LETTER TO EDITOR
Year : 2010 | Volume
: 53 | Issue : 1 | Page : 183--184
Duraiswami Ramanan, Reddy Nalaganta, KS Yadav Ram, Ravishankar Ramani
Department of Pathology, Military Hospital, Bhopal - 462031, MP, India
Pathologist, Military Hospital, 3 EME Center, Bairagarh, Bhopal - 462031, MP
|How to cite this article:|
Ramanan D, Nalaganta R, Yadav Ram K S, Ramani R. Amoebic meningo-encephalitis.Indian J Pathol Microbiol 2010;53:183-184
|How to cite this URL:|
Ramanan D, Nalaganta R, Yadav Ram K S, Ramani R. Amoebic meningo-encephalitis. Indian J Pathol Microbiol [serial online] 2010 [cited 2021 Oct 26 ];53:183-184
Available from: https://www.ijpmonline.org/text.asp?2010/53/1/183/59230
Central nervous system (CNS) infection with free-living amoebae is rarely encountered in clinical practice. We present a fatal case of meningoencephalitis caused by free-living amoebae.
A 46-year-old female was admitted to hospital with a history of headache and fever of three-day duration. She also complained of projectile vomiting and photophobia of since a day. There was no history of cough, neck stiffness, recent upper respiratory infection, chest pain, or breathlessness. There was no significant past, personal, or family history. The patient was a teacher and housewife. There was no history to suggest that the patient was immunocompromised. She gave no history of exposure/swimming in probably contaminated water.
The patient was febrile (38.8 o C) with tachycardia (110 beats per minute); blood pressure was 130/80 mm Hg; respiratory rate 22/minute. There was no rash or skin lesion, lymphadenopathy, pallor, or icterus.
CNS examination revealed that the patient was irritable, restless, and confused. Neck rigidity was detected and Kernigs' sign was positive. All deep tendon jerks were elicited; and plantar reflexes were extensor. There was no focal neurological deficit or papilloedema.
Systemic examination was normal.
Investigations revealed the hemoglobin 10.8 gm/dl T L count of 10,200 per dl. DL count was within normal limits. Biochemical parameters and routine urine analysis were within normal limits. Tests for HIV antibodies were not done.
Lumbar puncture was done. Cerebrospinal fluid (CSF) was turbid in appearance; RBC was 2600/dl; WBC was 1200/dl; predominant cells were neutrophil leukocytes; protein was 2.2 gm per l; sugar was 20 mg/dl (random blood sugar: 163 mg/dl); Gram's stain and Zeil Neilsen (ZN) stain did not reveal any organism/acid fast bacilli (AFB) or fungus. However, examination of fresh unstained CSF and Romanowsky stained slides revealed trophozoite forms of an amoeba [Figure 1].
These exhibited active amoeboid motility and binary fission in fresh specimens. Culture of CSF for amoeba was attempted on a non-nutrient agar plate seeded with Escherichia Coli; no growth of Acanthamoeba species was obtained. CSF cultures for pyogenic organisms and fungus were negative.
The patient was initially started on treatment with intravenous fluids, Sodium Penicillin 20 lakh units fourth hourly, Chloramphenicol 2 gm sixth hourly, Ceftoxime 2 gm sixth hourly, and Dilantin Sodium 100 mg stat. Subsequently, on confirmation of the causative organism being free-living amoebae, most likely Naegleria fowleri, Injection Amphotericin-B 1 mg/kg per day, Cap Rifampicin 1200 mg per day, and Tablet Septran 4 tabs twice daily, were administered.
Despite vigorous therapy, the patient did not respond to the treatment and succumbed to her illness 48 hours after admission. Autopsy was not carried out as permission was denied by the next of kin.
Free-living amoebae are ubiquitously present and are capable of causing human disease. Naegleria fowleri, Acanthamoeba species, and Balamuthia mandrillaris are known to cause CNS infection in immune-compromised and rarely immune-competent hosts. , Naegleria fowleri causes a primary meningoencephalitis with acute onset disease, characterized by severe headache, high fever, nausea, vomiting, and meningismus. Photophobia and palsies of the third, fourth, and sixth cranial nerves are common. Rapid progression to seizures and coma may follow, and most patients die within a week.  Infection with Acanthamoeba species follows a more indolent course and occurs typically in chronically ill or debilitated patients. Infection with Balamuthia mandrillaris follows a typically subacute course and occurs in immune-competent hosts. CSF examination reveals mononuclear pleocytosis, elevated protein levels, and normal to low glucose levels.
Our patient presented with acute onset of illness rapid progression and succumbed to the infective disease. The CSF examination was suggestive of acute bacterial meningitis. The causative amoeba was identified both in fresh wet preparations as well as in smears stained by Romanowsky stains. The acute clinical onset and CSF picture mimicking acute bacterial meningitis suggests that the causative organism was Naegleria fowleri though not established unequivocally.
Amoebic encephalitis is almost always fatal because of delay in diagnosing the disease and the lack of optimal antimicrobial therapy. Low clinical suspicion and mis-identification of the organism in CSF as reactive histiocytes lead to low detection of the condition.  The disease mimics bacterial, tuberculous or viral meningoencephalitis. Furthermore,
Awareness of the organism as a causal agent is essential to identify in routine wet preparations and Romanowsky stained slides of CSF. Some investigators have explored the use of serological and molecular diagnostic techniques for diagnosis of Acanthamoeba encephalitis. 
Various drug regimens have been tried in the treatment of Acanthamoeba encephalitis (combinations of Amphotericin-B, Rifampicin, Ketoconazole, Fluconazale, and Trimethoprim-Sulfadiazine/Sulfamethoxazole), but therapeutic success has been elusive.
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