Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxic shock syndrome, caused by an exotoxin of staphylococcus aureus is very rare in children. On admission, beside the shock, abdominal problems as vomiting, diarrhoea and a developing adynamic ileus were outstanding in our patient. Not before additional symptoms as staphylococcal pneumonia with bacteriemia occurred and later desquamation of palms and feet, diagnosis of toxic shock syndrome could be confirmed.
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PMID:[Toxic shock syndrome in a 6-year-old male]. 207 65

Toxic shock syndrome is uncommon in the prepubertal age group. Two children presented with pyrexia, macular erythroderma, vomiting, hypotension and rapid deterioration of consciousness. One child had severe neurological involvement. The diagnosis of toxic shock syndrome was established in both cases by the exclusion of other causes and by culturing staphylococcus aureus. We postulate that the neurological manifestations were caused by a direct neurotoxic action of the staphylococcal-produced toxin. Both children made a complete recovery.
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PMID:Toxic shock syndrome (TSS) in children. 356 76

Tumoricidal responses and tumor regressions have been observed after plasma perfusion over Staphylococcus aureus Cowan I (SAC), or purified protein A immobilized on solid supports. This system was initially studied in a single human patient and then extended to dogs with spontaneous mammary carcinoma, an excellent model of human breast cancer. In the single patient and dogs with mammary tumors, perfusion of plasma over protein A bearing staphylococcus resulted in tumor necrosis and tumor regression. Tumor reduction or growth retardation with similar perfusion systems has been noted in various feline and rodent tumor models. Tumoricidal responses were also observed in canine tumors after perfusion over commercial protein A which was immobilized in a collodion charcoal matrix (PACC). These responses were amplified when a subtherapeutic and nontoxic dose of cytarabine was given after perfusion. Similar tumor reduction in murine and feline tumor models has been noted after perfusion of autologous serum over protein A immobilized on various other solid supports. The PACC perfusion system was extended to five consecutive patients with advanced breast adenocarcinoma. Four of five patients showed tumor regression after perfusion of small volumes of autologous or homologous plasma over PACC. Patients also experienced pyrexia, nausea, vomiting, and significant cardiopulmonary toxicity. Detailed hemodynamic studies of these effects showed that the major pathophysiology involved a decline in total peripheral resistance associated with an increase in cardiac output. With reduction of immobilized protein A quantity and diminution in plasma perfusion rate, the cardiopulmonary toxicity associated with treatments was diminished. Chemotherapy given as FAC to a single patient shortly after concluding perfusion therapy resulted in rapid regression of residual large tumor masses. Studies focusing on the mechanism of the tumoricidal responses have examined changes in sera after incubation or perfusion over immobilized SAC or PACC. Major findings include (1) the identification of protein A leaching from PACC and SAC after serum perfusion and appearing in the effluent as Clq binding oligomers composed predominantly of IgG and protein A but also containing IgA, IgM and C3 with a molecular weight range of 600,000 to 2,000,000; (2) the identification of C3a anaphylatoxins in serum perfused over PACC or SAC; (3) the recognition that several enterotoxins, in particular enterotoxin B are present in commercial protein A preparation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Protein A and staphylococcal products in neoplastic disease. 390 35

Thirty-one children with primary peritonitis were studied. Most of them had been healthy prior to the onset of peritonitis and only one had nephrotic syndrome. There were 27 girls and four boys. The predominant organism in girls was pneumococcus, and in boys staphylococcus. The causative organisms, identified in 27 children, were all Gram positive. Most of the children were between four and 10 years of age. The onset of their illness was sudden with fever, vomiting and abdominal pain. Since in recent years, primary pneumococcal peritonitis has been the commonest type of peritonitis in young girls, our earlier policy of routine laparotomy for peritonitis was given up and in girls aged between four and ten, an attempt at initial pre-operative diagnosis was made by Gram's staining of peritoneal aspirate or vaginal swab. If Gram positive peritonitis was diagnosed, early cases were treated with antibiotics alone and late cases with antibiotics and minilaparotomy for drainage of pus. There was one death. Morbidity and mortality were higher when the period without treatment exceeded one week. The contribution of pre-operative diagnosis by Gram's staining to the provision of optimum treatment is emphasized.
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PMID:Primary peritonitis in children. 619 8

The toxic shock syndrome in a 14-year old girl is described. This syndrome occurs most frequently - but not exclusively - in the teens and young women during the first days of menstruation, if tampons are used. The patients are acutely ill with high fever, diarrhea and/or vomiting, with a rash, with loss of consciousness, and signs of shock (occasionally shock lung syndrome and renal insufficiency). During convalescence desquamation of hands and feet shows up. Patients with much less severe symptoms have been seen. The primary lesion is a local infection (e.g. vaginitis) with staphylococcus aureus, the symptoms being caused by staphylococcal toxins. Early recognition and immediate therapy are important for a better prognosis. The therapy consists of removal of the tampon, i.v. fluids including albumin, and the administration of a beta-lactamase-resistant antibiotic.
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PMID:[Toxic shock syndrome in a 14-year-old girl]. 672 95

The toxic-shock syndrome (TSS) is a recently recognized syndrome characterized by sudden onset of high fever, vomiting, and diarrhea with rapid progression to hypotension and shock. It is caused by one or more not yet clearly defined exotoxins from staphylococcus aureus. The disease primarily affects young women using tampons during their menstrual periods, although it occurs also in non-menstruating women and in men. In these cases extragenital staphylococcus aureus infections are found. Since 1981 the toxic-shock syndrome associated with menstruation has occurred less frequently, whereas the non-menses-related toxic-shock syndrome appears with similar frequency. The syndrome resembles Kawasaki disease (mucocutaneous lymph node syndrome) in several aspects, namely fever, rash with subsequent desquamation, and cardiovascular involvement. However, shock, which is prominent in toxic-shock syndrome, is not usually seen in Kawasaki disease.
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PMID:[Toxic shock syndrome]. 684 Oct 81

Staphylococcus aureus and Streptococcus pyogenes produce a lot of toxins, some of them responsible for specific diseases. Staphylococcal food poisoning is due to ingestion of enterotoxin containing food. Seven toxins have been isolated so far. Generalized exfoliative syndrome is related to exfoliatin. Young children are particularly affected. The disease consists in a cutaneous exfoliation usually limited with a favourable outcome. The mucus membranes are not involved. The nose or pharynx are the most usual portal of entry. Staphylococcus aureus is not grown from the bullae. Severe extensive forms have been observed particularly in neonates (Ritter's disease). Bullous impetigo is also due to exfoliatin. It consists in the presence of a restricted number of cloudy bullae, from which staphylococcus can be grown. It is a mild disease with a favourable outcome within a few days. Scarlet fever is related to the streptococcal erythrogenic toxins. The classic form of the disease is presently rare. This disease may be related to staphylococcus as a complication of arthritis, osteomyelitis or wound super-infection. Bacteremia is usual. Staphylococcal scarlet fever is not related to exfoliatin as previously believed, but to enterotoxins or TSST-1, so it seems to be an abortive form of toxic shock syndrome. Toxic shock syndrome is defined as a multi organ failure syndrome with a rapid onset, fever, rash followed by desquamation, vomiting and diarrhea, hypotension, conjunctivitis and strawberry tongue. The disease is related to an infection or colonisation with a toxin (TSST-1) producing strain of Staphylococcus aureus. Enterotoxins (mainly C) may be involved. The disease may occur in childhood, sometimes after superinfection of varicella. The mortality is low (5%) and mainly due to ARDS or cardiac problems. Erythrogenic toxins produced by Streptococcus pyogenes are involved in a streptococcal form of toxic shock syndrome with a quite similar presentation. In most cases however, a cutaneous or soft tissue infection is at the origin. Necrotizing fasciitis complicating varicella is a classic cause in children. Bacteremia is often observed. The mortality rate is as high as 60%. The streptococcal strains involved in north america use to produce the toxin erythrogenic A, the european cases seem to be more related to strains secreting the B toxin with a dysregulation of the mechanisms which control the secretion of the toxin. Staphylococcus strains producing the Panton and Valentine leucocidin are responsible for chronic or relapsing furonculosis and above all for a very severe necrotizing pneumonia observed in children and young adults presenting as an acute respiratory distress syndrome with leucopenia, hemoptysis and shock carrying a heavy mortality rate. Besides these specific diseases, staphylococcal and streptococcal toxins may be involved in some syndromes of unknown origin, in which the intervention of superantigens seems very likely. Kawasaki syndrome is among them as strains producing staphylococcal and streptococcal toxins have been grown from patients with Kawasaki syndrome. In the same way, the intervention of toxins is suspected in the determination of sudden infant death syndrome and atopic eczema.
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PMID:[Clinical aspects of streptococcal and staphylococcal toxinic diseases]. 1158 25

Toxic-shock-syndrome (TSS) is an acute febrile, exanthematous illness caused by toxins such as toxic-shock-syndrome-toxine-1 (TSST-1) and other endotoxines from staphylococcus aureus with an incidence of 0,5 per 100.000 inhabitants. Patients with menstrual toxic-shock-syndrome (menstrual-TSS) usually have TSS associated with menstruation and use of a vaginal device such as tampons. Other patients with non-menstrual toxic-shock-syndrome (non-menstrual-TSS) have a focus of staphylococcal infection such as a surgical wound infection or soft tissue abscess. TSS usually presents with fever, pharyngitis, diarrhoea, vomiting, myalgia and may progress rapidly (within hours) to signs of hypovolaemic hypotension and shock. In some cases TSS is associated with multisystem failure including shock, renal failure, myocardial failure and adult respiratory distress syndrome. In its acute phase the diagnosis of TSS is often uncertain because of its initial symptoms are non-specific and numerous conditions need to be considered in the differential diagnosis. But obviously less incidence, the signs and symptoms of toxic-shock-syndrome should be recognised early to permit successful therapy. The site of infection should be adequately drained and treated with antimicrobial therapy. Possible complications including ARDS and myocardial failure require a thorough understanding of its underlying pathophysiology to ensure appropriate intensive-care treatment. Only if appropriate therapy is instituted as early as possible, most of patients will be able to survive their toxic-shock-syndrome. In other cases TSS can be a rapidly progressive and perhaps lethal ending disease because of possible multiple organe failure such as ARDS.
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PMID:[Special features of intensive care of toxic shock syndrome. Review and case report of a TSST-1 associated toxic-shock syndrome with adult respiratory distress syndrome and multiple organ failure from a staphylococcal panaritium]. 1450 8

The paper presents the case of a 4-year-old child who was admitted with the diagnosis Dg: Pleuropneumonia lat. sin, while in the further course as a suspicion due to progressive flow as staphylococcus pneumonia. The illness is complex in terms of treatment. The diagnosis was set based on the history of illness, its clinical course, laboratory findings, radiology tests. The boy was hospitalized in January in current year with symptoms (coughing, vomiting and fever) that have been lingering for the past two days. The boy has been treated with a ternary antibiotic therapy (cephalosporin of third generation parenterally with aminoglycosides, plus anti-staphylococcus therapy). In laboratory findings Sedimentation rate increased 88/134 WBC 75 thousands. Radiologically extended pleuropneumonia on the left side. In sputum staphylococcus aureus was isolated. In the further course of hospitalization, due to the development of progressive form of staphylococcus pneumoniae with a fever of up to 39 degrees, pale aspect and dyspnoic patient with anemia and with complications in the form of cysts, ruptures and pneumothorax, with a thoracic drainage performed. In the further course, the cysts were gradually absorbed, while the thoracic drain was grafted. Clinically, the child was looking better. We continued the anti-staphylococcus therapy (stanicide), to which the child reacted well clinically and radiologically. Auscultatory breathing on the left side was audible. The last follow-up and the last rtg pulmo et cor 6 months after the outbreak of illness with a complete regression of the foregoing changes.
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PMID:[Staphylococcus pneumonia--complications]. 1758 82

Infectious aneurysms constitute 4% of all intracranial aneurysms. The microorganisms responsible are most commonly streptococcus viridans, staphylococcus aureus and combined bacterial infections. Nonetheless, cases with no reproduction in their cultures are rather frequent. A 6-year-old patient admitted with complaints of sudden headache, nausea, vomiting and high temperature. Intracerebral hematoma and saccular aneurysm located at the distal posterior cerebral artery were diagnosed as a result of the laboratory investigations and neuroradiological examinations. Infectious aneurysm was considered due to the clinical findings, morphology and location of the aneurysm. Although the causative microorganism was detected in blood culture, no focus could be detected. The aneurysm was hindered by endovascular intervention. In this manuscript, we discuss the infrequently seen childhood infectious aneurysm in the light of the pertinent literature.
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PMID:Endovascular treatment of primary infectious aneurysm in childhood: a case report. 1838 78


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