Naeglaria & Acanthamoeba PDF

Free living amoeba By Dr/ Ragaa Ahmed Lecturer of Medical Parasitology Faculty of Medicine- Helwan University Potentially Pathogenic Free Living Amoebae  They are widely distributed in environment. Mostly they are not harmful to human. They prefer water with a temper...

Free living amoeba By Dr/ Ragaa Ahmed Lecturer of Medical Parasitology Faculty of Medicine- Helwan University Potentially Pathogenic Free Living Amoebae  They are widely distributed in environment. Mostly they are not harmful to human. They prefer water with a temperature higher than average e.g. public swimming pools, warm waste water from factories or power stations, bonds, brackish water and in moist soil. They are mostly opportunistic parasites. They include: 1- Naegleria fowleri Primary amoebic meningeoencephalitis (PAM) 2- Acanthameba Granulomatous amoebic encephalitis (GAE) Amoebic keratitis Naegleria fowleri Brain eating amoeba Primary amebic meningeoencephalitis (PAM)  Geographical Distribution Reported in some parts of the world. Habitat in Nature Water (fresh, brackish & salt), moist soil, decaying vegetation. Morphology N. fowleri is an ameboflgellate, with 3 forms: § Amoeboid trophozoite – Active infective stage: Motile, feeding, has single nucleus, with large big karyosome,it is about 15 u. §Flagellate trophozoite form with anterior nucleus, it never feeds nor reproduces. §Cyst inactive resistant stages: rounded with single nucleus, Double walled, 7-15 u Life cycle  Mode of infection: through nasal route Swimming in or sniffing of contaminated water Inhalation of contaminated air. Habitat: CNS From life cycle Definitive host: human Diagnostic stage: Amoeboid trophozoite form Infective stage: Amoeboid trophozoite form  Pathogenesis 1. Amoeboid trophozoite invades the nasal mucosa and cribriform plate and reaches the brain along the olfactory nerves. 2. Flagellate & cyst give rise to Amoeboid form prior of invasion, which is the only form detectable in brain tissue. 3. Naeglaria produces diffuse meningio-encephalitis with many neutrophiles, hemorrhagic inflammation and necrosis of brain tissue.  N. fowleri Encephalitis Primary amebic meningeoencephalitis (PAM) gross pathology Focal hemorrhage Focal necrosis Frontal brain hemorrhage and necrosis  Clinical picture Pam is an acute fulminant 1. There is fever, 2. Disturbance in the rapidly fatal disease that headache, nausea & sense of smell or taste affects mostly children vomiting, stiffness of neck can occur. and young adults and convulsions. 3. The patient enters in 4. The entire course coma and death occurs usually takes 3 – 6 days. early.  Diagnosis 1. History of swimming mainly. 2. CSF examination: Microscopic examination reveals amoeboid forms. Suspension in fresh water incites transformation into flagellate forms that confirm the diagnosis. Culture on suitable medium.  Treatment 1. At present, there is no complete treatment. 2. Amphotericin B can be given IV or intrathecally. Prevention and control 1. Avoidance of swimming in contaminated water. 2. Proper chlorination of public water supplies & pools.  Acanthamoeba Granulomatous Amoebic Encephalitis (GAE) Acanthamoeba Keratitis Morphology Trophozoite § 25 to 30 μm.- spiky projections § finely granular cytoplasm, § nucleus -a large central nucleolus. Cyst § Double-walled ,irregular outline with wrinkled surface. § 20 μm in diameter. § nucleus -a large central nucleolus Morphological stages of Acanthamoeba Life cycle  Mode of infection: not strongly associated with swimming GAE: 1ry infection occurs in 1.the lower respiratory tract through inhalation of contaminated air and 2. ulcerated skin & mucosa then to brain. Acanthamoebic keratitis: Corneal trauma, exposure to contaminated water, wearing contaminated contact lens or usage of home made saline. Habitat: CNS and Cornea (eye). From life cycle possibly in kiney, uterus and pancreas. Definitive host: human Diagnostic stage: trophozoite and cyst forms Infective stage: trophozoite and cyst forms  Granulomatous amoebic encephalitis (GAE) pathogenesis 1ry infection occurs in the lower respiratory tract and ulcerated skin & mucosa. Invasion of CNS (2ry infection) by blood spread causes single or multiple focal granulomatous lesions in the brain & other affected organs. In AIDS patients, disseminated infection can developed. Unlike Naeglaria, it causes focal granulomatous lesions in the brain. Single or multiple focal space occupying lesions are produced.  Clinical picture of GAE Takes subacute or chronic course (weeks to months and may extend to years) Manifested by nausea & vomiting, altered mental state, headache. Convulsions and stiffness of the neck. Manifestations of space occupying lesion. In AIDS patients, the disease may be fulminating resembling Naeglaria infection.  Diagnosis of GAE CSF examinationreveals the parasite. Culture on suitable media. Treatment of GAE There is no complete satisfactory treatment. However, there are some re-ported successful regimens: Excision of focal lesion & treatment with Ketoconazole. Penicillin & Chloramphenicol  Acanthamoebic keratitis pathogenesis & clinical picture Acanthamoeba cause chronic progressive ulcerative keratitis. Corneal ulceration may progress to perforation. In AIDS patients, infection may cause endophthalmitis. The infection is characterized by severe ocular pain and affection of vision. Acanthameba keratitis pathogenesis K.ELSHEWY  Acanthameba keratitis clinical pattern Superficial Deep keratitis Painful red eye keratitis with with with itching decreased visual opacification acuity and blindness  Diagnosis of Acanthamoebic keratitis Identification of trophozoites & cysts in corneal scraping directly and after culture. Treatment of Acanthamoebic keratitis Oral Itraconazole combined with topical Miconazole. Corneal transplant.  Control of Acanthamoeba species Proper care of contact lenses. Avoidance of exposure of the eye to contaminated water. Treatment of ulcerated skin and mucosa. Special care to immunosuppressed patients.