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Home , Amoebic brain abscess

PARASITIC OF THE , WITH AN UPDATE ON FREE-LIVING AMOEBIC INFECTIONS 'NR de Silva, 2MKdeS Wijesundera Professor of Parasitology, Faculty of Medicine, University of Kelaniya, 2EmeritusProfessor of Parasitology, Faculty of Medicine, University of Peradeniya.

the central nervous system, and the disease entities associated with these infections. h the central nervous system (CNS) of humans frequent site of primary by parasites, Parasitic infections of the CNS: causative agents

tations when the CNS is involved. The second coccidia (Table I),while a range of nematodes, cestodes this article deals at greater length with the and trematodes are also known to cause neurological ae that are known to cause primary infections of disorders (Table 2).

Amoebic Primary amoebic rneningo- spp Granulomatous amoebic encephalitis, keratitis Balamufhia mandrilafls Granulomatous amoebic encephalitis

Trypanosoma bruceirhodesiense Encephalitis (in Human African Trypanosomiasis or sleeping sickness) and T.b. gambiense Tr~panosomacruzi Encephalitis

Msceral larva migrans Eosinophiliimeningo -encephalitis or encephalitis

Onchocerca volvulus a Encephabpathy

Neurocysticercosis gives rise to epilepsy, or organic Echinococcus granulosus Hydatid cyst of the brain or Echinococcus rnultilocularis Alveolar echinococcosis Cerebral sparganosis,

Schisfosomajaponlcum Schistosoma mansoni Paragonimus westerinani Seizures

I 49 (primary or re-activated infection) is well known to cause nwml~imldisease in immunmm~romisedPatients, Among the other trematodes, Paragonimus westerm particularlythosewith organ bns~lanband HIV/AIDS. causing paragonimiasisis a major cause of neurologi Cases of ence~halo~ath~temporally related to mass disease in the Far East, due to cyst formation in ecto tw&nent with i~ermedinfor onchocerciasis have been sits in the brain and presents as intracranial spa reported; most of these cases recovered without serious mupying lesions. consequence (Boussinesq et al2003). Fatalities usually occurinthosewhoarecdnfectedwith Loaloaand have Chronic helminth infections such as hydatidosis, a high microfilaraemia. A similar fatal encephalopathy a,so present with the features tients slowgrowing, sp has desa'bed in pa with loawho occupying lesion in the nervous system. have been treated with DEC (Kamgno et al2008).

Angiostrongylus cantonensis is the most common cause of eosinophilic worldwide. The rat is the definitive host of the parasite and humans are infected by ingesting third-stage larvae, which develop in a molluscan intermediate host, usually slugs or snails the CNS, in many zoonotic infections, helminth larva (Bunnag, 1999). migrate to brain tissue and persist there.

system include dementia, meningo-encephalitis, Florida (Intalapaporn et al, 2004). There are now

(Finsterw & Auer, 2007). A review of the literature from as aetiological agents of human disease. These are the early 50's to the present date found 29 cases of ~~l~~j~fowl8* brain involvement in toxocariasis (MoreiraSilva et al, Acanthamoeba spp 2004). Of these 28 cases, 20 reported different clinical and laboratory manifestations of eosinophilic meningitis, . ~%~amuthiamandriliaris encephalitis, or radiculopathy. r

The presence of encysted larval stages in the brain may Together, they are known to Muse three distinct clini also cause patients to present with seuures such as in syndromes neurocysticerwsis and in trichinellosis. Neuroqeti- Primary amoebic (P~,,,,) cenx>sis, infection ofthe brain parenchyma with the land 'I .- stage of ~d~is a common cause of focaland ,.,# -9bG~ulomatous amoebic encephalitis (GAE) generalised seizures of late onset, but it less commonly Amoebic keratitis (AK)

th GAE and AK. B. mandrillaris vomiting, altered mental status, and seizures (Kraff,

,i. * - L .- ;:a:: arily soil amoebae that are sluggishly motile. The cysts have a polyhedral shape d off into surface waters and as such are found and a double wall. They are about 15 pm in diameter. ty of warm stagnant or slow The widespread, ubiquitous presence of these organisms g surface water bodies. Recently these amoebae means that humans are frequently exposed to them, also been detected in ground water such as wells but the parasite usually finds it difficult to colonise et al, 2008). In Sri Lanka, Naegleria spp. have been humans. Organisms may enter through the nasal the Kandy area and irrigation passages into the lower respiratory tract, through in the Dry Zone (Wijesundera et al 1996, ulcerated or broken skin or the eye. Infections usually occur in the patients who are immunocompromisedor nly N. fowleri is known as a debilitated in some other way. They are of a chronic type, other species N. italica and with a marked granulomatous reaction. traliensis are now recognized as potential 02). The Naegleria isolated is a leptomyxid free-living i Lankan waters is yet to be speciated. , first described as causing disease in 1990. This species is also found worldwide, in soil and water, but eri is thermo~hilic,growing at temperatures upto the particular ecological niche occupied by the parasite The trophozoite stages thrive in large bodies of is as yet unknown. It was first isolated from the brain of water such as found in heated swimming pools a mandrill baboon at the San Diego Wild Animal Park. ination does not affect its Several reported cases of 5. mandrillaris had initially It is a facultative pathogen capable of living many been diagnosed as being due to Acanfhamoeba. tions without infecting a host. A wide range of Following the development of an immunofluorescence ns can be hosts to these assay, a number of human cases of 6. mandrillaris meningoencephalitis were diagnosed retrospectively (Intalapaporn et at, 2004). morphological forms: the is the feeding, growing, As with other amoebae, B. mandrillaris has two form; the flagellate tr0phozoite~which is morphological forms: the trophozoite and the cyst. and the dormant cyst stage. The amoebic Trophozoites, which range in size from 12 to 60m, are O - 30 bmin diameters has uninucleated with a large, densely staining nucleolus. There may be two or thee nucleoli in some trophozoites. Cysts may be more readily visualised with either GMS ically has 2 flagellae and a or periodic acid-schiffstains. They range in size from 6 nucleus, is found in the surface layers of warm to 30pm and appear to be double-walled and three- s of water. The 'yst ' Wherical with a walled by light and electron microscopy, respectively. wall; it is about IOpm in diameter and is also lmmunofluorescence studies are required for differentiating between B. mandri//aris and ccurs while bathing or Acanfhamoeba. e in the infected waters The parasites may enter the human host through the nasal tissue and thence via the lower respiratory tract to enter the meninges and circulation or through ulcerated or broken &in.Both 'paces' The amoebic forms may be found in the brain tissue of infected in tissue and CSF. The individuals. nally seen in the CSF. CSF, transformation A singlecase of amoebic thought to be due pitated and visualised to Sappinia diploidea, a soil-living amoeba, was reported in 2001 (Gelman st al, 2001). More recent work using newly developed real-time polymerase chain reaction assays, has suggested that the organism is most likely to be S. pedata. This amoeba had previously been found only in environmental sources, such as soil and tree bark (Qvarnstrom et al, 2009). . fowleri, the Acanthamoeba spp that infect s are also found worldwide, feeding on bacteria. The clinicalconditions ecessarily associated with warm Primary amoebic meningoencephalitis (PAM) caused by N. fowleri has a worldwide distribution.

However, disease is rare and to date only 200 cases large (20 - 40 pm in diameter), have been documented. The majority of cases are from single nucleus and its surface is covered with tiny developed countries, probably due to availability of tions that look like spines (acanthopodia). It is reference diagnostic facilities. A few cases have been

51 reported in India and Thailand (Shenoy et at, 2002). thalamus, diencephalon, brain stem and posterio Although the free-living organism been found in Sri Lanka, The chronic inflammatory, granulomatous resp no cases of PAM have been reported in Sri Lanka to characterised by multi-nucleated giant cells. date. trophozoites and cysts present in lesions.

Classically, the disease occurs in healthy young adults The onset of changes in mental status is usua or teenagers with a history of swimming in the type of insidious, with focal neurological deficits, seizures, water-body known to be favoured by N. fowlerilt appears and visual abnormalities. The duration of i likely that although many people are exposed to varies, but is usually about a month. Skin lesions infection, for unknown reasons, only a few actually be seen at the original site of infection. develop disease. Invasion of the brain through the olfactory bulb and cribriform plate results in a rapidly Multiple, non-enhancing lesions may be seen on progressive, purulent haemorrhagicnecrosis of the frontal Lumbar puncture is contra-indicated; in any cortex, starting with the olfactory bulbs. The pathology amoebae are not found in CSF. Diagnosis is u is very similar to that of purulent bpterial meningitis. made at autopsy, and brain sections will s The incubation period in PAM ranges from a few days to granulomatous lesions with amoebae and cys about 2 weeks. Patients may complain of distortions in Concurrent skin lesions may be biopsied to make taste and smell at the onset of the illness. They soon indirect diagnosb. The differentiation betwe develop clinical features of acute meningitis, with fever, Acanthamoeba and Balamufhia in tissue sectio headache, vomiting and neck stiffness. Illness rapidly requires immunohistochemistry. progresses to deep coma, and convulsions may occur. Patients usually die within a week of onset of symptoms. As with PAM, GAE is also nearly uniformly fats Diamidines such as pentamidine, propamidine ha The CSF usually has a high white cell count, shown the greatest in vitro activity. Azole antifun predominantlywith polymorphs. It also has a high protein and some aminoglycosides such as neomycin content and low glucose levels. Trophozoites are not paromomycin have also been tried, but with 11 easily seen in a Gram stain; they are better visualized success. with iron haematoxylin stain. A wet mount of CSF may show n'lotile trophozoites. Definitive diagnosis requires Amoebic keratitis caused by infection wi direct demonstration of organism. Formation of the rapidly Acanthamoeba spp is usually associated with mi motile biflagellate form may be precipitated by addition trauma to the eye or use of contact lenses.Espe of a drop of distilled water to the CSF; this may be risk factors include soaking contact lenses in homema observed in an unstained, wet mount, under a regular saline solutions, swimming with contact lenses, an microscope. of extended wear contact lenses. The organism has isolated from a Sri Lankan patient with central cor Although the clinical features and pathological changes ulceration (wijesundera et 2001 1. resemble those of purulent bacterial meningitis, PAM does not usually respond to anti-bacterial agents. The initial clinical features of amoebic keratitis inclu However, systemicand intrathecal amphotericin B have the sensation of a foreignbody in eye, tear been used in patients who have survived. Adjunctive photophobia and ocularpain. In full-blown infections, i therapies with rifampicin, mi~nazole,SU~~~SOX~ZO~~ have dendriform keratitis, hypopyon, increased intra-ocu also been tried, but the benefit remains unknown. Most pressure, and anterior nodular scleritis may cases described the in literature to date, have been fatal. Laboratory diagnosis may be made by examining scrapings. Wet mounts can show motile trophozoit Granulomatous Amoebic Encephalitis has also been and cysts, while fixed slides can be stained with Giem reported worldwide. one hundred and fifty-six human or periodic Acid Schiff reagent or calcofluor white cases GAE have been from 956 through visualize the amoebae. If the patient uses contact tense 1997 at the Centers for Disease Control and Prevention the contact lens and storage system should also (Atlanta, GA) 63 of them caused by 6. mandrillaris examined for the presence of amoebae. Acanthamoe (Intalapaporn, 2004). UnlikePAM, GAE due keratitis is curable if detected early. The affected are ~canfhamoebais a disease of immuno-suppressed or of cornea should be debrided. Specific treatment w otherwise debilitated patients. Balamuthia Can also topical propamidine, together with neosporin an cause GAE in patients who are otherwise healthy. The miconazole is required for about 1 month. mode of acquisition of infection is not always clear. Acanthamoebae may be present as a commensal in References upper respiratory tract of normal individuals. 1. Alibhoy AT, Fernando R, Perera F. A case of cereb When Acanthamoeba spp or B. mandrillaris enters a sparganosis. Ceylon Medical Journal 2007; 52: 93 human host, the primary foci are usually in lungs and 2. Blair B,Sarker P, Bright KR, Marchiano-Cabral F, Ger skin. The organisms spread haematogenously from there CP. Naegleria fowleri in well water. Emerging lnfectio to CNS. The brain involvement is frequently patchy: Diseases 2008; 14: 1491-501.

52 Boussinesq M, Gardon J, Gardon-Wendel N, Chippaux infected with Loa loa and Plasmodium spp. Am J Trop JP. Clinical picture, epidemiology and outcome of Loa- Med Hyg 2008; 78: 546-51. associated serious adverse events related to mass 12. Kraft R. Cysticercosis: an emerging . ivermectin treatment of onchocerciasis in Cameroon. Am Fam Physician 2007; 75: 91-6, 98. Filaria J 2003; 2 (Suppl 1): S4. 13. Moreira-Silva SF, Rodrigues MG, Pimenta JL, Gomes Bunnag T. Chapter 114. Angiostrongyliasis. In: Hunter CP, Freire LH, Pereira FEL. Toxocariasis of the central GW & Strickland GT (eds) Hunter's Tropical Medicine. nervous system: with reports of two cases. Revista da 8th ed. Philadelphia, WB Saunders Company, 1999, Sociedade Brasileira de Medicina Tropical 2004; 37: pp 793-6. 169 -74. De Jonckheer JF. A century of research on the amoebo- flagellate genus Naegleria. Acta Protozoo/ogica 2002; 14. Qvarnstrom Y, da Silva AJ, Schuster FL, Gelman BB, Visvesvara GS. Molecular confirmation of Sappinia 41 : 309-42. pedata as a causative agent of amoebic encephalitis. Drabick JJ. Chapter 99. Free-living amoebic infections. J Infect Dis Apr 2009 15; 199(8): 11 39-42. In: Hunter OW 'Strickland OT (eds) Hunter's 15. Ross AGP, Bartley PB. Sleigh AC, et al. Schistosorniasis. Medicine. 8th ed. Philadelphia, WB Saunders N Engl J Med 2002; 346: 1212 -20. Company, pp 705-7. . Finsterer J, Auer H. Neurotoxocarosis. Rev lnst Med 16. Shenoy S, Wilson G, Prashanth HV, Vidyalaksmi K, 7iop S Paulo 2007; 49: 279-87. Dhanashree B, Bharath R. Primary meningo- encephalitis by Naegleria fowleri: first reported case Gelman BB, Rauf SJ, Nader R, Popov V, Borkowski J, from Mangalore, South India. Journal of Clinical Chaljub G, Nauta HW, Visvesvara FS.~mOe~c--1Wicrobiofogyf60~389--~------encephalitis due to Sappinia JAMA 2001 285(19): 2450-1. 17. Warhurst DC. Chapter 78. Potentially pathogenic free- living ameobae. In: Cook G & Zumla A (eds)-Manson's Gunarathna JANS. Prevalence of Naegleria species in Tropical Diseases, 22nd edition. 2008. London: water bodies of Maho and Nikaweratiya Divisional Saunders. Secretariat divisions. Dissertation submitted for MSc in Medical Microbiology, University of Peradeniya, 2009. 18 Wijesundera MdeS, lddawela P, Wijesundera S. Isolation of Acanthamoeba spp from patients with . Intalapaporn P, Suankratay C, Shuangshoti S, keratitis in Sri Lanka. University of Peradeniya Annual Phantumchinda K, Keelawat S, Wilde H. Balamuthia Research Sessions 2001; pp.99. mandrillaris meningo-encephalitis: the first case in 19. Wijesundera NLS, Ranaweera RLAR & Wijesundera South East Asia. Am J Trop Med Hyg 2004; 70: 666-9. MdeS. Preliminary studies on pathogenic free living , Kamgno J, Boussinesq M, Labrousse F, Nkegoum B, amoebae in water samples in Kandy. 6th Academic Thylefors BI, Mackenzie CD. Case report: Sessions of the Sri Lanka College of Microbiologists encephalopathy after ivenectin treatment in a patient 1996. . Boussinesq M, Gardon J, Gardon-Wendel N, Chippaux infected with Loa loa and Plasmodium spp. Am J Trop JP. Clinical picture, epidemiology and outcome of Loa- Med Hyg 2008; 78: 546-51. associated serious adverse events related to mass iverrnectin treatment of onchocerciasis in Cameroon. 12. Kraft R. Cysticercosis: an emerging parasitic disease. Filaria J 2003; 2 (Suppl 1): S4. Am Fam Physician 2007; 75: 91-6, 98. 13. Moreira-Silva SF, Rodrigues MG, Pimenta JL, Gomes . Bunnag T. Chapter 114. Angiostrongyliasis. In: Hunter GW & Strickland GT (eds) Hunter's Tropical Medicine. CP, Freire LH, Pereira FEL. Toxocariasis of the central 8th ed. Philadelphia, WB Saunders Company, 1999, nervous system: with reports of two cases. Revista da pp 793-6. Sociedade Brasileira de Medicina Tropical 2004; 37: 169-74. . De Jonckheer JF. A century of research on the amoebo- flagellate genus Naegleria. Acta Protozoologica 2002; 14. Qvarnstrom Y, da Silva AJ, Schuster FL, Gelman BB, 41: 309-42. Visvesvara GS. Molecular confirmation of as a causative agent of amoebic encephalitis. . Drabick JJ. Chapter 99. Free-living amoebic infections. J Infect Dis Apr 2009 15; 199(8): 11 39-42. In: Hunter GW & Strickland GT (eds) Hunter's Tropical 15. Ross AGP, Bartley PB, Sl&gh AC, et al. Schistosomiasis. Medicine. 8th ed. Philadelphia, WB Saunders Company, pp 705-7. N Engl J Med 2002; 346: 1212-20. : Finsterer J, Auer H. Neurotoxocarosis. Rev lnsf Med 16. Shenoy S, Wilson G, Prashanth HV, Vidyalaksmi K, Trop S Paulo 2007; 49: 279-87. Dhanashree B, Bharath R. Primary meningo- encephalitis by Naegleria fowleri: first reported case . Gelman BB, Rauf SJ, Nader R, Popov V, Borkowski J, from Mangalore, South India. Journal of Clinical Chaljub G, Nauta HW, Visvesvara GS. Amoebic Microbiology 2002; 40: 309-10. encephalitis due to Sappinia diploidea. JAMA 2001 285(19): 2450-1. 17. Warhurst DC. Chapter 78. Potentially pathogenic free- living ameobae. In: Cook G & Zumla A (eds)-Manson's Gunarathna JANS. Prevalence of Naegleria species in Tropical Diseases, 22nd edition. 2008. London: water bodies of Maho and Nikaweratiya Divisional Saunders. Secretariat divisions. Dissertation submitted for MSc 18. Wijesundera MdeS, lddawela P, Wijesundera S. in Medical Microbiology, University of Peradeniya, 2009. Isolation of Acanthamoeba spp from patients with W lntalapaporn P, Suankratay C, Shuangshoti S, keratitis in Sri Lanka. University of Peradeniya Annual Phantumchinda K, Keelawat S, Wilde H. Balamuthia Research Sessions 2001; pp.99. mandrillaris meningo-encephalitis: the first case in South East Asia. Am J Trop Med Hyg 2004; 70: 666-9. 19. Wijesundera NLS, Ranaweera RLAR & Wijesundera MdeS. Preliminary studies on pathogenic free living I. Kamgno J, Boussinesq M, Labrousse F, Nkegoum B, amoebae in water samples in Kandy. 6th Academic Thylefors BI, Mackenzie CD. Case report: Sessions of fhe Sri Lanka College of Microbiologists encephalopathy after iverrnectin treatment in a patient 1996.

ACINETOBACTER BAUMANNII-ASUCCESS STORY OF A NOSOCOMIAL PATHOGEN Sujatha Pathirage Consultant Microbiologist, National Institute of Health Sciences, Kalutara.

'he most important representative of the genus tract infections, nosocomial meningitis. However, its icinetobacter, ~cinetobacter'baumannii,has emerged predominant role is as agent of nosocomial pneumonia, s one of the most troublesome pathogen for healthcare particularly ventilator associated pneumonia in patients lstitutions globally. It has a remarkable ability to up- confined to hespital intensive care units (ICU). In more gulate or acquire resistant determinants. Acinetobacter recent times, infection involving central nervous system, laumannii resistant to all known antibiotics have now skin and soft tissue, and bone have emerged as highly een reported, signrfying a sentinel event which need problematic for certain institutions. rompt action by the international healthcare community. ding in synergy with this emerging resistant profile is Microbiology le uncanny ability of A. baumannii to survive for The genus Acinetobacter, as currently defined, comprises mlonged periods throughout hospital environment, thus gram-negative, strictly aerobic, non fermenting, non otentiating its ability for nosocomial spread (Peleg AY fastidious, non motile, catalasepositive, oxidase negative It al). bacteria with a DNA G+C content of 39% to 47%. Acinefobacter species of human origin grow well on qcinetobacter spp have been implicated in variety of solid media that are routinely used in clinical iosocomial infections, including bacteraemia, urinary microbiology laboratories. These organisms form