| Patient Education |
|
Click here for patient education.
|
|
You are in: eMedicine Specialties >
Gastroenterology > Colon
Shigellosis
Article Last Updated: Feb 5, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 10  
Author: Joyann A Kroser, MD, Clinical Associate Professor of Medicine, Department of Internal Medicine, Division of Gastroenterology, Drexel University College of Medicine
Joyann A Kroser 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
Editors: 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; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Aaron Glatt, MD, Professor of Clinical Medicine, New York Medical College; Chief Medical Officer, Departments of Medicine and Infectious Diseases, New Island Hospital; Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine; 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
Author and Editor Disclosure
Synonyms and related keywords:
bacillary dysentery, Shigella organisms, Shigella boydii, Shigella dysenteriae, Shigella sonnei, Shigella flexneri
Background
Shigella organisms cause bacillary dysentery, a disease that has been described since early recorded history.
Pathophysiology
Shigella species 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, invasion of the colonic epithelium, which is dependent on a plasmid-mediated virulence factor, and 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 15,000 cases of shigellosis are reported 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. Shigella boydii and Shigella dysenteriae occur more commonly internationally. In impoverished countries, Shigella flexneri and S dysenteriae cause more than 600,000 deaths per year.
Mortality/Morbidity
Infection with Shigella species may be associated with extragastrointestinal complications.
- 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 greater than 50%. Hemolytic uremic syndrome is characterized by acute hemolysis, renal failure, uremia, and disseminated intravascular coagulation.
Race
No racial differences exist.
Sex
No sexual predilection exists in Shigella infections. Reiter syndrome, 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. Reiter syndrome 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.
History
- Acute bloody diarrhea
- Tenesmus
- Passage of mucus
- Fever (1-3 d after exposure)
- 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
- Shigella sonnei and Shigella flexneri cause 90% of the cases of shigellosis.
- S dysenteriae has produced epidemic shigellosis.
Amebiasis
Cholera
Clostridium Difficile Colitis
Colon Cancer, Adenocarcinoma
Crohn Disease
Salmonellosis
Ulcerative Colitis
Yersinia Enterocolitica
Lab Studies
- Fecal leukocytes and erythrocytes
- Mildly elevated hematocrit, sodium, and urea nitrogen are indicative of volume depletion.
- Leukocytosis is rare.
- Positive findings on stool culture of a fresh fecal specimen
- In patients who are immunocompromised (eg, because of HIV), blood cultures rarely may be helpful.
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
- Mucus depletion
- Occasional crypt abscesses
Medical Care
- Fluid and electrolyte supplement: Oral rehydration solutions are preferable.
- General supportive care
- Treat high fever in children.
- Avoid narcotic-related antidiarrheals.
- Antibiotic treatment is indicated in most patients.
Consultations
Consult a gastroenterologist or infectious diseases expert if the infection is prolonged or the patient experiences a severe course that is unresponsive to antibiotics.
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. Ampicillin was widely used in the past but is no longer an effective empiric treatment in the United States because of antibiotic resistance.
Drug Category: Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
| Drug Name | Trimethoprim-sulfamethoxazole (Bactrim, Septra, Bactrim DS, Cotrim) |
|---|
| Description | 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. |
|---|
| Adult Dose | SMX 800 mg/160 mg TMP PO bid for 5 d |
|---|
| Pediatric Dose | <2 months: Do not administer
>2 months: SMX 25 mg/kg PO bid for 5 d and 5 mg TMP/kg PO bid |
|---|
| Contraindications | Documented hypersensitivity; megaloblastic anemia due to folate deficiency |
|---|
| 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 |
|---|
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
|---|
| 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 |
|---|
| Drug Name | Ciprofloxacin (Cipro) |
|---|
| Description | Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth. |
|---|
| Adult Dose | 500 mg PO bid for 5 d |
|---|
| Pediatric Dose | Not recommended |
|---|
| Contraindications | Documented hypersensitivity |
|---|
| 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) |
|---|
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
|---|
| 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 |
|---|
Complications
Prognosis
- Postinfection carriage generally is less than 3-4 weeks.
- Mild cramps and diarrhea may continue for many days to weeks after treatment.
Patient Education
- Careful handwashing and stool precautions should prevent dissemination.
Medical/Legal Pitfalls
- Physicians should be cognizant that travelers from North America or Europe who acquire shigellosis or other bacterial dysenteries in Southeast Asia or the Indian subcontinent may return home with organisms resistant to multiple drugs.
- Shigellosis is a public health concern, and S dysenteriae causes epidemic shigellosis.
- Al-Abri SS, Beeching NJ, Nye FJ. Traveller's diarrhoea. Lancet Infect Dis. Jun 2005;5(6):349-60. [Medline].
- Banerjee S, LaMont JT. Treatment of gastrointestinal infections. Gastroenterology. Feb 2000;118(2 Suppl 1):S48-67. [Medline].
- Dupont HL, Edelman R, Kimmey M. Infectious diarrhea: from E coli to Vibrio. Patient Care. 1990;30:18-43.
- Kroser JA, Metz DC. Evaluation of the adult patient with diarrhea. Prim Care. Sep 1996;23(3):629-47. [Medline].
- Murphy GS, Bodhidatta L, Echeverria P. Ciprofloxacin and loperamide in the treatment of bacillary dysentery. Ann Intern Med. Apr 15 1993;118(8):582-6. [Medline].
- Policar M. Shigellosis. In: Ferri's Clinical Advisor: Instant Diagnosis and Treatment. 2005;752-754.
- Wolf DC, Gianella RA. Invasive pathogens. Consultations in Gastroenterology. 1996;381-384.
Shigellosis excerpt Article Last Updated: Feb 5, 2007
|
