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Abstract Background: Cat scratch disease (CSD) is an infectious disorder caused by Bartonella henselae. The infection usually presents as local lymphadenopathy, fever, and mild constitutional symptoms. Systemic or severe disease is reported in 5-20% of patients with CSD. We report a case of disseminated CSD with osteomyelitis and hepatosplenic disease and a review of the literature. Case report: A previously healthy 5-year-old male presented with prolonged fever and abdominal pain, followed by low back pain. The serologic test showed positive IgG for B. henselae and IgM and IgG for Epstein Barr virus (EBV). The abdominal ultrasound showed hepatic and splenic hypoechoic lesions, and the magnetic resonance imaging (MRI) revealed spondylitis of the D6 vertebra. He received treatment with azithromycin for 4 weeks and rifampicin for 6 weeks. The symptoms disappeared, and the abdominal ultrasound was normal nine months later. Conclusions: Disseminated CSD is infrequent. The diagnosis requires a high rate of suspicion. Laboratory findings of Bartonella infection are often non-specific. Serologic test, polymerase chain reaction of B. henselae in blood or biopsied material of the site of involvement and imaging test can be performed to confirm the diagnosis. The diagnosis of disseminated B. henselae was based on significantly elevated blood titers, radiologic findings, and epidemiologic history. Treatment of CSD depends on the disease presentation. Azithromycin is used as a first-line agent for lymphadenopathy. The optimum treatment and its duration have not been established in atypical or complicated CSD, including patients with osteomyelitis and hepatosplenic disease.
Resumen Introducción: La enfermedad por arañazo de gato (EAG) es una patología infecciosa originada por Bartonella henselae. Habitualmente se presenta como linfadenopatía local, fiebre y síntomas constitucionales leves. El 5-20% de los pacientes con EAG manifiestan una afectación sistémica. Se presenta un caso de EAG diseminada, con osteomielitis y enfermedad hepatoesplénica, y se hace una revisión de la literatura sobre la EAG. Caso clínico: Paciente de sexo masculino de 5 años, previamente sano, que presentó fiebre prolongada y dolor abdominal, seguidos de dolor en la parte baja de la espalda. En la serología, presencia de IgG frente a B. henselae y de IgM e IgG frente al virus de Epstein-Barr. En la ecografía abdominal se observaron lesiones hipoecoicas en el hígado y el bazo, y la resonancia magnética mostró espondilitis de D6. Recibió tratamiento con azitromicina 4 semanas y rifampicina 6 semanas. Los síntomas desaparecieron y la ecografía abdominal a los 9 meses fue normal. Conclusiones: La EAG diseminada es infrecuente. El diagnóstico requiere un alto grado de sospecha. Los hallazgos de laboratorio en la infección por Bartonella suelen ser poco específicos. Para confirmar el diagnóstico pueden hacerse serología, reacción en cadena de la polimerasa para B. henselae en sangre o en biopsia de tejidos afectados, y estudios de imagen. El diagnóstico de EAG diseminada se basa en títulos elevados en la sangre, hallazgos radiológicos e historia epidemiológica. El tratamiento depende de la forma de presentación. En los casos de linfadenopatía se utiliza azitromicina. En la EAG atípica o complicada, que incluye osteomielitis y afectación hepatoesplénica, no están bien establecidos el tratamiento ni su duración.
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Manifestations of serious disease in chronic schistosomiasis such as portal hypertension, collateral circulation and hepatosplenomegaly are ascribed to T cell-dependent obstructive granuloma formation with subsequent fibrosis principally in the liver. Collagen synthesis and tissue fibrosis may also result from indirect effects of T cell dependent macrophage activation but also from direct effects of eggs productions. Mature eggs are known to be a rich source of "immunopathologic" antigens. It is proposed that antibodies, through their effects on both mature and immature eggs, may markedly decrease opportunities for expression of immunopathologic responses. The hypothesis is that antibodies of certain specificities and certain istotypes can inhibit embryonation of immature and/or effect early or accelerated destruction of mature eggs. The disease modulating consequences of these stem from inhibition of sustained production and release of immunopathologic antigens. The anti-immunopathologic effects being termed "anti-embryonation immunity" (directed against immature eggs) and "anti-miracidial immunity" (accelerated desctruction of mature eggs). On theoretical grounds, sensitization of hosts for anti-embryonation immunity would be a particularly effective means of vaccinating against severe hepatosplenic disease. Such a vaccination strategy could also lead to reduced transmission of infection. It should also inhibit production of egg products with effects in the liver such as hepatotoxicity and promotion of collagen synthesis. The hypothesis emphasizes the consequences of the immune responses on the source of immunopathologic antigens (i.e the egg) in modulation of granuloma formation and disease abatement. The alternative, and in our view, less attractive strategy of vaccination for anti-immunopathology, is to promote immuregulatory responses (e.g. suppressor T cells) which operate to inhibit immunopathologic effector cells and antibodies.(Summary)