From cat scratch disease to endocarditis, the possible natural history of Bartonella henselaeinfection

In May 2005, a 43-year-old man was admitted to the hospital with mitral regurgitation. In 1981, he had been in a car crash and developed a destructive nosocomial Staphylococcus aureus endocarditis of the mitral valve. A bioprosthesis was inserted which failed in 1988 and was replaced. In May 2005, regurgitation through the valve was once again detected and the patient was hospitalized for a further valve replacement. The patient was afebrile and had a systolic murmur over the mitral area. He had no leukocytosis (leukocyte count was 3.63 × 10⁹/l with 50.2% neutrophils). The low neutrophil count corrected itself spontaneously. The erythrocyte sedimentation rate (16/43 mm) and C-reactive protein (<5 mg/l) was normal and hepatic enzymes were elevated (ALT: 69 IU/L; normal ≤ 40 IU/L). Three routine blood cultures were negative (Bactec, Becton Dickinson, Sparus, Maryland) and no rheumatoid factor was detected. Transthoracic echocardiography revealed mitral insufficiency but there were no vegetations and IE was not considered as a possible diagnosis. However, no transesophageal echocardiography was performed. Histology of the prosthetic valve removed at surgery using reported methods [17, 18], revealed an IE with a vegetation containing micro-organisms that stained with Warthin-Starry and Giemsa [19] (Figure 1). Standard cultures of cardiac valve tissue remained sterile, but with cell-cultures (human endothelial cell) a strain of B. henselae was isolated in 3 weeks [20]. Also, DNA of B. henselae was demonstrated to be present in the valve by PCR and sequencing with primers for the eubacterial 16S rRNA gene [21] and Bartonella ITS region [3] Genotyping of the B. henselae strain was carried out using the multi-spacer typing (MST) method as previously described [22]. Sequences obtained from the nine studied spacers classified the strain within MST genotype five, previously described to contain cat isolates from various countries including France, Germany and USA [22]. Serum tested retrospectively was found to contain antibodies to B. henselae and B. quintana at an IgG titer of 1:200 [14], which is not suggestive of IE. However, western blotting was positive for antibodies to B. henselae and B. quintana and showed a reactivity pattern typical for endocarditis [13] (Figure 2). Immunoblotting with a serum sample adsorbed with B. henselae confirmed the diagnosis of B. henselae IE.

The diagnosis of IE was made retrospectively based on the combination of histology of the cardiac valve lesions, culture of Bartonella from the valve, presence of a predisposing heart condition, and serological evidence of Bartonella infection. Without the histology of the valve the patient would not have had a positive score using the Duke criteria; he would only have had 2 minor criteria. After surgery, the patient recovered rapidly with routine post-surgical amoxicillin administration for 4 days, followed by gentamycin for 15 days and doxycycline for 1 month [23].

Retrospectively, it was found that six months before the patient had had suspected lymphoma of an inguinal lymph node. Histology of the node, however, showed a necrotizing lymphadenitis suggested of CSD. Numerous microabscesses containing fragmented neutrophils were observed in homogenous necrotic areas. These necrotic regions were surrounded by a ring of macrophages and epithelioid histiocytes to form stellate inflammatory granulomas (Figure 1). No bacteria were detected by immunohistochemical examination or Warthin-Starry staining. Unfortunately, the lymph node sample was not available for PCR analysis to confirm the diagnosis of CSD.

The patient did not own a cat but reported a single contact with a stray cat that scratched him one month before the enlargement of the inguinal lymph node. We report the development of IE after a likely episode of CSD in a patient with a mechanical mitral cardiac valve. In previous studies [16], B. henselae was described in patients who have regular contact with cats and with pre-existing valvulopathies [24, 25], but to the best of our knowledge the progression of CSD to IE has not previously been reported.