|Year : 1984 | Volume
| Issue : 2 | Page : 125-8
Primary amoebic meningo-encephalitis caused by Acanthamoeba (report of two cases).
AA Gogate, BN Singh, LP Deodhar, HI Jhala
A A Gogate
|How to cite this article:|
Gogate A A, Singh B N, Deodhar L P, Jhala H I. Primary amoebic meningo-encephalitis caused by Acanthamoeba (report of two cases). J Postgrad Med 1984;30:125-8
|How to cite this URL:|
Gogate A A, Singh B N, Deodhar L P, Jhala H I. Primary amoebic meningo-encephalitis caused by Acanthamoeba (report of two cases). J Postgrad Med [serial online] 1984 [cited 2023 Mar 31 ];30:125-8
Available from: https://www.jpgmonline.com/text.asp?1984/30/2/125/5472
The first account of four fatal human cases of meningo-encephalitis caused by aerobic free-living amoebae came from Australia. Fowler and Carter thought that these cases were probably due to Acanthamoeba. The term primary amoebic meningoencehalities (PAM) was suggested by Butt, to distinguish human disease from that caused by Entamoeba histolytica. Most of the workers still use the term PAM for amoebic meningoencephalitis caused by both Acanthamoeba and Naegleria. So far only 23 cases of human meningo-encephalitis caused by Acanthamoeba have been reported in the literature.,
Cleland et al saw, on three occasions, A. rhysodes (Hartmanella rhysodes) in CSF and cultured it from a man in Nigeria who had a five year history of excessive sleeping and a confusional illness with convulsions. The patient partially recovered from the disease. There was a rising, serum titre of immobilizing antibody against the strain of amoeba isolated. They suggested that this was a case of chronic amoebic meningoencephalitis.
Martinez, used the term PAM for the acute haemorrhagic necrotising meningoencephalitis caused by Naegleria. The portal of entry of amoebae was through the olfactory neuroepithelium. He suggested the name granulomatous amoebic encephalitis (GAE) for the chronic disease caused by Acanthamoeba. It usually occurred in chronically ill and debilitated persons and immunologically impaired patients, some receiving immunosuppressive therapy. In some reported human cases immuno-deficiency was not found, and the disease was acute.
The present communication describes two fatal human cases of amoebic meningo-encephalitis in which A. rhysodes and A. culbertsoni were seen in CSF, were cultured and detected in post-mortem tissue sections.
A 15 year old female was referred to the Lokamanya Tilak Municipal General Hospital, Sion, Bombay with a history of vomiting, nausea and fever. Six months earlier, she gave a history of jaundice. Her general condition was fair; the chest was clear; the pulse was 102 per min and B.P., 100/70 mm Hg. The case was diagnosed as acute gastritis with hepatomegaly. On the second day, the patient was drowsy and semiconcious. Lumbar puncture showed blood stained CSF with the following findings: proteins were 300 mg% and globulins increased; cells were 160/cmm with 35% polymorphs and 60% lymphocytes. There were 4-6 RBCs per high power field. On the third day, the patient was in precomatose condition when CSF was tapped again. It was blood stained and contained 125 mg sugar, 600 mg% chlorides and 320 mg% proteins. Blood glucose level was 150 mg%.
The patient was in deep coma on the fourth day and expired after cardio-vascular failure before receiving any specific treatment. She had been given ampicilin and neomycin before death. Post-mortem diagnosis was encephaitis with chronic hepatitis.
The CSF collected on the second and the third day was processed for bacteriological studies. No bacteria could be detected not isolated. The CSF after low speed centrifugation was used for wet and hanging drop preparations. Motile amoebae were seen in the CSF collected on the third day. For culture of amoebae from CSF, non-nutrient agar seeded with Escherichia cob was used, as described by Singh. The strain of amoeba was identified as
The amoebae were identified on the basis of following criteria:
1. Temperature for growth: 25°C, 37°C and 42°C.
2. Type of cyst: morphology, size, double walled or single walled; whether pores present or absent.
3. Type of locomotion: pseudopodia, lobopodia, acanthopodia; rate of movement.
4. Trophozoite: size; type of ectoplasm and endoplasm; presence, number and size of vacuoles
5. Flagellate stage: present or absent.
6. Aerobic or anaerobic growth.
7. Nuclear structure and nuclear division.
8. Animal pathogenecity.
Brain sections showed a fibrinopurulent meningeal reaction. The cellular component of the exudate comprised of polymorphonuclear and mononuclear inflammatory cells in roughly equal proportions, together with a number of amoebae. The amoebae at places were plentiful. They were found in large numbers clustered around the Wood vessels. The brain substances at places showed some invasion, inflamation or complete purulent and haemorrhagic disruption. There were areas of necrotising hemorrhages at places showing amoebae. No cysts were seen in brain sections.
Sections of the liver showed normal architecture. At places, mononuclear inflammatory cells were seen in the portal areas. No amoebae could be found in liver sections.
A 19 year old man was admitted to the Lokamanya Tilak Municipal General Hospital, Sion, Bombay with a history of irrelevant talk for 2 days, headache and vomiting. He had a high fever with rigors and profuse sweating. The patient was drowsy and had a confused behaviour. He was diagnosed as a case of pyogenic meningitis. CSF showed 90 mg% proteins and 150 mg% sugar. Cells were 276/cmm with 80% polymorphs and 20% lymphocytes. No bacteria could be isolated from the CSF.
After 2 days, the carotid angiogram was done. No haematoma or collection of blood or any space occupying lesion was detected. On the third day, the patient was semiconscious. The CSF showed motile amoebae. When cultured on non-nutrient agar with E. coli, the strain of amoebae was identified to be A. culbertsoni. The CSF was blood stained and contained 90 mg% sugar, 170 mg% proteins and 650 mg% chlorides. WBC count was 1700/cmm. The patient became comatose and died on the same day. He had been treated with chloramphenicol before his death.
At post-mortem, the brain weighed 1200 g. It was soft, oedematous and congested. The meninges were hazy. There was a purulent exudate with haemorrhages at places.
In stained brain sections necrotizing haemorrhage was a striking feature. There was severe encephalitic inflammatory reaction. Numerous amoebae were seen within the tissue substance. [Fig. 1] and [Fig. 2] . No cysts could be detected. The liver and other organs showed no evidence of amoebic infection.
Pathogenicity of amoebae isolated from the CSF in mice
For the pathogenicity test in mice, clonal cultures of amoebae were made from single cysts by the use of micropippets. Twenty thousand amoebae were inoculated intranasally per mouse by the method described by Singh and Das Twelve mice weighing 12 to 15 g were inoculated intranasally with A. rhysodes and another 12 with A. culbertsoni. All the mice died within 6 to 10 days with typical symptoms of meningoencephalitis. Smear preparations of the brain tissues showed motile amoebae. Cultures of amoebae from the brain tissue were positive on non-nutrient agar supplied with E, colt and the brain ;section also revealed amoebae.
Willaert et al have identified A. culbertsoni retrospectively in a case of amoebic meningo-encephalitis, previously reported by Jager and Stamm by the use of indirect immunofluorescence antibody test. This was the first record of the presence of A. culbertesoni in the CSF of fatal case of human meningo-encephalitis. So far, there is no record of A. rhysodes causing fatal human disease, although some strains of A. rhysodes have been found to be pathogenic to mice when given intranasally.` The work presented here suggests that the presence of cysts in fixed human brain section is not necessarily a criterion to diagnose meningo-encephalitis caused by Acanthamoeba. Our findings further suggest that the disease caused by Acanthamoeba can also be acute as in the case of Naegleria.
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