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Acanthamoeba meningoencephalitis in an immunocompetent patient


Debasish Biswal1, Bijay Ranjan Mirdha1



Introduction

Acanthamoeba spp. are free living amoeba capable of causing granulomatous amoebic encephalitis (GAE). It is also an important cause of severe keratitis among contact lens wearers and may also cause cutaneous lesions, particularly in immunocompromised individuals. Species known to infect humans include A. byersi, A. castellani, A. culbertsoni, A. hatchetti, A. healyi, A. astroonyxix, A. divionensis, A. polyphaga.

Acanthamoeba spp. are ubiquitous in the environment and have been found in a variety of sites, including soil, fresh, brackish and sea water; field grown vegetables, sewage, swimming pools, contact lens supplies, medicinal pools, dental treatment units, dialysis machines; heating, ventilating and air conditioning systems; tap water, mammalian cell cultures and vegetables.


Clinical presentation of Acanthamoeba infections:

1. GAE is of chronic onset and progressively worsens over a period of weeks to months. The signs and symptoms are typical of meningoencephalitis and encephalitis with varying degree of neurological involvement. See Table 1 for cases reported in India.
2. Acanthamoeba keratitis is associated with the use of contact lens. Corneal ulceration and scarring become apparent if not treated. See Table 2 for cases reported in India.
3. Rarely it can cause cutaneous acanthamoebiasis, which presents as a single/ disseminated chronic skin lesions, initially appear as reddish nodules and later it is crusted or ulcerated. These may occur with or without concurrent CNS disease.
4. It also can cause disseminated infection that typically causes inflammation of lungs or sinuses and/or skin infections but has the potential to spread to brain.


Table 1. Granulomatous amoebic encephalitis cases reported in India since 1990.
table1
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Table 2. Acanthamoeba keratitis reported in India since 1990.
table2
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Patient description

A 19-years old female patient complained of fever (102°F/38.9°C), vomiting, headache for 2 weeks and episodic abnormal neurological manifestations and disorientation for a period of 1 week.

On physical examination, she showed abnormal behaviour in the form of agitation and her Glasgow coma score (GCS) was 13/15 with E4V3M5 although other vital parameters were normal. A lumbar puncture showed clear cerebrospinal fluid (CSF) and wet-mount examination showed 6-8 lymphocytes and three sluggishly motile structures in two different high power microscopic fields (Fig. 2). Motile structures were producing spinous protrusions in random directions suggestive of free-living amoeba (FLA). Microbiological culture of CSF for FLA, bacteria, fungi and Mycobacterium tuberculosis were all negative besides blood culture for bacteria and fungi. Multiplex bacterial PCR assay for Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b was negative. Serological assay against Hepatitis C virus (HCV), HIV 1 & 2, Hepatitis B virus surface antigen (HBsAg) and autoimmune encephalitis panel were all negative.

We also investigated the patient for haematological parameters. Total leukocyte count (TLC) of the patient was 9500/cubic millimetres of blood with neutrophils 62%, lymphocytes 31%, monocytes 4%, eosinophils 3%, All the parameters were within normal limits.

CSF was subjected to conventional PCR assay which showed an amplified product of 180 bp corresponding with that of genus Acanthamoeba (Fig. 1). All imaging findings were insignificant. Cytological and biochemical analysis of CSF depicted total cells of 35 with 100% being lymphocytes, protein of 1500 mg/dl, glucose of 46 mg/dl, ADA (adenosine deaminase) of 15.1 U/L. There was no history of exposure to fresh water bodies and swimming. A diagnosis of infection due to Acanthamoeba species was made.


Treatment

The patient was treated with fluconazole, miltefosine, metronidazole and ceftriaxone, however she died after 12 days of admission.
















































































































































































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figure1
Figure 1. 1.5% agarose gel electrophoresis showing 180 bp band corresponding to that of Acanthamoeba genus.
[please click on the image to enlarge]


figure2
Figure 2. Wet mount examination of CSF on light microscope showed sluggishly motile structures with spine like projections.
[please click on the image to enlarge]



Figure 3. Still shot from the film showing wet mount examination of CSF under the light microscope with 6-8 lymphocytes per high power field and sluggishly motile structures with spine like projections. Published on the official WJOMI YouTube channel: https://youtu.be/zLcNHLe0Gpk
[please click on the image to play film]


Conclusion

Considering his illness, two other panel of markers were used to exclude auto-immune encephalitis, if at all. Following auto immune encephalitis marker panel was found to be negative a) NMOSD (Neuromyelitis optica spectrum disorder) and MOG (Myelin oligodendrocyte glycoprotein) with NMO Aquaporin 4 Ab+ MOG antibodies (Immunofluorescence); b) Auto-immune encephalitis mosaic (NMDA, VGKC, AMPA 1&2, GABA: Immunofluorescence).

No other immune disorders were detected in this apparently healthy patient.


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Conflict of interest: none declared.

Authors’ affiliations:
1 Department of Microbiology, All India Institute of Medical Sciences, New Delhi, India.

Corresponding author:
Bijay Ranjan Mirdha
Professor, Department of Microbiology
All India Institute of Medical Sciences
New Delhi
India
e-mail: mirdhabr@hotmail.com

To cite this article: Biswal D, Mirdha BR. Acanthamoeba meningoencephalitis in an immunocompetent patient. World J Med Images Videos Cases 2022; 8:e44-53.

Submitted for publication: 15 August 2022
Accepted for publication: 28 September 2022
Published on: 31 October 2022





















































































































































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