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FOODBORNE ILLNESS-SHIGELLA

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) "Food poisoning" results from bacterial transmission via contaminated food. Shigella may also be transmitted via contaminated water (as in the case with the majority of Shigella infections worldwide), or by direct fecal-oral transmission, resulting in local diarrheal outbreaks. The genus Shigella are made up of small, nonmotile, gram-negative rods that have morphologic and biochemical characteristics that are similar to E. Coli. There are 4 major subgroups of Shigella: S. dysenteriae (group A), S. flexneri (group B), S. boydii (group C), S. sonnei (group D). S. sonnei is the most common cause of Shigella infection in the United States. S. dysenteriae is more frequently found in the developing countries, where it causes severe illness.

Specific Substances

    1) Shigella (synonym)
    2) Food poisoning shigella (synonym)
    3) S. boydii (synonym)
    4) S. dysenteriae (synonym)
    5) S. flexneri (synonym)
    6) S. sonnei (synonym)
    7) Shigella food poisoning (synonym)
    8) Spoiled food, shigella (synonym)

Available Forms Sources

    A) SOURCES
    1) TRANSMISSION
    a) "Food poisoning" results from bacterial transmission via contaminated food. Shigella may also be transmitted via contaminated water (as in the case with the majority of Shigella infections worldwide), or by direct fecal-oral transmission, resulting in local diarrheal outbreaks (Pavia, 2003; Center for Food Safety and Applied Nutrition (CFSAN), 2012). Transmission may occur by food, fingers, feces, flies, and fomites (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) SUSCEPTIBLE POPULATION
    a) Anyone exposed to food contaminated with Shigella is at risk for developing symptoms, but the very young (children 6 months to 5 years of age), the elderly, and the immunocompromised (eg, AIDS patients) are at risk of developing a more severe illness. Risk of outbreaks are high in daycare centers, where close quarters and poor hand hygiene result in rapid transmission. Other populations at risk for non-food-bourne outbreaks can include: custodial care centers, Native Americans living on reservations, international travelers, homosexual men, and those in housing that has poor sanitation (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Centers for Disease Control and Prevention, 2008; Pavia, 2003; Centers for Disease Control and Prevention, 2001).
    3) TIME TO ONSET
    a) 8 to 50 hours (Center for Food Safety and Applied Nutrition (CFSAN), 2012). The incubation period can be as long as 5 days (Pavia, 2003).
    4) DURATION
    a) The illness is generally self-limiting. Symptoms generally resolve in 5 to 7 days. The organism can continue to be shed by the individual for several weeks after clinical symptoms have resolved (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Centers for Disease Control and Prevention, 2008; Pavia, 2003; Centers for Disease Control and Prevention, 2001).
    5) FOOD CONTAMINATION
    a) BEAN DIP
    1) 406 cases of drug resistant S. sonnei shigellosis were identified in 10 states in persons who had eaten a commercially available 5-layer bean dip. S. sonnei isolates from this outbreak were resistant to both ampicillin and trimethoprim-sulfamethasoxazole (Kimura et al, 2004).
    b) LETTUCE
    1) 347 persons in adjacent Texas counties had positive stool cultures for Shigella sonnei. Exposure was traced back to consumption of shredded lettuce at three restaurants, all of whom purchased the lettuce from a single processor. One food handler at the processing plant had a history of diarrhea, but no workers had positive stool cultures. The authors postulate that this worker did pass Shigella to the lettuce at the time of the outbreak (Davis et al, 1988).
    c) MEAT SALAD
    1) In a series of 72 outbreaks, the most common vehicle was meat salad (63%) (Black et al, 1978).
    d) MILK PRODUCTS
    1) Milk products are common vehicles (Black et al, 1978).
    e) OYSTERS
    1) Shigella sonnei infection in 24 persons was traced to consumption of raw oysters. The oysters were all harvested by one boat, on which one crew member had a positive stool culture for Shigella sonnei. The crew members, lacking toilets on the boats, often dumped buckets of human waste overboard, which may have contaminated the oysters in this case (Reeve et al, 1989).
    f) PARSLEY
    1) Chopped, uncooked parsley from a farm in Mexico was implicated in several restaurant-related outbreaks of S. sonnei shigellosis involving more than 400 people in several US states and in Canada. One child who ate parsley-containing food from a kiosk at a food fair was found to be the index patient at an outbreak at a daycare center, in which 5 secondary cases were reported (Centers for Disease Control and Prevention, 1999).
    g) STEWED APPLES
    1) Exposure was traced back to consumption of stewed apples (Martin et al, 1986; CDC, 1983a),
    h) VEGETABLES
    1) Exposure following consumption of vegetables (potato salad, mashed potatoes) and tossed salad has been reported (Martin et al, 1986; CDC, 1983a),
    i) WATERMELON
    1) Epidemics due to watermelon ingestion have been reported (Fredlund et al, 1987).
    6) INTENTIONAL/BIOTERRORISM
    a) Twelve lab workers developed severe diarrheal illness after eating pastries placed in the staff break room that had been intentionally contaminated with S. dysenteriae type II from the laboratory's stock strain. Eight patients had S. dysenteriae type II isolated from stool and 4 required hospitalization (Kolavic et al, 1997).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) CAUSATIVE ORGANISM
    1) The genus Shigella are made up of small, nonmotile, gram-negative, non-sporeforming, rods that have morphologic and biochemical characteristics that are similar to E. Coli. There are 4 major subgroups of Shigella: S. dysenteriae (group A), S. flexneri (group B), S. boydii (group C), S. sonnei (group D). Shigellosis (also known as bacillary dysentery) is the illness caused by Shigella.
    B) TOXIN
    1) Shiga toxin: A protein synthesis inhibitor produced by Shigella dysenteriae type 1 (Sd1). Shiga toxin is responsible for the increased severity of symptoms caused by S. dysenteriae infection, and is associated with hemolytic uremic syndrome.
    C) EPIDEMIOLOGY
    1) Shigella is the sixth most frequent cause of foodborne illness in the United States. S. sonnei is the most common cause of Shigella infection in the United States and in other developed countries. This results in an estimated 450,000 cases of gastroenteritis each year. In the developing world, S. flexneri is predominant and there are approximately 163 million cases of Shigellosis annually, resulting in 1.1 million deaths. S. dysenteriae serotype 1 (Sd1) is more frequently found in the developing countries, where it causes severe illness. Mild or severe form of infection may occur with S. boydii and S. flexneri.
    D) TARGET POPULATION
    1) Anyone exposed to food contaminated with Shigella is at risk for developing symptoms, but the very young (children 6 months to 5 years of age), the elderly, and the immunocompromised (eg, AIDS patients) are at risk of developing a more severe illness. Risk of outbreaks are high in daycare centers, where close quarters and poor hand hygiene result in rapid transmission. Other populations at risk for non-food-bourne outbreaks can include: custodial care centers, Native Americans living on reservations, international travelers, homosexual men, and those in housing that has poor sanitation.
    E) MECHANISM
    1) Bacterial invasion of intestinal enterocytes, disrupting cell function and inciting an inflammatory response.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) The illness is generally self-limiting. Symptoms can vary in severity from mild to severe, but usually begin with fever, malaise, anorexia, and occasionally vomiting or headache, followed by diarrhea. The diarrhea is most commonly watery and copious, but in severe cases can progress within hours or days to a true dysentery form, characterized by high fever, crampy abdominal pain, tenesmus, mucosal ulceration, and frequent small volume stools containing mucous and blood. Febrile seizures can occur early in the disease in children, most frequently in those less than 2 years old. Leukocytosis may occur. Hemolytic Uremic Syndrome (HUS) is a rare complication of S. dysenteriae type 1 infection, characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure.
    2) CHRONIC SYMPTOMS
    a) Reiter's syndrome, or reactive arthritis, is a rare, late complication of S. flexneri infection, consisting of a triad of arthritis, urethritis, and iritis.
    3) ROUTE OF EXPOSURE
    a) "Food poisoning" results from bacterial transmission via contaminated food (eg, raw vegetables, chicken salad, dairy products, poultry). Shigella may also be transmitted via contaminated water (as in the case with the majority of Shigella infections worldwide), or by direct fecal-oral transmission, resulting in local diarrheal outbreaks.
    4) TIME TO ONSET
    a) 8 to 50 hours. The incubation period can be as long as 5 days.
    5) DURATION
    a) Symptoms generally resolve in 5 to 7 days. The organism can continue to be shed by the individual for several weeks after clinical symptoms have resolved.

Laboratory Monitoring

    A) Obtain a CBC with differential.
    B) Monitor serum electrolytes and renal function.
    C) Stool culture confirms the diagnosis. If available, the suspected food may be cultured.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) Treatment is primarily symptomatic and supportive. Initial assessment must determine the magnitude and type of dehydration. Rapid correction of deficits and careful monitoring of intake and output are essential. Patients with mild fluid deficits can often be managed with oral fluid therapy consisting of clear liquids or specially formulated electrolyte solutions. Oral rehydration is not appropriate in children with severe circulatory collapse or intractable vomiting. In the moderately to severely dehydrated patient with normal renal function, initial rehydration should take place over 30 to 45 minutes with normal saline. This should be followed by maintenance fluids or a repeat bolus if there is evidence of ongoing hypovolemia.
    2) Treat fever with antipyretics (acetaminophen or ibuprofen).
    3) ANTIBIOTIC THERAPY: Microbial resistance is common. Although shigellosis is a self-limited disease, antibiotic treatment has been shown to decrease the duration of illness and person-to-person spread. Treatment with antibiotics should be considered in patients with severe symptoms, profound dehydration, electrolyte abnormalities, and grossly bloody stool. Fluoroquinolones, azithromycin, ceftriaxone, and cefixime are the drugs of choice when susceptibilities are unknown.
    a) CIPROFLOXACIN: DOSE: ADULTS: 500 mg orally twice daily for 5 days. CHILDREN: Avoid unless other therapies are contraindicated.
    b) AZITHROMYCIN: DOSE: ADULTS: 500 mg orally on day 1 followed by 250 mg orally daily for days 2 to 5. CHILDREN: 12 mg/kg orally as a single dose on day 1, followed by 6 mg/kg orally daily for days 2 to 5.
    c) CEFIXIME: DOSE: ADULTS: 400 mg/day orally daily. CHILDREN: 8 mg/kg/day orally in 2 divided doses.
    d) CEFTRIAXONE: DOSE: ADULTS: 1 to 2 g IV or IM daily. CHILDREN: 50 mg/day IV or IM as single dose for 3 days.
    e) Treatment with ampicillin and trimethoprim-sulfamethoxazole (TMP-SMX) is generally not recommended in cases where susceptibilities are unknown due to widespread microbial resistance.
    4) ANTIDIARRHEALS should be avoided.
    5) SEIZURES: Are generally self limited. Treat fever with antipyretics. If seizures persist or recur, treat with benzodiazepines.
    B) ANTIDOTE
    1) None.
    C) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild diarrhea may be treated on an outpatient basis if close follow-up care is available.
    2) OBSERVATION CRITERIA: Patients with severe symptoms should be sent to a healthcare facility for evaluation and treatment.
    3) ADMISSION CRITERIA: All persons with significant toxicity, dehydration, electrolyte abnormalities, or baseline immunocompromised state should be admitted for intravenous rehydration and antibiotic therapy. Patients at risk for dehydration who cannot be relied upon for adequate follow-up should be admitted.
    4) CONSULT CRITERIA: Consult a nephrologist if hemolytic-uremic syndrome develops.
    D) PITFALLS
    1) Because early symptoms and signs are nonspecific, they may be attributed to other conditions.
    E) TOXICOKINETICS
    1) The incubation period is usually 24 to 48 hours following exposure to contaminated food or water, but can be as short as 12 hours or as long as 5 days. Symptoms usually resolve in 5 to 7 days. The organism may continue to be shed for several weeks after symptoms have resolved.
    F) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis includes other bacterial (eg, E. coli) or nonbacterial (eg, viruses, plants or mushrooms ingestion) causes of acute gastroenteritis; exposure to chemicals (eg, insecticides, pesticides).

Range Of Toxicity

    A) TOXICITY: INFECTIVE DOSE: A small inoculum (10 to 200 cells) is able to produce infection, depending on the age and condition of the host.

Clinical Effects

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) The genus Shigella are made up of small, nonmotile, gram-negative, non-sporeforming, rods that have morphologic and biochemical characteristics that are similar to E. Coli. There are 4 major subgroups of Shigella: S. dysenteriae (group A), S. flexneri (group B), S. boydii (group C), S. sonnei (group D). Shigellosis (also known as bacillary dysentery) is the illness caused by Shigella.
    B) TOXIN
    1) Shiga toxin: A protein synthesis inhibitor produced by Shigella dysenteriae type 1 (Sd1). Shiga toxin is responsible for the increased severity of symptoms caused by S. dysenteriae infection, and is associated with hemolytic uremic syndrome.
    C) EPIDEMIOLOGY
    1) Shigella is the sixth most frequent cause of foodborne illness in the United States. S. sonnei is the most common cause of Shigella infection in the United States and in other developed countries. This results in an estimated 450,000 cases of gastroenteritis each year. In the developing world, S. flexneri is predominant and there are approximately 163 million cases of Shigellosis annually, resulting in 1.1 million deaths. S. dysenteriae serotype 1 (Sd1) is more frequently found in the developing countries, where it causes severe illness. Mild or severe form of infection may occur with S. boydii and S. flexneri.
    D) TARGET POPULATION
    1) Anyone exposed to food contaminated with Shigella is at risk for developing symptoms, but the very young (children 6 months to 5 years of age), the elderly, and the immunocompromised (eg, AIDS patients) are at risk of developing a more severe illness. Risk of outbreaks are high in daycare centers, where close quarters and poor hand hygiene result in rapid transmission. Other populations at risk for non-food-bourne outbreaks can include: custodial care centers, Native Americans living on reservations, international travelers, homosexual men, and those in housing that has poor sanitation.
    E) MECHANISM
    1) Bacterial invasion of intestinal enterocytes, disrupting cell function and inciting an inflammatory response.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) The illness is generally self-limiting. Symptoms can vary in severity from mild to severe, but usually begin with fever, malaise, anorexia, and occasionally vomiting or headache, followed by diarrhea. The diarrhea is most commonly watery and copious, but in severe cases can progress within hours or days to a true dysentery form, characterized by high fever, crampy abdominal pain, tenesmus, mucosal ulceration, and frequent small volume stools containing mucous and blood. Febrile seizures can occur early in the disease in children, most frequently in those less than 2 years old. Leukocytosis may occur. Hemolytic Uremic Syndrome (HUS) is a rare complication of S. dysenteriae type 1 infection, characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure.
    2) CHRONIC SYMPTOMS
    a) Reiter's syndrome, or reactive arthritis, is a rare, late complication of S. flexneri infection, consisting of a triad of arthritis, urethritis, and iritis.
    3) ROUTE OF EXPOSURE
    a) "Food poisoning" results from bacterial transmission via contaminated food (eg, raw vegetables, chicken salad, dairy products, poultry). Shigella may also be transmitted via contaminated water (as in the case with the majority of Shigella infections worldwide), or by direct fecal-oral transmission, resulting in local diarrheal outbreaks.
    4) TIME TO ONSET
    a) 8 to 50 hours. The incubation period can be as long as 5 days.
    5) DURATION
    a) Symptoms generally resolve in 5 to 7 days. The organism can continue to be shed by the individual for several weeks after clinical symptoms have resolved.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER may be noted early in the course. Fever can be seen without gastrointestinal symptoms (Schulman, 1988).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) COUGH
    1) WITH POISONING/EXPOSURE
    a) Cough and rhinorrhea have been associated with Shigella infections (Drachman, 1974).
    B) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) Pneumonia has been associated with Shigella sonnei dysentery (Margolin & Engelhard, 2003), and has been reported in an HIV-infected patient (Miller et al, 2005).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) In children, seizures associated with high fever may occur early in the course. In most cases, the seizures are generalized and self-limited (less than 10 min) (Ashkenazi et al, 1987). Meningismus and respiratory symptoms may also be present (Barkin, 1985; Edelman & Levine, 1980; Leibovici & Yahav, 1986)
    b) CASE REPORT: A 4-year-old child with shigellosis developed high fever (41 degrees C) and seizures (status epilepticus for 40 minutes) and awoke from a coma being blind, deaf, and mute. The child regained auditory and visual function, but some neurologic deficits persisted (van Dongen et al, 1993).
    c) INCIDENCE: Historically, seizures have been reported in 10% to 45% of pediatric patients with shigellosis, regardless of the severity of gastroenteritis symptoms. It has been estimated that 24% of individuals with shigellosis developed neurologic symptoms prior to the onset of gastrointestinal symptoms (Diercks et al, 2000).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Abdominal cramps, occasional vomiting and loss of appetite may occur (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Pavia, 2003).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Patients present with rapid onset of fever, severe crampy abdominal pain, and diarrhea. Stools are often profuse and watery, but may progress to a true dysentery form, characterized by high fever, crampy abdominal pain, tenesmus, and frequent small volume stools containing mucous and blood. Significant fluid losses often occur (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Pavia, 2003).
    b) Diarrhea symptoms can be so severe (ie, mucosal ulceration, rectal bleeding, severe dehydration) as to require hospitalization in immunocompromised, young children or the elderly (Center for Food Safety and Applied Nutrition (CFSAN), 2012; CDC , 2000) .
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain may occur in the lower right quadrant, mimicking appendicitis (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Schulman, 1988). However, there are several reported cases of true appendicitis, with and without perforation, occurring concomitantly with shigella dysentery (Nussinovitch et al, 1993).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) URETHRAL FINDING
    1) WITH POISONING/EXPOSURE
    a) REITER'S SYNDROME, also known as Reactive arthritis, is a late complication of S. flexneri infection. A triad of arthritis, urethritis, and iritis, this rare complication may occur in adolescents and adults with HLA-B27 status. Symptoms include burning with urination, joint pain, backache, and conjunctivitis (CDC , 2000; Simon et al, 1981).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEFT SHIFTED WHITE BLOOD CELLS
    1) WITH POISONING/EXPOSURE
    a) In Shigella infections, the WBC count is usually less than 10,000/mm(3), with a marked shift to the left; a high band count and high band to neurophil ratio is common (Ashkenazi et al, 1983).
    b) An elevated leukocyte count may be seen without gastrointestinal symptoms (Schulman, 1988).
    B) HEMOLYTIC UREMIC SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Hemolytic uremic syndrome (HUS) is a rare but important complication of S. dysenteriae type 1 infection (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Pavia, 2003), reported in 1% to 4% of children. It is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure, and is attributed to vasculopathy mediated by shiga toxin (Pavia, 2003).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERYTHEMA NODOSUM
    1) WITH POISONING/EXPOSURE
    a) Erythema nodosum and reactive arthritis were reported in two patients after having S. flexneri gastroenteritis (Neithercut et al, 1984). A similar case was described in a 13-year-old boy (Tami, 1985).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) ARTHRITIS
    1) WITH POISONING/EXPOSURE
    a) Reactive arthritis, or Reiter's syndrome, is a late complication of S. flexneri infection. A triad of arthritis, urethritis, and iritis, this rare complication may occur in adolescents and adults with HLA-B27 status. Symptoms include burning with urination, joint pain, backache, and conjunctivitis (CDC , 2000; Neithercut et al, 1984; Simon et al, 1981).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain a CBC with differential.
    B) Monitor serum electrolytes and renal function.
    C) Stool culture confirms the diagnosis. If available, the suspected food may be cultured.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) WBC count is usually normal, with a marked shift to the left in the differential count.
    B) BLOOD/SERUM CHEMISTRY
    1) Monitor serum electrolytes and renal function.
    4.1.4) OTHER
    A) OTHER
    1) CULTURES
    a) The diagnosis of shigellosis is made by serological or molecular identification of cultures isolated from stool. Stool samples should be processed within a few hours, as shigella may become difficult to cultivate (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) Shigellae is difficult to isolate from foods. FDA has developed and implemented a molecular-based method (PCR) that targets a multicopy virulence gene (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) FECAL LEUKOCYTES
    a) Fecal leukocytes are present in most of cases of Shigella infection (Bitterman, 1983). However, this finding is not specific. Patients with early shigellosis may show few, if any, fecal leukocytes.
    b) METHYLENE BLUE STAINING: Microscopic evaluation of a methylene blue-stained stool smear may reveal sheets of leukocytes; this is not specific for Shigella species.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) All persons with significant toxicity, dehydration, electrolyte abnormalities, or baseline immunocompromised state should be admitted for intravenous rehydration and antibiotic therapy.
    B) Patients at risk for dehydration who cannot be relied upon for adequate follow-up should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild diarrhea may be treated on an outpatient basis if close follow-up care is available.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a nephrologist if hemolytic uremic syndrome develops.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with severe symptoms should be sent to a healthcare facility for evaluation and treatment.

Monitoring

    A) Obtain a CBC with differential.
    B) Monitor serum electrolytes and renal function.
    C) Stool culture confirms the diagnosis. If available, the suspected food may be cultured.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Emetics and purgatives are NOT indicated as the toxin is eliminated by vomiting and diarrhea.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) A CBC with differential may be useful in diagnosis.
    2) Monitor serum electrolytes and renal function.
    3) Stool culture confirms the diagnosis. If available, the suspected food source may be cultured.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) INTRAVENOUS REHYDRATION: In the moderately to severely dehydrated patient with normal renal function, initial rehydration should take place over 30 to 45 minutes with normal saline (children: 20 mL/kg; adults: 1 to 2 L). This should be followed by maintenance fluids or a repeat bolus if there is evidence of ongoing hypovolemia.
    2) ORAL REHYDRATION: Although oral rehydration requires careful management and must be administered slowly, this approach is appropriate for patients with mild diarrhea who have normal vital signs and minimal evidence of dehydration, and are willing to take fluids orally. Oral rehydration is not appropriate in children with severe circulatory collapse or intractable vomiting (Finberg, 1982).
    C) ANTIBIOTIC
    1) SUMMARY
    a) Although shigellosis is a self-limited disease, antibiotic treatment has been shown to decrease the duration of illness and person-to-person spread. Treatment with antibiotics should be considered in patients with severe symptoms, profound dehydration, electrolyte abnormalities, and grossly bloody stool. Fluoroquinolones, azithromycin, ceftriaxone, and cefixime are the drugs of choice when susceptibilities are unknown. Treatment with ampicillin and trimethoprim-sulfamethoxazole (TMP-SMX)is generally not recommended in cases where susceptibilities are unknown due to widespread microbial resistance (Centers for Disease Control and Prevention, 2008; Pavia, 2003).
    2) CIPROFLOXACIN
    a) In a double-blind, placebo-controlled trial, ciprofloxacin significantly reduced duration of fever and diarrhea in adults with acute diarrhea secondary to Shigella infection (Pichler et al, 1987).
    b) DOSE
    1) ADULTS: 500 mg orally twice daily for 5 days (Pavia, 2003).
    2) CHILDREN: Avoid unless other therapies are contraindicated.
    3) AZITHROMYCIN
    a) Azithromycin is recommended by the American Academy of Pediatrics as treatment for shigellosis.
    b) DOSE
    1) ADULTS: 500 mg orally on day 1 followed by 250 mg orally daily for days 2 to 5.
    2) CHILDREN: 12 mg/kg orally as a single dose on day 1, followed by 6 mg/kg orally daily for days 2 to 5.
    4) CEFIXIME
    a) Cefixime has been shown to have in vitro activity against most strains of Shigella that are resistant to ampicillin or TMP-SMX (Martin et al, 2000).
    b) TREATMENT COURSE: In a study of 36 children with S. sonnei infection, as determined by positive stool cultures, children were treated with either 2- or 5-day courses of cefixime suspension (8 mg/kg/day given in a single daily dose) and found to have similar cure and clinical relapses. Despite similar cure rates, a higher rate of bacteriological failure (positive cultures at follow-up on day 7) was reported in the shorter course therapy. One limitation of the study was that the study group was based on an outbreak of S. sonnei and may not be generalizable to individuals in a nonepidemic setting (Martin et al, 2000).
    c) DOSE
    1) ADULTS: 400 mg/day orally daily (Pavia, 2003).
    2) CHILDREN: 8 mg/kg/day orally in 2 divided doses (Pavia, 2003).
    5) CEFTRIAXONE
    a) Ceftriaxone may be used for parenteral treatment of severe infections.
    b) DOSE
    1) ADULTS: 1 to 2 g IV or IM daily (Pavia, 2003).
    2) CHILDREN: 50 mg/day IV or IM as single dose for 3 days (Pavia, 2003).
    6) TRIMETHOPRIM/SULFAMETHOXAZOLE
    a) Treatment with trimethoprim-sulfamethoxazole (TMP-SMX), while effective in susceptible strains, are generally not recommended in cases where susceptibilities are unknown due to widespread microbial resistance (Centers for Disease Control and Prevention, 2008; Pavia, 2003).
    b) Trimethoprim-sulfamethoxazole (TMP-SMX) is effective for the treatment of susceptible strains of S. flexneri and S. sonnei in children and adults (Prod Info BACTRIM(TM) double strength tablets, oral tablets, 2010; Prod Info SEPTRA (R) oral tablets, double strength tablets, suspension, grape suspension, 2007).
    c) DOSE
    1) ADULTS: 160 mg TMP and 800 mg SMX orally twice a day (Pavia, 2003)
    2) CHILDREN: 10 mg/kg TMP and 50 mg/kg SMX daily orally in 2 divided doses (Pavia, 2003).
    7) AMPICILLIN
    a) Oral ampicillin was once the treatment of choice, but now resistance is almost universal (Pavia, 2003). It should only be used if the implicated strain is know to be susceptible to ampicillin.
    b) DOSE
    1) ADULTS: 500 mg orally 4 times a day (Pavia, 2003)
    2) CHILDREN: 100 mg/kg/day orally divided every 6 hours (Pavia, 2003).
    D) ANTIDIARRHEAL
    1) SUMMARY: In general, antidiarrheal agents (ie, loperamide or diphenoxylate with atropine) are likely to make the illness worse and are not recommended (CDC , 2000).
    E) SEIZURE
    1) Seizures are generally self limited. Treat fever with antipyretics. If seizures persist or recur, treat with benzodiazepines.

Range Of Toxicity

Summary

    A) TOXICITY: INFECTIVE DOSE: A small inoculum (10 to 200 cells) is able to produce infection, depending on the age and condition of the host.

Maximum Tolerated Exposure

    A) INFECTIVE DOSE: A small inoculum (10 to 200 cells) is able to produce infection, depending on the age and condition of the host (Center for Food Safety and Applied Nutrition (CFSAN), 2012; CDC , 2000).

Pharmacology Toxicology

Toxicologic Mechanism

    A) The genus Shigella are made up of small, nonmotile, gram-negative, non-sporeforming, rods that have morphologic and biochemical characteristics that are similar to E. Coli (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Haddad et al, 1998). Shigellosis (also known as bacillary dysentery) is the illness caused by Shigella (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    B) There are 4 major subgroups of Shigella: S. dysenteriae (group A), S. flexneri (group B), S. boydii (group C), S. sonnei (group D) (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    C) Shigella is the sixth most frequent cause of foodborne illness in the United States. The mildest form of shigellosis is produced by S. sonnei. It is the most common cause of Shigella infection in the United States and in other developed countries (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Centers for Disease Control and Prevention, 2008; Haddad et al, 1998). This results in an estimated 450,000 cases of gastroenteritis each year (Centers for Disease Control and Prevention, 2008). S. dysenteriae is more frequently found in the developing countries, where it causes severe illness, including hemolytic uremic syndrome (HUS) (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Centers for Disease Control and Prevention, 2009).
    D) MECHANISM OF DISEASE
    1) Bacterial invasion of intestinal enterocytes, disrupting cell function and inciting and inflammatory response (Pavia, 2003). Shigella cells enter and attach to colonic epithelial cells of the intestinal mucosa and multiply intercellularly and spread to contiguous epithelial cells, causing tissue destruction (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) Shiga toxin: A protein synthesis inhibitor produced by Shigella dysenteriae type 1 (Sd1). Shiga toxin is responsible for the increased severity of symptoms caused by S. dysenteriae infection, and is associated with hemolytic uremic syndrome (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Pavia, 2003).

References

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