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Shigella Encephalopathy - A Case Report

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Shigella Encephalopathy - A Case Report

Dr Ira Shah.
Consultant Pediatrician, Mumbai.
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Shah I. Shigella encephalopathy. Pediatr Oncall J. 2006;3: 21.

Address for Correspondence
Dr Ira Shah, 1/B Saguna, 271/B St. Francis Road, Vile Parle (W), Mumbai 400056.
 
Abstract
Neurological complications are among the most common extra-intestinal manifestations of shigellosis. It is commonly associated shigella dysentry and not usually with shigella sonnei. We present a case of shigella encephalopathy in a 1 1/2 years old boy who suffered from Shigella sonnei infection.
 
Introduction
Common complications of shigella infection include encephalopathy and hemolytic uremic syndrome (HUS). It is commonly seen with Sh. dysenteriae (1). However both HUS and encephalopathy together are rare complications of Shigella. We report a 1 1/2 years old boy who had both encephalopathy and HUS following Shigella sonnei infection.
 
Case Report
One and a half years old male child born of non-consanguineous marriage presented with loss of milestones 1 month back. Patient had loose motions and fever a month back followed by generalized tonic clonic convulsions on second day of illness and oliguria on day 5 of illness followed by loss of all milestones. Patient had been admitted for same in a hospital and investigated. At the time of acute presentation, his stool examination revealed plenty of pus cells with 54-60 RBCs/hpf. His stool culture revealed shigella sonnei. His hemogram showed leucocytosis with WBC count of 33,000/cu mm [70% polymorphs, 28% lymphocytes, 1% eosinophils & 1% monocytes] with hemoglobin of 10.9 gm%, platelets of 7,60,000 cells/cu mm and ESR of 8 mm at end of 1 hour. His serum electrolytes, blood sugar were normal. His serum calcium on Day 1 of admission was 8.5 mg/dl which dropped to 7.3 mg/dl on second day at the time of convulsion while his serum sodium was 123 mEq/L. A CSF examination revealed 4 cells/cu mm (100% lymphocytes) with normal sugar and proteins. Initially his BUN and S. creatinine were normal, however on Day 5 of illness, his BUN increased to 52 mg/dl and S. creatinine increased to 2.2 mg/dl with hypokalemia (S. potassium = 1.9 mEq/L. A urine examination at that time revealed 4+ albuminuria with microscopic hematuria and granular casts. An ultrasound of the kidneys revealed medical renal disease. His hemogram still showed persistent leucocytosis (WBC count = 32,000/cu mm) with thrombocytopenia (Platelets = 88,000/cu mm) and hemoglobin = 11.9 gm%. His Reticulocyte count was 3.5% at that time. He was clinically diagnosed as a case of shigella sepsis with dysentery with encephalopathy with hemolytic uremic syndrome. He was treated with antibiotics and IV fluids following which his renal parameters normalized and diarrhea resolved and platelet count returned to normal and his urine output was adequate. He was discharged however he had lost all his milestones.

On presentation to us, he was neuroregressed and vision was diminished. He had hypertonia with brisk deep tendon reflexes and hepatomegaly. He was suspected as a case of shigella encephalopathy. His MRI brain revealed subcortical hyperintense signals involving bilateral frontoparietal lobes suggestive of post infective etiology. EEG was suggestive of diffuse cerebral slowing suggestive of severe encephalopathy. Metabolic work up for organic acidemias, urea cycle defects, lactic academia was normal [Urine aminoacidogram, plasma aminoacidogram, S. lactate & pyruvate, S. carnitine, S. ammonia, blood gases were normal]. He was thus diagnosed as a case of shigella encephalopathy with nephritis and advised physiotherapy and rehabilitation.
 
Discussion
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 (1). 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 (2). Among shigella species, however, shiga toxin is produced in substantial quantities only by shigella dysentry 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 (1). 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 (1). 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.
 
Funding
None
 
Conflict of Interest
None
 
References :
  1. Khan WA, Dhar U, Salam MA, Griffiths JK et al. Central nervous system manifestations of childhood Shigellosis: Prevalence Risk Factors and outcome. Pediatrics 1999;103:1-5.  [CrossRef]
  2. Somech R, Leitner Y, Spirer Z. Acute encephalopathy preceding shigella Infection. IMAJ 2001;3:384-385.  [PubMed]

Last Updated : 01 January 2006 Vol 3 Issue 1 Art #2

Cite this article as: :
Shah I. Shigella encephalopathy. Pediatr Oncall J. 2006;3: 21.
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