China
Africa
Explore chapters and articles related to this topic
Answers
Published in Samar Razaq, Difficult Cases in Primary Care, 2021
Lyme disease is caused by the spirochete bacterium Borrelia burgdorferi. B. burgdorferi is transferred to humans via the hard tick Ixodes dammini, which feeds on animals infected with the bacterium. Introduction of the bacterium into the human bloodstream via tick saliva occurs during a tick bite. Patients may recall this tick bite and the resultant macular lesion that appears at the site of the bite. This lesion then expands over the course of a week and develops into the characteristic rash of Lyme disease: erythema chronicum migrans. While this is occurring the patient may suffer from a prodromal phase in which there is fever and general malaise. The appearance of the typical rash should raise suspicions and trigger appropriate investigations that may include serology (to look for antibodies against the bacterium) and culture from appropriate fluid or tissue. Untreated, there is a significant risk of developing the late manifestations of Lyme disease, which include neurological abnormalities (e.g. meningitis, cranial neuropathy, peripheral neuropathy), heart disease (e.g. myocarditis, pericarditis, atrioventricular block) and rheumatological disease such as arthritis and fatigue. Rarely, the eyes, liver, spleen and testicles may also be involved. Doxycycline is the first-choice antibiotic. Summer forest walkers should be advised to cover up well and remove attached ticks promptly. Q fever is another bacterial zoonosis caused by the bacterium Coxiella burnetii.
Pneumonitis In Rickettsial Infections
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Treatment for Q fever is available in the form of chloramphenicol and tetracycline (this drug should not be given to patients less than 9 years old because of its tooth-staining properties). Although it is unclear whether antimicrobials alter the course of Q fever, therapy is warranted for ill patients. Drug should be continued for several days after the patient becomes afebrile.
Coxiella
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Immunological tests (e.g., indirect immunofluorescence [IFA], enzyme-linked immunosorbent assay [ELISA]0, complement fixation test [CFT], and immunohistochemistry [IHC]) detect antibodies to phase antigens and represent a valuable approach for Q fever diagnosis and monitoring. An IFA titer of antiphase II IgG ≥200 and IgM ≥50, a fourfold increase in IgG between two samples with 2–4 weeks interval and seroconversion (rise in IgG and IgM against phase II antigen) are diagnostic features of acute Q fever. A rise in IgG and IgA against phase I antigen and phase I IgG ≥800 (if >1,600, 100% predictive of chronic infection) suggest chronic Q fever. A phase I IgG of 1:800 is one of the major modified Duke criteria for endocarditis. IHC may be used for confirmation of Q fever endocarditis from biopsy of cardiac valves, aortic grafts, and liver and is informative when blood cultures are negative [38,39].
New insights in Coxiella burnetii infection: diagnosis and therapeutic update
Published in Expert Review of Anti-infective Therapy, 2020
Cléa Melenotte, Matthieu Million, Didier Raoult
Q fever is a severe worldwide disease caused by Coxiella burnetii that can lead to major epidemic outbreaks, as reported in the Netherlands with more than 4000 cases in 4 years and nearly 118 deaths, among which 86 were Q fever-related [1,2]. C. burnetii-persistent focalized infection is still challenging physicians, first, because diagnosis of persistent infection can be difficult without symptoms, but mainly because no recent international recommendations have been stated to standardize the therapeutic strategy and improve clinical outcomes. The last two decades have seen new diagnostic tools that have revolutionized clinical practice, polymerase chain reaction, and the 18F-FDG-PET/CT-scan imaging [3–7]. This has allowed us to identify new C. burnetii-infectious foci and not to miss persistent infections, even if serological levels are low (15).
A contemporary 16-year review of Coxiella burnetii infective endocarditis in a tertiary cardiac center in Queensland, Australia
Published in Infectious Diseases, 2018
Mark R. Armstrong, Kate L. McCarthy, Robert L. Horvath
Q fever is a worldwide zoonotic disease caused by the obligate intracellular bacterium Coxiella burnetii. Q fever was first described in Brisbane, Australia, in 1935 by Derrick with the identification of the pathogen in tissue from infected abattoir workers [1] and its later isolation in 1937 by Burnet [2]. Coxiella burnetii is able to persist in the environment and resides in a wide variety of animal hosts. In Australia C. burnetii is known to be endemic in livestock in Queensland and New South Wales. One study showed that 16.8% of beef cattle in Queensland were sero-positive for Q fever [3]. Queensland has the highest human Q fever notification rate in Australia, followed by New South Wales [4]. From 2003 to 2005, notifications in Queensland and New South Wales for Q fever comprised 86% of all cases in Australia, and accounted for 83% of hospitalizations due to Q fever [5]. In 2015 notification rates in Queensland were 5.3/100,000 and in New South Wales 3.4/100,000, both higher than the national notification rate of 2.5/100,000 [6].
Chronic Q fever vertebral osteomyelitis, an underrecognized clinical entity
Published in Infectious Diseases, 2021
S. B. Buijs, J. M. Weehuizen, J. J. Oosterheert, S. E. van Roeden
No studies have been published on optimal treatment of chronic Q fever vertebral osteomyelitis. In fact, no randomized trials are available on optimum treatment strategies in chronic Q fever in general [9,10]. Since chronic Q fever is a rare entity, data are scarce and treatment advice is based on observational studies. The current advice is to treat chronic Q fever for 18 months at least (independent of focus of infection), and 24 months in case of infected prosthetic material [9,10].