Nineteen transfusion-dependent beta-thalassemia major patients were included in the study. Six of these patients underwent chelation therapy with desferrioxamine by subcutaneous infusion (50 mg/kg/12 hr) and 13 received intravenous infusion (50 mg/kg/6 hr or 100 mg/kg/24 hr). BUN, creatinine, creatinine clearance, beta 2-microglobulin, urinary beta 2-microglobulin and urinary growth hormone excretion were evaluated during desferrioxamine treatment. Thirteen out of nineteen patients presented tubular damage indicated by increased excretion of urinary beta 2-microglobulin. 85% (11 of 13) of these patients showed more serious tubular damage, as demonstrated by concurrent increased urinary growth hormone excretion. Moreover, a positive correlation between urinary growth hormone excretion and urinary beta 2-microglobulin was observed (P < 0.05).

We observed 12 very preterm infants (10 males) with a peculiar respiratory syndrome characterized by early onset soon after birth and by a biphasic course. The severe first phase was characterized by a clinical pattern mimicking the idiopathic respiratory distress syndrome of prematurity. Gradually, respiratory symptoms decreased and assisted ventilation with oxygen therapy was reduced. In the second phase, a significant worsening of respiratory signs and the appearance of apneic spells were observed. Chest X-ray showed hypoexpansion of the lungs and the prevalence of a fine reticular pattern. Chlamydia trachomatis was identified in this second phase in conjunctival and pharyngeal swabs and/or on tracheal aspirates. Our data suggest that in the very preterm infants, chlamydial infection shows different clinical and laboratory features if compared with Chlamydia trachomatis pneumonia of infants born at term.

We have recently observed a Chlamydia trachomatis infection presumably of intrauterine origin in a male infant delivered by cesarean section (CS) because of maternal gestosis at 30 weeks of pregnancy. The infant weighed 900 g and was referred to a neonatal intensive care unit soon after delivery with respiratory distress syndrome (RDS). Chest X-ray showed right sided pneumothorax and, subsequently, bilateral hypoexpansion and diffuse granularity. The infant required intubation and assisted ventilation for nine days. Blood culture and superficial swabs yielded no bacteria. On the 22nd day of life the infant's condition deteriorated. He developed progressive respiratory difficulties with tachypnea, mild sternal and intercostal retractions, inspiratory stridor and diminished air penetration to the lung. Chest-X-ray again showed severe hypoexpansion. White blood count was 4 600/mm3 with 3% eosinophils. Chlamydia trachomatis was detected in the baby's pharynx and conjunctiva, in the mother's cervix and in the father's urethra by two methods: direct immunofluorescence test with monoclonal antibodies (IF) and specimen culture on cycloheximide treated McCoy cells (1). For the IF we used fluorescein-labelled monoclonal antibodies against the 15 human serological variants of C. trachomatis (2). No bacteial or viral agents were isolated. The baby improved rapidly on oral erythromycin and was discharged at 100 days of age in good condition.Considering the two episodes of respiratory disease suffered by our patient in the newborn period, a chlamydial etiology of the late neonatal disease was likely, also in view of the prompt response to specific antimicrobial therapy, whereas the early respiratory picture was more consistent with hyaline membrane disease. However, it is difficult to exclude with certainty a contributing role of Chlamydia also in the first episode, in view of the observation by M%rdh (3) and Ushijima (4) on RDS to congenital chlamydial infection.On the basis of these preliminary observations it seems justified to search for chlamydial infection in preterm infants with atypical RDS, even if delivered by CS (5). Direct immunofluorescence with monoclonal antibodies for Chlamydia trachomatis may allow a rapid diagnosis and an appropriate treatment. Regina Elena, 324 00161 Rome Italy REFERENCES I. 2.3. 4. 5. RipaKT, Mkdh PA. Cultivation of Chlamydia trachomatis in cycloheximide-treated McCoy cells. J Clin Microbiol 1977; 6: 328-31. Tam MR, Stamm WE, Handsfield HH et al. Culture-independent diagnosis of Chlamydia trachomatis using monoclonal antibodies. N Engl J Med 1984; 310: 114650. Mirdh PA, Johansson PJH, Svenningsen N. Intrauterine lung infection with Chlamydia trachomatis in a premature infant. Acta Paediatr Scand 1984; 73: 569-72. Ushijima H, Hashira S, Shinozaki T, Fujii R. Chlamydia trachomatis infection. Acta Paediatr Scand 1985; 74: 604. La Scolea LJ, Paroski JS, Burzynski L , Faden H S . Chalamydia trachomatis infection in infants delivered by caesarean section. Clin Pediatr 1984; 23: 118-20.

The mode ofthis patient's infection is uncertain. We think that in walking barefoot she may have trodden in contaminated faeces from an infected person or pet. For a local dog or cat to be chronically infected it would have to have been imported from an endemic area, but larvae might persist and develop in warm, moist soil even in an English summer. It is unlikely that larvae would exist in the soil on contaminated vegetables imported from warmer climes. Orogenital transmission of strongyloidiasis has been suggested,3 but this patient denied any sexual contact.

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