Q Fever Endocarditis in the United States

Kimbrough, Robert C.

doi:10.7326/0003-4819-91-3-400

Cited by 98 publications

(41 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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: 98%

Chronic Q Fever in the United States

Karakousis¹,

Trucksis

Dumler

2006

J Clin Microbiol

View full text Add to dashboard Cite

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...

show abstract

mentioning

confidence: 98%

Chronic Q Fever in the United States

Karakousis¹,

Trucksis

Dumler

2006

J Clin Microbiol

View full text Add to dashboard Cite

show abstract

“…Acute Q fever is an influenza-like illness that usually is self-limiting and effectively treated by antibiotics (11). In contrast, chronic Q fever is a severe, sometimes fatal disease, and patients have responded poorly to various antibiotics (8,20). Endocarditis is the most common chronic manifestation, while vascular infection, bone infection, and chronic hepatitis are also reported (21).…”

mentioning

confidence: 99%

Identification and Characterization of an Immunodominant 28-Kilodalton Coxiella burnetii Outer Membrane Protein Specific to Isolates Associated with Acute Disease

Zhang

Russell

et al. 2005

Infect Immun

View full text Add to dashboard Cite

Coxiella burnetii causes acute Q fever in humans and occasional chronic infections that typically manifest as endocarditis or hepatitis. Isolates associated with acute disease were found to be distinct from a group of chronic disease isolates by a variety of biochemical parameters and in a guinea pig fever model of acute disease, suggesting a difference in virulence potential. We compared antigenic polypeptides among C. burnetii isolates and found an immunodominant 28-kDa protein in acute group isolates but not in chronic group isolates (T. Ho, A. Hotta, G. Q. Zhang, S. V. Nguyen, M. Ogawa, T. Yamaguchi, H. Fukushi, and K. Hirai, Microbiol. Immunol. 42:81-85, 1998). In order to clone the adaA gene, the N-terminal amino acid sequence of adaA was determined and a 59-bp fragment was amplified from Nine Mile phase I DNA by PCR. The putative gene fragment was used to screen a lambda ZAP II genomic DNA library, and an open reading frame expressing a 28-kDa immunoreactive protein was identified. Sequence analysis predicted a gene encoding an ϳ28-kDa mature protein with a typical signal sequence. The adaA (acute disease antigen A) gene was detected in acute group C. burnetii isolates but not identified in chronic group isolates by PCR and Southern blotting. A typical signal peptide was predicted in adaA, and specific antibody to adaA reacted with the purified membrane fraction of acute group isolates by Western blotting, suggesting that adaA is exposed on the outer surface of C. burnetii. adaA was overexpressed in pET23a as a fusion protein in Escherichia coli to develop anti-recombinant adaA (anti-radaA) specific antibody, which recognized a ϳ28-kDa band in acute group isolates but not in chronic group isolates. In addition, immunoblotting indicates that radaA reacted with sera derived from animals infected with acute group isolates but did not react with sera from animals infected with chronic group isolates. These results support the idea that an adaA gene-targeted PCR assay and an radaA antigen-based serodiagnostic test may be useful for differential diagnosis of acute and chronic Q fever.

show abstract

“…burnetii has been isolated from an extremely wide range of animals and arthropods in many countries (1,10,23). The differentiation of C. burnetii isolates is very important for the diagnosis and treatment of the various manifestations of Q fever and for epidemiological investigations.…”

mentioning

confidence: 99%

“…Acute Q fever is a flu-like illness which is self-limiting and easily treated with antibiotics when an appropriate diagnosis is made. Chronic Q fever is a severe disease that requires prolonged antibiotic therapy because the infection can result in endocarditis (10) or granulomatous hepatitis (23). C. burnetii is also a zoonotic pathogen that causes abortions in several domestic animals including goat, sheep and cattle (1).…”

mentioning

confidence: 99%

Differentiation of Coxiella burnetii by Sequence Analysis of the Gene (com1) Encoding a 27‐kDa Outer Membrane Protein

Zhang

Yamaguchi

et al. 1997

Microbiology and Immunology

View full text Add to dashboard Cite

The gene (coml) encoding a 27-kDa outer membrane protein in 21 strains of Coxiella burnetii from a variety of clinical and geographical sources was sequenced for strain differentiation. The coml gene was highly conserved among all the strains tested but there were several differences in nucleotide and deduced amino acid sequences. Based on the coml gene-specific nucleotides and deduced amino acids, the 21 strains were divided into four groups. Group 1 contained 14 strains originating from ticks, cattle and human cases of acute Q fever. Groups 2 and 3 included 2 and 3 strains, respectively, originating from human cases of chronic Q fever. Group 4 contained 2 strains originating from a human case of acute Q fever and a goat with abortion. The results indicated that the strains originating from ticks, cattle and human cases of acute Q fever differed at the molecular level from those of human chronic Q fever. This study suggests that a sequence analysis of the coml gene can be used for strain differentiation of C. burnetii.

show abstract

Q Fever Endocarditis in the United States

Cited by 98 publications

References 13 publications

Chronic Q Fever in the United States

Chronic Q Fever in the United States

Identification and Characterization of an Immunodominant 28-Kilodalton Coxiella burnetii Outer Membrane Protein Specific to Isolates Associated with Acute Disease

Differentiation of Coxiella burnetii by Sequence Analysis of the Gene (com1) Encoding a 27‐kDa Outer Membrane Protein

Contact Info

Product

Resources

About