Q fever is a zoonotic disease caused by Coxiella burnetii, a pathogen in a wide range of animals and humans. The main reservoir for the pathogen is domestic animals such as cattle, sheep and goats. 

Causative agent

Q fever is caused by an obligate intracellular polymorphic bacillus, Coxiella burnetii, which has a cell membrane similar to Gram negative bacteria.


Q fever is a worldwide zoonosis, which may occur in sporadic as well as epidemic forms. However, it may be an emerging disease, probably related to climate change.


This disease causes significant reproductive losses in both cattle and small ruminants, due to losses from abortion in small ruminants and infertility in cattle.


The main route of transmission of the disease is inhalation of the bacteria from the infected environment and ingestion of contaminated food or water with discharge of infected animals. Ticks act both as vectors and as reservoirs of the causative agent of Q fever, but this is not the most important route of infection for livestock. Infected animals usually shed the agent intermittently in milk, feces and urine with no outward signs of disease and should be regarded as possible sources of human infection.

Clinical signs

In cows, ewes and goats, Q fever has been associated with late abortion and reproductive disorders such as premature birth and weak offspring and with infertility and mastitis in cattle. Although mortality is a rare outcome of the acute form of the disease, the major clinical manifestation of chronic form of Q fever is endocarditis with case fatality in untreated cases exceeding 10%.


The aim of vaccination against C. burnetii is to reduce shedding and the risk of abortion.

C. burnetii has two antigenic forms: the pathogenic phase I, isolated from infected animals or humans, and the attenuated phase II, obtained by repeated in-ovo passages. An LPS (lipopolysaccharide) change occurs during serial passages: phase I cells, with full-length LPS chains, change to intermediate phases with decreasing LPS chain lengths and then to phase II, with truncated LPS.

To date, only inactivated vaccines are available against C. burnetii. To generate an appropriate immune response while minimizing the safety hazards, efficient vaccine production should be targeted at vaccines containing phase I antigen. It is used as preventive measure (minimize the disease’s clinical impact and reduce or eliminate C. burnetii excretion in vaccinated animals).

For further information, view our Small Ruminant Reproductive Multivalent Vaccine programme.