Salmonella And Shigella Case File
Eugene C.Toy, MD, Cynthia Debord, PHD, Audrey Wanger, PHD, Gilbert Castro, PHD, James D. Kettering, PHD, Donald Briscoe, MD
CASE 19
A 48-year-old man presents to the emergency room with 2 days of crampy abdominal pain, nausea, vomiting, diarrhea, and fever. He has not had any blood in his stool. He denies contact with anyone with similar symptoms recently. He has not eaten any raw or unprocessed foods recently. The only food that he did not prepare himself in the past week was a breakfast of eggs “sunny-side up” and bacon that he had at a diner the day before his symptoms started. On examination, he is tired appearing; his temperature is 37.7°C (99.9°F); and his heart rate is 95 beats per minute while he is lying down, but it increases to 120 beats per minute when he sits up. His blood pressure is 145/85 mm Hg while lying down and 110/60 mm Hg when sitting. The physician interprets this as a positive “tilt test,” indicating significant volume depletion. His mucous membranes appear dry. His abdominal exam is notable for diffuse tenderness but no palpable masses, rebound, or guarding. A rectal exam reveals only heme-negative watery stool.
◆ What is the most likely etiologic agent of this infection?
◆ What are the most common sources of human infections with this organism?
ANSWERS TO CASE 19: Salmonella AND Shigella
Summary: A 48-year-old man with acute gastroenteritis has fever, a positive tilt test, abdominal pain, and diarrhea after eating eggs a day before.
◆ Most likely etiology of infection: Salmonella
◆ Most common sources of infection: Undercooked poultry, eggs, dairy products, or foods prepared on contaminated work surfaces
CLINICAL CORRELATION
This individual has the acute onset of diarrhea and vomiting. The first priorities as with any patient are the ABC’s: airway, breathing, circulation. Circulatory status is assessed by monitoring the pulse rate and blood pressure, which may be normal at rest, but abnormal on changing of position. This patient had a rise in 10 beats per minute heart rate from the lying to the sitting position, and a fall of 10 mm Hg of blood pressure. This constitutes a positive tilt test and may indicate a volume depletion of 10–25 percent. Thus, the first therapeutic goal would be volume repletion, such as with intravenous normal saline.
In humans, most cases of nontyphoidal Salmonella result from ingesting contaminated food products. Poultry, eggs, dairy products, or other foods prepared on contaminated work surfaces are the most common sources. Fecal-oral spread is common among children. Live animals, especially exotic pets such as reptiles, have also been identified as sources of infection. Host gastric acid is a primary defense against the organism, and conditions or medications that reduce gastric acidity may predispose to infection. The primary site of invasion of Salmonella is the M (microfold) cells in the Peyer’s patches of the distal ileum. M cells internalize and transfer foreign antigens from the intestinal lumen to macrophages and leukocyte. The infection can then spread to adjacent cells and lymphoid tissue. Host inflammatory responses usually limit the infection to the gastrointestinal (GI) tract, but bacteremia can occur. Bacteremia is more common in the children, elderly patients, or those with immune deficiencies, such as AIDS. Gastroenteritis is the most common clinical manifestation of Salmonella infection. Nausea, vomiting, nonbloody diarrhea, fever, and abdominal cramps starting 8–48 hours after ingestion of contaminated food are typical. The illness is generally self-limited and will last from 2 to 7 days.
Enteric fever, or typhoid fever, is a more severe form of gastroenteritis with systemic symptoms that are caused by either Salmonella typhi or Salmonella paratyphi. Symptoms include chills, headache, anorexia, weakness, and muscle aches; and later fever, lymphadenopathy, and hepatosplenomegaly; and in a third of patients a maculopapular rash (rose spots). Symptoms persist for a longer period of time than nontyphoidal gastroenteritis as does the carrier state in a small percentage of infected patients.
Gastroenteritis caused by Salmonella can mimic the signs and symptoms of other forms of infections such as Shigella. Infection with Shigella produces predominantly diarrhea, sometimes grossly bloody as a result of invasion of the mucosa. The infection is also usually self-limited; however, dehydration can occur if diarrhea is severe.
APPROACH TO SUSPECTED Salmonella AND Shigella INFECTION
Objectives
- Know the structure, characteristics, and clinical diseases associated with salmonella.
- Know the virulence, epidemiology, and pathogenesis of salmonella infections.
- Know the structure, characteristics, and clinical diseases associated with shigella.
- Know the virulence, epidemiology, and pathogenesis of shigella infections.
Definitions
Rose spots: Papular rash usually on the lower trunk leaving a darkening of the skin, characteristic of typhoid fever.
Fecal leukocytes: White blood cells found in the stool, nonspecific finding of an invasive process.
Hepatosplenomegaly: Enlargement of both the liver and the spleen which can be a feature of many diseases, including typhoid fever.
DISCUSSION
Characteristics of Salmonella and Shigella
Salmonella are motile, facultative anaerobic, nonspore-forming, gramnegative bacilli that are part of the family Enterobacteriaceae. The genus Salmonella consists of more than 2400 serotypes capable of infecting almost all animal species. However, S. typhi and S. paratyphi only colonize humans. Salmonella is protected from phagocytic destruction by two mechanisms: an acid tolerance response gene, which protects it both from gastric acid and from the acidic pH of the phagosome, and Salmonella-secreted invasion proteins (Sips or Ssps). These rearrange M-cell actin, resulting in membranes that surround and engulf the Salmonella and enable intracellular replication of the pathogen with subsequent host cell death.
Shigella is a nonmotile gram-negative bacilli that is also part of the family Enterobacteriaceae. There are 40 serotypes of Shigella that are divided into four groups or species, based on biochemical reactivity. Shigella dysenteriae is group A, Shigella flexneri is group B, Shigella boydii is group C, and
Shigella sonnei is group D. Virulence mechanisms of Shigella include their ability to invade the intestinal mucosa and production of shiga toxin, which acts to destroy the intestinal mucosa once the organism has invaded the tissue. Some strains of Escherichia coli are closely related to Shigella species and are also capable of producing shiga toxin.
Diagnosis
The diagnosis of gastroenteritis is based on the patient’s age, risk factors, exposures, and symptoms. Collection of stool and blood cultures, if fever and other systemic symptoms are present, is necessary for the definitive diagnosis. A direct exam for fecal leukocytes and occult blood may initially help narrow down the differential diagnosis. For example, blood in the stools usually indicates invasive bacterial infection. In cases of bacterial gastroenteritis, final diagnosis is made by culture of the stool for enteric pathogens such as Campylobacter, Shigella, and Salmonella. Although culture of Campylobacter requires specialized media and incubation conditions, both Salmonella and Shigella grow rapidly on routine microbiologic media. Because of the fact that stool contains many organisms that are normal flora, stools are also cultured onto selective media to aid in more rapid diagnosis.
Both Salmonella and Shigella are nonlactose fermenters that appear as clear colonies on MacConkey agar. The use of a medium that contains an indicator for production of H2S helps differentiate the two genera. Shigella does not produce H2S and appears as clear or green colonies on a media such as Hektoen enteric (HE) agar, whereas Salmonella appears black as a result of production of H2S. This is only presumptive and further biochemical testing needs to be performed because other organisms also produce black colonies on HE agar. The diagnosis of Shigella can also be made by testing for Shiga toxin directly in the stool. This cannot differentiate Shigella from the enterohemorrhagic E. coli that also produce shiga toxin and are associated with hemolytic uremic syndrome.
Treatment and Prevention
Nontyphoid Salmonella gastroenteritis is usually not treated because it is a self-limited disease, and antibiotics have not been shown to alter the course of the infection. Primary treatment should be supportive including fluid replacement if necessary. Antibiotic treatment is recommended for treatment of bacteremia, long-term carriers, or typhoid fever. Amoxicillin, sulfamethoxazole and trimethoprim (SMX-TMP), or, in areas where antibiotic resistant strains are prevalent (India, Asia and Africa), quinolones can be used. The specific choice of antimicrobial agent should be based on susceptibility testing of the patient’s isolate.
In the case of infection caused by Shigella, antibiotic therapy has been shown to be useful, especially in the prevention of person-to-person spread of the disease. Quinolones can also be used to treat, although Shigella therapy should be based on antimicrobial susceptibility testing of the isolate.
Prevention of disease caused by enteric pathogens is based on control of the contaminated source in the environment and good personal hygiene. The thorough cooking of poultry and cooking eggs until the yolk is hard can kill Salmonella and prevent infection. A vaccine does exist for prevention of typhoid fever, which is useful for travelers to endemic areas of the world. The efficacy of the vaccine is thought to be between 50 and 80 percent.
COMPREHENSION QUESTIONS
[19.1] In which of the following sites is S. typhi most likely to be found during the carrier state?
A. Blood
B. Gallbladder
C. Kidney
D. Liver
E. Spleen
[19.2] A 4-year-old has fever and diarrhea. Blood culture grows a gramnegative rod. This is most likely to be which of the following?
A. Group B Streptococcus
B. Listeria species
C. Salmonella species
D. Shigella species
[19.3] Which of the following is a frequent cause of osteomyelitis in patients with sickle cell anemia?
A. Group A Streptococcus
B. Group B Streptococcus
C. Salmonella species
D. Streptococcus pneumoniae
[19.4] Which of the following is mismatched?
A. Ecthyma gangrenosum – Pseudomonas aeruginosa
B. Halophilic – Salmonella typhi
C. K1 antigen – neonatal meningitis caused by Escherichia coli
D. Red pigment – Serratia marcescens
E. Severe dehydration – Vibrio cholerae
Answers
[19.1] B. The feces of persons who have unsuspected subclinical disease or are carriers is a more important source of contamination than frank clinical cases that are promptly isolated. The high incidence of Salmonellae in commercially prepared chickens has been widely publicized, possibly related to the use of animal feeds containing antimicrobial drugs that favor the proliferation of drug-resistant Salmonellae and their potential transmission to humans. Permanent carriers usually harbor the organisms in the gallbladder or biliary tract and, rarely, in the intestine or urinary tract.
[19.2] C. Enterocolitis is the most common manifestation of Salmonella infection. In the United States, S. typhimurium and S. enteritidis are prominent, but enterocolitis may be caused by more than 1400 strains of Salmonella. Bacteremia is rare (2–4 percent) except in immunodeficient persons. Stool cultures may remain positive for Salmonella weeks after clinical recovery. Streptococci and Listeria stain grampositive, and Shigella organisms rarely, if ever, enter the blood stream from the intestines.
[19.3] C. Hematogenous infections account for about 20 percent of cases of osteomyelitis and primarily affect children, in whom the long bones are infected. More than 95 percent of these cases are caused by a single organism, with Staphylococcus aureus accounting for 50 percent of the isolates. Group B streptococci and E. coli are common during the newborn period and group A streptococci and Haemophilus influenzae in early childhood. Salmonella species and S. aureus are major causes of long-bone osteomyelitis complicating sickle cell anemia and other hemoglobinopathies. Septic arthritis may be encountered in sickle cell disease with multiple joints infected. Joint infection may result from spread of contiguous osteomyelitis areas. Salmonella infection is seen more often in osteomyelitis than in septic arthritis.
[19.4] B. Organisms requiring high salt concentrations are called halophilic. Usually, this refers to microorganisms that are capable of living or surviving in an ocean or saltwater area. Vibrios are especially well known for this ability. Salmonella typhi (typhoid fever) multiply in intestinal lymphoid tissue and are excreted in stools. They are hardy survivors in water sources, but they do not survive in halophilic conditions as well as Vibrios.
MICROBIOLOGY
PEARLS
❖ Shigella is a common cause of gastroenteritis, which
can be bloody as a result of the ability of the organism
to invade the mucosa. Because of the low inoculum required for
infection, person-toperson transmission may occur in close contacts.
❖ Salmonella nontyphi is associated with a self-limited
diarrhea associated with ingestion of contaminated food
products such as undercooked eggs.
❖ Salmonella and Shigella are nonlactose fermenters that are
differentiated in the laboratory by production of H2S; the appearance of black colonies on Hektoen enteric agar
result from Salmonella species.
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REFERENCES
Dupont HL. Shigella species (bacillary dysentery) In: Mandell GL, Bennett JE,
Dolin R, eds. Principles and Practice of Infectious Diseases, 5th ed.
Philadelphia, PA: Churchill Livingstone, 2000:2363–69.
Mandell GL, Bennett, JE, Dolin, R eds. Principles and Practice of Infectious
Disease. 5th ed. Philadelphia, PA: Churchill Livingstone, 2000:2344–63.
Miller SI, Pegues DA. Salmonella species, including salmonella typhi. In:
Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious
Diseases, 5th ed. Philadelphia, PA: Churchill Livingstone, 2000.
Murray PR, Rosenthal KS, Pfaller MA. Enterobacteriaceae. In: Murray PR,
Rosenthal KS, Pfaller MA. Medical Microbiology, 5th ed. St. Louis, MO:
Mosby, 2005:266–80.
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