Neurological complications are among the most common extra intestinal manifestations of shigellosis and can occur in as many as 45% of hospitalized patients. Headache, nuchal rigidity, confusion, memory loss, lethargy, hallucinations or delirium may manifest as acute encephalopathy in shigellosis. Alterations in consciousness including seizures, delirium and coma are known to occur during shigella infection. Shiga toxin has been postulated to play a role in the pathogenesis of altered sensorium in Shigellosis. Among shigella species, however, shiga toxin is produced in substantial quantities only by shigella dysentriae type. Studies have found that fever and metabolic alterations are known to lead to seizures and unconsciousness in shigellosis. Hyponatremia, hypoglycemia, hyperkalemia, elevated creatinine are found to be associated with encephalopathy. Similarly, our patient had hyponatremia and elevated creatinine at the time of encephalopathy. The duration of acute encephalopathy may last from 12 hours to 12 days and complete neurological recovery is achievable. However, a fatal encephalopathy is seen when associated with hyponatremia as was seen in our patient whereby there was loss of all previously attained milestones. A particularly lethal toxic encephalopathy of shigellosis known as Ekiri (in Japanese “epidemic dysentery”) is no longer a public health problem. It has been found that shorter duration of illness is also associated with unconsciousness as was seen in our patient.

Diagnosis is established by isolating the organism from stool specimens or rectal swab. Treatment of shigellosis with antibiotics and preventing development of seizures or unconsciousness by control of fever and rectifying metabolic alterations would reduce the neurological complications of shigellosis.