease control. A review on the published information regarding Q fever as a disease with impact for veterinary public health and public health is presented.
TopRisk Factors For Coxiellosis: A One Health Approach
Awareness of the excretion routes of C. burnetii from infected domestic animals is vital to pinpoint transmission routes, and thus, prevent human infection and allow the implementation of effective and reasonable preventive measures. Transmission to humans mainly occurs through inhalation of contaminated aerosols from the environment, such as dust or tick feces (Klemmer et al., 2018), thus making Q fever, essentially, an airborne disease, although some studies refer the evidence that C. burnetii may be a food-borne pathogen (Benson, Brock, & Mather, 1963; Cerf & Condron, 2006; Gale, Kelly, Mearns, Duggan, & Snary, 2015) throughout experiments obtained in which contaminated milk was fed to volunteers, causing seroconversion but any clinical disease (Benson et al., 1963) or through the consumption of unpasteurized milk (Gale et al., 2015). Domestic ruminants’ excretion of C. burnetii is considered to be the main source of environmental contamination and a key cause of human infection (Roest et al., 2012; van den Brom, van Engelen, Roest, van der Hoek, & Vellema, 2015), as referred. In the Netherlands, after one of the largest Q fever outbreaks, airborne presence of Coxiella burnetii showed to be associated with goat kidding season, and with spatial variation/distance/size of goat farms (de Rooij et al., 2016; van der Hoek et al., 2010).
Shedding of C. burnetii occurs in feces, milk, and mostly, in placental membranes and birth fluids of aborted mammal fetuses, as well as, in stillbirths and healthy infected neonates (Roest et al., 2012; van den Brom et al., 2015). Subclinically infected animals also shed the organism, but with considerably lower bacterial loads than those observed in animals that underwent abortion (Roest et al., 2012).
During abortion and parturition of infected ruminants, there is a massive excretion of bacteria from birth products. A previous study has found that around 109 bacteria/gram of placenta were excreted during abortions in ruminants (Khalili, Sakhaee, & Babaei, 2012), whereas birthing of healthy neonates, from infected mothers, revealed a lower quantity (Rodolakis, 2009). Infectious biological excretions are desiccated in the environment, aerosolize, thus becoming airborne and available to be inhaled, allowing for transmission and infection. Environmental surroundings, dust in windy days and fomites (inanimate objects, such as gloves, coveralls, rags, etc.), that have been exposed to contaminated materials, may also result in sources for transmission (The Center for Food Security and Public Health [CFSPH], 2017).
Although C. burnetii has been isolated from milk, udder tissue and corresponding lymph nodes, the transmission of Q fever to humans, via ingestion of contaminated unpasteurized dairy products, still remains controversial (Eldin et al, 2017; Galiero et al., 2016). Nonetheless, shedding of C. burnetii in milk should be considered an important vehicle of infection for farmers, veterinarians and for dairy workers in general. Shedding in milk seems to vary in quantity and duration between animal species (Guidi et al., 2017; Mangili et al., 2016).
When comparing two excretion routes (via vaginal mucus and milk), domestic ruminants (cattle, goats and sheep) exhibit different patterns. Milk shedding seems to be more regular in cattle and goats. Ewes shed more quantity in vaginal mucus and in a more prolonged manner than goats. Both, sheep and goats, can shed C. burnetii in subsequent pregnancies (Arricau-Bouvery & Rodolakis, 2005; Berri, Souriau, Crosby, & Rodolakis, 2002; Berri, Rousset, Champion, Russo, & Rodolakis, 2007).