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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper discusses the epidemiological and some clinical characteristics of 61 patients who were diagnosed as having anthrax at the Department of Infectious Diseases, University Hospital Split in the period from January 1, 1956, to December 31, 1987. The pathogenesis of the disease is also reviewed. Clinical diagnosis was confirmed in 36 (59.02%) patients, 32 (52.46%) were diagnosed by microscopic examination of Gram's stained smears and 4 (6.56%) patients by cutaneous lesion fluid culture. In 54 (88.52%) patients the disease presented as a malignant pustule and in 7 (11.48%) as a malignant edema. Only 3 patients had clinical signs of septicemia, but the diagnosis was not confirmed by positive blood cultures in none of these patients. The subjects contracted the infection either by a direct contact with a diseased animal or indirectly by contaminated products of animal origin or by hematophagic insects in approximate ratio 8:2:1. No mode of infection was identified in 27 (44.26%) patients. The male/female and professional/nonprofessional anthrax ratio was 1:1. The majority of children were in the 0-9-year and 30-39-year age groups. Most of the patients were treated with penicillin, and the others with tetracyclines or a combination of antibiotics. Serum was applied in 29 (47.54%) patients. Only one patient died (1.64%). Three different modes of infection are described in the last four treated patients.
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PMID:[Epidemiologic and clinical characteristics of anthrax in patients at the University Hospital in Split 1956-1987]. 823 17

73 cases of anthrax were recorded by the Health Office in the Sivas region in the last 4 years. This paper presents a rare and severe clinical form of anthrax displaying diagnostic difficulties. Six women aged between 16-46 were diagnosed as having throat anthrax and treated in the Infectious Diseases Department of Cumhuriyet University. The lesions were localized on the tonsils in 5 cases and on the base of the tongue in 1 case. The main clinical features were sore throat, dysphagia, fever, regional lymphadenopathy on the neck and toxemia. Three patients died with toxemia and sepsis. The diagnosis was confirmed by the isolation of Bacillus anthracis.
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PMID:Primary throat anthrax. A report of six cases. 377 69

Of 35 cases diagnosed as anthrax during 1.9.1981 - 1.12.1982, 18 were females (51,4%) and 17 were males (48,6%), the mean age was 39,7. All of the women were housewives, 14 male patients were farmers, 1 was a tradesman, 1 a worker, and 1 a butcher. It was localised on the skin in 31 cases (88,6%) and in the throat in 4 cases (11,4%). Penicillin was used for treatment. In one of the cases with throat localisation, sepsis developed, leading to death.
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PMID:[A review of 35 anthrax cases]. 688 96

From May 21 to June 4, 1993, a collaborative training project involving U.S. Army veterinary personnel, the Lao-American Integrated Rural Development Project, and the Lao Department of Livestock and Veterinary Services occurred in the Houa Muang District of Houa Phan Province in northeastern Laos. The project focus was control of the major animal diseases of economic or public health importance in the area to include, but not limited to, hemorrhagic septicemia, anthrax, swine fever (hog cholera), and Newcastle disease. The project provided Lao veterinary personnel and villagers with didactic training and field demonstrations in disease control practices. Supplies and equipment necessary to continue disease control activities were provided to the district at the conclusion of the training and field demonstrations. The project was designed to be compatible with disease reporting and surveillance systems at district, province, and national levels and be exportable to other districts and provinces. In addition to disease-control efforts, blood and fecal parasite surveys were conducted.
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PMID:Lao People's Democratic Republic Veterinary Public Health Project. 787 Mar 20

Hemorrhagic lymphadenitis of the intrathoracic lymph nodes and mediastinitis are shown to be the primary septical focus, this indicating an inhalation route of the contamination with development of pulmonary anthrax. The alterations in the gastrointestinal tract and central nervous system are considered to be secondary resulting from lymphohematogenic generalization of the anthraxic sepsis. The attention is drawn to the morphological signs of the immunodepression and the inhibition of granulocytic reaction. It is noted that the epidemic outburst of the pulmonary anthrax is without analogs and its development may be the result only of a massive penetration of bacteria into the atmosphere.
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PMID:[Pathology of anthrax sepsis according to materials of the infectious outbreak in 1979 in Sverdlovsk (various aspects of morpho-, patho- and thanatogenesis)]. 798 34

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

Anthrax is caused by Bacillus anthracis, a gram-positive spore-forming bacterium. Septicemia and toxemia rapidly lead to death in infected mammal hosts. Currently used acellular vaccines against anthrax consist of protective antigen (PA), one of the anthrax toxin components. However, in experimental animals such vaccines are less protective than live attenuated strains. Here we demonstrate that the addition of formaldehyde-inactivated spores (FIS) of B. anthracis to PA elicits total protection against challenge with virulent B. anthracis strains in mice and guinea pigs. The toxin-neutralizing activities of sera from mice immunized with PA alone or PA plus FIS were similar, suggesting that the protection conferred by PA plus FIS was not only a consequence of the humoral response to PA. A PA-deficient challenge strain was constructed, and its virulence was due solely to its multiplication. Immunization with FIS alone was sufficient to protect mice partially, and guinea pigs totally, against infection with this strain. This suggests that spore antigens contribute to protection. Guinea pigs and mice had very different susceptibilities to infection with the nontoxigenic strain, highlighting the importance of verifying the pertinence of animal models for evaluating anthrax vaccines.
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PMID:Anthrax spores make an essential contribution to vaccine efficacy. 1179 96

The authors explain the anthrax pathogeny as necessary base to treat the systemic anthrax, that it can be secondary to a terrorist aggression, that until now it causes death to damaged people. For fear that a contamination with anthracis spores by a terrorist aggression, it is imposed to administrate chymeprotection to damaged people, because once it is appeared the symptoms of the systemic illness, the antibiotics don't stop the process evolution. For that reason, we think it is important to know the process pathogeny, where it can be found the keys for effective treatment of carbuncle sepsis.
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PMID:[Carbuncle (anthrax) as biological weapon]. 1205 61

Anthrax is a severe bacterial infection that occurs when Bacillus anthracis spores gain access into the body and germinate in macrophages, causing septicemia and toxemia. Anthrax toxin is a binary A-B toxin composed of protective antigen (PA), lethal factor (LF), and edema factor (EF). PA mediates the entry of either LF or EF into the cytosol of host cells. LF is a zinc metalloprotease that inactivates mitogen-activated protein kinase kinase inducing cell death, and EF is an adenylyl cyclase impairing host defences. Inhibitors targeting different steps of toxin activity have recently been developed. Anthrax toxin has also been exploited as a therapeutic agent against cancer.
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PMID:Anthrax toxin: a tripartite lethal combination. 1243 80

The pathogenesis of acute respiratory melioidosis mice and hamsters is described. Inhaled organisms giving rise to lesions seemed to be first engulfed by the mononuclear alveolar phagocytes, but in less than 1 day polymorphonuclear cells made their appearance. In spite of this defense reaction, the bacteria continued to multiply and their products caused focal necrosis. These foci enlarged and gave rise to septicemia, toxemia, and eventually death, which usually occurred in 3 to 10 days depending on the dose. Melioidosis, is, therefore, an acute septicotoxemic disease resembling plague and anthrax in this respect. In hamsters the disease process developed more rapidly than in mice and death occurred sooner. The course of the disease in hamsters was sometimes complicated by intraglomerular deposits resembling "fibrinoid," which were similar to those of the generalized Shwartzman phenomenon. This phenomenon may have been an indirect cause of both the perifocal hemorrhage and the extremely large number of bacteria in some of the hamster lesions. When low infecting doses of organisms were employed, mice, but not hamsters, developed a chronic type of disease, lasting 2 to 8 weeks. This was characterized by large abscesses in the spleen or lung, marked proliferation of mononuclear phagocytes and plasma cells, and increased immunity against reinfection (about 40-fold against respiratory challenge). When mice and hamsters inhaled high infecting doses of organisms, a peracute disease resulted with death in 1 to 3 days. Increased numbers of bacteria were observed in the lesions, and the histological changes in the spleen resembled those following the intravenous injection of Malleomyces pseudomallei toxin or the intramuscular injection of large doses of cortisone. These changes were characterized by a swelling of the phagocytes of the white pulp with nuclear debris. The peracute, the acute, and the chronic forms of melioidosis in mice are similar to analogous clinical forms found in man.
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PMID:Melioidosis: pathogenesis and immunity in mice and hamsters. I. Studies with virulent strains of Malleomyces pseudomallei. 1348 Dec 62


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