弓形虫病六例报告

成人弓形虫感染大多不发病,只是在机体抵抗力下降时才可能发病,但女性感染者如怀孕可通过胎盘传播给胎儿,引起胎儿先天性弓形虫感染。据统计世界各地均有弓形虫感染,法国人群弓形虫感染的阳性率高达80%左右,我国在8%以下,北京地区母亲感染弓形虫后其婴儿感染率为12.6%[1],弓形虫感染是引起小儿神经系统先天畸形及精神发育障碍的重要原因之一。此病临床表现复杂多样,部分医生对此病认识不足,易误诊和漏诊,延误治疗。我院1994~2006年收治6例幼儿弓形虫病,现报告如下。1临床资料1·1一般资料本组6例中,男4例,女2例;年龄分别为18天、26天、34天…     

弓形虫病误诊一例

【病例】　女 ,68岁。因反复全身淋巴结肿大 30天入院。患者 30天前无明显诱因出现全身淋巴结肿大 ,轻触痛 ,伴低热、食欲缺乏、全身乏力 ,自服克拉维酸钾 (阿莫西林 ) 7天后淋巴结缩小 ,但未完全消失 ,自行停药。1周后病人全身淋巴结又复肿大 ,症状同前 ,遂去当地县医院就诊。查血白细胞 8 6× 1 0 9/L ,中性粒细胞 0 68,淋巴细胞 0 30 ,血红蛋白 1 3 0g/L ;红细胞沉降率5mm/h。B超检查颈部淋巴结示有低回声区 ;腹部B超检查肝、胆、胰、脾、肾未见异常。期间病人继续服用克位维酸钾 ,疗效差 ,为进一步诊治入我院。病人既往无喂养猫、狗…     

弓形虫病120例分析

弓形虫病又称弓形体病,是由弓形虫所引起的一种人兽共患性寄生虫病,分布范围广,对人类危害大.近些年来,随着人们经济水平的提高,个人及家庭饲养宠物的增多,临床上弓形虫病的发生亦呈上升趋势.由于弓形虫感染人体后可入侵全身多种脏器,引起复杂的临床症状且无特异性,明确诊断比较困难,误诊率高.     

弓形虫病漏误诊原因探析

自 196 4年报道首例弓形虫病 (Toxoplasmosis)以来 ,已近 36年 ,但该病的临床诊断率仍很低。截止 1992年底我国报道仅 12 0例左右。由于该病的特殊性 ,误诊是临床一个不可忽视的问题。本文就 4 1例弓形虫病的诊断进行讨论和分析。1　临床资料1.1　一般资料　近 2年内 ,我们诊治     

弓形虫病淋巴结炎22例临床病理分析

弓形虫进入人体后随血液侵入全身器官及组织,可引起多个器官或单个器官的病变.近年来我们应用免疫组化技术诊断弓形虫病淋巴结炎22例,现分析讨论如下.     

眼弓形虫病一例误诊

【病例】　女,3 4岁。因左眼视力下降伴黑影1周就诊。专科检查:视力右5 0 ,左4 7;右眼部检查正常;左眼前节无异常;眼底视盘正常,黄斑部轻度水肿,中心反光消失,未见出血渗出灶,初诊为左眼“中心性浆液性视网膜脉络膜病变(中浆病)”,予血管扩张剂、B族维生素等治疗。1周后症状加     

弓形虫病研究90年

弓形虫的发现至今已九十年，经过各国学者的研究，特别是在第二次世界大战期间，经过美国一些学者的深入研究，弓形虫病(Toxoplasmosis)作为医学上的一个疾病，逐步被人们所认识和接受。50年代中期我国开始研究此病，50年来取得了很大成绩。     

定量PCR在弓形虫病诊断中的研究进展

弓形虫病是一种严重危害人类健康的人兽共患寄生虫病.应用定量PCR对弓形虫进行定量检测,为弓形虫病的诊断提供了一条快速、准确、灵敏的途径.现就定量PCR技术诊断弓形虫病所用目的基因、定量PCR的类型以及在弓形虫病诊断中的应用作一综述.     

Helicobacter pylori and Helicobacter heilmannii in children. A Bulgarian study

The aim of the study was to evaluate the prevalence of Helicobacter pylori and Helicobacter heilmannii among 321 children. Gram staining, urease test and culture were performed. Of all patients, 52.6% were H. pylori positive and 0.3% were H. heilmannii positive. H. pylori infection was associated with chronic gastritis in 57.1%, with duodenal ulcer in 75% and with non-ulcer dyspepsia in 25.6%. This infection was more frequent in children aged 11-18 years than in younger patients. Rapid urease test, culture and direct Gram staining showed 42.3, 96.5 and 78.2% sensitivity and 93.2, 100 and 84.6% specificity, respectively. H. pylori was detected in 60.2% of fresh versus 52.8% of frozen specimens and in 64.8% in gastric biopsy versus 25% in gastric mucus specimens. H. pylori growth was detected after nine to 10 days in 6.2% and after 11 days in 1.2%. Culture exhibited the best accuracy of the three diagnostic methods. Frozen biopsy specimens gave reliable H. pylori detection unlike gastric mucus specimens. Eleven days of incubation for H. pylori is recommended. The study confirms an early acquisition of H. pylori infection in Bulgaria. The incidence of H. heilmannii infection in childhood is uncommon but clinically important.     

尿幽门螺杆菌抗体测定在幽门螺杆菌感染诊断中的价值

目的：探讨幽门螺杆菌（Hp)抗体阴性用于排除近期Hp感染的临床价值。方法：Hp感染诊断采用^13C尿素呼气试验、快速尿素酶试验和W－S银染色，Hp抗体测定采用Hp抗体测定层析板。结果：31例Hp感染患10分钟阳性率87．1％（27／31），30分钟阳性率96．7％（30／31），56例无Hp感染患假阳性率19．7％（11／56）。对Hp感染诊断敏感性96．78％，特异性80．3％。对Hp感染阳性组以Hp抗体，^13C尿素呼气试验阳性率最高，Hp感染阴性组以Hp抗体阳性率最高。46例阳性病例中仅1例^13C尿素呼气试验阳性，W－S银染色、快速尿素酶试验均阴性。结论：Hp抗体阴性基本可排除近期有Hp感染，可避免病人作进一步的无益检查。     

Compound efflux in Helicobacter pylori

Susceptibility testing with a variety of structurally unrelated compounds showed that hefC in Helicobacter pylori is involved in multidrug efflux. This efflux was shown to depend on the proton motive force, as demonstrated by ethidium bromide accumulation experiments. Thus, H. pylori contains an active multidrug efflux mechanism.     

Helicobacter pylori infection in Finland

Helicobacter pylori causes chronic gastritis worldwide and it is the most important single factor in peptic ulcer disease. Up to half of H. pylori infected individuals develop atrophic gastritis over years and decades. H. pylori infection has also been classified as a class I carcinogen in human gastric cancer. Most infections are obtained in childhood, in Finland mainly before the age of 7 years but the exact transmission routes are not known. The infection shows an age-dependent pattern, the infection being rare among children but gradually becoming more prevalent among older age groups. As new infections are few in adults and the infection only rarely disappears without effective anti-microbial therapy, the occurrence of the infection in the old actually reflects the prevalence of the infection in their childhood. In developed countries, such as Finland, a rapid decline of H. pylori prevalence rate has been demonstrated. In order to speed up this natural decline of the infection, a unique population based 'screen and treat' project was started in Vammala, a semiurban south-western community in Finland. In this survey, young inhabitants were offered diagnosis and treatment for H. pylori.     

Helicobacter pylori infection in Finland

Helicobacter pylori causes chronic gastritis worldwide and it is the most important single factor in peptic ulcer disease. Up to half of H. pylori infected individuals develop atrophic gastritis over years and decades. H. pylori infection has also been classified as a class I carcinogen in human gastric cancer. Most infections are obtained in childhood, in Finland mainly before the age of 7 years but the exact transmission routes are not known. The infection shows an age‐dependent pattern, the infection being rare among children but gradually becoming more prevalent among older age groups. As new infections are few in adults and the infection only rarely disappears without effective antimicrobial therapy, the occurrence of the infection in the old actually reflects the prevalence of the infection in their childhood. In developed countries, such as Finland, a rapid decline of H. pylori prevalence rate has been demonstrated. In order to speed up this natural decline of the infection, a unique population based ‘screen and treat’ project was started in Vammala, a semiurban south‐western community in Finland. In this survey, young inhabitants were offered diagnosis and treatment for H. pylori.     

A Redox Basis for Metronidazole Resistance in Helicobacter pylori

Metronidazole resistance in Helicobacter pylori has been attributed to mutations in rdxA or frxA. Insufficient data correlating RdxA and/or FrxA with the resistant phenotype, and the emergence of resistant strains with no mutations in either rdxA or frxA, indicated that the molecular basis of H. pylori resistance to metronidazole required further characterization. The rdxA and frxA genes of four matched pairs of metronidazole-susceptible and -resistant strains were sequenced. The resistant strains had mutations in either rdxA, frxA, neither gene, or both genes. The reduction rates of five substrates suggested that metabolic differences between susceptible and resistant strains cannot be explained only by mutations in rdxA and/or frxA. A more global approach to understanding the resistance phenotype was taken by employing two-dimensional gel electrophoresis combined with tandem mass spectrometry analyses to identify proteins differentially expressed by the matched pair of strains with no mutations in rdxA or frxA. Proteins involved in the oxireduction of ferredoxin were downregulated in the resistant strain. Other redox enzymes, such as thioredoxin reductase, alkyl hydroperoxide reductase, and superoxide dismutase, showed a pI change in the resistant strain. The data suggested that metronidazole resistance involved more complex metabolic changes than specific gene mutations, and they provided evidence of a role for the intracellular redox potential in the development of resistance.Metronidazole (Mtr) is an important component of therapeutic regimens that currently are used to treat many microbial infections. Metronidazole is considered a prodrug whose uptake and activation requires intracellular reduction, resulting in the production of cytotoxic short-lived radicals and other reactive species (29). 5-Nitroimidazole is activated via interactions with redox systems capable of reducing the low-potential (−415 mV) nitro group in position 5 of the imidazole ring (29). This property makes metronidazole effective against organisms in a low-intracellular-redox state, such as anaerobic bacteria and protozoa, as well as some microaerophiles, such as Campylobacter spp. and Helicobacter pylori (16).Helicobacter pylori is found in the gastric mucous layer or adhering to the epithelial lining of the human stomach and is one of the most prevalent infections in humans (1, 19, 39). The frequent use of metronidazole has resulted in increased resistance to the antibiotic by H. pylori. The emergence of resistant isolates that do not respond to the drug fostered an interest in understanding the primary causes of resistance to metronidazole in this bacterium. Extensive investigations of H. pylori established that the main causes of metronidazole resistance are mutations in the gene rdxA or frxA (6, 7, 14, 15). However, insufficient data correlating the oxygen-insensitive nitroreductase RdxA and/or the NAD(P)H flavin oxidoreductase FrxA with the resistant phenotype and the fact that a small percentage of resistant strains do not have mutations in either rdxA or frxA indicated that the molecular basis of H. pylori resistance to Mtr has not been characterized completely.Early studies showed that the oxygen tension has a large impact on the resistance of H. pylori to Mtr (23, 31-33), and several investigations have linked the activities of specific oxidoreductases to the Mtr-susceptible phenotype of the bacterium (9, 23, 36). Three disulfide reduction activities, which use dithiobis-2-nitrobenzoic acid (DTNB), oxidized glutathione (GSSG) and NADH, or ferredoxin (Fdx) and NADH as substrates, were identified in H. pylori (12). Metronidazole inhibited disulfide reduction competitively in each of the three activities, and the measured inhibition constants of Mtr for the reduction of different substrates indicated that the effects of Mtr were stronger in susceptible strains than in resistant ones (12). The presence of DTNB, GSSG, or Fdx inhibited Mtr reduction in situ, indicating that these substrates competed with Mtr as acceptors in redox reactions catalyzed by the corresponding disulfide reductases and suggesting that the enzymes participated in the reduction of Mtr (12). These results indicated a possible role in Mtr activation by enzymes catalyzing redox reactions that modulate the intracellular redox status, and that in metronidazole-susceptible strains, the cellular machinery regulating the redox status maintains an intracellular potential sufficiently low to activate metronidazole-reducing pathways (12).In this study, four matched pairs of susceptible and resistant strains with different mutations in their rdxA and frxA genes were investigated. The redox state of the cells and the metabolic reduction of five substrates were measured. A more global approach was required to understand the resistant phenotype; thus, changes in the proteome of a matched pair of strains with no mutations in rdxA or frxA and changes induced in the proteome of the Mtr-resistant strain subjected to Mtr were investigated using two-dimensional gel electrophoresis and mass spectrometry (MS).     

A clinician's guide to managing Helicobacter pylori infection

Helicobacter pylori infection is chronic and very common. Its clinical consequences vary widely, ranging from being asymptomatic and clinically insignificant in many cases to causing dyspepsia, peptic ulcer disease, and gastric malignancy in others. Care must be used in deciding whom to test for H pylori infection, as a positive result mandates treatment, making broad-based screening impractical.