Cellabs血液檢測(cè)沙眼衣原體檢測(cè)卡

廣州健侖生物科技有限公司

廣州健侖生物科技有限公司長(zhǎng)期供應(yīng)可替寧檢測(cè)試劑盒，其牌子是美國(guó)NOVABIOS,國(guó)產(chǎn)創(chuàng)侖

廣州健侖生物科技有限公司與cellabs達(dá)成代理協(xié)議，歡迎廣大用戶咨詢訂購(gòu)。

Cellabs血液檢測(cè)沙眼衣原體檢測(cè)卡

我司還提供其它進(jìn)口或國(guó)產(chǎn)試劑盒：登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲(chóng)病、違禁品濫用、肺炎球菌、軍團(tuán)菌、化妝品檢測(cè)、食品安全檢測(cè)等試劑盒以及日本生研細(xì)菌分型診斷血清、德國(guó)SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。

歡迎咨詢

歡迎咨詢2042552662

二維碼掃一掃

【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(hào)二期2幢101-3室
【企業(yè)文化】

宿主經(jīng)過(guò)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(chóng)體，但不能殺傷初次感染的成蟲(chóng)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(chóng)病的基本病變是由蟲(chóng)卵沉著組織中所引起的蟲(chóng)卵結(jié)節(jié)。蟲(chóng)卵結(jié)節(jié)分急性和慢性兩種；急性由成熟活蟲(chóng)卵引起，結(jié)節(jié)中央為蟲(chóng)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(rùn)，形成急性蟲(chóng)卵結(jié)節(jié)。急性蟲(chóng)卵結(jié)節(jié)形成10天左右，卵內(nèi)毛蚴死亡，蟲(chóng)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(zhǎng)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(chóng)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(jiàn)的異位損害則在肺及腦。1．腸道變病 成蟲(chóng)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(chóng)日本血吸蟲(chóng)下層產(chǎn)卵，故活組織檢查時(shí)發(fā)現(xiàn)蟲(chóng)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(jiàn)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(jiàn)有痢疾癥狀，此時(shí)，大便檢查易于發(fā)現(xiàn)蟲(chóng)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(chóng)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(jī)械性梗阻。由于闌尾炎組織也常有血吸蟲(chóng)卵沉著，闌尾粘膜受激及營(yíng)養(yǎng)障礙，易發(fā)生闌尾炎。2．肝臟病變 蟲(chóng)卵隨門(mén)靜脈血流入肝，抵達(dá)于門(mén)靜脈小分枝，在門(mén)管區(qū)等處形成急性蟲(chóng)卵結(jié)節(jié)，故在肝表面和切面可見(jiàn)粟?；蚓G豆大結(jié)節(jié)，肝竇充血，肝竇間隙擴(kuò)大，竇內(nèi)充滿漿液，有嗜酸性粒細(xì)胞及單核細(xì)胞浸潤(rùn)；肝細(xì)胞可有變性，小灶性壞死與褐色素沉著。晚期可見(jiàn)門(mén)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(mén)靜脈分支管壁增厚，管腔內(nèi)血栓形成。由于肝內(nèi)門(mén)靜脈阻塞，形成門(mén)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(chóng)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.