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51.
Objective To investigate the clinical features of 3 cases of Burkholderia pseudomallei septicemia in Guangxi Province.and therefore to improve its diagnosis and treatment. Method The clinical features.treatment and prognosis of 3 cases of acute septicemic melioidosis admitted to this hospital from October 2006 to December 2008 were retrospectively analyzed. Results The 3 male patients were local farmers,with an average age of (42 ±2)years.Two of them had a history of frequent trauma and contact with polluted water.and another had a history of exposure to the dust and soil.All patients had an acute onset,manifested as septicemia with chills,high-grade fever,anemia and weight loss.At the same time,the disease was often complicated with multiple organ abscesses.The pus wag characterized by smelling like mud.One case wag manifestated with lung abscess.with right calf skin pyogenic infection,and the another case was with liver,spleen,pancreas and mediastinal abscess,and the third presented with right facial and ankle soft tissue abscess.The leukocyte counts[(11.6 ±0.5)×10~9/L]and neutrophils[(8.3±0.4)×10~9/L] in 2 patients were slightly increased,but decreased in the other patient.There were significant increase of erythrocyte sedimentation rate(63.5±2.7)mm/1 h and c-reactive protein (155 ±4)mg/L,and liver dysfunotion and elevated blood glucose occurred in 3 patients.Chest radiology and CT showed a number of patchy infiltrates,consolidation,and nodules with varying sizes in the upper lung lobes.Abscess in other organs mainly occurred in liver,spleen.and skin.The final diagnosis was confirmed as infection with Burkholderia pseudomallei by repeated blood or pus culture.The isolated Burkholderia pseudonmallei wag sensitive to carbapenem,and β-lactam+β-lactamage inhibitors.One patient was treated effectively with Imipenem,and other 2 patients with β-lactam+β-lactamage inhibitors.After 3-4 days of treatment with antibiotics,the body temperature of these patients gradually decreased,and the intravenous drug wag used as long as 4 to 8 weeks.and a total course of antibiotic therapy would continue for 4 to 6 months. Conclusions Human melioidosis exists in the south and southwest of Guangxi.Repeated blood or pus culture can confirm the diagnosis.A relatively long course of antibiotic treatment with β-lactam/β-lactamage inibitors or carbapenem is recommended.  相似文献   
52.
Burkholderia mallei is the etiologic agent of glanders in solipeds (horses, mules and donkeys), and incidentally in carnivores and humans. Little is known about the molecular mechanisms of B. mallei pathogenesis. The putative carboxy-terminal processing protease (CtpA) of B. mallei is a member of a novel family of endoproteases involved in the maturation of proteins destined for the cell envelope. All species and isolates of Burkholderia carry a highly conserved copy of ctpA. We studied the involvement of CtpA on growth, cell morphology, persistence, and pathogenicity of B. mallei. A sucrose-resistant strain of B. mallei was constructed by deleting a major portion of the sacB gene of the wild type strain ATCC 23344 by gene replacement, and designated as strain 23344DeltasacB. A portion of the ctpA gene (encoding CtpA) of strain 23344DeltasacB was deleted by gene replacement to generate strain 23344DeltasacBDeltactpA. In contrast to the wild type ATCC 23344 or the sacB mutant 23344DeltasacB, the ctpA mutant 23344DeltasacBDeltactpA displayed altered cell morphologies with partially or fully disintegrated cell envelopes. Furthermore, relative to the wild type, the ctpA mutant displayed slower growth in vitro and less ability to survive in J774.2 murine macrophages. The expression of mRNA of adtA, the gene downstream of ctpA was similar among the three strains suggesting that disruption of ctpA did not induce any polar effects. As with the wild type or the sacB mutant, the ctpA mutant exhibited a dose-dependent lethality when inoculated intraperitoneally into CD1 mice. The CD1 mice inoculated with a non-lethal dose of the ctpA mutant produced specific serum immunoglobulins IgG1 and IgG2a and were partially protected against challenge with wild type B. mallei ATCC 23344. These findings suggest that CtpA regulates in vitro growth, cell morphology and intracellular survival of B. mallei, and a ctpA mutant protects CD1 mice against glanders.  相似文献   
53.
Polyphosphate is a linear chain of phosphate residues and is present in organisms ranging from bacteria to humans. Pathogens such as Mycobacterium tuberculosis accumulate polyphosphate, and reduced expression of the polyphosphate kinase that synthesizes polyphosphate decreases their survival. How polyphosphate potentiates pathogenicity is poorly understood. Escherichia coli K-12 do not accumulate detectable levels of extracellular polyphosphate and have poor survival after phagocytosis by Dictyostelium discoideum or human macrophages. In contrast, Mycobacterium smegmatis and Mycobacterium tuberculosis accumulate detectable levels of extracellular polyphosphate, and have relatively better survival after phagocytosis by D. discoideum or macrophages. Adding extracellular polyphosphate increased E. coli survival after phagocytosis by D. discoideum and macrophages. Reducing expression of polyphosphate kinase 1 in M. smegmatis reduced extracellular polyphosphate and reduced survival in D. discoideum and macrophages, and this was reversed by the addition of extracellular polyphosphate. Conversely, treatment of D. discoideum and macrophages with recombinant yeast exopolyphosphatase reduced the survival of phagocytosed M. smegmatis or M. tuberculosis. D. discoideum cells lacking the putative polyphosphate receptor GrlD had reduced sensitivity to polyphosphate and, compared to wild-type cells, showed increased killing of phagocytosed E. coli and M. smegmatis. Polyphosphate inhibited phagosome acidification and lysosome activity in D. discoideum and macrophages and reduced early endosomal markers in macrophages. Together, these results suggest that bacterial polyphosphate potentiates pathogenicity by acting as an extracellular signal that inhibits phagosome maturation.

In metazoans, cells such as macrophages use phagocytosis to obtain nutrients, remove cell debris, and engulf and kill pathogens (1). Phagocytosis begins by recognition of particles by cell-surface receptors and engulfment of the ingested particle to form a phagosome. Ingested material in the phagolysosome is then degraded by lysosomal acid, enzymes, and oxygen radicals (2, 3). Many successful pathogens, including Mycobacterium tuberculosis, Legionella pneumophila, Neisseria gonorrhoeae, and Streptococcus pyogenes, have evolved countermeasures to evade phago-lysosomal killing, allowing the pathogen to live in the arrested phagosome (48). One commonly used countermeasure is to inhibit phagosome acidification and fusion with lysosomes (911). How pathogens inhibit this process is poorly understood.Polyphosphate is a linear chain of phosphate residues present in all kingdoms of life (12). Polyphosphate metabolism is associated with the virulence of pathogens such as Burkholderia mallei, M. tuberculosis, Salmonella enterica, Shigella flexneri, and Pseudomonas aeruginosa (1317). In a wide range of bacteria, including pathogens, polyphosphate is synthesized from ATP by an essential enzyme polyphosphate kinase (PPK), and polyphosphate levels are maintained by exopolyphosphatase (PPX), an enzyme that degrades polyphosphate by removing terminal phosphate residues (1822). PPK mutants of many pathogens display decreased growth, reduced sensitivity to stress and starvation, decreased survival, reduced invasiveness, defects in quorum sensing, and defects in other features associated with virulence (13, 14, 23, 24). However, the role of PPK in the survival of pathogenic bacteria is not clearly understood.The eukaryotic social amoeba D. discoideum uses phagocytosis to uptake nutrients such as bacteria (25). D. discoideum cells accumulate extracellular polyphosphate, and, as the local cell density increases, the extracellular polyphosphate concentration increases (26). To anticipate starvation when a colony of cells is about to overgrow its food supply, the concomitant high extracellular polyphosphate concentration inhibits proliferation (26). The G-protein–coupled receptor glutamate receptor-like protein D (GrlD) binds, and helps cells sense, polyphosphate (26, 27).Since not digesting nutrients might be a way to inhibit D. discoideum proliferation, we examined whether polyphosphate might inhibit phagosome maturation in D. discoideum and human macrophages. In this report, we show that both exogenous polyphosphate and polyphosphate released from bacteria inhibit phagosome maturation in D. discoideum and that this effect is conserved in human macrophages.  相似文献   
54.
58岁的老年男性患者,因"反复双髋疼痛20 d"入院。于当地医院多次行"双髋切开引流术"后转诊某院,于该院行分泌物、关节液培养结果示假鼻疽伯克霍尔德菌,先后采取抗菌药物治疗、换药、置管冲洗引流术等保守治疗均失败,复查双髋X线片示双髋关节已严重破坏,行双侧髋关节切除旷置与二期全髋关节置换术,同时予以敏感抗菌药物治疗。术后随访2年,关节功能恢复,未见感染复发。因此,在临床慢性化脓性关节炎治疗中,首先需要积极行细菌培养鉴定,选用敏感抗菌药物,其次需要严格把握手术适应证,针对骨与关节感染,应及时彻底清创灌洗引流,关节严重破坏或功能丧失者可行一二期关节置换。  相似文献   
55.
目的分析类鼻疽的临床特点,并探讨其诊断及治疗的方法。方法回顾性分析某院2012年3月—2017年2月收治的有明确病原学依据的35例类鼻疽患者。结果 35例类鼻疽患者在入院时2例(5.7%)因有外院培养结果而确诊,3例(8.6%)高度疑似患者主要有相对典型的临床特点,误诊30例(85.7%),疑似患者入院后均经各种标本培养检出类鼻疽伯克霍尔德菌确诊;采用抗感染、外科穿刺引流(11.4%)及手术(20.0%)治疗,病情好转或痊愈26例(74.3%),放弃治疗2例(5.7%),死亡7例(20.0%)。临床首发症状以发热(88.6%)最常见,其次为咳嗽(34.3%)、气促(28.6%)、腹痛(14.6%)、上下肢痛(11.4%)、关节痛(5.7%);感染部位居前五位的分别为血液(85.7%)、肺(54.3%)、脾(20.0%)、皮肤软组织(20.0%)、肝(14.3%);以血培养出类鼻疽伯克霍尔德菌最为常见,占85.7%,其次为各种穿刺液(37.1%)、痰(20.0%)。结论类鼻疽的临床特点复杂多样,误诊率高,早期确诊和及时、合理、足疗程的治疗可降低病死率和复发率。  相似文献   
56.
本实验用类鼻疽特异抗原和壁膜抗原分别免疫金黄地鼠和家兔,然后攻击金黄地鼠,观察家兔腹腔巨噬细胞对细菌的吞噬作用。实验证明这两种抗原具有刺激机体产生免疫保护的作用,吞噬能力的增强是免疫保护的一个因素,吞噬能力不依赖于抗体产生的水平。  相似文献   
57.
A 79-year-old man with underlying alcoholic liver cirrhosis presented with complaints of a fever, abdominal pain, and difficulty walking. A diagnostic work-up revealed liver atrophy and chylous ascites, and spontaneous bacterial peritonitis (SBP) was diagnosed based on the cell and neutrophil counts. The Burkholderia cepacia complex (Bcc) was detected on blood and ascitic fluid cultures. Although broad-spectrum antibiotic therapy was initiated, the infection was difficult to control, and the patient died of multiple organ failure. Bcc is often multidrug-resistant and difficult to treat. SBP caused by Bcc has been rarely reported and may have a serious course, thus necessitating caution.  相似文献   
58.
Phylogenetic analysis of a clinical isolate associated with subclinical Burkholderia pseudomallei infection revealed probable exposure in the British Virgin Islands, where reported infections are limited. Clinicians should consider this geographic distribution when evaluating possible infection among persons with compatible travel history.  相似文献   
59.
60.
Background: In the end of 2009, a large number of patients with cancer undergoing chemotherapy at the day care unit of a private hospital in Mumbai, India developed Burkholderia cepacia complex (BCC) blood stream infection (BSI). Objective: The objectives were to identify the source of the outbreak and terminate the outbreak as rapidly as possible. Materials and Methods: All infection control protocols and processes were reviewed. Intensive training was started for all nursing staff involved in patient care. Cultures were sent from the environment (surfaces, water, air), intravenous fluids, disinfectants and antiseptics and opened/unopened medication. Results: A total of 13 patients with cancer with tunneled catheters were affected with BCC BSI. The isolates were of similar antimicrobial sensitivity. No significant breach of infection control protocols could be identified. Cultures from the prepared intravenous medication bags grew BCC. Subsequently, culture from unused vials of the antiemetic granisetron grew BCC, whereas those from the unopened IV fluid bag and chemotherapy medication were negative. On review, it was discovered that the outbreak started when a new brand of granisetron was introduced. The result was communicated to the manufacturer and the brand was withdrawn. There were no further cases. Conclusions: This outbreak was thus linked to intrinsic contamination of medication vials. We acknowledge a delay in identifying the source as we were concentrating more on human errors in medication preparation and less on intrinsic contamination. We recommend that in an event of an outbreak, unopened vials be cultured at the outset.  相似文献   
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