History

Fact Explanation
Acute onset blood and mucus diarrhoea. Shigella is an invasive enteropathogen which causes a mucosal inflammatory response in the intestine which usually involves the release of cytolethal cytotoxins resulting in epithelial cell loss and ulceration [1].
Cramping type abdominal pain. It is associated with acute inflammation of the intestinal mucosal wall [2].
Tenesmus. As a result of proctitis [3].
Fever. It occurs as part of the acute inflammatory response to infection of the colon [4].
Vomiting. Damage of the gut mucosa triggers the release of serotonin from enterochromaffin cells which acts on 5-HT receptors which in turn mediates vomiting [5].
Symptoms usually last 5-7 days. Bacillary dysentery diarrhoea is usually a self-limiting condition [6].
References
  1. CASBURN-JONES A. C. and M. J. G. FARTHING. Management of infectious diarrhoea. Gut[online] 2004, 53(2): 296-305. [viewed 30 April 2014] available from: DOI: 10.1136/gut.2003.022103
  2. JENNISON A. V. and N. K. VERMA. Shigella flexneri infection: pathogenesis and vaccine development. FEMS Microbiology Reviews[online] 2004, 28: 43–58. [viewed 30 April 2014] available from: DOI: 10.1016/j.femsre.2003.07.002
  3. DE VRIES Henry J.C. 2013 European Guideline on the management of proctitis, proctocolitis and enteritis caused by sexually transmissible pathogens. International journal of STD & AIDS[online] 2013. [viewed 30 April 2014] available from: DOI: 10.1177/0956462413516100
  4. SANDYK R. and M. J. BRENNAN. Fulminating encephalopathy associated with Shigella flexneri infection. Archives of disease in childhood[online] 1983, vol 58(1): 70-71. [viewed 30 April 2014] available from: DOI: 10.1136/adc.58.1.70
  5. CUBEDDU L. X., et al. Antiemetic activity of ondansetron in acute gastroenteritis. Alimentary Pharmacology & Therapeutics[online] 1997, 11: 185–191. [viewed 30 April 2014] available from: DOI: 10.1046/j.1365-2036.1997.97269000.x
  6. BYERS Patricia A., Herbert L. DUPONT and Millicent C. GOLDSCHMIDT. Antimicrobial susceptibilities of shigellae isolated in Houston, Texas, in 1974. Antimicrobial agents and chemotherapy[online] 1976, vol 9(2): 288-291. [viewed 3 May 2014] available from: DOI: 10.1128/AAC.9.2.288

Examination

Fact Explanation
Lower abdominal tenderness. Due to inflammation of the colonic wall [1].
Dry and sunken eyes, dry mouth, reduced skin turgor and other features of dehydration. Due to the associated fluid loss as a result of the diarrhoea [2].
Pyrexia. It occurs as part of the acute inflammatory response to infection of the colon [3].
References
  1. JENNISON A. V. and N. K. VERMA. Shigella flexneri infection: pathogenesis and vaccine development. FEMS Microbiology Reviews[online] 2004, 28: 43–58. [viewed 30 April 2014] available from: DOI: 10.1016/j.femsre.2003.07.002
  2. THAPAR Nikhil and Ian R. SANDERSON. Diarrhoea in children: an interface between developing and developed countries. The Lancet[online] 2004, 363(9409): 641-653.[viewed 30 April 2014] available from: DOI: 10.1016/S0140-6736(04)15599-2
  3. SANDYK R. and M. J. BRENNAN. Fulminating encephalopathy associated with Shigella flexneri infection. Archives of disease in childhood[online] 1983, vol 58(1): 70-71. [viewed 30 April 2014] available from: DOI: 10.1136/adc.58.1.70

Differential Diagnoses

Fact Explanation
Viral gastroenteritis. it presents as watery, non-bloody diarrhoea [1].
Crohn's disease. It presents with frequent relapses [2].
Amebiasis Since it is of gradual onset, weight loss is a common feature. Bleeding without diarrhoea is also common [3].
Salmonellosis. The blood which is associated with diarrhoea is less than that of shigellosis [4].
Campylobacter enteritis. Vomiting is rare and abdominal pain and discomfort which is severe may persist even after the diarrhoea has stopped [5].
Cholera. It presents with massive watery diarrhoea of great volume and can present with features of hypotension within 12 hours of onset of symptoms [6].
References
  1. ACHESON David, et al. Foodborne viral gastroenteritis: challenges and opportunities. Clinical infectious diseases[online] 2002, vol 35(6): 748-753. [viewed 2 May 2014] available from: DOI: 10.1086/342386
  2. GRIFFITHS Anne M., et al. Growth and clinical course of children with Crohn's disease. Gut[online] 1993, vol 34(7): 939-943. [viewed 2 May 2014] available from: DOI: 10.1136/gut.34.7.939
  3. PETRI William A. and Upinder SINGH. Diagnosis and management of amebiasis. Clinical infectious diseases[online] 1999, vol 29(5): 1117-1125. [viewed 2 May 2014] available from: DOI: 10.1086/313493
  4. ACHESON David and Elizabeth L. HOHMANN. Nontyphoidal salmonellosis. Clinical Infectious Diseases[online] 2001, vol 32(2): 263-269. [viewed 2 May 2014] available from: DOI: 10.1086/318457
  5. BUTZLER J.P. Campylobacter, from obscurity to celebrity. Clinical Microbiology and Infection[online] 2004, 10: 868–876. [viewed 2 May 2014] available from: DOI: 10.1111/j.1469-0691.2004.00983.x
  6. REIDL J. and K. E. KLOSE. Vibrio cholerae and cholera: out of the water and into the host. FEMS Microbiology Reviews[online] 2002, 26: 125–139. [viewed 2 May 2014] available from: DOI: 10.1111/j.1574-6976.2002.tb00605.x

Investigations - for Diagnosis

Fact Explanation
Stool full report revealing red blood cells and leukocytes. Shigella is an invasive enteropathogen which causes a mucosal inflammatory response in the intestine which usually involves the release of cytolethal cytotoxins resulting in epithelial cell loss and ulceration [1].
Positive findings in stool culture. The infected individual excretes the organism in stools [2].
Elevated hematocrit in full blood count. As a result of the intravascular fluid depletion due to diarrhoea [3].
References
  1. CASBURN-JONES A. C. and M. J. G. FARTHING. Management of infectious diarrhoea. Gut[online] 2004, 53(2): 296-305. [viewed 30 April 2014] available from: DOI: 10.1136/gut.2003.022103
  2. GUPTA Amita, et al. Laboratory-confirmed shigellosis in the United States, 1989–2002: epidemiologic trends and patterns. Clinical Infectious Diseases[online] 2004, vol 38(10): 1372-1377. [viewed 30 April 2014] available from: DOI: 10.1086/386326
  3. THAPAR Nikhil and Ian R. SANDERSON. Diarrhoea in children: an interface between developing and developed countries. The Lancet[online] 2004, 363(9409): 641-653.[viewed 30 April 2014] available from: DOI: 10.1016/S0140-6736(04)15599-2

Investigations - Fitness for Management

Fact Explanation
Renal function tests such as serum electrolytes and blood urea levels. To look for evidence of renal compromise so that complications such as pulmonary edema can be prevented during fluid resuscitation by maintaining the appropriate fluid requirement [1].
References
  1. BELLOMO Rinaldo, et al. Acute renal failure–definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical care[online] 2004, vol 8(4): R204. [viewed 3 May 2014] available from: DOI: 10.1186/cc2872

Management - General Measures

Fact Explanation
It is mainly supportive with fluids and antipyretics. Shigellosis is a self-limiting condition [1].
Antipyretics. Eg: Paracetomol 10-15mg/kg/dose 6 hourly. Fever occurs as part of the acute inflammatory response [2].
Oral rehydration sloutions. Mild dehydration: 50 ml/kg over 4 hours moderate dehydration: 100ml/kg over 4 hours. To compensate for the fluid and electrolyte losses associated with diarrhoea [3].
Avoid antimotility drugs. They are known to cause prolonged fever in those with shigellosis [4].
References
  1. BYERS Patricia A., Herbert L. DUPONT and Millicent C. GOLDSCHMIDT. Antimicrobial susceptibilities of shigellae isolated in Houston, Texas, in 1974. Antimicrobial agents and chemotherapy[online] 1976, vol 9(2): 288-291. [viewed 3 May 2014] available from: DOI: 10.1128/AAC.9.2.288
  2. SANDYK R. and M. J. BRENNAN. Fulminating encephalopathy associated with Shigella flexneri infection. Archives of disease in childhood[online] 1983, vol 58(1): 70-71. [viewed 30 April 2014] available from: DOI: 10.1136/adc.58.1.70
  3. THAPAR Nikhil and Ian R. SANDERSON. Diarrhoea in children: an interface between developing and developed countries. The Lancet[online] 2004, 363(9409): 641-653.[viewed 30 April 2014] available from: DOI: 10.1016/S0140-6736(04)15599-2
  4. THIELMAN Nathan M. and Richard L. GUERRANT. Acute infectious diarrhea. New England Journal of Medicine[online] 2004, vol 350(1): 38-47. [viewed 30 April 2014] available from: DOI: 10.1056/NEJMcp031534

Management - Specific Treatments

Fact Explanation
Ciprofloxacin. 20mg/kg twice daily. Antimicrobial therapy shortens the average duration of diarrhoea, decreases the duration of fever and tenesmus, and reduces the excretion of infectious organisms [1].
Nalidixic acid. 55mg/kg/day for 5 days. Antimicrobial therapy shortens the average duration of diarrhoea, decreases the duration of fever and tenesmus, and reduces the excretion of infectious organisms [1].
Trimethoprim and sulfamethoxazole. 5mg/kg and 25 mg/kg respectively, twice a day for 3 days. Antimicrobial therapy shortens the average duration of diarrhoea, decreases the duration of fever and tenesmus, and reduces the excretion of infectious organisms [1].
Antibiotic treatment should be used mainly for immunocompromised patients and malnourished children. Therapy with broad-spectrum antibiotics may facilitate the emergence of drug resistance among bacterial enteric pathogens that spread easily from person to person, such as Shigella [2].
References
  1. THIELMAN Nathan M. and Richard L. GUERRANT. Acute infectious diarrhea. New England Journal of Medicine[online] 2004, vol 350(1): 38-47. [viewed 30 April 2014] available from: DOI: 10.1056/NEJMcp031534
  2. GUERRANT Richard L., et al. Practice guidelines for the management of infectious diarrhea. Clinical Infectious Diseases[online] 2001, vol 32(3): 331-351. [viewed 3 May 2014] available from: DOI: 10.1086/318514