Pathogenic and potentially pathogenic amoebae

Question 1

General information about Amoebae

Answer 1

• Move by pseudopodia
• Feed by phagocytosis
• Heterogenous
• Divided into parasitic and free-living
• Many form cysts

Question 2

final host of Entamoeba histolytica

Answer 2

dog, cat,human, pig

ZOONOTIC!

Question 3

location of Entamoeba histolytica

Answer 3

• Forma minuta in colon - non-invasive
• Forma magna in liver - invasive

Question 4

Morphology of Entamoeba histolytica

Answer 4

• Body delimited by plasma membrane - higly variable size and shape
• Vesicular nucleus
• Chromatin granules attached to nuclear membrane
• Forma minuta: cyst with 4 nuclei, non-invasive, rod-haped
• Forma magna: no cyst, invasive

Question 5

Transmission of Entamoeba histolytica

Answer 5

Fecal oral - salad, water, flies

Question 6

Pathogenesis of Entamoeba histolytica

Answer 6

• Small necrotic foci, ulcers, dysentery
• Liver: fatal disease
• Mucoid bloody diarrhea

Dysentery: infection of intestine resulting in mucoid bloody diarrhea

Question 7

Life cycle of Entamoeba histolytica

Answer 7

Direct

• mature cysts are transmitted from host to host
• Ingestion of cyst –> excyst in SI & trophozoite enter colon where they multiply by binary fission
• New cysts are relesed with feces
• Multiply in colon for months without causing any harm, but may invade intestinal wall & cause disease (enter blood, liver, lung, brain)

Question 8

Clinical signs of Entamoeba histolytica

Answer 8

• Asymptomatic
• Progressive invasive disease - intestinal / hepatic abcess

Question 9

Diagnosis of Entamoeba histolytica

Answer 9

• Coproscopy
• Abcess aspiration
• Amoeba (extraintestinal, pulmonary, cutaneous)
• Culture
• Serology

Question 10

Treatment of Entamoeba histolytica

Answer 10

• Metronidazole

Question 11

Control of Entamoeba histolytica

Answer 11

• Clean & boil food and water

Question 12

Morphology of Naegleria fowleri

Answer 12

• Amoeboid trophozoite, cyst, flagellated form

Question 13

Location of Naegleria fowleri

Answer 13

• Brain, blood, tissue
• Trophozoite: human tissue
• Flagellated form: cerebrospinal fluid

Question 14

Transmission of Naegleria fowleri

Answer 14

enter nasal cavity in water

Question 15

Clinical signs of Naegleria fowleri

Answer 15

• Primary amoeboid meningoencephalitis, sore throat, headache, nausea, vomit, fever

Question 16

Life cycle of Naegleria fowleri

Answer 16

• Trophozoite enter nasal cavity in freshwater / pools
• Migrate to brain via olfactory nerve - brain-eating amoeba: phagocytize RBCs & WBCs, destroy tissue
• Trophozoite is infective stage, and can turn into cyst and flagellated form in poor conditions
• IP: 3-7 days

Question 17

Pathogenesis of Naegleria fowleri

Answer 17

Fatal disease

• Primary Amoebic Meningoencephalitis
• Acute inflammation, necrosis of brain tissue, haemorrhage and oedema.
• Releases cytotoxic molecules and uses suckers (amoebastomes) to ingest brain cells. Symptoms develop within 1-9 days.
• Often infect young, immunocompetent, healthy indiviuals.
• Nearly 100% fatal.

Question 18

Diagnosis of Naegleria fowleri

Answer 18

• Biopsy
• CT

Question 19

Treatment of Naegleria fowleri

Answer 19

No treatment, few survives

only 4 have survived

Question 20

morphology of Acanthamoeba culbertoni

Answer 20

Trophozoite & cyst stage

Question 21

location of Acanthamoeba culbertoni

Answer 21

repiratory system

Question 22

transmission of Acanthamoeba culbertoni

Answer 22

enter water trough eye or mouth

Question 23

Clinical signs of Acanthamoeba culbertoni

Answer 23

Granulomatous amoebic encephalitis and keratitis

Question 24

Acanthamoeba culbertoni

Question 25

Pathogenesis & life cycle of Acanthamoeba culbertoni

Answer 25

It effects immunodeficient and weak individuals. * Enter through skin wounds, respiratory tract, or contaminated contact lenses. * Can enter bloodstream, cross BBB, & invade CNS. * Exists in trophozoite form (active) and cyst form (resistant). **Granulomatous Amoebic Encephalitis** * slow chronic infection of the brain and spinal cord. * Perivascular cuffing, granuloma formation and necrosis. * Induce strong immune response. * Fatal.