Cases reported "Cystic Fibrosis"

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11/28. Disseminated scedosporium apiospermum infection in a cystic fibrosis patient after double-lung transplantation.

    scedosporium apiospermum is a saprophytic ubiquitous filamentous fungus. It can cause a wide spectrum of diseases, from localized to invasive infections. S apiospermum has been described as one of the major fungal agents of chronic colonization of airways in cystic fibrosis (CF) patients. Invasive infections due to S apiospermum are only rarely reported in CF after lung transplantation. A 26-year-old woman with CF and chronic bronchial colonization by S apiospermum developed bilateral chorioretinitis and subcutaneous nodules 4 weeks after double-lung transplantation (LTx). Isolates of S apiospermum from sputum samples before and after LTx and from vitreal fluid were typed by random amplification of polymorphic dna (RAPD). The patient was treated with voriconazole (VRC). The patient improved with VRC given orally for 6 months. Two days after VRC discontinuation, she developed sub-acute meningitis (isolation of S apiospermum from the cerebrospinal fluid). She was again given VRC, but died 23 days later from uncontrolled fungal infection. molecular typing of clinical isolates of S apiospermum performed by RAPD demonstrated that all isolates belonged to the same genotype. S apiospermum is a frequent, but late colonizing fungal agent in CF patients. In the case of LTx, these patients can develop invasive infection due to the colonizing strain, as confirmed by molecular typing.
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12/28. Aspergillus bronchitis in cystic fibrosis.

    aspergillus fumigatus, a widely distributed spore-bearing fungus, is commonly grown in sputum cultures of patients with cystic fibrosis (CF). A fumigatus may cause allergic bronchopulmonary aspergillosis (ABPA), a complex condition that leads to worsening of airway inflammation and progressive damage and is diagnosed by specific criteria. In this report, we present six CF patients with respiratory deterioration that did not respond to appropriate antibiotic treatment. All had had A fumigatus in sputum cultures but did not fulfill the criteria of ABPA. Treatment with antifungal agents was followed by improvement in clinical condition. We suggest that in patients with CF, A fumigatus should be considered as a pathogen that may directly cause respiratory exacerbations. Antifungal therapy should be considered when deteriorating respiratory function is not responding to antibacterial therapy and A fumigatus is growing in sputum cultures.
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13/28. An unusual case of munchausen syndrome by proxy.

    An 11-year-old boy was presented by his father with a long and plausible history of cystic fibrosis. The diagnostic test for cystic fibrosis, the sweat test, was normal and excluded the diagnosis. The medical history was later found to be false, and the child to be well. By definition, the case met the criteria for munchausen syndrome by proxy with fabrication of symptoms on behalf of another in order to deceive medical personnel. Unusual features included the illness chosen, the father as the parent falsifying illness, his failure to pursue unnecessary investigations and treatment, and the ease with which he relinquished the diagnosis of cystic fibrosis.
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14/28. munchausen syndrome by proxy simulating cystic fibrosis.

    The case of a child with apparent cystic fibrosis whose many signs, symptoms, and laboratory results were convincingly portrayed by his mother is presented. The mother falsified the history, and cunningly altered sweat tests and stool fat analyses, and stole sputum from patients with cystic fibrosis to make her child appear to have cystic fibrosis. This case of munchausen syndrome by proxy highlights the extent to which the diagnosis of cystic fibrosis rests on reliable history and laboratory data and emphasizes the extremes to which perpetrators of this form of child abuse may go to make their case. Medical personnel must educate civil authorities about this syndrome and the dangers it represents to the child.
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15/28. Respiratory infections may reflect deficiencies in host defense mechanisms.

    Serious respiratory tract infections are rare in the healthy individual and most of the nuisance morbidity that occurs results from nasopharyngeal viral infections that many people get once or twice a year. The economic impact from these upper respiratory tract infections is appreciable, however, in terms of absenteeism from school or work, but unfortunately there is little that can be done to ward them off in a practical way. pneumonia is an infrequent lifetime experience for most non-smoking adults and when it occurs, unusual circumstances may pertain--a particularly virulent microorganism is in circulation, or perhaps one has been exposed to a newly recognized germ, such as has occurred with legionella species in the past 8 years or so. What protects us the great majority of the time is a very effective network of respiratory tract host defenses. These include many mechanical and anatomical barrier mechanisms concentrated in nose and throat; mucociliary clearance, coughing and mucosal immunoglobulins in the conducting airways and in the air-exchange region of the alveolar structures, phagocytes, opsonins, complement, surfactant and many other factors combine to clear infectious agents. The ability to mount an inflammatory response in the alveoli may represent the maximal and ultimate expression of local host defense. In some way these host defenses are combating constantly the influx of micro-organisms, usually inhaled or aspirated into the airways, that try to gain a foothold on the mucosal surface and colonize it. But many general changes in overall health such as debility, poor nutrition, metabolic derangements, bone marrow suppression and perhaps aging promote abnormal microbial colonization and undermine the body's defenses that try to cope with the situation. It is a dynamic struggle. The departure from normal respiratory health may not be obvious immediately to the patient or to the physician and repeated episodes of infection or persisting symptoms of cough, expectoration and sinus or ear infections may develop before serious assessment of the situation is taken and appropriate diagnosis gotten underway. Obvious explanations for respiratory infections may be apparent and, nowadays, side effects from antineoplastic chemotherapy or immunosuppressive therapy for a variety of diseases that create an immunocompromised host are common. In a few subjects, especially young adults who present with a cumulative history of frequent but mild infections in childhood and youth, a subtle deficiency in host defenses may exist and have been partially masked because of attentive pediatric medical care and prompt use of broad spectrum antibiotics.(ABSTRACT TRUNCATED AT 400 WORDS)
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16/28. Cutaneous necrotizing venulitis in patients with cystic fibrosis.

    Palpable purpura was noted to occur late in the course of some patients with cystic fibrosis. Skin biopsy specimens showed necrotizing venulitis characterized by a perivenular infiltrate composed of neutrophilic leukocytes, fibrin, hypogranulated mast cells, and endothelial cell necrosis. Circulating immune complexes were detected. Recurrent pulmonary infections and the chronic administration of therapeutic agents provide sources of potential antigens.
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17/28. moxalactam-tobramycin-resistant pseudomonas aeruginosa isolates in patients with cystic fibrosis.

    in vitro studies have shown synergistic killing activity against pseudomonas aeruginosa (PA) with the combination of an aminoglycoside and moxalactam, a new beta-lactam agent. We describe three patients with cystic fibrosis (CF) with PA isolates that were resistant to all single-agent antibiotics, but sensitive to the combination of moxalactam-tobramycin. Initially, all patients had a good clinical response to this combination. However, during a second course of therapy, there was clinical deterioration coincident with the rapid emergence of moxalactam-tobramycin-resistant PA isolates.
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18/28. Allergic bronchopulmonary aspergillosis complicating cystic fibrosis in childhood.

    Allergic bronchopulmonary aspergillosis, known to be associated with cystic fibrosis in older patients, occurred in 7 young atopic children with cystic fibrosis. The diagnosis was suggested by the onset of, or the increase in, asthmatic symptoms accompanied by major chest x-ray changes ranging from total collapse of a lung or lobe to extensive but changing areas of consolidation. Each of the children had a blood eosinophilia, positive type I skin tests to aspergillus fumigatus, and reversible airways obstruction. Most had a positive type III skin test and circulating precipitins to A. fumigatus, with raised IgE levels which contained specific antibodies to the fungus on radioallergosorbent (RAST) test. None had advanced suppurative chest disease of cystic fibrosis. None was given specific antifungal agents; two received systemic treatment with corticosteroids, the other received additional drugs for their asthma. Two developed total collapse of one lung, one child being only 2 years old. Five have had recurrences of pulmonary shadowing typical of allergic aspergillosis but are not showing significant progression of their cystic fibrosis lung disease. Our experience suggests that there should be an increased awareness of this condition, particularly its association with extensive pulmonary collapse or consolidation in children with cystic fibrosis who are atopic.
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19/28. Isolation of Pseudomonas cepacia in cystic fibrosis patient.

    Pulmonary infection on cystic fibrosis (CF) patients are associated with a limited qualitative number of microorganisms. During the colonization process, staphylococcus aureus usually precedes pseudomonas aeruginosa. This latter is at first non-mucoid, being replaced or associated to a mucoid morphotype which is rare in other diseases. In 1980, Pseudomonas cepacia appeared as an important agent in CF pulmonary infections with a mean frequency of about 6.1% isolations in different parts of the world. The primus colonization mainly occurs in the presence of pre-existent tissue lesions and the clinical progress of the disease is variable. In some patients it can be fulminant; in others it can cause a gradual and slow decrease in their pulmonary functions. The concern with this germ isolation is justified by its antibiotic multiple resistance and the possibility of direct transmission from a colonized patient to a non-colonized one. We reported the first case of P. cepacia infection in a CF patient in our area. The microbiological attendance to this patient had been made from 1986 to 1991 and the first positive culture appeared in 1988. The sensitivity profile showed that the primus colonization strain was sensitive to 9 of 17 tested antibiotics, however in the last culture the strain was resistant to all antibiotics. These data corroborate the need for monitoring the bacterial flora on CF patients respiratory system.
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20/28. Pseudomonas cepacia empyema necessitatis after lung transplantation in two patients with cystic fibrosis.

    lung transplantation is an accepted modality for patients with cystic fibrosis (CF) who have end-stage respiratory failure. The postoperative course of these patients is often complicated by serious infections with organisms such as pseudomonas aeruginosa and Pseudomonas cepacia that may be multiply resistant to conventional antimicrobial agents. We describe two patients with CF who, after double lung transplantation, developed the unusual complication of empyema and empyema necessitatis due to P cepacia that was resistant to all tested antibiotics.
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