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Shigellosis-Disentri Basiler

• • • • S. dysentriae(serogroup A) S. flexneri (serogroup B) S. boydii (serogroup C) S. soneii (serogroup D)

. dikode pada kromosom bakteri dan ShET-2 dikode pada plasmid virulens.Patofisiologi • Sifat virulensi dasar: Invasi sel epitel kolon (dikodekan pada plasmid besar yang menyebabkan sintesis kelompok polipeptida). • Fase diare berair dapat disebabkan oleh enterotoksin unik. enterotoksin shigella 1 (ShET1). dibantu oleh sintesis lipopolisakarida dan sintesis shigotoksin(eksotoksin kuat penghambat sintesis protein).

• A variety of cell wall adhesins (def) enable the bacterium to make a more intimate contact with mucosal cells.• Symptoms of shigellosis include diarrhea. Pathogenicity • In the outer membrane of the gram-negative cell wall. . Within 1-2 days this progresses to Abdominal cramps and tenesmus (def). the lipopolysaccharide functions as an endotoxin . Classic shigellosis presents itself as lower abdominal cramps and stool abundant with blood and pus develops as the Shigella invade the mucosa of the colon. with or without bloody stool. abdominal cramps. • Initial profuse watery diarrhea typically appears first as a result of enterotoxin. and fever. The incubation period is 1-3 days. bloody stool.

(M cells are phagocytic cells in the mucous membrane whose function is to sample microbes from the intestinal lumen and pass them on to the lymphoid tissue of the Peyer's patch in order to activate the immune defenses against intestinal microbes). Now they move through the host cell and spread to adjacent host cells by a unique process called actinbased motility whereby actin filaments polymerize at one end of the bacterium producing comet-like tails that propel the Shigella through the cytoplasm of the host cell.It is thought that Shigella first transit the mucous membrane of the colon by passing through M cells (see Fig. . 1). the actin filaments push the Shigella across that membrane and into the adjacent cell (see Fig. those epithelial cells die and provoke a strong inflammatory response leading to the symptoms of dysentery. When they reach the boundary of that cell. Once across the mucosa. As the Shigella grow and spread within the epithelial cells. 1). 1). Once inside they escape from the vacuole into the cytoplasm and multiply. the Shigella use invasins (def) to enter the epithelial cells from the underside (see Fig.

• Shigella survive phagocytosis by inducing a programmed cell death called apoptosis in macrophages. In some people it also damages glomerular endothelial cells (def)causing hemolytic uremic syndrome (HUS). • S. dysenteriae produce Shiga toxin that disrupts host cell protein synthesis resulting in damage to the intestinal epithelium. .

Shigella Passing Through the Mucous Membrane and Invading Mucosal Epithelial Cells .

Imunitas seluler juga memainkan beberapa peran dalam proteksi. .Respon imun IgA sekretori dan antibodi serum berkembang dalam beberapa hari sampai beberapa minggu sesudah infeksi dengan Shigella. identifikasi determinan proteksi utama terhadap infeksi selanjutnya tetap belum jelas. Ada bukti bahwa proteksi adalah spesifik serotip. tetapi ada juga kesan bahwa tingkat proteksi silang terhadap semua shigella menyertai infeksi dengan serotip tertentu. walaupun tampaknya kecil. Walaupun antilipopolisakarida maupun antibodi polipeptida plasmid antivirulens telah diuraikan.

mukosa rapuh. ulserasi. kematian sel epitel. . • Edema mukosa setempat atau diffus. dan terjadi edema submukosa. pseudomembran.Patologi • Kolon terutama kolon distal. • Mikroskop: ulserasi. infiltrasi PMN dan mononuklear meuas dari lapisan mukosa sampai lapisan muskularis. pankolitis. perdarahan dan eksudat.