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)

A 76-year-old white male presented with progressive malaise, weight loss and dyspnea at rest. Echocardiography revealed a circular pericardial effusion and global hypokinesia. Pericardiocentesis showed a purulent exudate and microbiologic examination revealed Mycobacterium bovis fully sensitive to isoniazid, streptomycin, ethambutol, rifampin, and pyrazinamide. By spoligotyping the isolate could be further differentiated to M. bovis ssp. caprae. Antimycobacterial therapy was initiated but 3 weeks later the patient's circulation and renal function deteriorated and he died with clinical signs of sepsis despite intensive care treatment. Pericarditis is a rare manifestation of tuberculosis and can be fatal even when diagnosed and treated appropriately. In low incidence countries diagnosis is often delayed and even overlooked.
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PMID:Pericarditis as primary manifestation of Mycobacterium bovis SSP. caprae infection. 1452 18

A nontuberculous Mycobacterium ulcerans-like organism was identified as the causative agent of an epizootic of mycobacteriosis in a colony of African tropical clawed frogs, Xenopus (Silurana) tropicalis, at the University of California, Berkeley. Diverse clinical signs of disease were observed, including lethargy, excess buoyancy, coelomic effusion, cutaneous ulcers, and granulomas. Visceral granulomas, ulcerative and granulomatous dermatitis, coelomitis, and septicemia were common findings at necropsy. Identification of M. ulcerans-like organisms was based on molecular and phenotypical characteristics. The findings of this investigation indicate that this M. ulcerans-like organism is a primary cause of morbidity and mortality in aquatic anurans and should be considered in the differential diagnosis of coelomic effusion in amphibians. Furthermore, if this Mycobacterium species ultimately is identified as M. ulcerans, X. tropicalis should be considered a potential source of this important public health pathogen.
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PMID:Characterization of a Mycobacterium ulcerans-like infection in a colony of African tropical clawed frogs (Xenopus tropicalis). 1525 78

Late-onset sepsis (after 3 days of life) is a frequent a complication found in very low birth weight (VLBW, 1000 to 1500 g) premature infants. We report the second case of late-onset sepsis caused by an uncommon pathogen, Mycobacterium abscessus.
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PMID:Late-onset Mycobacterium abscessus sepsis in a very low birthweight premature infant: diagnostic and therapeutic challenges. 1531 74

Streptococcus (S.) suis and Mycobacterium avium ssp. paratuberculosis (MAP) differ substantially in their host specificity and tissue tropism. S. suis is a facultative pathogen in swine, which mainly colonises the upper respiratory tract and can cause meningitis, septicemia, arthritis and pneumonia. In contrast, MAP is an obligatory pathogen causing paratuberculosis in ruminants, and shows high tropism for the intestinal tract. Both pathogens are able to invade and persist in host cells. In S. suis, the significance of invasion for pathogenesis is a matter of controversial discussions. In vitro it has been shown that S. suis is internalized by epithelial cells and survives intracellularly for at least 24 h. However, at present there is no evidence that S. suis invades epithelial cells also in vivo. In MAP, on the other hand, persistence in macrophages is generally considered a crucial step in pathogenesis, but it remains to be elucidated, how it contributes to pathophysiology of the disease. The two pathogens exemplify how intracellular invasion and persistence might play different roles in pathogenesis. In S. suis, intracellular life may represent only a transient retreat phase, whereas in MAP it is the predominant in vivo niche of the pathogen.
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PMID:Intracellular invasion and persistence: survival strategies of Streptococcus suis and Mycobacterium avium ssp. paratuberculosis. 1558 27

The postmortem records of 160 white-tailed deer (Odocoileus virginianus) submitted for necropsy examination from 59 separate Pennsylvania captive deer farms over a 3.5-year period were reviewed to determine the primary cause of death of each animal. The most common causes of death were bronchopneumonia (39 cases), enterocolitis (30 cases), malnutrition (13 cases), and trauma (11 cases). Other causes of mortality included severe gastrointestinal parasitism (6 cases), cellulitis with septicemia (5 cases), degenerative myopathy (4 cases), ruminal acidosis (4 cases), and nephritis (4 cases). The cause of death was undetermined in 13 of the 160 animals. Arcanobacterium pyogenes (19 cases), Fusobacterium necrophorum (10 cases), Escherichia coli (7 cases), and Mannheimia haemolytica (4 cases) were the most commonly isolated bacteria from the pneumonic lungs. Bacterial agents associated with enterocolitis included Clostridium perfringens (15 cases), E. coli (12 cases), and Mycobacterium avium subsp. paratuberculosis (2 cases). The majority (52.2%) of the death loss in white-tailed deer of known ages occurred in animals 1 year of age or less, with 46.2% of the bronchopneumonia cases and 50.0% of the enterocolitis cases occurring during this time period. Cases of degenerative myopathy, myocardial degeneration, hepatic necrosis, meningoencephalitis, peritonitis, and urolithiasis considered severe enough to be the primary cause of death appeared early in life, affecting deer 6 months of age or less in all cases. In conclusion, bronchopneumonia, enterocolitis, malnutrition, and trauma were considered the most common causes of death in confined white-tailed deer in this study.
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PMID:A retrospective study of mortality in Pennsylvania captive white-tailed deer (Odocoileus virginianus): 20000--2003. 1558 66

The Infectious Disease Control Act enacted in Germany in 1.1.2001 led to a duty of notification also for institutes of pathologic-anatomical diagnostics. All reports within 45 months after enacting concerning diseases and agents being subject to registration were evaluated. Among the notifiable diseases with fatal outcome ( section sign 6) belonged 3 cases of Meningococcus sepsis, 13 of tuberculosis und 5 cases of Creutzfeldt-Jacob disease. During lifetime 54% of tuberculosis cases remained undetected. Notifiable agents ( section sign 7.1) concerned 92 times Mycobacterium-tuberculosis-complex, twice Influenza Virus and one case of Cryptosporidiosis and Giardia lamblia each. Six Echinococcus granulosus cysts were reported ( section sign 7.2). Notification needs exact diagnosis of infectious diseases and agents being subject of registration. By this pathologists participate in the control of infectious diseases.
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PMID:[The duty of notification for pathologists according to the infectious disease control act. Tuberculosis as dominating disease]. 1576 98

We looked at mycobacterial infections occurring after a kidney transplant to determine incidence, risk factors, and outcomes. Of 3921 kidney transplants performed between 1984 and 2002, 18 (0.45%) (10 men, eight women; 11 cadaveric donor, seven living donor graft) were identified as having mycobacterial infection at some time posttransplant. Mean age at transplant was 38.3 years. Racial background was: Caucasian (n = 12), African-American (n = 2), Native Indian (n = 2), Hispanic (n = 1), and Middle Eastern (n = 1). The majority had a kidney alone (n = 14). Four recipients had simultaneous transplant of a second organ: pancreas (n = 2), islets (n = 1), and liver (n = 1). None of the 18 recipients had documented mycobacterial infection pretransplant. One recipient had a positive Mantoux test at the time of transplant and then developed pulmonary tuberculosis 4 months posttransplant; the remaining 17 patients had either negative (n = 10) or unavailable (n = 7) pretransplant Mantoux results. Mean time to infection was 3.2 years (range 1 week to 12 years). The most common site of infection was respiratory (n = 8). Other sites included musculoskeletal (n = 4), skin (n = 3), gyn (n = 1), and other (n = 2). Only three of the infections were with mycobacterial tuberculi; the others were with avium (n = 5), chelonae (n = 2), or other nontuberculous mycobacteria. Risk factors included previous TB exposure, occupational exposure, or accidental soft tissue injury. Soft tissue infections often presented as chronic unhealed wounds and required extensive surgical debridements. With mean follow-up of 12.5 years since transplant and 9.2 years since infection, 13 of the recipients are alive and well; causes of death included cardiovascular (n = 3) and sepsis (n = 2).
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PMID:Mycobacterial infections after kidney transplant. 1584 80

Toll-like receptor 2 (TLR2) is a member of the TLR family, which plays a central role in the innate immune response to a wide variety of microorganisms. Animal studies have shown that TLR2-knockout mice are more susceptible to septicemia due to Staphylococcus aureus and Listeria monocytogenes, meningitis due to Streptococcus pneumoniae, and infection with Mycobacterium tuberculosis, suggesting that functional TLR2 polymorphisms may impair host response to a certain spectrum of microbial pathogens. In humans, 2 polymorphisms in the exon part of TLR2, which attenuate receptor signaling, enhance the risk of acute severe infections, tuberculosis, and leprosy. Because gram-positive bacteria have became the first cause of severe infections, including septic shock, knowledge of the role that alteration or lack of TLR2 function plays in the pathogenesis of infectious diseases could contribute to the design of new therapeutic strategies, including prevention, pharmacological intervention, and vaccine development.
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PMID:The importance of Toll-like receptor 2 polymorphisms in severe infections. 1623 39

Even in developed countries, tuberculosis still contributes significantly to morbidity and mortality. The most frequent causative agent is Mycobacterium tuberculosis, while infections due to other mycobacterial species are usually associated with immunocompromised patients. In the following, we describe the case of a previously healthy man who underwent laparotomy for suspected adrenal carcinoma. Peritoneal "cancerous nodules" turned out to be tuberculous granulomas. After surgery the patient developed a protracted septic shock and died 6 days after surgery. Isolation and identification of the causative agent yielded Mycobacterium microti, an uncommon species of the M. tuberculosis complex. No other pathogen could be isolated during the clinical course, which finally led to the diagnosis of Landouzy septicemia (sepsis tuberculosa acutissima).
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PMID:Landouzy septicemia (sepsis tuberculosa acutissima) due to Mycobacterium microti in an immunocompetent man. 1625 76

Tumor necrosis factor (TNFalpha), a cardinal early mediator of the innate host inflammatory response, has been an attractive target for therapeutic intervention in human sepsis. However, pooled data from 12 completed randomized controlled trials show only a very modest impact on mortality in a highly heterogeneous population of patients. To gain insight into the preclinical in vivo biology of TNFalpha that might aid in better identifying appropriate patient populations for therapeutic intervention, we undertook a systematic review of published reports of preclinical studies assessing the consequences of neutralization of TNFalpha in models of acute infection or inflammation. We identified 143 reports incorporating 484 unique experimental comparisons in seven different animal species. The effects of neutralization of TNFalpha in these were quite variable. Neutralization of TNFalpha was beneficial in endotoxemia, or after systemic challenge with gram-negative organisms, Staphylococcus aureus, or Group B streptococci. On the other hand, neutralization was detrimental in infections caused by Streptococcus pneumoniae, Candida spp., or intracellular pathogens such as Listeria and Mycobacterium tuberculosis, and in models of pneumonia. Treatment was more efficacious when delivered before infectious challenge, and the therapeutic signal increased as the baseline mortality in the placebo group increased. Evidence of neutralization of TNFalpha bioactivity, and of attenuation of inflammation, was typically accompanied by evidence of impairment of antimicrobial defenses. Multiple specific and nonspecific therapeutic strategies were identified. We conclude that the beneficial effects of TNF in systemic inflammation occur at the cost of impaired antimicrobial defenses, and that a better understanding of the consequences of neutralization of TNFalpha in vivo could aid in better defining optimal patient populations for therapeutic intervention.
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PMID:Neutralization of tumor necrosis factor in preclinical models of sepsis. 1637 82


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