Cases reported "Meningococcal Infections"

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1/6. meningococcal infections and meningitis: what is new?

    Meningococcal infection is one of the very few severe bacterial infections, in this era, that still can kill a relatively healthy child within minutes. Fortunately, it is a relatively rare disease. Rural practitioners may see one affected child once every 2-3 years, but once seen they will never forget it. The present article gives some examples of case scenarios along with a brief overview of the problem, with emphasis on early diagnosis, prevention and possible future developments.
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2/6. Invasive meningococcal disease presenting as Henoch-Schonlein purpura.

    Henoch-Schonlein purpura (HSP) is an acute systemic form of vasculitis that has been associated with a number of viral and bacterial infections. Described here are the cases of two children with invasive meningococcal disease who presented with clinical and laboratory findings typical of HSP. Meningococcal infection may have been the trigger for the manifestation of HSP in these patients.
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3/6. Selective C7 complement deficiency causing recurrent meningococcal infection.

    We report on two sisters both with complete absence of the 7th component of complement. This congenital immunodeficiency disorder is associated with recurrent bacterial infection, especially that due to Neisseria species. These cases illustrate many of the well-recognised features of this disorder, but in one patient the illness was complicated by infective endocarditis due to N. meningitidis, a feature not previously reported.
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4/6. Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells.

    The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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5/6. The hemorrhagic fevers of Southern africa with special reference to studies in the South African Institute for Medical research.

    In this review of studies on the hemorrhagic fevers of Southern africa carried out in the South African Institute for Medical research, attention has been called to occurrence of meningococcal septicemia in recruits to the mining industry and South African Army, to cases of staphylococcal and streptococcal septicemia with hemorrhagic manifestations, and to the occurrence of plague which, in its septicemic form, may cause a hemorrhagic state. "Onyalai," a bleeding disease in tropical africa, often fatal, was related to profound thrombocytopenia possibly following administration of toxic witch doctor medicine. Spirochetal diseases, and rickettsial diseases in their severe forms, are often manifested with hemorrhagic complications. Of enterovirus infections, Coxsackie B viruses occasionally caused severe hepatitis associated with bleeding, especially in newborn babies. Cases of hemorrhagic fever presenting in February-March, 1975 are described. The first outbreak was due to marburg virus disease and the second, which included seven fatal cases, was caused by rift valley fever virus. In recent cases of hemorrhagic fever a variety of infective organisms have been incriminated including bacterial infections, rickettsial diseases, and virus diseases, including Herpesvirus hominis; in one patient, the hemorrhagic state was related to rubella. A boy who died in a hemorrhagic state was found to have congo fever; another patient who died of severe bleeding from the lungs was infected with leptospira canicola, and two patients who developed a hemorrhagic state after a safari trip in Northern botswana were infected with trypanosoma rhodesiense. An illness manifested by high fever and melena developed in a young man after a visit to zimbabwe; the patient was found to have both malaria and marburg virus disease.
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6/6. properdin deficiency in a family with fulminant meningococcal infections.

    Three males in a large family showed a selective deficiency of properdin (P). One of the P deficient individuals died from a fulminant infection with neisseria meningitidis group C. The family history revealed three previous cases of similar infections with a fatal outcome. The deficiency did not appear to be associated with repeated bacterial infections. The pattern of inheritance suggested an X-linked mode of transmittance. However, heterozygous carriers were not clearly distinguished in the family. P deficient serum supported immune haemolysis in a normal fashion. Alternative pathway functions, such as the activation of C3 by inulin or zymosan, lysis of guinea-pig erythrocytes in agarose gel and opsonization of endotoxin coated oil particles, were grossly impaired in P deficient serum while efficient C3 activation was produced by addition of cobra venom factor.
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keywords = bacterial infection
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