Nocardia infection in lung transplant recipients.

BACKGROUND: Nocardia is responsible for infection in both normal and immunocompromised hosts. Organ transplant recipients are increasingly recognized as a sub-group of immunocompromised patients in whom nocardia is an important pathogen. The frequency of nocardia in organ transplant recipients varies between 0.7% and 3%. Nocardia infection has largely been reported in heart, kidney and liver transplant recipients. Presentations of nocardia in lung transplant recipients have been restricted primarily to case reports. The present study reviews the clinical and epidemiologic characteristics of nocardia infection in lung transplant recipients at our institution. METHODS: A retrospective cohort study of 473 lung transplant recipients from January 1991 to November 2000 was done at a university hospital. Patient demographics, immunosuppressive regimen at the time of isolation of nocardia species, use of trimethoprim-sulfamethoxazole for Pneumocystis carinii prophylaxis, rejection episodes in the preceding 6 months, concurrent pathogens, site of infection, radiologic findings and treatment and outcome were recorded. RESULTS: Nocardia infection was found in 2.1% (10 of 473) of our lung transplant recipients. Median time of onset was 34.1 months after transplantation. Nocardia species included N farcinica in 30% (3 of 10), N nova in 30% (3 of 10), N asteroides complex in 30% (3 of 10) and N brasiliensis in 10% (1 of 10) of patients. Post-transplant diabetes was present in 50% (5 of 10) of patients. The primary indication for lung transplantation was emphysema in 40% (4 of 10). Native lung involvement was noted in 75% (3 of 4) of patients with single lung transplant. Breakthrough nocardia infection were noted in 6 patients who were receiving trimethoprim-sulfamethoxazole prophylaxis for P carinii pneumonia; all breakthrough isolates remained susceptible to trimethoprim-sulfamethoxazole. Overall mortality was 40% (4 of 10). All patients (3 of 3) with infection due to N farcinica, except 1 (1 of 7) with infection due to other nocardia species, died. Seventy-five percent (3 of 4) of deaths were attributable to nocardia infection. CONCLUSIONS: Nocardia infection tended to involve the native lung in single lung transplant recipients. Trimethoprim-sulfamethoxazole for P carinii prophylaxis at the doses given was not protective against nocardiosis in these patients. Infection with N farcinica was associated with poor outcome. Thus, species identification and extended courses of antibiotics based on antimicrobial susceptibility testing are important in management of these patients.     

Mucous metaplasia of the pleura.

A case of mucous metaplasia of mesothelium in an 80 year old woman is described. Its cause is unknown, but it is important not to confuse it with secondary tumour.     

THE EFFECT OF SOME α2-ADRENOCEPTOR AGONISTS AND ANTAGONISTS ON GASTROINTESTINAL TRANSIT IN MICE: INFLUENCE OF MORPHINE, CASTOR OIL AND GLUCOSE

1. The effects of graded doses of the α₂-adrenoceptor agonists clonidine, tizanidine and BHT-920, and the α₂-adrenoceptor antagonists yohimbine and idazoxan, on gastrointestinal transit were investigated in mice using the charcoal meal test. 2. The agonists produced significant and dose-dependent decreases in gastrointestinal transit, and the antagonists produced the opposite effect. In affecting the gastrointestinal transit, clonidine (1 mg/kg) was as effective as tizanidine (12 mg/kg) and BHT-920 (40 mg/kg), while yohimbine (2 mg/kg) was as effective as idazoxan (1 mg/kg). 3. Morphine (2, 4 and 8 mg/kg) significantly inhibited gastrointestinal transit. This effect was significantly reversed by the co-administration of yohimbine (2 mg/kg) and idazoxan (1 mg/kg). 4. The acute administration of glucose (5.04 g/kg, i.p.) potentiated the inhibition of gastrointestinal transit produced by clonidine (1 mg/kg) and BHT-920 (40 mg/kg). Glucose treatment, however, had no significant effect on the increase in gastrointestinal transit induced by yohimbine (2 mg/kg) or idazoxan (1 mg/kg). 5. Castor oil (0.25 mL/mouse, orally) induced diarrhoea in saline-treated animals within about 45 min. Clonidine (1 mg/kg), tizanidine (12 mg/kg) and BHT-920 (40 mg/kg) delayed the occurrence of diarrhoea to 2.1, 1.2 and 1.4 h, respectively.     

Damage control surgery for abdominal trauma.

OBJECTIVE: To review the physiology, indications, technical aspects, morbidity, and mortality of damage control surgery. DESIGN: Retrospective study of published papers. SETTING: Teaching hospital, United Arab Emirates. INTERVENTIONS: A MEDLINE search on damage control surgery for the years 1981-2001. Further articles were retrieved from the references of the original articles. RESULTS: The indications for damage control surgery are: the need to terminate a laparotomy rapidly in an exsanguinating, hypothermic patient who had developed a coagulopathy and who is about to die on the operating table; inability to control bleeding by direct haemostasis; and inability to close the abdomen without tension because of massive visceral oedema and a tense abdominal wall. The principles of damage control surgery are: Phase I: laparotomy to control haemorrhage by packing; shunting, or balloon tamponade, or both; control of intestinal spillage by resection or ligation of damaged bowel, or both. Phase II: physiological resuscitation to correct hypothermia, metabolic acidosis, and coagulopathy. Phase III: planned reoperation for definitive repair. Damage control surgery is appropriate in a small number of critically ill patients who are likely to require substantial hospital resources; it has a high mortality (mean 45%, range (10%-69%). CONCLUSION: Damage control surgery offers a simple effective alternative to the traditional surgical management of complex or multiple injuries in critically injured patients. Phases I and II can be done at a rural hospital before transfer to a major trauma centre for definitive repair.     

Clinical efficacy of codergocrine mesylate in children with learning difficulties

A double-blind placebo-controlled study in children showed codergocrine mesylate to be effective in improving cognitive functions and behavioural symptoms associated with learning disorders. Forty randomly grouped children of either sex were given an increasing dosage of codergocrine mesylate and followed up for 12 weeks. A significant improvement was noted in speech (acquisition of new words, comprehensibility/meaningfulness of speech), sociability, attention/concentration, comprehension and memory. Improvement in behaviour (emotional lability and cooperativeness) was also noted. Problems of assessing cognitive progress in very young children with culturally appropriate methods were encountered.