|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 2 | Page : 176-177
Guillain-Barre syndrome in a case of typhoid fever: A less common scenario
Department of General Medicine, Institute of Post-Graduate Medical Education and Research, Kolkata, West Bengal, India
|Date of Web Publication||16-Mar-2015|
Department of General Medicine, Institute of Post-Graduate Medical Education and Research, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chakrabarti S. Guillain-Barre syndrome in a case of typhoid fever: A less common scenario. CHRISMED J Health Res 2015;2:176-7
|How to cite this URL:|
Chakrabarti S. Guillain-Barre syndrome in a case of typhoid fever: A less common scenario. CHRISMED J Health Res [serial online] 2015 [cited 2021 Oct 19];2:176-7. Available from: https://www.cjhr.org/text.asp?2015/2/2/176/153272
Guillain-Barre syndrome (GBS) is a rare complication of typhoid fever and very few case reports are available in literature. The author reports a case of typhoid fever, which was complicated by GBS.
A 43-year-old male presented to the out-patient department with high grade, continuous fever for the last 18 days. He also had severe bifrontal headache and other constitutional symptoms during this period. No history of altered sensorium, projectile vomiting, cough or altered bowel habits was present. On examination, he was febrile and had mild pallor. Vitals were stable; mild non-tender hepatomegaly (2 fingers below right costal margin) was present. No signs of meningeal irritation were noted, and fundoscopy was normal. Complete blood counts revealed normocytic, normochromic anemia with normal other parameters. Serum biochemistry was normal. Blood culture showed no growth but IgM typhi-Dot ELISA was positive in high titers. A diagnosis of typhoid fever was made, and he was started on injection Ceftriaxone and fever diminished in intensity. On the 8 th day of admission, he developed acute onset, painless, rapidly progressive weakness involving all 4 limbs simultaneously. Weakness was complete within 24 hours with no bladder-bowel involvement. Examination revealed flaccid quadriparesis - reduced motor power (3/5) in all 4 lower limbs along with global hypoflexia. Autonomic instability was absent. Rest of the neurological and other system examination was normal. Serum CPK was sent, which came out to be normal. Suspecting development of GBS, cerebrospinal fluid (CSF) examination was done, which revealed albumin-cytological dissociation (7 cells/cm 3 ; all lymphocytes with protein of 154 mg/dl and sugar 56 mg/dl). Nerve conduction study revealed demyelinating type of polyradiculoneuropathy. As weakness was rapidly progressing and threatened bulbar involvement, IVIg in recommended dosages was instituted along with intensive supportive care and physiotherapy. Muscle power started to return after 5 days of therapy. On the 15 th day of admission, power in all 4 limbs improved to 4/5. A final diagnosis of typhoid fever complicated by GBS was made. He was discharged the next day and advised follow-up in Neurology OPD.
Neurological manifestations of typhoid fever are not common but may be diverse. Central or peripheral nervous system or both may be affected.  Encephalopathy is probably the most common neurological complication of typhoid fever.  Aphasia, benign intracranial hypertension and cerebellar ataxia are other possible manifestations. ,, Cranial nerve palsies in the form of palatal palsy and abducens palsy have been noted.  The exact pathogenesis of these neurological manifestations is only postulatory till now. Probably toxemia and metabolic dysregulation along with non-specific cerebral changes like edema and hemorrhage are responsible for the neurological manifestations. , Vasculitis or some ill-defined immune-mediated mechanisms may also be responsible.  GBS following typhoid is extremely uncommon and only few case reports are available in literature. ,,,, A plausible mechanism for GBS in typhoid fever is the generation of IgM antibodies against the bacterial capsule by a non-T cell-mediated mechanism, which cross-react with myelin gangliosides.  The importance of this case report is to highlight upon the fact that a diagnosis of GBS should always be kept in mind whenever a patient of typhoid fever develops weakness. In contrast to the usual benign course of uncomplicated typhoid fever, development of GBS can dramatically change the course as without prompt diagnosis and institution of management, the condition may be life-threatening.
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