Data from Camilleri, 201 5; DuPont, 201 4.
Judicious use of antimicrobial agents is warranted. For moderate to severely ill women, some recommend empirical treatment with ciprofloxacin, 500 mg twice daily for 3 to 5 days. Speciic pathogens are treated as needed when identiied (see Table 54-4). Syndromes for which treatment is usually unnecessary include those caused by Escherichia coli, staphylococcal species, Bacilus cereus, and Norwalk-like virus. Severe illness caused by Salmonela spp is treated with ciprofloxacin or trimethoprim-sulfamethoxazole; by Campylobacter spp with azithromycin; by Clostridium diicile with oral metronidazole or vancomycin; and by Giardia spp and Entamoeba histoytica with metronidazole (DuPont, 2014; Rocha-Castro, 2016).
his anaerobic gram-positive bacillus is transmitted by the fecal-oral route. It is the most frequent nosocomial infection in the United States. In 2011, 453,000 cases of C dicile and 29,000 associated deaths were reported by the Centers for Disease Control and Prevention (CDC) (Lessa, 2015). he most important risk factor is antibiotic use, and the highest risk is with aminopenicillins, clindamycin, cephalosporins, and luoroquinolones. Other risk factors include inlammatory bowel disease, immunosuppression, advanced age, and gastrointestinal surgery. Most cases are hospital-acquired, however, community-acquired cases are becoming common (Leler, 2015). With severe colitis, the infection-related mortality rate is 5 percent.
Diagnosis is by enzyme immunoassay for toxins in the stool, or by DNA-based tests that identiy toxin genes. Only patients with diarrhea should be tested, and posttreatment testing is not recommended. Prevention is by soap-and-water hand washing, and infected individuals are isolated. Treatment is oral vancomycin or metronidazole. The risk of recurrence after an initial episode is 20 percent. Fecal microbial transplantation may become standard for recurrent clostridial colitis.
Two presumably noninfectious forms of intestinal inlammation are ulcerative colitis and Crohn disease. Diferentiation between these is important because treatment difers. That said, they both share common features, and sometimes are indistinguishable if Crohn disease involves the colon. he salient clinical and laboratory features shown in Table 54-5 permit a reasonably confident diagnostic diferentiation in most cases. he etiopathogenesis is enigmatic in both, but a genetic predisposition is suspected. Inlammation is thought to result from dysregulated mucosal immune function in response to commensal microbiota, with or without an autoimmune component (Friedman, 2015).
TABLE 54-5. Some Shared and Diferentiating Characteristics of Inflammatory Bowel Disease
Hereditary More than 100 disease-associated genetic loci-a third shared; Jewish predominance; familial in 5-10% of cases; Turner syndrome; immune dysregulation
Other Chronic and intermittent with exacerbations and remissions; extraintestinal manifestations: arthritis, erythema nodosum, uveitis
Major symptoms Diarrhea, tenesmus, rectal bleeding, cramping pain; Fibrostenotic-recurrent RLQ colicky pain; fever chronic, intermittent bladder, interenteric Bowel involvement Mucosa and submucosa of large bowel; usually begins Deep layers small and large bowel; at rectum (40% proctitis only); continuous disease commonly transmural; discontinuous involvement; strictures and fistulas