In Australia epidemiologcal studies revealed a widespread incidence of the Rickettsia burneti. The native rodent, the bandicoot, was found to be susceptible, and evidence of latent infection was found in other bush animals, in water rats, other native rats, and also in cows. The Rickettsia burneti was isolated from ticks (haemaphysalis humerosa) collected from the bandicoots, and the faeces of these infected ticks were found to be highly infectious and capable of infecting guinea pigs when applied to the skin. In Derrick's opinion, this tick, the H. humerosa, is the vector among bandicoots. This tick was readily infected with the R. burneti by feeding on infected guinea pigs. The infection was transmitted from larvae to nymph, and from nymph to adult. The R. burneti were found to be confined to the lumen of the gut and faeces were heavily infected. Three other ticks could also be infected— rhipecephalus sanguinius, ixodes holocyclus, and haemaphysalis bispinosa—by feeding on infected guinea pigs, and could transmit infection to their host. Each, therefore, is a potential vector, and Derrick's conclusion is that the haemaphysalis bispinosa is the probable source of the human infection in Queensland and that the mode of infection is by inhalation of infected faecal dust from these ticks.

In Italy the possible route and sources of infection were examined in detail in some of the northern Italian epidemics, and although no vectors, such as ticks or fleas, were incriminated, it was found that the disease often made its appearance in units occupying farm billets and where men were living in close proximity to animals such as cattle, rats, and also pigeons. Various forms of mites were discovered in several of these billets, but it was thought that cases probably occurred by inhalation infection arising from the dust and droppings. The complete absence of any insect bites in any of the cases, and also the uniform picture of pulmonary involvement, suggested that the route of infection was via the upper respiratory tract, such as probably occurred in the laboratory infection with the same agent (Robbins and Rustigan, 1946), and which is also seen in at least laboratory infections with other rickettsial diseases such as epidemic murine and scrub typhus. It was also found that many of the civilian population in the area where these cases occurred showed a high level of antibody to Q fever, suggesting that the infection was endemic in the local population.

In the New Zealand hospital cases most of the patients came from a British infantry training depot where men were living in hutments and where there was a rapid turnover of personnel. The page 587 staff of the hospital escaped lightly. A strict isolation technique was carried out in the wards until the temperature had been normal for a week, or until productive cough had ceased. The regimental aid post orderly, who treated men daily from the infantry training depot, and the hospital librarian who visited the wards, both contracted the disease, but no case occurred among nurses who were nursing the cases.