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The case of a 14-y-old girl who presented with a mass in her left breast after having contact with a guinea pig is presented. The diagnosis of cat-scratch disease was made by detection of Bartonella henselae DNA by PCR analysis of abscess aspirate.
Restriction endonuclease analysis of the PCR-amplified 16S-23S rRNA gene spacer region was used to investigate the prevalence of Bartonella henselae variants in samples from cat-scratch disease (CSD) patients. Analysis of spacer PCR fragments from 27 Bartonella DNA-positive samples from Dutch patients with CSD with AluI revealed two restriction fragment length polymorphism (RFLP) patterns, patterns A and B. Twenty samples yielded B. henselae pattern A, and 7 samples yielded B. henselae pattern B. Three samples from North American patients with CSD were shown to contain B. henselae with RFLP pattern B. To be able to detect and differentiate Bartonella DNA in clinical material more sensitively and faster, two B. henselae PCRs which amplify part of the 16S rRNA gene and which can discriminate between two B. henselae variants were developed. Thirty-two of 41 Bartonella DNA-positive samples from Dutch patients with CSD contained type I B. henselae, 7 samples contained type II B. henselae, and two samples were negative in both type-specific PCRs. Two samples from North American patients with CSD both contained type II B. henselae. A 100% correlation was found between the AluI spacer RFLP pattern and the 16S rRNA PCR type. We have shown that Dutch patients with CSD contain a limited number of B. henselae variants, suggesting that, in contrast to systemic bartonellosis, CSD in immunocompetent patients is caused by a limited number of B. henselae variants.
We present a patient diagnosed as having tuberculous lymphadenitis after lymph node biopsy and referred for tuberculous therapy. On review, because of recent cat exposure, she was tested for cat scratch disease (CSD), but serological tests for Bartonella henselae were negative. However, the diagnosis of CSD was confirmed, and tuberculosis excluded, by polymerase chain reaction techniques. This case serves as a reminder that CSD may mimic tuberculosis histologically and that sensitive molecular diagnostic tests are available.
A 6-y-old girl developed fever, soft-tissue mass in the right chest wall, osteomyelitis of the 10th rib and hepatic granuloma. Cat scratch disease was diagnosed by histological examination of the mass and serological tests. The patient was treated successfully with antibiotics and recovered completely, as shown by a 10 month follow-up.
A library of Bartonella (Rochalimaea) henselae DNA was constructed in the cloning vector lambda ZAPII and screened for expression of antigenic proteins by using a pool of sera from patients who had been diagnosed with cat scratch disease (CSD) and had antibodies to Bartonella spp., as determined by indirect fluorescent-antibody (IFA) assay. Ten immunoreactive phages were subcloned as recombinant plasmids by in vivo excision. All 10 recombinants expressed a protein of approximately 17 kDa when they were examined by immunoblot with the pool of human sera. Restriction endonuclease digestion of each recombinant plasmid indicated seven profiles, suggesting that cloning bias was not the reason for repeated isolation of clones expressing the 17-kDa antigen. The gene coding for the 17-kDa antigen was sequenced and shown to code for an open reading frame of 148 amino acids with a predicted molecular mass of 16,893 Da. The amino terminus of the deduced amino acid sequence was hydrophobic in nature and similar in size and composition to signal peptides found in gram-negative bacteria. The remainder of the deduced amino acid sequence was more hydrophilic and may represent surface-exposed epitopes. Further subcloning of the 17-kDa antigen as a biotinylated fusion protein in the expression vector PinPoint Xa-2 resulted in a 30-kDa protein that was highly reactive on immunoblots with individual serum samples from patients with CSD. The agreement between reactivity with the 30-kDa fusion protein on immunoblot analysis and the results obtained by IFA assay was 92% for IFA-positive sera and 88% for IFA-negative sera. The recombinant-expressed 17-kDa protein should be of value as an antigen for serologic diagnosis of CSD and Bartonella infections and warrants further study in attempts to develop a subunit vaccine to prevent long-term Bartonella infection in cats and the potential for further spread of these organisms to humans.
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Unilateral conjunctivitis with regional lymphadenitis has been designated Parinaud's oculoglandular syndrome (POGS). The cause has been attributed to various infectious agents, especially leptothrix and the unidentified agent of cat scratch disease (CSD). In 1983-84 the cause of CSD in lymph node and skin was established as small pleomorphic gram-negative bacilli. We now report identical bacteria in the conjunctival lesions of 9 of 24 patients with POGS. This confirms the belief that the CSD bacillus is a major cause of POGS.
A male two year old was admitted to the hospital with a one month history of fever. The physical examination was unrevealing. Abdominal ultrasound revealed multiple, circumscribed regions of low attenuation in the liver and a parapancreatic mass. Laparotomy and biopsy revealed multiple nodules in the liver. The histopathologic findings indicated the child had cat-scratch disease, which resolved with administration of gentamycin sulfate.
A 7-year-old boy was referred to us for evaluation of an enlarging neck mass. The results of his primary care physician's initial clinical examination suggested lymphadenopathy secondary to lymphadenitis, and the patient was treated over a 4-week period with two rounds of antibiotics. However, the mass did not resolve, and it subsequently became fluctuant. The patient was referred to our institution, where we diagnosed cat-scratch disease.
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Catch-scratch disease (CSD) is a self-limiting zoonotic illness. Encephalopathy is the most common neurologic manifestation of CSD. Neuroimaging is usually normal with occasional abnormalities reported in children involving the cerebral cortex and thalamus but not previously described in the basal ganglia. Here we report a 7-year-old boy with CSD encephalopathy who developed choreoathetosis with high intensity changes in basal ganglia on magnetic resonance imaging scan.
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