Q Fever Endocarditis in the United States

Gami, Apoor S.; Antonios, Vera S.; Thompson, Rodney L.; Chaliki, Hari P.; Ammash, Naser M.

doi:10.4065/79.2.253

Cited by 31 publications

(29 citation statements)

References 35 publications

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“…In the USA, C. burnetii is enzootic in ruminants and wild animals as in other parts of the world [105], but human infections due to C. burnetii are rare [48,105]. The most recent cases of Q fever have been described in Australia [50,148,186], Canada [87,94], France [125,165], Germany [58], Japan [160], Spain [34,135], Switzerland and the United Kingdom [117].…”

Section: Zoonotic Aspectmentioning

confidence: 99%

Is Q Fever an emerging or re-emerging zoonosis?

2005

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-Q fever is a zoonotic disease considered as emerging or re-emerging in many countries. It is caused by Coxiella burnetii, a bacterium developing spore-like forms that are highly resistant to the environment. The most common animal reservoirs are livestock and the main source of infection is by inhalation of contaminated aerosols. Although the culture process for Coxiella is laborious, advances on the knowledge of the life cycle of the bacterium have been made. New tools have been developed to (i) improve the diagnosis of Q fever in humans and animals, and especially animal shedders, (ii) perform epidemiological studies, and (iii) prevent the disease through the use of vaccines. This review summarizes the state of the knowledge on the bacteriology and clinical manifestations of Q fever as well as its diagnosis, epidemiology, treatment and prevention in order to understand what factors are responsible for its emergence or re-emergence. Coxiella burnetii / epidemiology / bacteriology / diagnostic / control

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Section: Zoonotic Aspectmentioning

confidence: 99%

Is Q Fever an emerging or re-emerging zoonosis?

2005

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“…Over 90% of Q fever endocarditis cases occur in persons with underlying heart disease, which may be congenital, rheumatic, degenerative, or syphilitic or may involve prosthetic valves (23). Whereas C. burnetii accounts for 3% of all endocarditis cases diagnosed in England and Wales (26) and at least 5% of cases in France (29), there have been only seven reported cases of Q fever endocarditis in the United States, including the patient presented here (1,4,10,13,27). However, the true number of chronic Q fever cases in the United States is unknown and is likely underrepresented in the literature, since many cases may have occurred prior to the advent of national reporting in 1999.…”

mentioning

confidence: 99%

“…Peripheral manifestations of endocarditis including digital clubbing, purpuric rash, hepatomegaly, splenomegaly, immune complex glomerulonephritis, and embolic phenomena are common (21). Cardiac vegetations are visible by echocardiography in as few as 12% of patients (23), as these vegetations tend to be smaller and located beneath endothelial surfaces (10). The organism may be cultured under special conditions, but isolation of C. burnetii by culture is generally not performed because of the high risk of infectivity to laboratory workers and the lack of sensitivity of the technique (25).…”

mentioning

confidence: 99%

“…As witnessed in these seven cases, the diagnosis of chronic Q fever may be delayed by many months because of the lack of specific signs and symptoms. Fever may be absent in more than 18% of cases, and vague constitutional symptoms, congestive heart failure, or valvular dysfunction may predominate (10). Peripheral manifestations of endocarditis including digital clubbing, purpuric rash, hepatomegaly, splenomegaly, immune complex glomerulonephritis, and embolic phenomena are common (21).…”

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confidence: 99%

“…Other less common clinical manifestations of acute Q fever include myocarditis, pericarditis, skin rash, and meningoencephalitis (23). Chronic Q fever may develop many months to years after initial infection, manifesting as bacterial culture-negative endocarditis in up to 75% of cases (10). Chronic Q fever occurs almost exclusively in patients with predisposing conditions, including those with heart valve lesions, vascular abnormalities, and immunosuppression (7).…”

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confidence: 99%

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Chronic Q Fever in the United States

Karakousis¹,

Trucksis

Dumler

2006

J Clin Microbiol

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Infections due to Coxiella burnetii, the causative agent of Q fever, are uncommon in the United States. Cases of chronic Q fever are extremely rare and most often manifest as culture-negative endocarditis in patients with underlying valvular heart disease. We describe a 31-year-old farmer from West Virginia with a history of congenital heart disease and recurrent fevers for 14 months who was diagnosed with Q fever endocarditis based on an extremely high antibody titer against Coxiella burnetii phase I antigen. Despite treatment with doxycycline, he continued to have markedly elevated Coxiella burnetii phase I antibody titers for 10 years after the initial diagnosis. To our knowledge, this case represents the longest follow-up period for a patient with chronic Q fever in the United States. We review all cases of chronic Q fever reported in the United States and discuss important issues pertaining to epidemiology, diagnosis, and management of this disease. CASE REPORTA 31-year-old farmer from West Virginia was admitted in June 1995 because of recurrent episodes of fever as high as 39°C, night sweats, paroxysmal coughing, chest pressure, decreased appetite, fatigue, and an 11-kg involuntary weight loss over the preceding 14 months. He had been treated several times for presumed bronchitis with various antibiotics, but his complaints had worsened since December 1994. His past medical history was significant for congenital heart disease, including dextrocardia, a double-outlet right ventricle, a ventricular septal defect, and severe pulmonary stenosis. As an infant, he had undergone operative placement of a right Blalock-Taussig shunt, and at age 12, he underwent surgery for closure of a ventricular septal defect and placement of a conduit between the right ventricle and pulmonary artery. At age 26, he underwent surgery for replacement with a 22-mm Hancock conduit. He participated in birthing his calves, one of which was stillborn around the time of the onset of his illness. He was treated empirically with penicillin, gentamicin, and vancomycin, and his fevers resolved.On physical examination, he was a thin, chronically ill-appearing white male. His vital signs were within normal limits, and he was afebrile. Cardiac examination revealed a grade 3/6 harsh systolic ejection murmur heard maximally at the right upper sternal border without radiation. The chest examination was normal. There was no hepatosplenomegaly, enlarged lymph nodes, or peripheral stigmata of endocarditis. Laboratory studies revealed the following results: hematocrit level was 41%; white blood cell count was 7.3 ϫ 10 9 white blood cells/ liter, with a differential cell count of 35% segmented neutrophils, 5% bands, and 54% lymphocytes; platelets were aggregated and uncountable; electrolyte panel and urinalysis were normal; erythrocyte sedimentation rate was 34 mm/h; and alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase levels were elevated at 198 U/liter, 244 U/ liter, and 196 U/liter, respectively. Serologies for hepatiti...

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Bacterial Diseases

Weese

BSc

2010

Companion Animal Zoonoses

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Q Fever Endocarditis in the United States

Cited by 31 publications

References 35 publications

Is Q Fever an emerging or re-emerging zoonosis?

Is Q Fever an emerging or re-emerging zoonosis?

Chronic Q Fever in the United States

Bacterial Diseases

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