Diagnosis of cat-scratch disease.
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A patient with AIDS developed subcutaneous nodules and associated osteolytic lesions with negative stains and cultures for bacteria, fungi and parasites. Flucloxacillin was not effective but treatment with vancomycin was associated with improvement. Six months later the patient became severely ill, with fever, malaise and multiple skin and laryngeal papules. Cat-scratch disease was diagnosed from the typical epithelioid angiomatosis seen in skin biopsies with bacterium-like structures in the Warthin-Starry stain. Retrospectively these typical structures were also seen in earlier biopsies. All lesions improved after therapy with erythromycin had been instituted.
In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.
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We report on a young patient with chronic cervical lymphadenopathy and serological and histological evidence for infection with Bartonella henselae and Toxoplasma gondii. Serological follow-up studies, including testing for avidity of Toxoplasma-specific immunoglobulin G antibodies, assisted in the determination of the cause of the acute lymphadenitis. Our results suggest that the clinical symptoms were most likely due to cat scratch disease rather than to acute toxoplasmosis.
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We describe a patient who presented with a massive chest-wall abscess after a severe debilitating illness that lasted 3 months. Steroid therapy, administered for 4 weeks, masked the slow development of an extensive axillary and chest-wall abscess. After multiple negative tests, the patient's prolonged illness was diagnosed as cat-scratch disease (CSD). An indirect fluorescent antibody test revealed that two convalescent serum samples were positive for IgG to Bartonella clarridgeiae, but no other Bartonella species. We also review 12 cases of severe chest and pulmonary disease due to CSD that were reported in the English-language literature. Thoracopulmonary findings associated with CSD, pathogenic mechanisms of bartonella infections, diagnostic criteria, and management of CSD are presented.
To evaluate the causative factor for multifocal chorioretinitis, papillitis, and recurrent optic neuritis. A 41-year-old patient presenting multifocal choroiditis, papillitis, and recurrent optic neuritis was evaluated with funduscopy, angiography (FA), optical coherence tomography (OCT), visual evoked potentials (VEP), and numerous blood laboratory tests. FA and OCT showed multifocal pigment epithelial detachments. VEP showed typical changes for optic neuritis and papillitis. Indirect fluorescent antibody assay disclosed Bartonella henselae. Although cat-scratch disease frequently presents with optic neuritis or neuroretinitis, additional multifocal chorioretinal lesions associated with serous pigment epithelial detachments may occur. In case of recurrent episodes, a detailed laboratory work-up is mandatory to define the appropriate diagnosis and treatment.
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Papular and nodular skin lesions that clinically resembled Kaposi sarcoma, but histologically showed a distinct epithelioid haemangioma-like appearance, were noted in seven patients with the acquired immunodeficiency syndrome. Clusters of bacteria that had the structure of gram-negative rods were identified within each of the vascular proliferations by electron microscopy. The bacteria did not stain with the Brown-Brenn, acid-fast, or other histochemical stains for infectious organisms, but did stain with Warthin-Starry--ie, the staining profile was that described for the cat scratch disease (CSD) bacillus. Immunoperoxidase staining, using antisera raised in rabbits against cultured CSD bacillus, showed a positive reaction with the bacterium in all five cases tested. The two surviving patients have both given histories of having been scratched by a cat. In several patients, the vascular lesions regressed after therapy with antibiotics appropriate for CSD bacillus infection.
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In patients who have history of lymphoma, a positive positron emission tomography (PET) scan is frequently considered as good evidence for relapse and/or persistent disease. Thus, lymph node biopsy is not always done to confirm the diagnosis of relapse or refractory lymphoma before a patient is subjected to further chemotherapy. We report a case of patient with history of T cell lymphoblastic lymphoma who presented again with inguinal lymphadenopathy and positive study on positron emission tomography suggestive of lymphoma relapse. This was pathologically proven to be cat scratch disease. This case suggests that in the immunocompromised patients who had history of lymphoma, infectious etiology should be ruled out for PET scan-positive lymphadenopathy.
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Richter's Syndrome is a highly refractory and usually fatal condition. It occurs as a result of transformation of chronic lymphocytic leukemia (CLL) or low grade lymphoma into highly aggressive lymphoma. Patients usually present with rapidly enlarging lymph nodes and systemic symptoms like night sweats, fever and weight loss. We are reporting a case of CLL presenting with similar symptoms. Initial suspicion of Richter's Syndrome proved wrong when lymph node biopsy did not reveal evidence of high grade lymphoma. Instead it showed findings consistent with cat scratch disease (CSD), later confirmed by serology. To our knowledge this is the first reported case of CSD in a patient with CLL.