The new imitator

P. Poovarasan1, Suresh Chelliah^1,*, S. Thilagavathy², V. Senthilvelmurugan³

¹Department of Pediatrics, Kauvery Hospital, Cantonment, Trichy, India

²Department of Microbiology, Kauvery Hospital, Cantonment, Trichy, India

³Department of Radiodiagnosis, Kauvery Hospital, Cantonment, Trichy, India

*Correspondence: chelliah.suresh@yahoo.in

Abstract

A 7-year-old obese child presented with fever, vomiting, irrelevant and slurred speech with abnormal movements of upper limbs. Acute CNS infection was considered and IV antibiotics and antivirals were started pending blood culture report. MRI Brain showed Cytotoxic Lesion of Corpus Callosum (CLOCCs). Covid IgG was positive raising a suspicion of MIS-C. Methylprednisolone was given. At around the same time. blood culture revealed growth of S.typhi. Antimicrobials other than Ceftriaxone were stopped. His sensorium gradually improved. Obtaining cultures before antibiotic use improve the chances of identifying the offending microorganism and guides appropriate care.

Background

In the days of the old, syphilis used to be called a great imitator. The authors present another imitator that was unmasked and overcome.

Case Presentation

A 7-year-old obese boy was brought to our emergency department with fever for 5 days following which he developed vomiting, irrelevant and slurred speech for 2 days, and abnormal movement of upper limbs. On examination, he was irritable, febrile, and oriented at times. He had abnormal, movement of both hands off and on. There was no neck stiffness. Deep tendon reflexes were brisk and planters were extensor. Acute meningoencephalitis and autoimmune encephalitis were considered.

Blood counts showed leukopenia and thrombocytopenia with elevated CRP and ESR. Serum urea and creatinine were normal. There was hyponatremia. IV antibiotics were started pending blood culture report.

MRI Brain done showed a Cytotoxic Lesion of Corpus Callosum (CLOCCs) (Fig. 1). CSF analysis was non-contributory. COVID IgG was positive. Serum ferritin, D-Dimer, and NT Pro BNP were elevated raising a suspicion of MIS-C. Echo showed mild global hypokinesia of LV, and normal coronary artery. Methylprednisolone was given and parents were counselled regarding the use of Intravenous immunoglobulin (IVIG).

Fig. 1. Cytotoxic Lesion of Corpus Callosum.

At around the same time, the growth of Gram-negative bacteria, later confirmed to be S. typhi was reported. Anti-microbials other than Ceftriaxone was stopped. His sensorium gradually improved. He was discharged after 7 days of Ceftriaxone. Cefixime was given for 7 days after discharge.

Discussion

The term ‘typhoid’ is derived from the Greek word ‘Typhos’ meaning smoke which further connotes apathy and confusion. Sir William Osler described typhoid as a semi-conscious state which is characterized by a blank stare with muttering, non-interactive, just arousable patient. Typhoid fever is caused by Salmonella enterica serovar typhi (S. typhi), a gram-negative bacterium. It is also caused by Salmonella paratyphi A, S. paratyphi B (Schotmulleri) and S. paratyphi C (Hirschfeldii). It infects 11 million to 20 million people every year in the world, resulting in 120,000 to 220,000 fatalities. India is burdened by the disease with 63,45,776 cases per year [1]. Encephalopathy usually occurs in the third week of illness. Older children and young adults are at higher risk of developing encephalopathy in enteric fever in comparison to young children [2]. Acute neuropsychiatric illness, spasticity, and clonus, ataxia, aphasia, cerebritis, meningitis are varied neurological presentations [3]. A higher risk of complication is seen among three categories of patients. First, patients whose antibiotic treatment for typhoid was started late. Second, patients with resistant strains, and third, the younger demographic. Complications of typhoid fever have been estimated to occur in 10 to 15% of hospitalized patients. Overall, the complications with the highest prevalence (95% CI) reported by three studies are encephalopathy, gastrointestinal bleeding, and nephritis, with a prevalence of 7.3, 5.7, and 4.8% respectively as reported in a meta-analysis [1].

CLOCCs demonstrate reduced diffusion from cytotoxic edema. They are usually ovoid and located in the splenium but may be more extensive with involvement of the body of the corpus callosum and the genu.

CLOCCs are secondary lesions associated with drug therapy, malignancies, infections, MIS-C, SAH, metabolic disorders, trauma, and other entities enteric fever, drugs, malignancy, infarction, demyelination, PRES (Posterior Reversible Encephalopathy Syndrome) and Cerebral fat embolism.

CLOCCs due to infarction and demyelination tend to appear asymmetrical, the former one usually appears after aneurysm clipping surgery. CLOCCs are frequently but not invariably reversible [4]. When they are present, the underlying cause should be sought and addressed.

Conclusion

Common illnesses are common. Appropriate cultures are mandatory before starting Antibiotics

Author Contributions

Poovarasan wrote the manuscript with valuable inputs from Senthil Velmurugan who was also instrumental in the diagnosis as was Thilagavathy. Suresh Chelliah was involved primarily, in the management, edited the article, and will act as guarantor.

References

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Starkey J, Kobayashi N, Numaguchi Y, et al. Cytotoxic lesions of the corpus callosum that show restricted diffusion: Mechanisms, causes and manifestations. RadioGraphics 2017;37(2).