eMedicine Specialties > Gastroenterology > Colon

Shigellosis

Joyann A Kroser, MD, Clinical Associate Professor of Medicine, Gastroenterology, and Hepatology, Drexel University College of Medicine

Updated: Aug 22, 2008

Introduction

Background

Shigella organisms cause bacillary dysentery, a disease that has been described since early recorded history.

Pathophysiology

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.

Frequency

United States

Approximately 450,000 cases of shigellosis are estimated to occur annually in the United States.

International

Shigellosis occurs worldwide, and it tends to occur whenever war, natural calamities (eg, earthquakes, floods), or unhygienic living conditions result in overcrowding and poor sanitation. S boydii and S dysenteriae occur more commonly internationally. Disease from Shigella species causes an estimated 1 million deaths and 165 million cases of diarrhea annually worldwide.

Mortality/Morbidity

• Bacteremia occurs primarily in malnourished children and carries a mortality rate of 20% as a result of renal failure, hemolysis, thrombocytopenia, gastrointestinal hemorrhage, and shock.
• Hemolytic uremic syndrome may complicate infections with Shigella species and Escherichia coli, and it carries a mortality rate of greater than 50%. Hemolytic uremic syndrome is characterized by acute hemolysis, renal failure, uremia, and disseminated intravascular coagulation.
• Metabolic disturbances: Hyponatremia secondary to syndrome of inappropriate antidiuretic hormone (ADH) secretion may occur.
• Leukemoid reaction: An elevated WBC count of 50,000/mm³ occurs in approximately 4% of patients, mainly in pediatric patients aged 2-10 years.
• Neurologic disease: Seizures, the most common neurologic complication, are always associated with fever and are generalized. They are typically nonrecurring and uncomplicated. Seizures are least common with S dysenteriae. The prevalence of seizures is approximately 10% across all ages.
• Encephalopathy with lethargy, confusion, and headache has been noted in up to 40% of children hospitalized with Shigella infections.
• Reactive arthritis (also known as Reiter syndrome) may occur.

Race

No racial differences exist.

Sex

No sexual predilection exists in Shigella infections.

Reactive arthritis, which is a triad of arthritis, urethritis, and conjunctivitis, occurs most commonly in men aged 20-40 years, and it occurs 2-4 weeks after infection with the Shigella species. Reactive arthritis is associated with the human leukocyte antigen (HLA)–B27 phenotype. The arthritis is asymmetrical and can be chronic and relapsing.

Age

Shigellosis is most common in children aged 6 months to 5 years.

Clinical

History

• 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)

Physical

• Lower abdominal tenderness
• Normal or increased bowel sounds
• Dehydration (occasional)

Causes

• S sonnei and S flexneri cause 90% of the cases of shigellosis.
• S dysenteriae has produced epidemic shigellosis.

Differential Diagnoses

Workup

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.

Procedures

• Sigmoidoscopy is not necessary in most cases of shigellosis.
• If distinguishing between dysentery and the acute presentation of idiopathic ulcerative colitis is urgently necessary, a colonic biopsy may be useful if it is performed within 4 days of the onset of symptoms.

Histologic Findings

• Intense neutrophilic and mononuclear cells infiltrating the lamina propria
• Hemorrhage
• Ulcers
• Mucous depletion
• Occasional crypt abscesses

Treatment

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.

Consultations

Consult a gastroenterologist or an infectious diseases expert if the Shigella infection is prolonged or if the patient experiences a severe course of shigellosis that is unresponsive to antibiotics.

Diet

Clear liquids followed by a low residue, lactose-free diet are recommended until symptoms of shigellosis resolve.

Medication

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.

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.

Dosing

Adult

Uncomplicated infections: 250 mg IM once; not to exceed 4 g
Severe infections: 1-2 g IV qd, or divided bid; not to exceed 4 g/d

Pediatric

Infants and children: 50 mg/kg/d IV/IM qd; not to exceed 1.5 g/d for 5 d

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity; hyperbilirubinemic neonates, particularly those who are premature

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, and promotion of non-susceptible organisms may occur with prolonged use or repeated therapy; caution in breast-feeding women; may displace bilirubin from albumin binding sites increasing the risk of kernicterus; caution with gallbladder, biliary tract, liver or pancreatic disease; or in patients with history of colitis or penicillin hypersensitivity

Ciprofloxacin (Cipro)

Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth.

Dosing

Adult

500 mg PO bid for 5 d

Pediatric

Not recommended

Interactions

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy

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.

Dosing

Adult

SMX 800 mg/160 mg TMP PO bid for 5 d

Pediatric

<2 months: Do not administer
>2 months: SMX 25 mg/kg PO bid for 5 d and 5 mg TMP/kg PO bid

Interactions

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenic purpura in the older population; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine; coadministration with MAOIs may increase toxicity of both agents

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, older population, patients receiving anticonvulsant therapy, patients with malabsorption syndrome); hemolysis may occur in G-6-PD deficient individuals; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation

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.

Dosing

Adult

Day 1: 500 mg PO
Days 2-5: 250 mg PO qd

Pediatric

<6 months: Not established
>6 months:
Day 1: 12 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 6 mg/kg PO qd; not to exceed 250 mg/d

Interactions

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Site reactions can occur with IV route; bacterial or fungal overgrowth may result from prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function or prolonged QT intervals

Follow-up

Deterrence/Prevention

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 food
  • Food handlers must be treated with antibiotics and should not be involved in food preparation as long as stool cultures are positive for Shigella infection.
  • At least 48 hours of antibiotic treatment are usually required.

Complications

• Chronic carriers of shigellosis are unusual.
• See Mortality/Morbidity.

Prognosis

• Postinfection carriage is generally less than 3-4 weeks.
• Mild cramps and diarrhea may continue for many days to weeks after treatment of shigellosis.

Patient Education

• Careful handwashing and stool precautions should prevent the dissemination of shigellosis.

Miscellaneous

Medicolegal Pitfalls

• Physicians should be cognizant that travelers from North America or Europe who acquire shigellosis or other bacterial dysenteries in Southeast Asia or in the Indian subcontinent may return home with organisms resistant to multiple drugs.
• Shigellosis is a public health concern, and S dysenteriae causes epidemic shigellosis.

References

1. Al-Abri SS, Beeching NJ, Nye FJ. Traveller's diarrhoea. Lancet Infect Dis. Jun 2005;5(6):349-60. [Medline].

2. Banerjee S, LaMont JT. Treatment of gastrointestinal infections. Gastroenterology. Feb 2000;118(2 Suppl 1):S48-67. [Medline].

3. Dupont HL, Edelman R, Kimmey M. Infectious diarrhea: from E coli to Vibrio. Patient Care. 1990;30:18-43.

4. Kroser JA, Metz DC. Evaluation of the adult patient with diarrhea. Prim Care. Sep 1996;23(3):629-47. [Medline].

5. Murphy GS, Bodhidatta L, Echeverria P, et al. Ciprofloxacin and loperamide in the treatment of bacillary dysentery. Ann Intern Med. Apr 15 1993;118(8):582-6. [Medline].

6. Policar M. Shigellosis. In: Ferri's Clinical Advisor: Instant Diagnosis and Treatment. 2005:752-754.

7. Sivapalasingam S, Nelson JM, Joyce K, et al. High prevalence of antimicrobial resistance among Shigella isolates in the United States tested by the National Antimicrobial Resistance Monitoring System from 1999 to 2002. Antimicrob Agents Chemother. Jan 2006;50(1):49-54. [Medline].

8. Taneja N. Changing epidemiology of shigellosis and emergence of ciprofloxacin-resistant Shigellae in India. J Clin Microbiol. Feb 2007;45(2):678-9. [Medline].

9. Wolf DC, Gianella RA. Invasive pathogens. Consultations in Gastroenterology. 1996;381-384.

Keywords

shigellosis, dysentery, bacillary dysentery, diarrhea, bacterial infection, intestinal infection, Shigella organisms, Shigella boydii, Shigella dysenteriae, Shigella sonnei, Shigella flexneri, S dysenteriae, S flexneri, S sonnei, S boydii

Contributor Information and Disclosures

Author

Joyann A Kroser, MD, Clinical Associate Professor of Medicine, Gastroenterology, and Hepatology, Drexel University College of Medicine
Joyann A Kroser, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Pennsylvania Medical Society, Phi Beta Kappa, and Philadelphia County Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Ronnie Fass, MD, Director of GI Motility Laboratory, Tucson VA Medical Center, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of Arizona School of Medicine
Ronnie Fass, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Motility Society, American Society for Gastrointestinal Endoscopy, and Israel Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Aaron Glatt, MD, Professor of Clinical Medicine, New York Medical College; President and CEO, Former Chief Medical Officer, Departments of Medicine and Infectious Diseases, New Island Hospital
Aaron Glatt, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Infectious Diseases Society of America, International AIDS Society, and Society for Healthcare Epidemiology of America
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

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