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Cellabs血液檢測沙眼衣原體檢測卡

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【公司名稱】 廣州健侖生物科技有限公司
【】   楊永漢 
【】 
【騰訊 】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-3室
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宿主經(jīng)過初次感染產(chǎn)生抗感染抵抗力之后，在一定程度上能坡壞重復(fù)感染的蟲體，但不能殺傷初次感染的成蟲或阻止其產(chǎn)卵。這種現(xiàn)象稱為伴隨免疫。病理變化血吸蟲病的基本病變是由蟲卵沉著組織中所引起的蟲卵結(jié)節(jié)。蟲卵結(jié)節(jié)分急性和慢性兩種；急性由成熟活蟲卵引起，結(jié)節(jié)中央為蟲卵，周圍為嗜酸性包繞，聚積大量嗜酸性細(xì)胞，并有壞死，稱為嗜酸性膿腫，膿腫周圍有新生肉芽組織與各種細(xì)胞浸潤，形成急性蟲卵結(jié)節(jié)。急性蟲卵結(jié)節(jié)形成10天左右，卵內(nèi)毛蚴死亡，蟲卵破裂或鈣化，圍繞類上皮細(xì)胞，異物巨細(xì)胞和淋巴細(xì)胞，形成假結(jié)核結(jié)節(jié)，以后肉芽組織長入結(jié)節(jié)內(nèi)部，并逐漸被類上皮細(xì)胞所代替，形成慢性蟲卵結(jié)節(jié)。zui后結(jié)節(jié)發(fā)生纖維化。病變部位主要在結(jié)腸及肝臟，較多見的異位損害則在肺及腦。1．腸道變病 成蟲大多寄生于腸系膜下靜脈，移行至腸壁的血管末梢在粘膜及粘膜日本血吸蟲日本血吸蟲下層產(chǎn)卵，故活組織檢查時發(fā)現(xiàn)蟲卵多排列成堆，以結(jié)腸，尤其是直腸、降結(jié)腸和乙狀結(jié)腸為zui顯著，小腸病變極少，僅見于重度感染者。早期變化為粘膜水腫，片狀充血，粘膜有淺潰湯及黃色或棕色顆粒。由于潰湯與充血，臨床上見有痢疾癥狀，此時，大便檢查易于發(fā)現(xiàn)蟲卵。晚期變化主要為腸壁因纖維組織增生而增厚，粘膜高低不平，有萎縮，息肉形成，潰瘍、充血、瘢痕形成等復(fù)雜外觀。血吸蟲病變所形成的息肉有轉(zhuǎn)變?yōu)榘┠[可能，應(yīng)予重視。由于腸壁增厚，腸腔狹窄，可致機械性梗阻。由于闌尾炎組織也常有血吸蟲卵沉著，闌尾粘膜受激及營養(yǎng)障礙，易發(fā)生闌尾炎。2．肝臟病變 蟲卵隨門靜脈血流入肝，抵達于門靜脈小分枝，在門管區(qū)等處形成急性蟲卵結(jié)節(jié)，故在肝表面和切面可見粟?；蚓G豆大結(jié)節(jié)，肝竇充血，肝竇間隙擴大，竇內(nèi)充滿漿液，有嗜酸性粒細(xì)胞及單核細(xì)胞浸潤；肝細(xì)胞可有變性，小灶性壞死與褐色素沉著。晚期可見門靜脈周圍有大量纖維組織增生，形成肝硬變，嚴(yán)重者形成粗大突起的結(jié)節(jié)。較大門靜脈分支管壁增厚，管腔內(nèi)血栓形成。由于肝內(nèi)門靜脈阻塞，形成門靜脈高壓，引起腹水、脾腫大及食管靜脈曲張。3．脾臟病變 早期腫大，與成蟲代謝產(chǎn)物激有關(guān)。

After the host has developed an anti-infective resistance through a primary infection, it can, to a certain extent, be able to sway the re-infected worm body, but it cannot kill the first infected adult or prevent its production. This phenomenon is called concomitant immunity. Pathological changes The basic lesion of schistosomiasis is the egg nodule caused by the oocyst tissue. The egg nodule is divided into two kinds: acute and chronic; acute is caused by mature live eggs, the center of the nodule is an egg, surrounded by eosinophilic surrounding, accumulating a large number of eosinophils, and necrosis, called eosinophilic abscess, abscess Around the new granulation tissue and various cell infiltration, the formation of acute egg nodules. The acute egg nodule formed for about 10 days. The ovum within the egg died, the eggs were broken or calcified, surrounded by epithelial cells, foreign giant cells and lymphocytes, and formed pseudotuberculosis nodules. After that, the granulation tissue grew into the interior of the nodule, and gradually Replaced by epithelial cells to form chronic egg nodules. In the final nodule, fibrosis occurred. The lesions are mainly in the colon and liver, and the most common ectopic lesions are in the lungs and brain. 1. Intestinal disease adults mostly parasitize in the inferior mesenteric vein. The blood vessels that migrate to the intestine wall lay eggs in the mucosa and mucous membranes of the Japanese schistosome Schistosoma japonicum. Therefore, during biopsy, it was discovered that the eggs were mostly arranged in heaps to colon, especially the rectum. , descending colon and sigmoid colon is the most significant, minimal intestinal lesions, only seen in severely infected persons. The early changes were mucosal edema, flaking, and pale ulceration of the mucosa and yellow or brown granules. Due to ulceration and congestion, symptoms of diarrhea are clinically observed. At this time, stool examination is easy to detect eggs. The late changes are mainly the thickening of the intestinal wall due to fibrous tissue hyperplasia, mucosal uneven, with atrophy, polyp formation, ulcers, congestion, scar formation and other complex appearance. The polyps formed by schistosome lesions may turn into cancerous lesions and should be taken seriously. Due to thickening of the intestinal wall and narrowing of the intestinal lumen, mechanical obstruction can be caused. Because appendicitis tissue also often has schistosomiasis eggs, appendix mucosal stimulation and nutritional disorders, prone to appendicitis. 2. Liver lesions oocysts flow into the liver with portal venous blood and reach the small branch of the portal vein, forming acute egg nodules in the portal area, etc. Therefore, large nodules of miliary or mung bean are seen on the liver surface and section, hepatic sinus congestion, and hepatic sinusoids The gap is enlarged, the sinus is filled with serous fluid, with infiltration of eosinophils and monocytes; the liver cells may have degeneration, small focal necrosis, and brown pigmentation. In the late stage, a large number of fibrous tissue around the portal vein can be seen to form liver cirrhosis, and in severe cases, large nodules are formed. Larger portal vein branches thicken, and thrombus formation occurs in the lumen. Due to intrahepatic portal vein obstruction, portal hypertension is formed, causing ascites, splenomegaly, and esophageal varices. 3. Splenic lesions are swollen early and are associated with the metabolites of adult metabolites.

 

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