Editorial

Q fever in Thailand suggests additional vectors responsible for spread

An abstract, titled “Epidemiology of Q fever in Thailand,” was presented at the American Society of Tropical Medicine and Hygiene meeting in November by Padungtod and colleagues from the National Health Authorities in Bangkok and the CDC in the United States.

The researchers said Coxiella burnetii has been identified as a cause of Q fever endocarditis in Thailand, which prompted their study. They evaluated the prevalence of C. burnetii by phase 2 immunoglobulin G antibody determinations. The secondary goal was to identify animal reservoirs for C. burnetii in Thailand. They sampled different groups for C. burnetii for previous Q fever exposure by phase 2 elevated IgG titers. First, they studied Q fever seroprevalence in hospitalized patients with fever of unknown origin (FUO) in an academic hospital. Among these patients, 18% were seropositive, indicating past C. burnetii exposure. The researchers also obtained samples from dairy cattle, goats and dairy farm owners in farming communities in three provinces. Seroprevalence was low in cattle (4%) and goats (6%), but was higher in livestock farmers: 48% had elevated C. burnetii IgG antibodies. In contrast, wild deer/ruminants in zoos were screened, as well as zoo caretakers. None of the zoo animals were positive, but 12% of the caretakers were positive. This study raises more questions than it answers.

Burke A. Cunha

The investigators have done the initial work in trying to determine Q fever seroprevalence in select human groups and some animal reservoirs in Thailand. Since Q fever endocarditis has been described in Thailand, the investigators correctly reasoned that there must also be many asymptomatic C. burnetii cases, as well as some cases of acute Q fever community-acquired pneumonia (CAP). Since seroprevalence gives an indication of Q fever prevalence, determining the incidence of Q fever CAP would be helpful because chronic Q fever may follow acute Q fever CAP. Determination of the prevalence of the Q fever CAP would be predictive of the extent of chronic Q fever in Thailand.

Cause of atypical CAP

Q fever is a worldwide zoonosis whose transmission involves ticks and animals. In humans, airborne infections occur most frequently. As with most infectious diseases, exposure to Q fever results in seroconversion without clinically apparent disease. Alternately, acute Q fever usually presents as a zoonotic atypical CAP. Patients with acute Q fever and valvular heart disease are at high risk of later developing chronic Q fever endocarditis. Although Q fever, particularly chronic Q fever, is a well-known cause of FUO, the presence of antibodies in the hospitalized FUO population does not imply a causal relationship. Rather, seropositivity in a hospitalized FUO population is probably reflective of seropositivity in the hospitalized FUO age group.

Most domestic animals are hosts of C. burnetii, as are game birds (pigeons and sparrows), wild rodents and humans. Ticks are the natural reservoir of Q fever and are infected for life. Many different species are implicated. Tick feces may contain C. burnetii, which are able to survive in tick excreta for months in the environment. Tick excreta are probably responsible for Q fever transmission to domestic animals. The domestic animals primarily involved are cattle, goats, sheep, dogs and cats. Animal placenta/amniotic fluid contain large numbers of C. burnetii, which may contaminate soil and dairy products. Unpasteurized milk or cheese can support growth of C. burnetii for 1 to 2 months. Airborne spread of C. burnetii via infected dust from placenta is often responsible for the airborne transmission of Q fever, particularly from infected parturient cats. Q fever may also be acquired from contact with infected animals/products or consumption of contaminated milk/dairy products.

Seroprevalence studies needed

For these reasons, the study showed seropositivity rate in livestock farmers was much higher (48%) than in cattle (4%) or goats (6%), suggesting that other potential vectors are responsible for the farmer’s high seropositivity. Future seroprevalence studies are needed to determine the seroprevalence of the C. burnetii in sheep, dogs and cats in Thailand. Tick surveys should be done because one study showed seroprevalence of 50% in dog ticks. For completeness, wild rodents and birds should also be sampled. Future seroprevalence studies should also take into account geographical (rural vs. urban) and seasonal differences — Q fever has a seasonal distribution, with peak incidence after the rainy seasons by 3 months.

References:

Harris P. Epidemiol Infect. 2013;141:1034-1038.
Knobel DL. Am J Trop Med Hyg. 2013;88:513-518.
Liu L. Am J Trop Med Hyg. 2013;88:770-773.
Million M. Clin Infect Dis. 2013;57:836-844.
Padungtod P. Abstract #718. Presented at: 62nd Annual Meeting of the American Society of Tropical Medicine and Hygiene; Nov. 13-17, 2013; Washington, D.C.
Raoult D. J Infect. 2012;65:102-108.
Thompson M. Zoonoses Public Health. 2012;59:553-560.
Vilibic-Cavlek T. Vector Borne Zoonotic Dis. 2012;12:293-296.

For more information:

Burke A. Cunha, MD, MACP, is Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, N.Y., and Professor of Medicine, SUNY School of Medicine, Stony Brook, N.Y. Cunha is also a member of the Infectious Disease News Editorial Board.

Disclosure: Cunha reports no relevant financial disclosures.

An abstract, titled “Epidemiology of Q fever in Thailand,” was presented at the American Society of Tropical Medicine and Hygiene meeting in November by Padungtod and colleagues from the National Health Authorities in Bangkok and the CDC in the United States.

The researchers said Coxiella burnetii has been identified as a cause of Q fever endocarditis in Thailand, which prompted their study. They evaluated the prevalence of C. burnetii by phase 2 immunoglobulin G antibody determinations. The secondary goal was to identify animal reservoirs for C. burnetii in Thailand. They sampled different groups for C. burnetii for previous Q fever exposure by phase 2 elevated IgG titers. First, they studied Q fever seroprevalence in hospitalized patients with fever of unknown origin (FUO) in an academic hospital. Among these patients, 18% were seropositive, indicating past C. burnetii exposure. The researchers also obtained samples from dairy cattle, goats and dairy farm owners in farming communities in three provinces. Seroprevalence was low in cattle (4%) and goats (6%), but was higher in livestock farmers: 48% had elevated C. burnetii IgG antibodies. In contrast, wild deer/ruminants in zoos were screened, as well as zoo caretakers. None of the zoo animals were positive, but 12% of the caretakers were positive. This study raises more questions than it answers.

Burke A. Cunha

The investigators have done the initial work in trying to determine Q fever seroprevalence in select human groups and some animal reservoirs in Thailand. Since Q fever endocarditis has been described in Thailand, the investigators correctly reasoned that there must also be many asymptomatic C. burnetii cases, as well as some cases of acute Q fever community-acquired pneumonia (CAP). Since seroprevalence gives an indication of Q fever prevalence, determining the incidence of Q fever CAP would be helpful because chronic Q fever may follow acute Q fever CAP. Determination of the prevalence of the Q fever CAP would be predictive of the extent of chronic Q fever in Thailand.

Cause of atypical CAP

Q fever is a worldwide zoonosis whose transmission involves ticks and animals. In humans, airborne infections occur most frequently. As with most infectious diseases, exposure to Q fever results in seroconversion without clinically apparent disease. Alternately, acute Q fever usually presents as a zoonotic atypical CAP. Patients with acute Q fever and valvular heart disease are at high risk of later developing chronic Q fever endocarditis. Although Q fever, particularly chronic Q fever, is a well-known cause of FUO, the presence of antibodies in the hospitalized FUO population does not imply a causal relationship. Rather, seropositivity in a hospitalized FUO population is probably reflective of seropositivity in the hospitalized FUO age group.

Most domestic animals are hosts of C. burnetii, as are game birds (pigeons and sparrows), wild rodents and humans. Ticks are the natural reservoir of Q fever and are infected for life. Many different species are implicated. Tick feces may contain C. burnetii, which are able to survive in tick excreta for months in the environment. Tick excreta are probably responsible for Q fever transmission to domestic animals. The domestic animals primarily involved are cattle, goats, sheep, dogs and cats. Animal placenta/amniotic fluid contain large numbers of C. burnetii, which may contaminate soil and dairy products. Unpasteurized milk or cheese can support growth of C. burnetii for 1 to 2 months. Airborne spread of C. burnetii via infected dust from placenta is often responsible for the airborne transmission of Q fever, particularly from infected parturient cats. Q fever may also be acquired from contact with infected animals/products or consumption of contaminated milk/dairy products.

Seroprevalence studies needed

For these reasons, the study showed seropositivity rate in livestock farmers was much higher (48%) than in cattle (4%) or goats (6%), suggesting that other potential vectors are responsible for the farmer’s high seropositivity. Future seroprevalence studies are needed to determine the seroprevalence of the C. burnetii in sheep, dogs and cats in Thailand. Tick surveys should be done because one study showed seroprevalence of 50% in dog ticks. For completeness, wild rodents and birds should also be sampled. Future seroprevalence studies should also take into account geographical (rural vs. urban) and seasonal differences — Q fever has a seasonal distribution, with peak incidence after the rainy seasons by 3 months.

References:

Harris P. Epidemiol Infect. 2013;141:1034-1038.
Knobel DL. Am J Trop Med Hyg. 2013;88:513-518.
Liu L. Am J Trop Med Hyg. 2013;88:770-773.
Million M. Clin Infect Dis. 2013;57:836-844.
Padungtod P. Abstract #718. Presented at: 62nd Annual Meeting of the American Society of Tropical Medicine and Hygiene; Nov. 13-17, 2013; Washington, D.C.
Raoult D. J Infect. 2012;65:102-108.
Thompson M. Zoonoses Public Health. 2012;59:553-560.
Vilibic-Cavlek T. Vector Borne Zoonotic Dis. 2012;12:293-296.

For more information:

Burke A. Cunha, MD, MACP, is Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, N.Y., and Professor of Medicine, SUNY School of Medicine, Stony Brook, N.Y. Cunha is also a member of the Infectious Disease News Editorial Board.

Disclosure: Cunha reports no relevant financial disclosures.