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PubMed1998

Culture-negative endocarditis caused by Bartonella henselae.

A 4-year-old girl presented with clinical evidence of infective endocarditis involving her aortic valve, but blood cultures were sterile. Serologic studies and analysis of resected valve by immunohistochemistry and polymerase chain reaction established the diagnosis of Bartonella henselae endocarditis. Clinicians should be aware that B. henselae can cause apparent culture-negative endocarditis in children.

Antibodies, Bacterial↗
PubMed2000

Imaging of granulomatous lesions of the neck in children.

Cervical lymphadenopathy is the most common presentation of granulomatous inflammation of the neck in children and is usually caused by NTM infection. Although certain granulomatous infections have characteristic imaging features, there is considerable overlap in the imaging appearance of the various disorders. The diagnosis is usually based on a combination of clinical features, histopathologic examination, serologic tests, and culture results.

Cat-Scratch Disease↗
PubMed1985

Cellular composition of suppurative granulomas: an immunohistochemical study of suppurative granulomatous lymphadenitis.

The immunohistochemical findings from an investigation of suppurative granulomatous lymphadenitis (SGL) are presented. With a broad panel of monoclonal and polyclonal antibodies directed against B cells, T cells, monocytes/macrophages, HLA-DR antigens, and the transferrin receptor, early, nonsuppurative granulomas were found to consist of OKM1+ OKIa1+ OKT9+ epithelioid histiocytes and multinucleated giant cells, admixed with variable numbers of OKT4+ Leu-3a+ helper/inducer T cells. These nonsuppurative lesions were surrounded by distinctive cuffs of BA1+ B1+ sIgM+ sIgD+ OKIa1+ lymphocytes. In contrast, suppurative granulomas were bordered by palisades of OKM1+ OKIa1+ OKT9+ epithelioid histiocytes, admixed with some OKT8+ suppressor/cytotoxic T cells. These suppurative lesions lacked distinctive cuffs of B lymphocytes, but half of the lesions were surrounded by numerous plasma cells that expressed cytoplasmic IgA and IgG. Based on these immunohistochemical findings, it is concluded that a shift in the nature of the predominant intragranulomatous T-cell subset occurs during the successive phases of the immune response in SGL. The cause of the central necrosis and suppuration may be related to the excessive numbers of intragranulomatous OKT8+ T cells or to the formation of immune complexes by the surrounding plasma cells.

Antibodies↗
PubMedDate not supplied

The right answer.

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Bartonella↗
PubMed1998

[Down the claws!].

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Bartonella henselae↗
PubMed2001

Autoimmune haemolytic anaemia triggered by Bartonella henselae infection: a case report.

Bartonella henselae is a hitherto unidentified cause of autoimmune haemolytic anaemia. Here we report a case of Coombs-negative autoimmune haemolytic anaemia. The episode was preceded by exposure to a cat and a non-specific infectious syndrome. Concomitant serum titres of B. henselae antibodies were indicative of a recent infection. The case report suggests that B. henselae infection can trigger secondary autoimmune haemolytic anaemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1999

Characterization of Bartonella henselae-specific immunity in BALB/c mice.

BALB/c mice were inoculated with Bartonella henselae by both systemic and mucosal routes. Culture analysis of tissues from mice infected intraperitoneally with a high dose of B. henselae yielded positive results 24 hr after infection. However, culture analysis of blood taken between 6 hr and 7 days after infection from groups receiving live B. henselae were negative. Following intraperitoneal infection, B. henselae was detected by polymerase chain reaction in liver and mesenteric lymph nodes by 6 hr and up to 7 days after infection in liver, kidney and spleen tissue. Enzyme-linked immunosorbent assay (ELISA) of serum samples collected as early as 13 days after infection indicated humoral immune responses to B. henselae. Specific humoral responses remained through week 6. Analysis of faecal samples revealed induction of B. henselae-specific immunoglobulin A by day 28 after infection. In addition, B. henselae-specific cellular responses were indicated by a positive delayed-type hypersensitivity and a T helper 1 (Th1) (CD4+ T cell)-type cytokine response following in vitro stimulation of splenocytes. The significance and implications of these data in relation to B. henselae infections are discussed.

Animals↗