Cases reported "Sepsis"

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1/27. Immune deposit nephritis in infectious mononucleosis.

    A 22-year-old white male (L.V.) died of gram-negative septicemia complicating infectious mononucleosis (IM) that was associated with jaundice and oliguric renal failure. The kidney showed mesangial granular deposits of IgM and C3, mesangial electrondense deposits, and interstitial infiltrates of infiltrates of mononuclear cells, including atypical lymphocytes. Eluates obtained from kidney, spleen and liver contained Paul--Bunnell (PB) antibodies. Presence of PB antigens in these tissues was indicated by absorption of PB antibodies from IM sera, with the sediments resulting from tissue elutions. The IgM mesangial deposits were partially eluted with acid buffer at 56 degrees C and then reconstituted by incubation with IM sera or with immunoglobulins eluted from tissues of patient L.V. The presence in renal structures of PB antigens, IgM heterophile antibody, C3 and electron-dense deposits is consistent with the hypothesis that heterophile immune complexes were localized in the kidney and that they contribute in the pathogenisis of IM nephritis.
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2/27. Fournier's gangrene after unrelated cord blood stem cell transplantation.

    A 16-year-old boy with refractory acute myelogenous leukemia developed Fournier's gangrene as an early complication after two-antigen HLA-mismatched unrelated cord blood stem cell transplantation. On day 25 after the transplantation, he noted abrupt onset of penile swelling with miction pain. The penile inflammation rapidly extended posteriorly to involve the scrotum and perianal tissues, inferiorly to involve the thighs, and superiorly up the lower abdominal region within the next 36 h, and he died from sepsis on day 27. Fournier's gangrene presenting as a genitoperineal necrotizing fasciitis should be considered as a potential complication in umbilical-cord blood recipients in the cytopenic post-transplant phase.
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3/27. arizona hinshawii osteomyelitis with antecedent enteric fever and sepsis. A case report with a review of the literature.

    A case of arizona osteomyelitis of the spine which occurred 11 months after an episode of gastroenteritis and enteric fever is presented. As close biochemical and antigenic relative of salmonella, arizona infection produces a similar clinical course with gastrointestinal manifestations frequently preceding localized infections by several months. The boney lesion in the present case and in three of the four other cases of arizona osteomyelitis described in the literature was a chronic inflammation which may have a xanthomatous component. The bone destruction caused by arizona infection is less severe than that of tuberculosis or pyogenic osteomyelitis. Proposed treatment of arizona osteomyelitis consists of debridement of the localized infection and long term antimicrobial therapy.
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4/27. Unexpected response of hormone-refractory prostate cancer to treatment with an antileukemic chemotherapy regimen.

    Our patient was a 61-year-old man with hormone-refractory prostate cancer and a rapidly rising serum prostate-specific antigen level. During the course of therapy for prostate cancer, abnormal blood counts and subsequent bone marrow biopsy led to a diagnosis of acute lymphoblastic leukemia. He was treated with a chemotherapeutic regimen in standard use for lymphoblastic leukemia, which resulted in an unusual response of his prostate cancer, with declining serum prostate-specific antigen levels that had reached undetectable levels at the time of the patient's death from acute sepsis and leukemic relapse. autopsy showed minimal evidence of prostate cancer, localized to the prostate.
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5/27. purpura fulminans due to staphylococcus aureus.

    BACKGROUND: purpura fulminans is an acute illness commonly associated with meningococcemia or invasive streptococcal disease, and it is typically characterized by disseminated intravascular coagulation (DIC) and purpuric skin lesions. In this article, we report the first 5 cases (to our knowledge) of purpura fulminans directly associated with staphylococcus aureus strains that produce high levels of the superantigens toxic shock syndrome toxin-1 (TSST-1), staphylococcal enterotoxin serotype B (SEB), or staphylococcal enterotoxin serotype C (SEC). methods: Cases were identified in the Minneapolis-St. Paul, minnesota, metropolitan area during 2000-2004. S. aureus infection was diagnosed on the basis of culture results, and susceptibility to methicillin was determined. The ability of the isolated organisms to produce TSST-1, SEB, SEC, and Panton-Valentine leukocidin (PVL) was determined. TSST-1, SEB, and SEC levels were also quantified after in vitro growth of the organisms. RESULTS: In 3 of the 5 cases, the infecting S. aureus strain was isolated from the blood cultures. In 2 of the 5 cases, the infecting S. aureus strain was isolated only from the respiratory tract, indicating that purpura fulminans and toxic shock syndrome resulted from exotoxin and/or other host factors, rather than septicemia. One of these latter 2 patients also had necrotizing pneumonia, and the isolated S. aureus was a methicillin-resistant strain that produced both SEC and PVL. Only 2 of the 5 patients survived, and 1 of the survivors received activated protein c. CONCLUSIONS: Staphylococcal purpura fulminans may be a newly emerging illness associated with superantigen production. Medical practitioners should be aware of this illness.
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6/27. Interest of postmortem-collected specimens in the diagnosis of fulminant meningococcal sepsis.

    We reported the case of a child who died of purpura fulminans. The diagnosis of neisseria meningitidis serogroup C could be assessed using postmortem specimens collected up to 10 h after death. We were able to identify the bacteria by culture and/or PCR on samples without having autopsy performed. Soluble antigens were also detected in serum.
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7/27. Apparent increase in the incidence of invasive group A beta-hemolytic streptococcal disease in children.

    Recently, among adults, an increase in the incidence of invasive disease caused by group A beta-hemolytic streptococci (GABS) has been noted, as has the appearance of a severe illness called "toxic shock-like syndrome," also caused by GABS. We now report an apparent increase beginning in 1987 in the incidence of invasive disease caused by GABS in children. Among these patients the manifestations were varied. One child had signs and symptoms compatible with the streptococcal toxic shock-like syndrome. Among the GABS isolates from our patients, 8 (80%) of 10 evaluated for M-protein antigens were nontypeable. Further studies will be necessary to determine the relationship between serotypes and virulence of GABS. physicians should be aware of the possibility of an increasing incidence of invasive GABS disease in children, as well as its manifestations, which may include toxic shock-like syndrome.
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8/27. Humoral immune response to pneumococcal antigen 23-F in an asplenic patient with recurrent fulminant pneumococcaemia.

    Host defence mechanisms were analysed in a patient with three episodes of fulminant pneumococcaemia and one episode of bacteraemic epiglottitis with haemophilus influenzae type b. The first episode took place 11 years after splenectomy for blunt abdominal trauma. Investigations revealed several host defence mechanisms to be impaired. In addition to the patient's asplenia, an inherited C2-deficiency was noted. Assessment of IgG subclasses repeatedly revealed markedly low IgG4 concentrations. These were not due to an increased turnover of IgG4, as could be shown following infusion of intravenous IgG. In addition, IgG2 concentrations were low in the patient who lacked G2M(23). Opsonic mediating antibodies against type 23-F pneumococci were in the range of those of non-immune volunteers 6 months after vaccination with a 23-valent pneumococcal vaccine. These antibodies did not increase after a septic episode with 23-F capsular-type pneumococci. Neutrophil function was apparently normal.
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9/27. Fatal streptococcus suis septicemia in an abattoir worker.

    A 51-year-old abattoir worker became ill with high fever and was admitted to hospital late in the evening, where he died 4 h later. Smears of peripheral blood taken 7 h after death showed numerous cocci. Cultures of the blood grew beta-hemolytic streptococci exhibiting the biochemical properties of streptococcus suis II. A complete autopsy with extensive microscopical studies showed numerous bacteria in small vessels of several organs, but no bacterial colonisation of tissues, meningitis, or other relevant lesions were found. The group R antigen of the bacteria could be demonstrated by immunofluorescence in paraffin sections of the kidney and the adrenal gland. Two similar cases of fulminant fatal streptococcus suis II septicemia have been reported from denmark. This appears to be the first case observed in the Federal Republic of germany.
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10/27. Complete and partial deficiencies of complement factor d in a Dutch family.

    A young man suffering from recurrent Neisseria infections was shown to lack detectable serum complement factor d hemolytic activity. Addition to the patient's serum of purified factor D to a final concentration of 1 microgram/ml resulted in full restoration of the activity of the alternative pathway. Using an enzyme-linked immunosorbent assay, it was shown that the patient's serum did not contain measurable amounts of factor D antigen either. The sister, the father, as well as the parents of the mother had factor D levels within the normal range, and the factor D level of the mother was decreased. The capacity of the patient's serum, at concentrations up to 5%, to promote phagocytosis of escherichia coli by normal human granulocytes was low when compared to normal serum. Substitution of the patient's serum with purified factor D resulted in a full restoration of opsonic activity. This study describes the first complete deficiency of factor D, and demonstrates its possible relation to recurrent Neisseria infections.
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