Cases reported "Pneumonia, Viral"

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1/13. Familial cases of severe measles pneumonia.

    We report two cases of severe measles pneumonia. Patient 1, a 17-year-old boy who contracted measles in the acute phase of infectious mononucleosis caused by Epstein-Barr virus (EBV), transmitted the disease to patient 2, his father. Both patients presented severe pneumonia with bilateral diffuse micronodular shadows. Diagnoses were established in both patients by antibody titers for measles and reverse transcriptase-polymerase chain reaction (RT-PCR) of blood and throat swab. Multinucleated giant cells with intranuclear inclusion bodies were revealed in the transbronchial lung biopsy (TBLB) specimen of patient 2. Both patients recovered with pulse steroid therapy.
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2/13. Unusual presentation of measles giant cell pneumonia in a patient with acquired immunodeficiency syndrome.

    The typical clinical presentation of measles in a normal immunocompetent host includes cough, coryza, conjunctivitis, Koplik's spots, and rash. However, in an immunocompromised host, measles may have an atypical clinical presentation and may be commonly associated with severe pneumonia or encephalitis. We report a fatal case of measles pneumonia without any clinical features that suggest measles in a patient with acquired immunodeficiency syndrome.
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3/13. Giant cell pneumonia in a leukemic child in remission: a case report.

    Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles, especially in immunocompromised patients, whether their immune systems are affected primarily or whether they have acquired immune defects. As well as being uncommon, it is also atypical because of absence of the characteristic rash and of absent or low antibody titers against measles in most of the cases. It is known that cellular immunity is more important than humoral immunity in the host response to measles, so hypogammaglobulinemic patients with normal cellular immunity usually recover uneventfully from measles and also have the characteristic rash. We report a case with giant cell pneumonia that was confirmed by postmortem histopathological examination. We especially want to point out that even in the absence of rash, with the clinical and radiological features of pneumonia, measles should be considered in a patient, whether in remission or not, receiving immunosuppressive treatment.
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4/13. Human parainfluenza virus giant cell pneumonia following cord blood transplant associated with pulmonary alveolar proteinosis.

    Giant cell pneumonia secondary to human parainfluenza virus 3 has been reported only rarely in immunocompromised hosts. The few cases documented after bone marrow transplant have resulted in significant morbidity and mortality. To our knowledge, this entity has not been described following umbilical cord blood transplant. pulmonary alveolar proteinosis, a rare condition that has been reported with increasing frequency in association with immunocompromise and infections, has not been documented in the setting of either umbilical cord blood transplant or human parainfluenza viral infection. We report what we believe is the first documented case of giant cell pneumonia caused by human parainfluenza virus 3 in an umbilical cord blood transplant recipient. To our knowledge, a unique associated feature of this case, a pulmonary alveolar proteinosis-like reaction, has not been reported previously in association with human parainfluenza virus pneumonia.
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5/13. Patterns of measles pneumonitis.

    As a result of the enlarging pool of unvaccinated children and young adults, there has been an increase in serious measles pneumonitis in our areas. We recently examined autopsy and/or lung biopsy material from five children with fatal measles pneumonitis. Two patients were immunocompromised because of either prematurity or acute leukemia and died 13-16 days following onset of symptoms. Both had classic giant cell pneumonitis, with readily demonstrable intranuclear inclusions. Three other children without known immunocompromise had a more prolonged course. The lungs of these patients lacked the classic pattern and displayed instead a spectrum of less specific findings ranging from organizing diffuse alveolar damage to interstitial pneumonia with giant cells, but without viral inclusions. An accompanying necrotizing bronchiolitis was also present. Electron microscopy and/or detection of elevated measles-specific immunoglobulin M was necessary to confirm the diagnosis in these apparently immunocompetent patients. We conclude that the histologic features of fatal or serious measles pneumonitis are variable and depend to some extent on the immunocompetence of the host as well as the duration and tempo of the disease. Ancillary studies may be necessary to establish the diagnosis in cases lacking classic histopathologic features.
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6/13. ribavirin response in measles pneumonia.

    A 9-year-old boy with Hodgkin's disease developed measles 1 month after completing eight courses of intensive anti-cancer chemotherapy. The atypical nature of the rash and the absence of Koplik's spots indicated a high risk of progression to fatal giant cell pneumonia. Seven days nebulised and intravenous ribavirin therapy produced apparent recovery. Two weeks later the child presented with measles giant cell pneumonia diagnosed on open lung biopsy. ribavirin therapy was again successful. The role of ribavirin in the treatment of measles in immunocompromised children is discussed.
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7/13. Giant cell pneumonia caused by varicella zoster virus in a neonate.

    A premature male neonate, born at the 25th gestational week, developed pneumonia six days after delivery and died. Postmortem examination of the lungs revealed giant cell pneumonia with intranuclear inclusion bodies; varicella zoster infection was confirmed by immunoperoxidase stain using monoclonal antibody to varicella zoster virus and electron microscopic examination. In previously reported necropsy cases of numerous giant-cell formation in the lung is not mentioned. Therefore, the unusual features prompting this report include the absence of skin lesions in this mother and infant and the presence of giant cell pneumonia, not previously reported in varicella zoster infection.
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8/13. Measles pneumonia in childhood leukemia.

    Fatal measles pneumonia developed in a 7-year-old boy who was in complete remission from acute lymphoblastic leukemia. There was no detectable antibody titer in two specimens taken eight days apart. measles virus was grown from a lung biopsy taken shortely after hospital admission. Classical measles had been diagnosed in the patient and his siblings nine months previously. Immunosuppressed children who do not develop an antibody rise after a measles infection are at risk of later development of measles giant cell pneumonia. Suggestions are offered for the prevention of this often fatal complication.
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9/13. 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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10/13. Measles giant cell pneumonia in childhood leukemia in remission.

    A four-year old girl had acute lymphoblastic leukemia in remission with immunosupressive chemotherapy and complicated giant cell pneumonia. Investigations by light and electron microscopy and immunoperoxidase study of autopsy material disclosed measles virus nature of the penumonia, although there was no typical rash of the disease. Similar giant cells were seen in the gastric and colon mucosa, and the other of Warthin-Finkeldey type in the spleen, and lymph nodes of pulmonary hiluses. To the best of our knowledge, this is the first discription of gastric giant cells with inclusion of measles virus.
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