الفهرس 
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Abstract
Typhoid fever continues to be a global health problem, with an estimated 16–22 million cases of typhoid and 200,000 to 600,000 deaths occur annually. In Egypt, in 2006 the incidence of typhoid fever was 59/100,000 persons/year which remain Egypt as a country with medium incidence. Shortly after bacteria adhere to the apical epithelial microfold cells, profound cytoskeletal rearrangements occur in the host cell, disrupting the normal epithelial brush border and inducing formation of membrane ruffles that reach out and enclose adherent bacteria in large vesicles. Salmonellae encode a type III secretion system (T3SS) within Salmonella pathogenicity island 1 (the SPI-1 T3SS), which is required for bacteria-mediated endocytosis and intestinal epithelial invasion. It do its function through the translocation of virulence proteins (SipA, SipB, SipC, SipD, SipE, SopE, SopE2 and SopB) directly from the bacterial cytoplasm into the host cell and also through synthesis and polarized secretion of inflammatory mediators and neutrophil chemoattractants, including IL-8 which directs the recruitment and transmigration of neutrophils into the gut lumen.
Shortly following invasion of the gut epithelium, invasive salmonellae encounter and enter macrophages present in the submucosal space and Peyer’s patches which is essential for salmonella survival, replication and dissemination within the host cell and induction of systemic disease. Once in the intracellular environment within the macrophage, Salmonellae induce the expression of numerous genes that allow evasion of the antimicrobial defenses, and persist within a vacuolar compartment. The bacterium within macrophage is presented to the underlying lymphoid tissue. Invading microorganisms translocate to intestinal lymphoid follicles and are transported to draining mesenteric lymph nodes and also into the circulation.
As some bacteria die, they release endotoxins (LPS) which induce the expression of genes encoding inflammatory cytokines (TNF-α, IFN-, IL-1, IL-2, IL-6 and IL-8), adhesive proteins and enzymes, which up-regulate host defense systems including the initiation of antigen-specific adaptive immune responses.
Early diagnosis of typhoid fever and institution of appropriate treatment are essential for optimal management and outcome, especially in children. The vast majority of cases (more than 90%) can be managed at home with oral antibiotics and close medical follow-up for complications or failure to response to therapy. However, patients with persistent vomiting, severe diarrhea and abdominal distension may require hospitalization and parenteral antibiotic therapy. The general principles of management of typhoid include (1) general nursing and supportive care (adequate bed rest, soft and easily digestible diet, adequately hydration and antipyretics as required) (2) antibiotic therapy. Fluoroquinolones antibiotics are the most effective class of agents, and azithromycin has proved effective in the treatment of uncomplicated typhoid fever in adults and children. β-lactam antibiotics aminopenicillins (amoxicillin and ampicillin) and extended spectrum third generation cephalosporins (ceftriaxone, cefotaxime, cefpodoxime and cefixime) also used. Co-trimoxazole was widely used for the treatment of typhoid fever but with widespread resistance and an inferior efficacy, finally chloramphenicol which is the first successful therapy and still widely prescribed in developing countries for the treatment of typhoid fever.