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A patient on disopyramide developed disopyramide toxicity when treated concurrently with azithromycin. Evidence of toxicity included an elevated serum disopyramide level and ventricular tachycardia requiring cardioversion. The azalide antibiotic presumably inhibited dealkylation of disopyramide to its major metabolite, mono-N-dealkyldisopyramide. Physicians should avoid using azithromycin in patients on disopyramide. If this drug combination is unavoidable, disopyramide levels must be closely monitored.
A series of 10 monoclonal antibodies reacting with Afipia felis antigens were selected from mice immunized with live organisms of the reference strain ATCC 53690. Immunoblotting against SDS-PAGE-separated A felis sonicate allowed the antibodies to be classified into three groups: 1) 168-4, -6, -7 and -10 reacted with a 53 kDa antigen, 2) 168-1, -3 and -9 reacted with both 53 kDa and 60 kDa antigens, and 3) 168-2, -5 and -9 reacted with other antigens. Antibodies of group 1 did not cross-react with other Afipia species or 36 unrelated bacteria, whereas those of groups 2 and 3 reacted with other Afipia species and some unrelated bacteria. Immunoblots of crossed immunoelectrophoretic patterns of A. felis sonicate against rabbit antiserum showed that antibodies of groups 1 and 2 bound to the same precipitin arcs. Antibodies of group 1 reacted with a species-specific epitope on the 53 kDa antigen, while those of group 2 reacted with other epitopes shared by the 53 kDa and 60 kDa antigens. The binding of antibodies of group 1 to A. felis sonicate was inhibited by post-infection rabbit serum, whereas no inhibition was observed for antibodies of group 2. The species-specific epitope of the 53 kDa antigen and the early appearance of antibodies against this epitope after infection suggest that this antigen can be used in a serodiagnostic test for A. felis infection.
To investigate the role of B. henselae in patients with symptoms suggesting neuroborreliosis, serum and cerebrospinal fluid samples were tested with serological and PCR methods. Among 17 examined patients, in 12 cases Borrelia burgdorferi infections were detected, in 1 case Bartonella henselae infection was ascertained, and in two patients mixed B. burgdorferi and B. henselae infections were found. These results indicate that mixed infections should be taken into consideration in establishing diagnosis of neurological disorders. Further study of this conclusion is needed.
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A 55-year-old male was admitted to our hospital because of fever and left submaxillary, right axillary, and left inguinal lymphadenopathy. A presumptive diagnosis of rickettsiosis was made and treatment with oral doxycycline was started. Lymphadenopathy was partialy resolved after antibiotics treatment. Ablation of the left inguinal node was done and histopathological examination showed non-Hodgkin's lymphoma. Lymphadenopathy was resolved by chemotherapy. The second patient, a 40-year-old male, developed a tender submandibular node. Excisional biopsy of the node was performed to eliminate lymphoma. Histopathological examination revealed granulomatous lymphadenitis with follicular hyperplasia. The patients had no history of cat contact, but owned a dog. Diagnosis of both cases was confirmed by the detection of IgG antibodies to Bartonella henselae with an enzyme immunoassay. Our findings suggest that dogs are implicated in B. henselae infection and can serve as a reservoir of the organism as well as cats. In the abscence of other bacterial and especially after exposure to dogs, B. henselae should be included as possible cause of lymphadenopathy.
Two patients were reported as having been infected with Bartonella henselae after having contact with a dog. Both of the patients owned a dog, but had no contact with cats. One patient was a 10-year-old boy who had experienced a fever of 38-39 degrees C for 11 days, as well as having bilateral cervical lymphadenopathy. The boy's serum IgM antibodies to B. henselae were negative on the 6th and 16th day of his illness, whereas his IgG value, using indirect fluorescence antibody (IFA) method, was found to be elevated from 1:256 to 1:1,024. B. henselae DNA was detected, by PCR method, in swabs from the gingiva and buccal membrane of the dog with which the boy had been in contact. The boy was first treated with cefdinir (300 mg daily) for 6 days without beneficial effect. He responded, however, to minocycline (100 mg daily) with symptom resolution in four days. The other patient was a 64-year-old man who had experienced a fever of 38-39 degrees C for 27 days, as well as having right inguinal lymphadenopathy. The man's serum IgM antibody to B. henselae was negative, although his IgG value, determined by IFA, was 1:1,024. In addition, B. henselae DNA was detected, by PCR method, in parafin-embedded tissue obtained from the biopsied inguinal lymph nodes. The man was treated with cefazolin (2 g daily). His fever resolved, but his lymph nodes remained swollen. After a regimen of erythromycin (1,200 mg daily), the swelling in his inguinal lymphnodes gradually disappeared. Careful review of suspected CSD victims' history of contact with animals is important in making a prompt diagnosis of B. henselae infection.
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The isoprenoid quinone contents of seven strains of "Afipia felis," the type strains of "A. clevelandensis" and "A. broomeae," and reference strains of three unnamed "Afipia" genospecies were determined by reverse-phase high-performance liquid chromatography. The quinone profiles of all "Afipia" strains were essentially identical, with ubiquinone 10 as the major component. The identity of ubiquinone 10 was confirmed by mass spectrometry.
We report the case of a human immunodeficiency virus-negative woman who developed native valve endocarditis of the aortic valve due to Bartonell henselae infection. The diagnosis was established using serology and PCR analysis of excised aortic valve tissue.
We report the first description of osteomyelitis due to Bartonella henselae genotype I in an immunocompetent middle-aged woman. The diagnosis was established by serology, histopathology, and PCR analysis of osseous and lymph node tissues. The mycobacteria growth indicator tube inoculated with the lymph node aspirate was used for PCR analysis.
Six children presented during one year with clinical features of infectious mononucleosis, but with laboratory findings of leucocytosis with neutrophilia, increased erythrocyte sedimentation rate, and hypergammaglobulinaemia. Serology for Epstein-Barr virus, cytomegalovirus, adenovirus, and Toxoplasma gondii was negative, while anti-Bartonella henselae IgM with high IgG titre (>/=1/1024) was present in all. All children had contact with kittens. No specific treatment was administered and all recovered.
Cervicothoracic lesions are not uncommon in children. All cervicothoracic lesions except superficial lesions extend from the neck to the thorax through the thoracic inlet. Evaluation of this area involves multiple imaging modalities: plain radiography, ultrasonography, nuclear medicine, computed tomography, and magnetic resonance (MR) imaging. However, MR imaging is the method of choice for assessing the full extents of cervicothoracic lesions and their relationships to neurovascular structures. Cervicothoracic lesions can be classified as congenital lesions, inflammatory lesions, benign tumors, malignant tumors, and traumatic lesions. Lymphangioma is the most common cervicothoracic mass in children; other congenital lesions include hemangioma, thymic cyst, and vascular anomalies. Inflammatory adenopathy reactive to tuberculosis, mononucleosis, tularemia, cat-scratch fever, infection with human immunodeficiency virus, or other upper respiratory tract infections can manifest as cervicothoracic lesions; tuberculous abscesses and abscesses of other origins can also be seen. Lipoma, lipoblastoma, aggressive fibromatosis, and nerve sheath tumors (either isolated lesions or those associated with neurofibromatosis) can also occur as cervicothoracic masses. Malignant cervicothoracic tumors include lymphoma, thyroid carcinoma, neuroblastoma, and chest wall tumors (rhabdomyosarcoma, Ewing sarcoma, and neuroectodermal tumor). Traumatic cervicothoracic lesions include pneumomediastinum of traumatic origin, traumatic pharyngeal pseudodiverticulum, esophageal foreign-body granuloma, and cervicothoracic hematoma.
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Explore the source record for details and available documents.
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Explore the source record for details and available documents.