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TISSUE PARASITE: AMOEBA NAEGLERIA FOWLERI


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NAEGLERIA FOWLERI is a free living Amoeba found in?
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Distributed world wide, they are found in soil, lakes, brackish water, hot springs, heated swimming pools.

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TISSUE PARASITE: AMOEBA NAEGLERIA FOWLERI - Details

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NAEGLERIA FOWLERI is a free living Amoeba found in?
Distributed world wide, they are found in soil, lakes, brackish water, hot springs, heated swimming pools.
Contraction of NAEGLERIA FOWLERI?
They gain entry via nasal mucosa during swimming, travel along the olfactory nerve and gain entry to the brain via the cribiform plate.
NAEGLERIA FOWLERI cause PAM where cases are fetal, symptoms include?
Headaches, fever, rigid neck, mental confusion coma and eventually death.
The life cycle of NAEGLERIA FOWLERI
1)cyst in water, 2) trophozoite dvelops, may becomem flagellated, 3)divide by binary division, promitosis, 4) penetration of nasal mucosa, 5) migrate olfactory nerve to the brain
The diagnostic stage of NAEGLERIA FOWLERI?
Trophozoite in csf and brain tissue, flagellated form occasionally in csf
The 3 stages in the life cycle of NAEGLERIA FOWLERI
Cyst, trophozoite and the flagellated forms
An individual went for a swim in a hot spring: a) what is the causative agent of the t disease he may contract? b) what is the disease ? c) what symptoms may develop in 1-2 days ? d) and within 9 days?
A)NAEGLERIA FOWLERI. b) PAM c) headaches, fever, nausea and vomiting d) meningeo-encephalitis, irrational behavior, coma leading to death
NAEGLERIA FOWLERI can be cultured on
Non-nutrient agar containing bacteria
Lab diagnosis of NAEGLERIA FOWLERI
Wet mount, CT and MRI of head, staining, fluorescent antibody immunofluorescent, indirect immunofluorescent
The pathology of PAM
Hemmorhage and Nercrosis. mainly in the frontal cortex.
Case 1b) in a public health discussion about case 1a) what preventative measure would you suggest and why?
Treat swimming pools with chlorine since NAEGLERIA FOWLERI, the causative agent of PAM is susceptible to chlorine.
In treating an infection with NAEGLERIA FOWLERI which medication is used?
AMPHOTERIUM B, MICONAZOLE AND RIFAMPIN ( wellz., administered how?)
The clinical diseases of ACANTHAMOEBA SPP. include?
A) granulomatous ameboc encephalitis GAE, b) disseminated granulomatous amebic disease c) amebic keratitis
What is the complication of infection of ACANTHAMOEBA SPP. once an immunocompromised patient was infected?
The organism can enter circulation and disseminate to brain and other organ.
The pattern of GAE if leptimeninges is involved?
1) infiltrates with equal number of polymorphonuclear cells, lymphocytes and macrophages 2) infiltrates predominantly of lymphocytes and macrophages
Usually unilateral diffuse punctuate, the epithelipathology include?
Dendritic epithelial lesions which leads to sternal infection leading to ring infiltrates formation.
Lab diagnosis of ACANTHAMOEBA SPP include
CSF wet prep for trophozoites, CT and culture
Culture for ACANTHAMOEBA SPP
Nutrient/non nutrient agar with E.coli or enterobacter aerogenes
Treatment of non keratic disease?
Pentamidine and azole compound: voriconazole, flucytosine, sulfadiazine, miltefosine, amikacin. these can be given topically, iv or intrathecally depending on the nature of the disease.
Treatment of keratitis?
Polyhexamethylenebiguanide (PHMB) chlorexinide,propamidine, hexamidine
Treatment in progressinve karatitis?
Penetrating karatoplasty.
TOXOPLASMA GONDII life cycle in non feline phase
1) Oocyst she in cat feces sporulate in 1-5 days 2) intermediate host ingest Oocyst contaminated food, water 3)Oocyst transform into TACHYZOITES. In nueral and muscle tissue, they develop into tissue Cyst. 4) cats become reinfected 5) human become infected.
Humans get infected by TOXOPLASMA GONDII by
1) ingestion of raw/ undercooked meat containing cyst 2) ingestion of Oocysts in contaminated water or food 3) blood transfusion or organ transplant (less common) 4) from mother to fetous 5)accidental sticks with contaminated needles or exposure of lesions/ mucosal surface to parasite
Pheline phase os life cycle of TOXOPLASMA GONDII
1) sex gametes mate to form Oocyts 2) Oocyst pass in cat feces 3) after 2-3 days Oocyst become sporozoites ingested by feline to continue life cycle
Human infection of TOXOPLASMA GONDII from cats occurs
Sporozoites infect humans when cleaing cat litter
High risk transmission if mother is infected
Lee than 6 months before conception
TOXOPLASMA GONDII bradyzoites and Oocyst are found in ?
Bradyzoites are found in tissue, Oocyst are found in cat feces
Host response include
Secretory IgA, cell death, necrosis and inflammatory response.
Pathology of tachyzoites and bradyzoites
Tachyzoites: cell death, necrosis, mononuclear inflammatory response. bradyzoites: yield only inflammatory response. cyst eventually rupture.
Infected organs in TOXOPLASMA GONDII include
Lymph nodes, eyes, brain. lungs, heart and GIT
Clinical features and pathology of TOXOPLASMA GONDII
1) in immunocompromised pts: toxoplasmic encephalitis most frequently seen in AIDS due to recrudescence. altered mantal status, seizures, fever and nerological findings. pneumonia, h. failure, liver failure and retinitis.
Clinical pathology in immunocompetent patients
80/90 % show no symptoms but lymphadenopathy, malaise, headahes, fever <40 degrees celcius. infectious mono syndrome. vary rare : fever polymyositis, encephalitis, pnemonia and myocarditis
Congenital toxoplasmosis include
Hypoxia, hypoglycemia, hydrocephalus, visual impairment and death
Lab diagnosis of TOXOPLASMA GONDII
Culture, serology, PCR, ELISA, Immunoassays. amniotic fluid analysis for B1 gene, igg/igm titres
Treatment of congenital TOXOPLASMA GONDII infection
PYRIMETHAMINE AND SULFADIAZINE FOR I YR
TRETEMENT OF TOXOPLASMOSIS IN IMMUNOCOMPETENT INDIVIDUAl
PYRIMETHAMINE AND SULFADIAZINE OR CLINDOMYCIN insever presentations.
Toxoplasmosis in immunocompromised individual
Primary prophylaxis (before infection): compromoxazole and pyrimethamine- sulfadiazine or depsone pyrimethamine or atovaqone.
Life cycle of T solium
1) eggs or gravid proglottis in feces( diagnostic/infective stage) 2) eggs/gravid proglottis eaten by pigs/human 3) oncospheres( infective) hatch, penetrate intestine and invade muscle. oncospheres develop into cystercerci in muscle of pigs and humans. 4) human ingest rew/ undercooked meat 5) scolex attach to intestine 6) adults in intestine
Clinical feature of infection f T. solium
NEUROCYSTICERCOSIS: Seizures,hydrocephalus, arachnoditis, headaches, nausea, vomiting, visual impairment, papilloedema
Treatment of T. solium infection
Control seizure, praziquantol, albendazole. corticosteroids, antiparasitic drugs may exacerbate inflammation. hydrocephalus, seizures
INfection caused by larva nematodes that migrate to tissue that cause intense eosiphillic respone?
Visceral& occular Larva migrans. most commonly caused by T. canis/ cati
Clinical features of Visceral and ocular larva migrans
Fever, malaise, anorexia, weight loss, cough, wheezing and rashes.
Treatment of viscera and ocular larva migrans
Infection is self limiting. use corticosteriods for inflammation and albenadiazole ofr larvae
Cutaneous larva migrans
Cuased by dog and cat hookworn ancylostoma braziliense.
Treatment of cutaneous larva migrans?
Treat with albendazole/ivermectin
The infective stage of T. solium
Oncospheres, eggs or gravid proglottis
Human infection with T. solium is by?
Ingestion of raw undercooked meat.