What are the possible systemic complications of shigellosis?

Updated: Aug 20, 2021
  • Author: Heba Rashid Ashraf, MD; Chief Editor: BS Anand, MD  more...
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Shigella bacteremia has a reported incidence of 0-7%. Signs that correlate with bacteremia are leukocytosis, hypothermia, temperature above 39.5ºC, severe dehydration, and lethargy. Bacteremia is more common among children than in adults, occurring primarily in those younger than 5 years. [27, 28]  In one study, among the 22 cases of bacteremia described in adults, one third of patients were older than 65 years, and more than half had an underlying disease (most commonly diabetes). [29]  However, infection with human immunodeficiency virus (HIV) does not appear to confer a significant predisposition to Shigella bacteremia.

Bacteremia is associated with an increased risk of death. [28]  Young malnourished children are at greatest risk. Additionally, the mortality rate associated with Shigella bacteremia may be higher in the setting of human immunodeficiency virus (HIV) infection. [30]  Antibiotic therapy is recommended in all patients who become bacteremic with Shigella.

Metabolic disturbances may occur. Substantial volume depletion is uncommon in shigellosis, because the stool volume is usually very low. In one study, hyponatremia, defined as serum sodium levels below 120 meq/L, was noted in 29% of patients hospitalized with diarrhea due to type 1 S dysenteriae.  [31]  However, the hyponatremia is generally caused by the syndrome of inappropriate antidiuretic hormone secretion, not volume depletion. Protein-losing enteropathy may also be observed. Increased catabolism secondary to fever, stool protein loss, decreased intake owing to anorexia, and malabsorption can exacerbate preexisting malnutrition.

Leukemoid reaction, defined as a white blood cell (WBC) count of 50,000/mm3 or more, has been observed in Bangladesh in approximately 4% of patients, most commonly in children between the ages of 2 and 10 years. In contrast, a study conducted in the United States found no association between disease severity and an elevated WBC count. [32]

Neurologic complications associated with Shigella infection may arise, of which seizures are the most common. These tend to be generalized seizures. Although they are not associated with specific neurologic deficits, they have been associated with a higher risk of death. Seizures occur almost exclusively among children younger than 15 years. The occurrence of seizures has been observed during infection with all serotypes of Shigella, and they are associated with fever (often >39ºC), an increased proportion of immature leukocytes, low serum sodium levels, and high serum potassium levels. Analysis of cerebrospinal fluid (CSF) obtained by lumbar puncture is typically normal, although up to 15% may demonstrate mild lymphocytic pleocytosis with up to 12 cells. [33]

In addition to seizures, other neurologic findings have been described in up to 40% of children hospitalized with Shigella infection, including encephalopathy with lethargy, confusion, and headache. [34]  Obtundation, coma, and posturing are rare. In cases of fatal encephalopathy, cerebral edema has been observed at autopsy.

A particularly lethal form of shigellosis, known as Ekiri syndrome, was responsible for 15,000 deaths per year in Japan during the pre-World War II era. Ekiri syndrome was associated with S sonnei infection, and was characterized by the rapid development of seizures and coma in patients with high fever and few dysenteric symptoms. The mechanism of the fulminant course of this disease remains unclear. [23]

Reactive arthritis is an uncommon complication that may follow S flexneri infection. It can occur alone or in association with conjunctivitis and urethritis. The arthritis is a sterile inflammatory arthritis. Symptoms develop 1-2 weeks following symptoms of dysentery, regardless of whether or not the dysentery was treated with antibiotics. Approximately 70% of patients with post-shigellosis reactive arthritis are HLA-B27 positive. [35]

Hemolytic-uremic syndrome (HUS) is a relatively uncommon disease; however, it is the most frequent cause of acute renal failure among infants and young children worldwide. About 90% of cases of pediatric HUS follow a diarrheal prodrome that is most commonly due to infection with enterohemorrhagic Escherichia coli (particularly type O157:H7) but that may also be induced by infection with type 1 S dysenteriae. [23, 36]

At the end of the first week and during the recovery phase of diarrheal or dysenteric symptoms, patients with HUS present with a combination of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure (initially oliguric and then anuric). These patients may be considered to have thrombotic thrombocytopenic purpura (TTP) if fever and transient neurologic symptoms are also present. Seizures occur in approximately 10% of affected patients, and stroke or cerebral edema occur in 5%.

The pathogenesis of HUS or TTP involves cytotoxic damage to the vascular endothelium. In most studies, Shiga toxin production by type 1 S dysenteriae is thought to be directly involved.

Other manifestations can also occur. In young girls, Shigella can cause vaginitis or vulvovaginitis, with or without diarrhea. [37]  Rarely, keratitis or conjunctivitis and acute myocarditis may develop. [38, 39]


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