Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are three clinical presentations of anthrax in humans: cutaneous (>95% of cases), orogastric and inhalational. The infectious form, the spore, enters the body and is thought to germinate within macrophages either at the site of inoculation (cutaneous or orogastric) or in the regional lymph node (inhalational). The bacillus then synthesizes its antiphagocytic capsule and the lethal and oedema toxins which interfere with the non-specific host defences leading to the characteristic locally destructive lesion and spread by lymphatics to the systemic circulation and other organs. The cutaneous form begins as a papule which progresses over several days to a vesicle and then ulcerates. There is often oedema, sometimes massive, probably due to the oedema toxin that surrounds the lesions which then develop a characteristic black eschar. The patient may be febrile with mild to severe systemic symptoms of malaise, headache and toxicity. Oropharyngeal anthrax presents with severe sore throat or an ulcer in the oropharyngeal cavity associated with neck swelling, fever, toxicity and dysphagia. Gastrointestinal anthrax begins with anorexia, nausea, vomiting and abdominal pain which may be similar to an acute abdomen. There may be diarrhoea and ascites, both of which may be haemorrhagic. Inhalational anthrax begins with non-specific symptoms of malaise, fever, myalgia and non-productive cough. After a period of 2-3 days, this is followed by a sudden onset of severe respiratory distress associated with diaphoresis, cyanosis and increased chest pain. There may be a widened mediastinum and pleural effusions on chest X-ray. Death follows in 24-36 h from respiratory failure, sepsis and shock. The diagnosis of anthrax is easy if it is considered. The organism is readily observed by Gram or Wright stain in local lesions or blood smear and can be easily cultured from the blood and other body fluids. However, because of its rarity, it is not often included in the differential diagnosis and in inhalational disease the diagnosis is rarely made until the patient is moribund. More rapid diagnostic tests are under development. Penicillin, combined with supportive care, remains the mainstay of treatment, although the organism is susceptible in vitro to many antibiotics. In recent years, there have been significant advances in our knowledge of the organism and its toxins and it is anticipated that similar progress will be made in the future in developing more rapid diagnostic tests and new modalities of treatment.
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PMID:Clinical aspects, diagnosis and treatment of anthrax 1047 74

A 34-year-old woman presented two weeks after a visit to Burma with fever peaking up to 39 degrees C, chills, non-productive cough, headache, muscle pain, shortness of breath and a painful swelling on the left lower leg. She was treated immediately with intravenous amoxycillin-clavulanic acid. The Gram negative causative agent of melioidosis, Burkholderia (previously Pseudomonas) pseudomallei, was cultured from samples taken beforehand. The patient then received ceftazidime. She recovered. In view of the risk of relapse she was treated with amoxycillin-clavulanic acid for a further six months. Melioidosis is endemic in Southeast Asia and Northern Australia. It is rarely seen outside these areas. The clinical spectrum of the disease is wide and varies from fulminating sepsis to a subclinical disease and may affect any organ system, usually the lungs. The mortality of the septicaemic form after adequate treatment is 40%. Surviving patients have a high relapse rate (4-20%). Melioidosis can become chronic with formation of abscesses or can remain subclinical for many years, probably because the microorganism can survive within phagocytic cells with a risk of reactivation at moments of immunosuppression. The optimal treatment consists of ceftazidime intravenously for at least two weeks followed by an eradication phase consisting of oral antibiotics for at least 3 months.
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PMID:[Melioidosis]. 1198 Mar 74

Background. Group A streptococcal (GAS) meningitis is rarely seen in the antenatal period, but it is associated with significant mortality. We present a case of a mid-trimester woman who developed fulminant meningitis following a rapid onset atypical presentation of infection with this organism. Case. A multiparous 23(+5)-week woman presented with a 10-day history of a non-productive cough associated with pyrexia. Within minutes of her admission she collapsed and lost consciousness; sepsis was suspected and cross-specialty care was initiated. She was managed empirically in extremis with broad-spectrum antibiotics and mannitol with 3% hypertonic saline for suspected infection and raised intracranial pressure, respectively. Despite intensivist management, a CT head revealed diffuse oedema with coning of the cerebellar tonsils. Brainstem death was certified within 19 hours of admission and fetal death ensued. Postmortem bacteriology confirmed GAS meningitis. Conclusion. Through raising awareness of this patient and her disease course, we hope that future policy decisions, primary care, and hospital level management will be informed accordingly for treatment of pregnant women with suspected GAS infection.
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PMID:Maternal and Fetal Death following Group A Streptococcal Meningitis in Mid-Term Pregnancy. 2488 15