TISSUE PARASITE: AMOEBA NAEGLERIA FOWLERI
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TISSUE PARASITE: AMOEBA NAEGLERIA FOWLERI - Leaderboard
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. |
| NAEGLERIA FOWLERI is an organism that alternated between Amoebic form and flagellated form, which form is found in tissue? | Amoebic form is found in tissue. |
| 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 |
| NAEGLERIA FOWLERI divides by binary division with nuclear membrane intect, the process is known as | Promitosis |
| 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 |
| Diagnosis of this disease is usually during autopsy where csf show motile organism. | PAM caused by NAEGLERIA FOWLERI |
| NAEGLERIA FOWLERI can be cultured on | Non-nutrient agar containing bacteria |
| Which form of NAEGLERIA FOWLERI will be found in a) period of low nutrition? b) prolonged adverse condition? | A) flagellated form, b) cyst |
| Staining of csf sample being screened for NAEGLERIA FOWLERI can be done with? | H&E, Giemsa-Wright stain |
| 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 most common amoeba in soil and fresh water where cyst and trophozoites exist and is resistant to chlorine? | ACANTHAMOEBA SPP. |
| A patient wearing contact lens is most like to infected by this organism due to swimming? | ACANTHAMOEBA SPP. |
| The clinical diseases of ACANTHAMOEBA SPP. include? | A) granulomatous ameboc encephalitis GAE, b) disseminated granulomatous amebic disease c) amebic keratitis |
| The form of infection of ACANTHAMOEBA SPP. that involves the skin, sinus and pulmonary infection is ? | Disseminated granulomatous amebic disease |
| The disease caused by ACANTHAMOEBA SPP. that is a sight threatening disease that is mostly seen in contact lense wearers? | Amebic keratitis |
| Symptoms of foreign body sensation, sever occular pain, photophobia and blurred vision is common with? | Amebic keratitis |
| The mode of entry of ACANTHAMOEBA SPP.? | Respiratory tract. |
| 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 histology of GAE disease which may be absent in immunocompromised? | Parenchymal necrosis and granuloma |
| 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 |
| Axenic cultures are useful for ? | ACANTHAMOEBA SPP |
| In the cornea of an infected individual, which form of the organism are likely to be present with acute and mixed inflammatory infiltrates? | Cyst and trophozoite. (organism may be present without inflammatory infiltrates) |
| 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. |
| A patient infected with ACANTHAMOEBA SPP. is being treated with an azole compund, they are likely to have which form of the disease? | Non keratic disease |
| 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 |
| In transplantation transmission of TOXOPLASMA GONDII ,low risk transmission to fetus if mother is infected? | More than 6 months before conception |
| High risk transmission if mother is infected | Lee than 6 months before conception |
| Infected infants with TOXOPLASMA GONDII are usually asymptomatic. infant can later suffer from? | Chronic leaning difficulty and neurological sequelae |
| Most infected women are asymptomiatic so screening should occur? | In women who intend to become pregnant |
| 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. |
| Host response in immunocompromised individuals where Tarchyzoites persist? | Necrotisisnf encephalitis, pneumonia, myocarditis |
| 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 |
| Occular infection of TOXOPLASMA GONDII due to congenital infection show symptoms such as? | Blurred vision, scotoma, photophobia and glaucoma |
| Lab diagnosis of TOXOPLASMA GONDII | Culture, serology, PCR, ELISA, Immunoassays. amniotic fluid analysis for B1 gene, igg/igm titres |
| Acute/Prior infection of TOXOPLASMA GONDII is associated wiht which form of the parasite? | TACHYZOITES: acute infection BRADYZOITES: Prior infection |
| 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 |
| Diagnosis of T. solium include | CT. MRI and ELISA |
| 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 |
| In human: cystercercosis may develop in any organ but more common in? | Subcutaneous tissue, brain and eyes. |
| Human infection with T. solium is by? | Ingestion of raw undercooked meat. |
| The development of oncospheres into cysterci occurs in? | Muscles of pigs/humans |
| The diagnostic stage of t. solium | Egg/gravid proglottis |
| Disease caused by T. Solium | Cysticorcosis |