Microbiology and Epidemiology of Q fever
This section authored by Stephen Graves.
Q Fever is an infectious disease caused by the bacterium, Coxiella burnetii. It was named after Cox, an American microbiologist who first detected the microbe in a tick and Burnet, an Australian immunologist, who, in association with Derrick, first isolated the microbe from patients. Derrick, working in Brisbane, recognized Q Fever as new infectious disease, occurring amongst abattoir workers. He transmitted the infectious agent to guinea pigs, from whose tissues Burnet isolated the new microbe. Derrick called the illness "Q Fever" for "query" fever as it wasn't clear at that time (1935) what was causing the fever. The name stuck!
The microbe was originally classified as a "rickettsia" as it was a very small, Gram-negative bacterium, transmitted by an arthropod vector ( ie a tick ) and it was only able to grow inside animal cells both in vivo and in vitro. It was an obligate intracellular bacterium. It would not grow on agar. These were all features of the Rickettsiae group of bacteria.
However, many decades later, molecular examination of its genome showed that C.burnetii did not belong to the Rickettsiae group but was a member of the gamma subgroup of the Proteobacteriacea phylum. Its closest bacterial "relative" is Legionella spp. Q Fever and Legionnaire's Disease are caused by very similar bacteria. In fact Q Fever is more common in Australia than Legionnaire's Disease!
The infection is a zoonosis, meaning that patients become infected by exposure to animals carrying the bacterium. Infected animals may be mildly symptomatic ( eg goats may abort ) but mostly they are asymptomatic. The farmer may not realize that his herd is infected until he or one of his family or staff develop Q Fever. Patient to patient spread is very rare and hardly ever occurs. A cluster or outbreak of Q Fever is always related to a common animal source of infection. The animals most commonly involved in Australia are cattle, goats and sheep. However virtually all mammals can be infected and potentially pass it on to humans. Even dogs and cats have been involved in human infections. There is also a natural cycle of infection occurring in the Australian bush, involving several tick species and macropods ( eg kangaroos ), bandicoots, rodents, etc.
When a patient becomes infected from an infected animal it is usually from a parturient female as, during birthing, huge numbers of C.burnetii are excreted from its genital tract into the environment. The bacteria are then inhaled by a person nearby or downwind of the site.
The bacterium can produce a "spore-like" form, which is smaller, metabolically inert but still alive. It can survive for a long period in the environment, especially if the weather is dry and dusty. Wind blows these "spores" around for many kilometers. Thus persons who have no known connection with animals can often be infected with Q Fever. The risk of infection is higher in rural and regional parts of Australia, simply because there are more animals living in the shared environment with susceptible people. The patient inhales the bacterium into their lungs and it starts growing inside their alveolar macrophages and C.burnetii eventually spreads around their body and establishes a systemic infection, sometimes including infectious endocarditis.
Symptomatic Q Fever does not occur soon after exposure to an infected animal. It can take several weeks to months before the patient develops symptoms of infection. Thus it is very difficult to determine for sure the animal source of the infection, especially if the patient has had multiple animal exposures. The most recent exposure may not have been the at-risk exposure. Often the source of the Q Fever infection in a patient is never determined. The number of bacterial cells required to establish an infection in a human is very small. Inhalation of somewhere between 1 and 10 bacterial cells appear to be sufficient for some persons to become infected.
Strangely, some people can be exposed to C.burnetii and not become unwell. It is not clear why this is so but we know that it does occur. A person may have antibodies to C.burnetii in their serum ( ie they are "seropositive" ), indicating a definite exposure to C.burnetii at some time in their past. However, the person may not recall ever having had an illness compatible with Q Fever. In a few cases the antibodies may have been due to vaccination with the Q Fever vaccine, "Q-VAX".
Middle-aged men appear to be at the highest risk of infection. Women are definitely less susceptible to this infection, although if pregnant their risk increases somewhat. C.burnetii has a growth predilection for the trophoblast cells of the placenta.
While Queensland has the highest incidence of Q Fever in Australia, followed by New South Wales, the infection has been detected in all parts of Australia, including Tasmania. The number of notifiable cases is probably an underestimate of the true number of cases because some patients have a mild infection and do not seek medical help and some patients become sick but are not diagnosed as Q Fever by their doctor. Q Fever is very difficult to diagnose on clinical grounds alone. It has no pathognomic signs or symptoms. Laboratory investigations are nearly always required to make the correct diagnosis.
Serological studies of healthy Australian populations ( via blood bank sera ) suggest that about 5% of Australian people have antibodies to C.burnetii, implying that they have been exposure to the bacterium in the past. In many persons antibody levels decrease with time after exposure and after a decade or more antibodies are often no longer detectable in their serum by current laboratory assays. Nevertheless, these persons had been exposed. So the figure of 5% is also a likely underestimate of exposure risk.