Shigella organisms cause bacillary dysentery, a disease that has been described since early recorded history.
The disease is due to Enterobacteriaceae, the genus Shigella, that includes more than 100 serotypesClassification- There are four groups of shigellae described as follows:Group A: Shigella dysenteriae (10 serotypes)Group B: Shigella flexneri (6 serotypes)Group C: Shigella boydii (15 serotypes)Group D: Shigella sonnei.
Insufficient data exists, but conservative estimatessuggest that Shigella causes approximately 90 millioncases of severe dysentery annually, with at least100,000 of these resulting in death, mostly amongchildren in the developing world. Shigella also causesapproximately 580,000 cases annually among travelersand military personnel from industrialized countries.An estimated 18,000 cases of shigellosis occur annuallyin the United States. Infants, the elderly, and the infirmare susceptible to the severest symptoms of disease,but all humans are susceptible to some degree.Individuals with acquired immune deficiencysyndrome (AIDS) are more frequently infectedwith Shigella. Shigellosis is a more common andserious condition in the developing world; fatalityrates of Shigellosis epidemics in developing countriescan be 5–15%.
Shigellae are released from the patient or carrier with excrements. The microorganisms can survive in soil for 3 months, on soiled utensils, dishes, moist linens for weeks or even months, for several days on food (bread, meat); in milk they persist for 30 days or longer, in running water they can survive from several hours to 5-9 days. S sonnei and S flexneri cause 90% of the cases of shigellosis. S dysenteriae has produced epidemic shigellosis.
Shigella species (eg, Shigella dysenteriae, Shigella flexneri, Shigella sonnei, Shigella boydii) are aerobic, nonmotile, glucose-fermenting, gram-negative rods that are highly contagious, causing diarrhea after ingestion of as few as 180 organisms. Shigella species cause damage by 2 mechanisms, as follows: (1) invasion of the colonic epithelium, which is dependent on a plasmid-mediated virulence factor, and (2) production of enterotoxin, which is not essential for colitis but enhances virulence. The organism is spread by fecal-oral contact; via infected food or water; during travel; or in long-term care facilities, day care centers, or nursing homes.
Invasion of shigellaIn addition to the toxins, the invsasive properties of shigellaeare also very important for the development of pathology in theintestine. Intracellular parasites cause degenerative changes,desquamation and destruction of the epithelial cells .Toxaemia affects the CVS and CNS, causes disorders in thealimentary canal and in the first instance upsets the secretory,motor and absorption functions; water, mineral, protein,carbohydrate, fat and vitamin metabolisms are also affected.
Acute bloody diarrhea Crampy abdominal pain Tenesmus Passage of mucus Fever (1-3 d after exposure) Occasionally vomiting (35% prevalence) Self-limited course (3 d to 1 wk and rarely lasts as long as 1 mo)
Lower abdominal tenderness Normal or increased bowel sounds Dehydration (occasional)
Symptoms may range from mild abdominal discomfort to full-blown dysentery characterized by cramps, diarrhea, fever, vomiting, blood, pus, or mucus in stools or tenesmus. Onset time is 12 to 96 hours, and recovery takes 5 to 7 days. Infections are associated with mucosal ulceration, rectal bleeding, and drastic dehydration. Reiters disease and hemolytic uremic syndrome are possible sequelae that have been reported in the aftermath of shigellosis. Shigella can be transmitted through food, including salads (potato, tuna, shrimp, macaroni, and chicken), raw vegetables, milk and dairy products, and meat. Contamination of these foods is usually through the fecal-oral route. Fecally contaminated water and unsanitary handling by food handlers are the most common causes of contamination. Apart from hand-to-mouth infection, Shigellosis is transmitted through fomites, water and mechanical vectors like houseflies. The most common neurological symptom includes seizures.
1. Laboratory Studies: Fecal leukocytes and erythrocytes Mildly elevated hematocrit, sodium, and urea nitrogen are indicative of volume depletion in cases of shigellosis. Leukocytosis is rare. Positive findings on stool culture of a fresh fecal specimen In patients who are immunocompromised (eg, HIV), blood cultures are rarely helpful in cases of shigellosis.
2. Histologic Findings: Intense neutrophilic and mononuclear cells infiltrating the lamina propria Hemorrhage Ulcers Mucous depletion Occasional crypt abscesses Endoscopic view of colitis caused by shgellosis
Treatment consists mainly of replacing fluids and salts lost because of diarrhea. Oral replacement is satisfactory for most people, but some may need to receive fluids intravenously. In most cases, the disease resolves within four to eight days without antibiotics. Severe infections may last three to six weeks. Antibiotics, such as trimethoprim-sulfamethoxazole (Co- Trimoxazole),norfloxacin, ciprofloxacin or furazolidone, may be given when the person is very young or very old, when the disease is severe, or when there is a high risk of the infection spreading to other people. Additionally, ampicillin (but not amoxicillin) is effective in treating this disease. The severity of the symptoms and the length of time the stool contains Shigella are reduced with antibiotics. However, many strains of Shigella are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. Antidiarrheal drugs (such as diphenoxylate or loperamide) may prolong the infection and should not be used.
1. Medical Care: General supportive care of patients with shigellosis includes the following:  High fever in children should be treated. Narcotic-related antidiarrheals should be avoided. Antibiotic treatment is indicated in most patients. Antimotility agents should be avoided. They have the potential to worsen symptoms and may predispose to toxic dilation of the colon. For fluid and electrolyte supplementation, oral rehydration solutions are preferable.2. Diet: Clear liquids followed by a low residue, lactose-free diet are recommended until symptoms of shigellosis resolve.
Shigella infection produces a self-limited diarrheal illness that lasts 5-7 days and may not require antibiotics in individuals who are otherwise healthy. Antibiotic treatment is recommended for infirm or older patients, malnourished children, patients infected with HIV, food handlers, health care workers, and children in day care centers. For public health reasons, most experts recommend treating any person whose stool culture is positive for Shigella species. Moreover, antibiotics have been shown to decrease the duration of fever and diarrhea by about 2 days. The shorter duration of shedding with antibiotic therapy can reduce the risk of person-to-person spread. Ampicillin was widely used in the past but is no longer an effective empiric treatment in the United States because of antibiotic resistance. In fact, antibiotic resistance to Shigella species is widespread and increasing worldwide. Thus, antibiotic susceptibility testing is essential for the management of patients with suspected Shigella infection. Given the widespread resistance to ciprofloxacin as well as trimethoprim-sulfamethoxazole and azithromycin, a third-generation cephalosporin is appropriate empiric therapy in the setting of acute illness. The treatment of choice for HIV-infected patients is a quinolone for 5 days.
1. Antibiotics: Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. - Ceftriaxone (Rocephin): Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested. Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding have been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL. (1-2 g IV/IM qDay or divided BID for 4-14 days depending on type and severity of infection)
- Ciprofloxacin (Cipro): Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth. (Mild/Moderate/Severe: 500 mg PO q12hr for 5-7 days) - Trimethoprim-sulfamethoxazole (Bactrim, Septra, Bactrim DS, Cotrim): Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Reasonable DOC in the United States due to few resistant strains. Dosing may be based on TMP component. (Indicated for treatment of enteritis caused by susceptible strains of Shigella flexneri and Shigella sonnei DS tablet: 1 tab PO q12hr for 5 days 8-10 mg TMP/kg/day IV divided q6-12hr for up to 5 days)
- Azithromycin (Zithromax): Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected. Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues. Treats mild-to-moderate microbial infections. Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half- life.
A vaccine for shigellosis is not currently available. Until a vaccine is available, the following measures can help prevent the dissemination of shigellosis: Use of safe drinking water Chlorination of unreliable water sources Strict handwashing Refrigeration and proper preparation and cooking of foodFood handlers must be treated with antibiotics and should not be involved in food preparation as long as stool cultures are positive forShigella infection. At least 48 hours of antibiotic treatment are usually required.
Postinfection carriage is generally less than 3-4 weeks. Mild cramps and diarrhea may continue for many days to weeks after treatment of shigellosis.