Shigella Infection Clinical Presentation

  • Author: Jaya Sureshbabu, MBBS, DCh, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg); Chief Editor: Russell W Steele, MD   more...
 
Updated: Jul 22, 2010
 

History

  • Populations that are at high-risk for shigellosis include the following:
    • Children in daycare centers (< 5 y) and their caregivers
    • Persons in custodial institutions
    • International travelers
    • Homosexual men
    • People living in crowded conditions with poor sanitary facilities and inadequate clean water supply (eg, refugee camps, shelters for displaced people)
    • People with human immunodeficiency virus (HIV) infection[2]
  • Symptoms include the following:
    • Sudden onset of severe abdominal cramping, high-grade fever, emesis, anorexia, and large-volume watery diarrhea. Seizures may be an early manifestation.
    • Abdominal pain, tenesmus, urgency, fecal incontinence, and small-volume mucoid diarrhea with frank blood (fractional stools) may subsequently occur.
  • Signs include the following:
    • Elevated temperatures (as high as 106 º F) are documented in approximately one third of cases, and a generally toxic appearance is noticed.
    • Tachycardia and tachypnea may occur secondary to fever and dehydration. Depending on the degree of dehydration, dry mucous membranes, hypotension, prolonged capillary refill time, and poor skin turgor may be present.
    • Abdominal tenderness is usually central and lower, although it may be generalized.
  • Extraintestinal manifestations are as follows:
    • CNS symptoms include severe headache, lethargy, meningismus, delirium, and convulsions lasting less than 15 minutes, especially with S dysenteriae.[3] Severe toxic encephalopathy is rare, but lethal complications occur when initial symptoms are followed by sensory obtundation, seizures, coma, and death in 6-48 hours. The pathogenesis of neurologic manifestations during shigellosis is unclear. However, data now clearly demonstrate that Stx is not responsible.
    • Regarding HUS, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure have been reported with S dysenteriae because of vasculopathy mediated by Stx. The principal organ affected in Stx1-mediated HUS is the kidney. This is presumed to be the consequence of the high renal blood flow and abundant baseline expression and high inducibility of the Stx glycolipid receptor Gbe in the glomerular microcirculation. Manifestations of the disease arise due to 2 primary pathogenetic mechanisms: (1) direct Stx-mediated injury to vascular endothelial cells that leads to tissue ischemia and dysfunction and (2) a systemic inflammatory response triggered by Stx-mediated release of a wide range of cytokines and chemokines, including IL-6, IL-8, and tumor necrosis factor-alpha.
    • Septicemia is rare, except in malnourished children with S dysenteriae infection. Septicemia is sometimes caused by other gram-negative organisms and is related to loss of mucosal integrity by Shigella infection.
    • Profound dehydration and hypoglycemia is more common with S dysenteriae infection.
    • Shigellasepsis may be complicated with disseminated intravascular coagulation (DIC), bronchopneumonia, and multiple organ failure in lethal cases.
    • Arthritis, urethritis, conjunctivitis syndrome is commonly observed in adults carrying human leukocyte antigen (HLA)-B27 histocompatibility antigen.
    • Cholestatic hepatitis, if present, is usually mild.
    • Myocarditis is identified with cardiogenic shock, arrhythmias, and heart block.
    • Rectal prolapse, toxic megacolon, and intestinal obstruction may be present.
    • Shigellosis in the first 6 months of life is rare probably due to presence of antibodies to both virulence plasmid-coded antigens and lipopolysaccharides in the breast milk. Shigellosis in the neonatal period results from mother-to-infant fecal-oral transmission during labor and delivery, usually from asymptomatic mothers.
    • Symptoms usually begin on the third day of life.
    • Septicemia and chronic diarrhea are common.
    • Fever may be absent.
    • Diarrhea is not usually bloody.
    • Intestinal perforation and mortality are more common in this group than in older children.
  • Shigellosis in patients with HIV infection is often a protracted, chronic, relapsing disease (even when treated with antibiotics). Bacteremia is rare, although it can occur in immunocompromised or malnourished patients.
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Physical

  • Physical examination during acute illness reveals a febrile ill-appearing child. Fever with a temperature as high as 39-40 º C may be noted.
  • The patient's hydration status should be carefully assessed. Especially note dryness of the oral mucosa, lack of tears, decreased urine output, and loss of skin turgor.
  • Abdominal examination may reveal generalized mild-to-moderate tenderness with no guarding or rigidity.
  • In a child who presents with febrile seizures, careful neurologic examination is mandatory to exclude meningitis.
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Causes

  • The primary mode of transmission of Shigella infection is fecal-oral contamination by the gram-negative aerobic bacilli.
  • Contaminated food usually looks and smells normal. Food may become contaminated by infected food handlers who forget to wash their hands with soap after using the bathroom. Vegetables can become contaminated if they are harvested from a field with sewage in it.
  • Outbreaks of shigellosis have also occurred among men who have sex with men.
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Contributor Information and Disclosures
Author

Jaya Sureshbabu, MBBS, DCh, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg),  Consultant, Department of Pediatrics and Neonatology, Credence Institute for Womens Health and Fertility Research, Thiruvananthapuram

Jaya Sureshbabu, MBBS, DCh, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg), is a member of the following medical societies: Indian Academy of Pediatrics, Indian Medical Association, Royal College of Paediatrics and Child Health, Royal College of Physicians and Surgeons of Glasgow, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Coauthor(s)

Poothirikovil Venugopalan, MBBS, MD, FRCP(Glasg), FRCPCH,  Consulting Staff, Department of Child Health, University Hospital of North Tees and Hartlepool, UK

Poothirikovil Venugopalan, MBBS, MD, FRCP(Glasg), FRCPCH, is a member of the following medical societies: British Cardiac Society, Royal College of Paediatrics and Child Health, and Royal College of Physicians and Surgeons of Glasgow

Disclosure: Nothing to disclose.

Walid Abuhammour, MD  FAAP, Professor of Pediatrics, Michigan State University, Director of Pediatric Infectious Disease, Department of Pediatrics, Hurley Medical Center

Walid Abuhammour, MD is a member of the following medical societies: American Medical Association, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Glenn Fennelly, MD, MPH  Director, Division of Infectious Diseases, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Clinical Associate Professor of Pediatrics, Albert Einstein College of Medicine

Glenn Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Larry I Lutwick, MD  Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

References

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