Cases reported "Staphylococcal Infections"

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1/9. Recurrent staphylococcus aureus chalazia in hyperimmunoglobulinemia E (Job's) syndrome.

    PURPOSE: To report a case of recurrent staphylococcus aureus chalazia in a patient with hyperimmunoglobulinemia E syndrome (Job's syndrome). DESIGN: Case report. methods: Three separate surgical incisions and curettages of multiple, recurrent chalazia of the right upper eyelid were performed over a course of 3 months. Cultures and pathologic specimens were obtained. Postoperative treatment consisted of oral erythromycin and amoxicillin/clavulonate, topical tobramycin/dexamethasone ointment, and warm compresses. RESULTS: pathology of the tarsus confirmed the diagnosis of multiple chalazia. Cultures of the chalazia contents were positive for staphylococcus aureus. No further recurrence was observed following the third surgical procedure over a 3-month follow-up period. CONCLUSION: Characteristic staphylococcus aureus skin infections in immunodeficient patients with hyperimmunoglobulinemia E syndrome can involve the eyelids and may be recurrent despite appropriate medical and surgical therapy.
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2/9. Job's syndrome: a rare cause of recurrent lung abscess in childhood.

    A clinical syndrome characterized by recurrent staphylococcal infection of the skin and respiratory tract from birth was described in 1966 and referred to as Job's syndrome. Marked hyperimmunoglobulinemia E was later found to be associated with this syndrome. This article describes a case of Job's syndrome as a cause of recurrent lung abscess during childhood necessitating lung resection.
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3/9. A hyperimmunoglobulin E syndrome with normal chemotaxis in vitro and defective leukotaxis in vivo.

    A 26-yr-old male with a lifelong history of atopic dermatitis and recurrent severe staphylococcal abscesses was found to have hyperimmunoglobulinemia E. Evaluation of both the humoral and cellular aspects of chemotaxis in vitro showed both neutrophils and monocytes to be normal. However, quantitative neutrophil migration in vivo was significantly suppressed using the patient's own serum as the attractant. This defective migration in vivo was partially corrected by serum from normal donors as the attractant and also partially corrected following plasma infusion in this patient. Evaluation of quantitative leukocyte migration in vivo may be most useful in patients suspected of defects of leukocyte mobility.
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4/9. plasmapheresis treatment in patients with severe atopic keratoconjunctivitis.

    A 19-year-old woman with hyperimmunoglobulinemia E (the hyper-IgE syndrome [HIE]) and a 62-year-old man with atopic dermatitis experienced dramatic improvement in their chronic ocular symptoms and signs of atopic keratoconjunctivitis after plasmapheresis was instituted. Both patients had previously received topical and oral corticosteroids as well as topical cromolyn sodium without significant beneficial effect. The authors recommend a trial of plasmapheresis in selected patients with recalcitrant and debilitating atopic keratoconjunctivitis when standard therapy proves unsuccessful.
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5/9. Oral chloramphenicol therapy for multiple liver abscesses in hyperimmunoglobulinemia E syndrome.

    In a patient with Hyper-IgE-syndrome multiple liver abscesses developed in spite of prophylactic treatment with trimethoprim and sulfamethoxazol. Ultrasound confirmed the clinical diagnosis and percutaneous needle aspiration under ultrasonographic guidance and culture of the aspirated pus allowed specific antibiotic treatment by oral chloramphenicol alone without surgical drainage. The isolated Staph.aureus strain was resistant to trimethoprim and sulfamethoxazol.
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6/9. Defective leukocytotaxia and recurrent staphylococcal infecion: deficiency of leukocytotaxia and abnormal granulocytes associated with increase serum IgE levels in an adult with recurrent staphylococcal infection.

    A man who was suffering from recurrent staphylococcal infection had antecedent symptoms of severe pruritus. Laboratory investigations showed leukocytosis with eosinophilia, hyperimmunoglobulinemia of all fractions, but particularly of IgE, and a deficiency of cell-mediated immunity on in vivo testing. phagocytosis and bactericidal activity of polymorphonuclear leukocytes were normal, but a cellular and serum-associated defect in leukocytotaxia was present. Ultrastructural changes were observed in polymorphonuclear leukocytes. association of impaired leukocytotaxia and elevated levels of IgE is not uncommon. Recurrent bacterial infections in the patient described are probably related to defective chemotaxis.
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7/9. Defective neutrophil chemotaxis and hyperimmunoglobulinemia E-a reversible defect?

    An eleven-month-old boy is presented with chronic atopic dermatitis and recurrent infections of the skin and respiratory tract, including subcutaneous abscesses. Immunological studies disclosed a neutrophil chemotactic defect, blood eosinophilia and serum hyper IgE. The clinical and analytical data are similar to those of patients previously dermatitis reversed the chemotatic defect, the blood eosinophilia and the clinical symptoms.
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8/9. Recurrent staphylococcal abscesses associated with defective neutrophil chemotaxis and allergic rhinitis.

    Four patients with recurrent staphylococcal furonculosis and deep abscess formation were evaluated to determine if a defect in the host defense mechanism could account for the unusual incidence of infection. Each also suffered repeated allergic rhinitis, often preceding the onset of infection. A marked defect in neutrophil granulocyte chemotaxis occurred when the patients were symptomatic with rhinitis and abscess formation. Their mean chemotactic index ( /- SD) was 16 /- 6, while that of 25 control subjects was 70 /- 11. Neutrophil random migration, phagocytosis, bactericidal activity, and lymphocyte T-cell populations were normal, as were serum concentrations of IgA, IgG, IgM, and IgE. Serial neutrophil function tests revealed normal chemotactic responsiveness when the patients were symptom-free of allergic rhinitis and no longer having abscesses. Abnormal function returned, however, when symptoms recurred. These studies suggest that defective neutrophil function associated with allergic phenomena need not be accompanied by hyperimmunoglobulinemia E. Such defects may be intermittent, appearing when allergic symptomatology and infections develop.
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9/9. Severe staphylococcal disease associated with allergic manifestations, hyperimmunoglobulinemia E, and defective neutrophil chemotaxis.

    Neutrophil granulocyte function was determined in three patients with systemic staphylococcal infection, clinical manifestations of generalized allergic disease, and hyperimmunoglobulinemia E. Each of the patients had urticarial skin rashes before or at the time of development of staphylococcal suppurative lymphadenitis, pneumonia, or sepsis. Neutrophil chemotaxis, random migration, phagocytosis, and bactericidal capacity were assessed to determine if an abnormality in these functions might have contributed to the development of severe staphylococcal infections. Each of the three patients with generalized urticaria was found to have a marked defect in neutrophil chemotaxis. The mean chemotactic index of the patients was 12 /- 4, whereas that of 20 controls was 72 /- 11. Neutrophil random migration, phagocytosis, and bactericidal capacity were normal in each patient. The serum or plasma of the patients did not inhibit chemotaxis of control neutrophils and did not contain an increased concentration of the chemotactic-factor inactivator found in normal serum. Treatment of the neutrophils of these three patients with the competitive histamine H2 receptor blocking agent, burimamide, produced a significant increase in chemotactic responsiveness. These studies suggest the possibility of pharmacologic modification of neutrophil granulocyte function.
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