The natural habitat of shigellae is limited to the intestinal tracts of humans and other primates, where they produce bacillary dysentery.

Morphology and Identification

 A. Typical Organisms

 Shigellae are slender, nonmotile Gram-negative rods; cocco bacillary forms occur in young cultures.

B. Culture

Shigellae are facultative anaerobes but grow best aerobically. Convex, circular, transparent colonies with intact edges reach a diameter of about 2 mm in 24 hours.

C. Growth Characteristics

All strains of Shigella species ferment glucose. With the exception of Shigella sonnei, they do not ferment lactose. The inability of lactose fermentation distinguishes shigellae on differential media from other, lactose-fermenting members of the Enterobacteriaceae (eg, E. coli). Shigellae form acid from carbohydrates but rarely produce gas. They may also be divided into those organisms that ferment mannitol and those that do not (Table 1).

Table1. Pathogenic Shigella Species

Antigenic Structure

 Shigellae have a complex antigenic pattern. There is great overlapping in the serologic behavior of different species, and most of them share O antigens with other enteric bacilli.

The somatic O antigens of shigellae are lipopolysaccharides. Their serologic specificity depends on the polysaccharide. There are more than 40 serotypes. The classification of shigellae relies on biochemical and antigenic characteristics. The pathogenic species are S. sonnei, S. flexneri, S. dysenteriae, and S. boydii (Table 1)

Pathogenesis and Pathology

 Shigella infections are almost always limited to the gastrointestinal tract; bloodstream invasion is quite rare. Shigellae are highly communicable; the infective dose is low, on the order of 10² organisms (in comparison, the infectious dose for salmonellae and vibrios is usually 10⁵–10⁸). The essential pathologic process is invasion of the mucosal epithelial cells (eg, M cells) by induced phagocytosis, escape from the phagocytic vacuole, multiplication and spread within the epithelial cell cytoplasm, and passage to adjacent cells. Microabscesses in the wall of the large intestine and terminal ileum lead to necrosis of the mucous membrane, superficial ulceration, bleeding, and formation of a “pseudomembrane” on the ulcerated area. This consists of fibrin, leukocytes, cell debris, a necrotic mucous membrane, and bacteria. As the process subsides, granulation tissue fills the ulcers, and scar tissue forms.

Toxins

 A. Endotoxin

Upon autolysis, all shigellae release their toxic lipopolysaccharide. This endotoxin probably contributes to the irritation of the bowel wall.

B. Shigella Dysenteriae Exotoxin

 S. dysenteriae type 1 (Shiga bacillus) produces a heat-labile exotoxin that affects both the gut and the central nervous system. The exotoxin is a protein that is antigenic (stimulating production of antitoxin) and lethal for experimental animals. Acting as an enterotoxin, it produces diarrhea as does the E. coli Shiga-like toxin, perhaps by the same mechanism. In humans, the exotoxin also inhibits sugar and amino acid absorption in the small intestine. Acting as a “neurotoxin,” this material may contribute to the extreme severity and fatal nature of S. dysenteriae infections and to the central nervous system reactions observed in them (ie, meningismus and coma). Patients with S. flexneri or S. sonnei infections develop antitoxin that neutralizes S. dysenteriae exotoxin in vitro. The toxic activity is distinct from the invasive property of shigellae in dysentery. The two may act in sequence, the toxin producing an early nonbloody, voluminous diarrhea and the invasion of the large intestine, resulting in later dysentery with blood and pus in stools.

Clinical Findings

Members of the genus Shigella cause bloody as well as non-bloody diarrhea. After a short incubation period (1–4 days), there is a sudden onset of abdominal pain, fever, and watery diarrhea. A day or so later, as the infection involves the ileum and colon, the number of stools increases; each bowel movement is accompanied by straining and tenesmus (rectal spasms), with resulting lower abdominal pain. In more than half of adult cases, fever and diarrhea subside spontaneously within 2–5 days. However, in children and elderly adults, loss of water and electrolytes may lead to dehydration, acidosis, and even death. The illness caused by S. dysenteriae may be particularly severe.

On recovery, most persons shed dysentery bacilli for only a short period. Upon recovery from the infection, most per sons develop circulating antibodies to shigellae, but these do not protect against reinfection. Bloodstream infections rarely occur as a complication of shigellosis. Other sequelae of shigellosis include hemolytic uremic syndrome (HUS), typically associated with S. dysenteriae type 1, and Reiter’s chronic arthritis syndrome, associated with S. flexneri.

Diagnostic Laboratory Tests

 A. Specimens

For optimal organism recovery, fecal specimens should be collected during the early stages of the illness. Specimens include fresh stool, mucus flecks, and rectal swabs for culture. While whole stool is usually the preferred specimen for laboratory workup of diarrhea, rectal swabs with visible fecal staining present may be the preferred specimen for the isolation of shigellae.

B. Culture

 The materials are streaked on differential media (eg, MacConkey or EMB agar) and on selective media, such as Hektoen Enteric agar (Figure 1A) or xylose-lysine deoxycholate agar, which suppress other Enterobacteriaceae and Gram-positive organisms. Colorless (lactose-negative) colonies are inoculated into a TSI agar slant. Nonmotile organisms that fail to produce H₂S, that produce acid but not gas in the butt and an alkaline slant in TSI agar medium (Figure 1B) should be subjected to slide agglutination by specific Shigella antisera. It should be noted that Shigella species and E. coli cannot be reliably differentiated by MALDI ToF MS.

Fig1. A: Shigella species on Hektoen Enteric (HE) agar. B: Shigella species on TSI agar slant. Shigella spp. do not ferment lactose, salicin, or sucrose, and therefore appear as translucent, colorless colonies on HE agar. Shigella spp. ferment glucose, but not lactose and sucrose present in the TSI agar slant. Therefore, they produce an alkaline over acid (K/A) reaction and do not produce H₂S or gas. (Courtesy of S. Riedel.)

C. Serology

Healthy persons often have agglutinins against several Shigella species. However, serial determinations of antibody titers may show a rise in specific antibody. Serology is not used to diagnose Shigella infections.

D. Nucleic Acid Amplification Tests

There are several commercial NAATs that directly detect shigellae in fecal samples along with some of the other major enteric pathogens.

Immunity

Infection is followed by a type-specific antibody response. Injection of killed shigellae stimulates production of antibodies in serum but fails to protect humans against infection. IgA antibodies in the gut may be important in limiting reinfection; these may be stimulated by live attenuated strains given orally as experimental vaccines. Serum antibodies to somatic Shigella antigens are IgM.

Treatment

In general, shigellosis is a self-limited illness, and many patients recover without treatment within 5–7 days. Mortality is generally low in shigellosis, except in malnourished children, infants, and elderly patients. Severe dehydration, febrile seizures, septicemia, and pneumonia are potential complications of severe shigellosis. In general, oral fluid replacement is considered to be sufficient for treatment of uncomplicated shigellosis, but in high-risk patient populations intravenous fluid replacement may be required. Anti diarrheal medications (eg, loperamide and opiods) should be avoided in Shigella dysentery, as such medications may worsen the symptoms of the illness. Antibiotic treatment is recommended for the treatment of severe infections and to prevent secondary spread among people living in closed quarters (eg, family members) or during outbreaks. Because of widespread resistance in the United States, trimethoprim sulfamethoxazole and ampicillin are no longer recommended as first-line agents for treatment of shigellosis. Ciprofloxacin and ceftriaxone are effective antibiotics of choice; however, in recent years the Centers of Disease Control and Prevention (CDC) have identified emerging strains of Shigella species with potentially reduced susceptibility to ciprofloxacin. Ceftriaxone is commonly used for treatment of children with shigellosis. Finally, azithromycin has been shown as a useful antibiotic for treatment of antibiotic-resistant Shigella infections in adults and children.

Epidemiology, Prevention, and Control

 Humans are the only reservoir for Shigellae; the organisms are most commonly transmitted by “food, fingers, feces, and flies” from person to person. Sexual transmission of Shigella spp. has also been described among men who have sex with men (MSM). In general, a low infectious dose (10–100 organisms) is capable of causing disease. Shigellosis is a disease that occurs typically in situations where hygiene is compromised. In the United States, an estimated 500,000 cases of shigellosis occur every year, and up to 15% of these cases may be related to international travel. However, in comparison, an estimate 90 million cases occur, worldwide. Most cases of Shigella infection occur in children younger than 10 years of age. Shigellosis, caused primarily by S. sonnei, accounts for up to 85% of cases in the United States, and has become a common and important problem in daycare centers. S. flexneri is the predominant cause of shigellosis in developing countries. S. dysenteriae can spread widely and is a common cause of epidemic dysentery, with an associated high morbidity and mortality, particularly in developing countries. Because humans are the main recognized host of pathogenic shigellae, control efforts must be directed at eliminating the organisms from this reservoir by (1) sanitary control of water, food, and milk; sewage disposal and fly control; (2) isolation of patients and disinfection of excreta; (3) detection of subclinical cases and carriers, particularly food handlers; and (4) antibiotic treatment of infected individuals.

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مواضيع ذات صلة

Rapidly Growing Nontuberculous mycobacteria (RGM)

Slow-growing Nontuberculous Mycobacteria

Mycobacterium Tuberculosis Complex

Anaerobic Gram-Positive and Gram-Negative Cocci

The Salmonellae

Diseases Caused by Enterobacteriaceae Other than Salmonella and Shigella

Antigenic Structure of Enterobacteriaceae

Gram-Negative Rods

Gram-Positive, non–Spore- Forming Bacilli

Gram-Positive, Spore Forming Bacilli

Morphology and Identification of Enterobacteriaceae

Clinical Findings of Enterococci