Coxiella burnetii, agent de la fièvre Q

Abstract

Résumé : La fièvre Q est une zoonose de répartition mondiale excepté la Nouvelle-Zélande. Elle est due à une bactérie intracellulaire : Coxiella burnetii. Cette infection passe souvent inaperçue car la manifestation principale de la forme aiguë de la maladie est un syndrome pseudogrippal spontanément résolutif. C'est l'épidémie qui a eu lieu aux Pays-Bas qui a attiré l'attention sur cette maladie qui était moins étudiée auparavant. Cette synthèse résume la description de la bactérie (taxonomie, cycle intracellulaire et génomique) mais également la maladie (description, diagnostic, pathogénie et épidémiologie). Enfin, la vaccination de l'humain et des animaux est également analysée. Mots-clés : Coxiella burnetii, fièvre Q, épidémiologie, description, génomique.Abstract: Q fever is a zoonosis of worldwide distribution with the exception of New Zealand. It is caused by an intracellular bacterium, Coxiella burnetii. The disease often goes underdiagnosed because the main manifestation of its acute form is a general self-limiting flu-like syndrome. The Dutch epidemics renewed attention to this disease, which was less considered before. This review summarizes the description of C. burnetii (taxonomy, intracellular cycle, and genome) and Q fever disease (description, diagnosis, epidemiology, and pathogenesis). Finally, vaccination in humans and animals is also considered.

Seroprevalence and risk factors for <i>Coxiella burnetii</i>, the causative agent of Q fever in the dromedary camel (<i>Camelus dromedarius</i>) population in Algeria

“…Unfortunately, the ELISA cannot distinguish between active and old infections in animals. Although active infections can be confirmed by detecting C. burnetii DNA by using a conventional PCR assay (Boarbi, Fretin & Mori 2016 ; Muskens et al 2011 ), that technology was not available to us during this study.…”

Farming, Q fever and public health: agricultural practices and beyond

“…C. burnetii has a broad host range (with a role in dissemination or maintenance of the disease) and is found in unicellular organisms, invertebrates, birds and mammals [ 8 ]. Domestic ruminants are the primary reservoir for human infection, and the majority of human epidemics are related to exposure to small ruminant (sheep and goats) infected products (placenta membranes, birth fluids, animal excretions or contaminated dust) [ 9 , 10 ]. Transmission of infection from animals to humans is facilitated by the inhalation of contaminated aerosols.…”

“…The occurrence of human Q fever is mainly sporadic, most often limited to at risk individuals (abattoir workers, farmers, veterinarians), and rarely epidemic [ 9 , 10 ]. Modifications in farming practices, which also imply expansion of trading, have been related to Q fever epidemics in humans, particularly when the activity was implemented in an area in close proximity to the human population.…”

“…C. burnetii displays a wide range of cell type tropism including but not limited to monocyte and macrophages, trophoblasts, adipocytes and epithelial cells [ 10 , 49 , 50 ]. The bacterium internalizes by binding to the αvβ3 integrin of the targeted cell, and in monocyte/macrophages stimulates their activation through binding to Toll-like receptors (TLR) [ 51 ].…”

Molecular characterization of Coxiella burnetii in the slaughtered animals of Southern Iran

“…The reports have implied that farm animals including cattle, sheep, and goats, play a major role as reservoir of the infection, with high risk to the vulnerable populations including ranchers, veterinarian, butchers and personnel of slaughterhouses [5][6][7]. Transmission routes of the infection to human are including infected ticks, aerosols, direct contact with the infected animal fluids such as milk, urine, seminal fluid, contaminated tissues such as kidneys, mammary glands and lymph nodes [2,[8][9][10][11][12].…”