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Table of Contents    
Year : 2011  |  Volume : 59  |  Issue : 2  |  Page : 270-272

Magnetic resonance imaging findings in a fatal case of Salmonella typhi-associated encephalopathy: A case report and literature review

1 Department of Radiology, Christian Medical College & Hospital, Vellore, Tamil Nadu, India
2 Department of Neurological Sciences, Neurology Unit, Christian Medical College & Hospital, Vellore, Tamil Nadu, India
3 Department of Medicine, Christian Medical College & Hospital, Vellore, Tamil Nadu, India

Date of Submission16-Dec-2010
Date of Decision05-Jan-2011
Date of Acceptance06-Jan-2011
Date of Web Publication7-Apr-2011

Correspondence Address:
Munawwar Ahmed
Assistant Professor, Department of Radiology, CMC Hospital, Vellore, TN
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.79145

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 » Abstract 

We describe MRI findings in a fatal case of culture proven Salmonella typhi-associated encephalopathy. MRI findings included symmetrical diffuse abnormal signal in centrum semiovale, periventricular and deep white matter, splenium of corpus callosum and cerebellar deep white matter with central area of restricted diffusion. There was no contrast enhancement, significant edema or mass effect. Previous literature is also reviewed for imaging findings in Salmonella associated encephalopathy.

Keywords: Salmonella associated encephalopathy, demyelination, magnetic resonance imagaing

How to cite this article:
Ahmed M, Sureka J, Mathew V, Jakkani RK, Abhilash K. Magnetic resonance imaging findings in a fatal case of Salmonella typhi-associated encephalopathy: A case report and literature review. Neurol India 2011;59:270-2

How to cite this URL:
Ahmed M, Sureka J, Mathew V, Jakkani RK, Abhilash K. Magnetic resonance imaging findings in a fatal case of Salmonella typhi-associated encephalopathy: A case report and literature review. Neurol India [serial online] 2011 [cited 2022 May 23];59:270-2. Available from: https://www.neurologyindia.com/text.asp?2011/59/2/270/79145

 » Introduction Top

Non-infectious neurological complications of  Salmonella More Details typhi infection occur in 3-35% of patients, mostly in pediatric age group. Very few reports have described the imaging findings of Salmonella-associated encephalopathy (SAE). [1],[2] We describe magnetic resonance imaging (MRI) findings in a fatal case of SAE due to S. typhi. This is probably the first case report describing the bilateral diffuse symmetrical MRI brain findings in a fatal case of culture proven SAE.

 » Case Report Top

A 17-year-old female presented to the Emergency Department with high-grade fever of 3 days duration and altered mental status and seizures of 1 day duration. She had an episode of 1 day fever followed by papulo-vesicular rashes all over the body 12 days back which regressed spontaneously leaving scars and hyperpigmentation. She did not have any other history of prior co-morbidities. On examination, the patient was febrile, drowsy and disoriented, with a Glasgow Coma Scale (GCS) score of 13/15. There was increased tone in both the lower limbs with exaggerated deep tendon reflexes and extensor plantar response. Rest of the neurological examination was normal. A diagnostic possibility of varicella encephalitis was considered and she was started on intravenous (IV) acyclovir and dexamethasone empirically.

Laboratory tests showed the following: white blood cell count 4700 (neutrophils 81%, lymphocytes 17%, monocytes 2%); hemoglobin 10.9 g%; erythrocyte sedimentation rate (ESR) 5 mm first hour; platelet count 81,000/mm 3 ; and normal liver functions. Cerebrospinal fluid (CSF) showed cells 8 lymphocytes/mm 3 , protein level of 27 mg/dl, and glucose of 94 mg/dl. CSF gram stain and culture was negative for bacterial growth. CSF polymerase chain reaction (PCR) for varicella virus, cytomegalovirus, Epstein-Barr virus, herpes simplex 1 and 2 and adenovirus was negative. Serum rapid HIV Elisa test was negative. Tests for all the vasculitis markers were negative.

Blood culture taken at admission grew S. typhi on day 6 of hospitalization, with susceptibility to ciprofloxacin, co-trimoxazole, ampicillin and chloramphenicol and resistance to nalidixic acid. She was then treated with oral gatifloxacin, high dose of dexamethasone and mannitol. Her fever settled down but sensorium did not improve and she had further few episodes of seizures. Considering the possibility of SAE, MRI of brain was done on day 7 of her hospitalization. MRI revealed bilateral diffuse symmetrical hyperintense signal on long TR sequences involving the centrum semiovale, periventricular and deep white matter (WM) and splenium of corpus callosum (CC) with minimal subcortical and deep cerebellar WM involvement [Figure 1]a-c. Diffusion-weighted imaging (DWI) revealed central area of diffusion restriction in the involved areas [Figure 2]a and b. No abnormal enhancement was seen on post gadolinium study [Figure 3]. Considering the diagnosis of postinfectious demyelinating process, she was started on high doses of IV methylprednisolone. However, she continued to deteriorate and died on day 13 of her hospitalization.
Figure 1: (a, b) Axial FLAIR images show hyperintense signal in centrum semiovale, periventricular and deep WM and splenium of CC. Corresponding areas were hypointense on T1-weighted images (not shown). (c) Mild hyperintense signal was also present in the deep white matter of both cerebellar hemispheres

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Figure 2: (a, b) Axial DWI and ADC images show central area of diffusion restriction in centrum semiovale

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Figure 3: Axial T1-weighted post gadolinium image shows no enhancement in the hypointense areas

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 » Discussion Top

A wide spectrum of non-infectious neurological complications of typhoid fever include encephalopathy, neuropsychiatric disorder, cerebral edema, cerebellar ataxia,  Parkinsonism More Details, acute disseminated encephalomyelitis and brainstem encephalitis. Exact pathophysiology of these complications is not clear. Of the various mechanisms that have been proposed, immune mediated process and endotoxemia are the most widely accepted mechanisms. Early SAE is an uncommon and potentially fatal neurological complication. Pathologic findings in SAE are nonspecific and include cerebral edema, minimal ischemia, vasculitis, perivenous demyelination and cellular infiltrates. [3],[4]

The literature on imaging findings of SAE and other neurological complications is sparse. MRI findings include multifocal cerebellar subcortical WM hyperintense lesions in a case of acute cerebellar ataxia post typhoid fever [1] and focal areas of reversible restricted diffusion in the splenium of the CC and bilateral parietal subcortical WM in a patient with Salmonella enteridis-associated encephalopathy (non-typhoid fever). [2] These findings were attributed to cytotoxic edema. [2] Case reports with normal MRI brain and abnormal EEG [5],[6] and CT showing diffuse vasogenic cerebral edema have been reported. [7],[8] Bilateral symmetrical WM hypodensity with minimal gyral enhancement and no significant mass effect was described in a case of S. typhi-associated cerebritis. [9] All these patients had a good clinical recovery with treatment. In a series of eight patients with non-typhoidal SAE, MRI and CT showed diffuse cerebral edema without any focal lesion. [3] There were three fatalities in this series. These observations suggest that abnormal findings on MRI may not have any prognostic significance.

In the present patient, the MRI lesions were suggestive of demyelinating process. [10] However, we could not confirm it on histopathology or follow-up. We believe endotoxemia and/or sepsis may be the possible mechanisms in our patient as the temporal evolution of clinical features does not support the immune mediated mechanism. Mechanism of brain injury in sepsis-associated encephalopathy includes both inflammatory and non-inflammatory processes that induce blood-brain barrier breakdown, dysfunction of intracellular metabolism and brain cell death. [11] In conclusion, SAE can be of multiple pathophysiological mechanisms, and accordingly, the MRI findings can range from normal to diffuse white matter involvement including CC as in the present case.

 » References Top

1.Murthy JM, Kishore LT. Case report. MR findings in cerebellar ataxia after enteric fever. J Comput Assist Tomogr 1997;21:216-7.  Back to cited text no. 1
2.Kobuchi N, Tsukahara H, Kawamura Y, Ishimori Y, Ohshima Y, Hiraoka M, et al. Reversible diffusion-weighted MR findings of Salmonella enteritidis-associated encephalopathy. Eur Neurol 2003;49:182-4.  Back to cited text no. 2
3.Arii J, Tanabe Y, Miyake M, Mukai T, Matsuzaki M, Niinomi N, et al. Clinical and pathologic characteristics of nontyphoidal Salmonella encephalopathy. Neurology 2002;58:1641-54.  Back to cited text no. 3
4.Ramachandran S, Wickremesinghe HR, Perera MV. Acute disseminated encephalomyelitis in typhoid fever. Br Med J 1975;1:494-5.   Back to cited text no. 4
5.Uysal H, Karademir A, Kilinç M, Ertürk O. Salmonella encephalopathy with seizure and frontal intermittent rhythmic delta activity. Infection 2001;29:103-6.  Back to cited text no. 5
6.Ichikawa K, Kajitani A, Tsutsumi A, Takeshita S. Salmonella encephalopathy successfully treated with high-dose methylprednisolone therapy. Brain Dev 2009;31:782-4.  Back to cited text no. 6
7.van de Wetering J, Visser LG, van Buchem MA, van der Hoeven JG. A case of typhoid fever complicated by unexpected diffuse cerebral edema. Clin Infect Dis 1995;21:1057-8.  Back to cited text no. 7
8.El-Khoury M, Naoushi H, Sawaya R, Aoun E, Nassar NT, Sharara AI. Reversible encephalopathy secondary to paratyphoid infection and concomitant acute hepatitis A. South Med J 2005;98:723-5.  Back to cited text no. 8
9.Rajeshwari K, Yadav S, Puri RK, Khanijo CM, Sethi Y. Cerebritis in typhoid fever. Indian Pediatr 1995;32:1305-7.  Back to cited text no. 9
10.Smith AB, Smirniotopoulos JG. Imaging evaluation of demyelinating processes of the central nervous system. Postgrad Med J 2010;86:218-29.  Back to cited text no. 10
11.Iacobone E, Bailly-Salin J, Polito A, Friedman D, Stevens RD, Sharshar T. Sepsis-associated encephalopathy and its differential diagnosis. Crit Care Med 2009;37:S331-6.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3]

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