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1/8. Neonatal alloimmune neutropenia in premature monozygous twins.

    Alloimmune neonatal neutropenia (ANN) is an uncommon but potentially life-threatening disorder of the neonate and young infant. Hematologically, the mother's peripheral neutrophil count is normal. However, the passive transfer of maternal immunoglobulin g neutrophil-specific antibodies and the subsequent sensitization of fetal neutrophils can result in severe neutropenia in the neonate. Generally, ANN is a self-limiting condition, but with severe bacterial infection, mortality can be high. We present the clinical features of monozygous twins delivered at 33 weeks' postconception with this condition. This case report is unique in that it occurred in twins born prematurely and was attributable to antibodies against 2 neutrophil-specific antigens, NA1 and NB1. A brief review of the diagnosis, management, and treatment of ANN is presented.
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2/8. Human cytomegalovirus as a direct pathogen: correlation of multiorgan involvement and cell distribution with clinical and pathological findings in a case of congenital inclusion disease.

    The human cytomegalovirus (HCMV), a member of the herpesviridae, is the most frequent cause of congenital virus infections and a major cause of morbidity and mortality in immunocompromised patients. Due to the lack of an appropriate animal model, insight into the pathogenesis of HCMV infections originates primarily from in situ examination of HCMV-infected tissues. Although in immunocompromised adults such tests are complicated frequently by the presence of additional misleading pathogens, the absence of additional pathogens renders congenital inclusion disease the most suitable access for investigation of pathogenetic aspects of HCMV infections. Immunohistochemical examination of tissue sections from a boy with fatal congenital inclusion disease was undertaken to detect the extent of multiorgan and cell involvement. Adrenal gland, bone marrow, diencephalon, heart, kidney, liver, lung, pancreas, placenta, small bowel and spleen were included in this study. Detection of virus antigens from different phases of viral replication revealed that all investigated organs were infected by HCMV. Simultaneous detection of cell type specific marker molecules showed that a variety of cell types stained positive for HCMV antigens including endothelial cells, epithelial cells, smooth muscle cells, mesenchymal cells, hepatocytes, monocytes/macrophages and granulocytes. The lung, the pancreas, the kidneys and the liver were the major target organs with a high number of HCMV infected cells. This correlated with multiorgan failure as the cause of death and strongly indicates direct pathogenetic effects of HCMV.
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3/8. cytomegalovirus encephalopathy in an infant with congenital acquired immuno-deficiency syndrome.

    A female infant born pre-term to a hiv seropositive mother presented at birth with seropositivity for hiv and CMV viruria. At five months of age she developed an aids-related complex. Six months later she died from rapidly progressive diffuse encephalopathy. Post mortem examination revealed generalized CMV infection. Neuropathological examination showed a nodular encephalitis with occasional cytomegalic cells containing characteristic CMV inclusion bodies. There was no evidence of hiv encephalitis; immunostaining for hiv antigen (gp 41) was negative. opportunistic infections in infants with congenital AIDS are the exception. To our knowledge, only one case of CMV encephalitis in an infant with congenital AIDS has been reported previously. In that case, as in the present one, a reactivation of a congenital CMV infection is likely.
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4/8. Hypogammaglobulinemia in infants infected with human immunodeficiency virus.

    Two premature infants were infected with hiv via blood transfusions during the neonatal period. Although neither patient had serum antibody to hiv owing to severe hypogammaglobulinemia, hiv infection was confirmed by finding hiv antigen in the sera of both patients. These cases show that hiv infection can produce severe hypogammaglobulinemia, and illustrate the value of hiv antigen detection in the diagnosis of hiv infection in seronegative patients.
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5/8. measles pneumonia in a newborn.

    We report a 21-day-old preterm infant who had severe respiratory distress of 6 days' duration and whose lungs revealed a giant cell pneumonia at necropsy. measles antigen was demonstrated in mononuclear and multinucleated epithelial cells of the lung by immunoperoxidase staining. We recommend the immunostaining procedure to differentiate measles from other viruses, such as parainfluenza 2 or 3, and respiratory syncytial virus, all of which may produce giant cell pneumonias.
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6/8. Chronic respiratory disease in premature infants caused by chlamydia trachomatis.

    The relation between chronic respiratory disease and infection with chlamydia trachomatis in premature infants was investigated to ascertain the aetiological importance of intrauterine C trachomatis infection and chronic respiratory disease in premature infants. serum IgM antibodies against C trachomatis were determined by enzyme linked fluorescence assay. Sections of lung tissues obtained by biopsy and at necropsy were also tested for the presence of antigens using fluorescein conjugated monoclonal antibodies to C trachomatis. Of 16 sera from premature infants with chronic respiratory diseases clinically diagnosed as bronchopulmonary dysplasia or the Wilson-Mikity syndrome, five had IgM antibodies to C trachomatis L2 strain by enzyme linked fluorescence assay (titre greater than or equal to 1/500). Of 37 sera from premature infants with extremely low birth weights, two had IgM antibodies to C trachomatis. No specific IgM antibody was detected in 31 neonates who showed raised serum IgM concentrations but who did not have respiratory tract symptoms. C trachomatis was identified from two specimens of lung tissue obtained at necropsy from premature infants with chronic respiratory disease positive for IgM antibody. These findings indicate the aetiological importance of intrauterine C trachomatis infection in chronic respiratory disease in premature infants.
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7/8. Candida antigen detection in two premature neonates with disseminated candidiasis.

    Two premature neonates with birth weight less than 1,200 g developed systemic candidiasis during treatment with multiple antibiotics and parenteral hyperalimentation. Clinical findings included signs of necrotizing enterocolitis in one patient and multiple fungal renal cortical abscesses in the other. The Candida antigen, mannan, was present in the sera of both patients at the time of clinical deterioration. Multiple blood cultures and urine and stool samples from both patients grew candida albicans. Systemic antifungal therapy was given for a 6-week period and was associated with prolonged antigenemia despite negative findings on follow-up cultures. Antifungal therapy was stopped soon after antigen was no longer detected. Both patients recovered without evidence of further fungal infection. Candida antigen detection may be useful in the diagnosis and follow-up of premature infants with disseminated candidiasis.
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8/8. Bacterial-induced activation of erythrocyte T-antigen complicating necrotising enterocolitis: a case report.

    Erythrocyte Thomsen-Friedenreich crypt antigen (T-antigen) activation is not an uncommon event in infants with severe necrotising enterocolitis (NEC). Transfusion of these infants with blood products containing plasma carries the risk of causing intravascular haemolysis. T-antigen activation is easily detected using a rapid simple lectin agglutination test. Early recognition of T-antigen activation ensures the correct choice of plasma free transfusion therapy. We describe an infant with severe NEC complicated by T-antigen activation and haemolysis.
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