Background. Because person-to-person transmission of brucellosis is exceptional, physicians who care for patients with this disease are not considered to be at increased risk. A woman in her 24th week of pregnancy who had received a diagnosis of placenta previa presented to the hospital with massive vaginal bleeding and hypovolemic shock, requiring performance of an emergency Cesarean delivery. Two physicians who assisted the surgical delivery developed culture-proven Brucella melitensis infection. The organism was also recovered from cultures of blood samples obtained from the mother and the premature newborn. The mother had been observed since early pregnancy because of an undiagnosed febrile hepatitis, but no specific tests for brucellosis had been performed. Retrospective testing of serum samples obtained at the onset of disease were positive for Brucella antibodies, indicating that the disease could have been diagnosed earlier.Methods. Hospital records of the obstetric, intensive care, and surgical departments were examined to identify all staff members who took care of the mother and her offspring. The identified personnel were interrogated about exposure to potentially infective blood and fomites and were screened by blood cultures and serologic tests for Brucella species.Results. An additional physician who assisted in the resuscitation of the newborn had a blood culture positive for B. melitensis and a positive result of a diagnostic serological test. Ninety-five other members of the hospital staff, who were potentially exposed to the organism, were found to be uninfected. Conclusions. Although rare, transmission of B. melitensis from patients to medical personnel may occur. Strict adherence to universal precautions, especially during performance of medical procedures characterized by massive blood exposure, should be reinforced.

Fetal goiter is an extremely rare complication of pregnancy. Its incidence is 1 in 40,000 deliveries. Antithyroid maternal therapy is responsible for 10-15% of fetal congenital hypothyroidism and can be considered as the most frequent underlying cause for this condition. The frequency of fetal goiter that is associated with fetal hypothyroidism and normal maternal thyroid function, as in our case, is even less frequent. Fetal goiter is associated with increased rate of perinatal complications and long-term morbidity, due to peripartum complications including labor dystocia due to its mass effect, as well as neonatal airway obstruction that may lead to hypoxic-ischemic brain injury and death. We present, in this study, a case report of late antenatal fetal goiter in an euthyroid woman and a literature review of the diagnosis and treatment of these cases.

Although apnea is common in premature babies, there is a paucity of information concerning the pathophysiologic basis of these episodes and their relationship to other perinatal conditions such as hyperbilirubinemia. Unconjugated hyperbilirubinemia in premature infants, even in moderately high levels, may cause encephalopathy affecting brainstem functions and has been linked to increased incidence of apnea in these infants. Thus, there is a need to clarify mechanisms by which bilirubin may alter respiratory control and induce apnea of prematurity. In this study, bilirubin or placebo was infused i.v. in 9-d-old rat pups (n ϭ 36). Serum hyperbilirubinemia peaked in the first hours after bilirubin infusion. Twenty-four hours after bilirubin infusion, respiration was recorded by plethysmography at rest and under hypercapnic and hypoxic conditions. In treated pups, minute ventilation in room air was significantly reduced, hyperventilatory response to CO 2 was blunted, and hypoxic ventilatory depression was increased, compared with placeboinjected rat pups. Brainstem bilirubin deposition and immunoreactivity to bilirubin was detected in the brainstem on histologic analysis. We speculate that high serum bilirubin levels may cause prolonged inhibition of brainstem autonomic function and that this could underlie the exacerbation of apnea noted in premature babies who have experienced jaundice. A pnea is a frequent occurrence in premature babies, affecting up to 84% of infants weighing Ͻ1000 g at birth (1,2). The long-term implications of this phenomenon for human development are unclear; however, some studies have suggested an association between apnea of prematurity and abnormal motor and mental development (3-5). Apneic episodes are considered to be the consequence of immature respiratory control by neuronal networks within the brainstem. However, despite advances in the field of developmental respiratory neurobiology in recent years, the pathophysiologic basis of these episodes has not yet been completely elucidated and there is a paucity of information concerning their relationship to other widespread perinatal conditions such as hyperbilirubinemia.Hyperbilirubinemia of the newborn infant is very common, and the line separating physiologic and pathologic jaundice has been difficult to define (6). In severe cases this condition can be harmful due to the risk of bilirubin encephalopathy or development of kernicterus (7). In premature infants, in particular, bilirubin encephalopathy and kernicterus have been shown to occur at a lower threshold of serum bilirubin, compared with term babies (8,9). Furthermore, an association between moderate hyperbilirubinemia and poorer neurodevelopmental outcomes has been suggested in a large, retrospective multicenter study of premature infants (10). A preliminary observation from our laboratory by DiFiore et al. suggests that a significant relationship exists between apnea of prematurity and the prior occurrence (11) have also reported a correlation between bilirubin enceph...

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