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PTM4310 > Amoeba > Flashcards

Amoeba Flashcards

1
Q

Types of amoeba

A

Intestinal and free living

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2
Q

Intestinal ones are

A

E.Histolytica
E.Dispar
E.Coli
E.Gingivalis
E.Polecki
Endolimax Nana

Only E.Histolytica is pathogenic

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3
Q

Free living ones

A

Balamuthia Mandrillaris
Acanthamoeba spp
Naegleria Fowleri

All are opportunistic pathogens

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4
Q

E.Histolytica geographic distribution

A

Worldwide.
Especially is tropics and developing countries due to poor sanitation

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5
Q

E.Histolytica life cycle

A

Direct lifecycle, needs only a single human host

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6
Q

Habitat of E.Histolytica

A

The large intestines

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7
Q

Mode of transmission of E.Histolytica

A

Fecal oral route

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8
Q

Source of infection of E.Histolytica

A

Contaminated food and water (with cysts)

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9
Q

Means of diagnosis E.Histolytica

A

Intestinal amoebiasis:

Microscopic:
1) demonstration of actively motile trophozoites in freshly passed stool
2) troohzoites that have invested RBCs
3) iodine stained preparation for demonstrating cysts and dead trophozoites.

Macroscopic:
Brownish-black, foul smelling stool with blood and mucus

Serological tests: only tests positive if the infection is invasive.
Includes
IHA, ELISA, latex agglutination test (LA)

Stool culture: for chronic and asymptomatic amoebiasis

Extra intestinal:

-Radiology exam (USG, CT): demonstrates space occupying lesions
-serology tests: looks for Abs formed against E.Histolytica Ags.

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10
Q

Treating amoebiasis

A

1) luminal amoebcides: effective for liminal pathogens such as those in the intestines.
Includes:
Tetracycline
Iodoquinol
Paromomycin

2) tissue agents: for systemic infection
Includes
Emetine
Chloroquine

3) luminal and tissue agents: effective in both the tissue and in the gut lumen.

Includes
Tinidazole
Ornidazole
Metronidazole

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11
Q

Pleural amoebiasis

A

-extension from hepatic abscess through the diaphragm
-or direct spread from colon to the lower part of the right lung via the blood
-dyspnea, non-productive cough, pleuritic chest pain

Hepati-bronchial fistula: chocolate brown sputum

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12
Q

Hepatic amoebiasis

A

-Ulcers form in upper part of right lobe.

Seen as central necrotic tissue but normal peripheral hepatic tissue with invading amoebae.

May be multiple or solitary.

-jaundice occurs if the lesions are many or if they’re pressing against biliary tract

-amoebic hepatitis
-immune inflammatory reaction against trophozoites is what injures the liver

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13
Q

Preventing amoebiasis

A

Improve sanitation

Improve personal habits and hygiene

Health education

Detection and control of carriers. They should a wood handling food.

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14
Q

Amoeboma

A

Tumour-like masses of granulation tissue on the intestinal wall as a result of a chronic ulcer.

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15
Q

Other virulence factors for E.Histolytica

A

Amoebic lectin, cystine proteanise: inhibits complement factor C3 and ionophore

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16
Q

Colonic mucus glycoprotein

A

Can block attachment of trophozoites to epithelial cells and therefore prevent invasion.
So changes in the nature and quality of the mucus may influence virulence.

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17
Q

Perforation and perinitis

A

May occur if ulcer involves the muscle and series layers of the colon

18
Q

Clinical features of intestinal amoebiasis

A

Charcot-Leyden crystals present

Amoebic dysentery (but mostly just diarrhoea and vague abdominal symptoms)

Chronic involvement of caecum causes a condition that stimulate appendicitis.

19
Q

What are pathogenic free living amoeba?

A

Amphizoic - can multiply both in the body of the host and in the free environment

20
Q

What does NF cause

A

Primary amoebic Meningoencephalitis (PAM) by amoeboflagellate Naegleria (brain eating amoeba)

21
Q

What does acantamoeba cause?

A

Granulomous amoebic encephalitis (GAE) and Chronic amoebic keratitis (CAK)

22
Q

Balamuthia mandrillaris

A

Can also cause GAE

23
Q

Free living amoeba infections are mostly seen in…?

A

PAM and CAK: seen in healthy individuals.

GAE - in immunodeficiency

24
Q

Infectious species of the genus Naegleria

A

Naegleria Fowleri

PAM - brain infection that leads to destruction of brain tissue.

25
Q

NF global distribution

A

Worldwide, found in soil and water.
Thermophilic so it strives in warm freshwater bodies (such as rivers, lakes and springs) at low oxygen tension

26
Q

Morphology of NF

A

1) ameoboid trophozoite

round pseudopodia, spherical nucleus, pulsating vacuoles (for WBC and RBC engulfment)

feeding, growing and replicating form. Seen on the surface of vegetation, soil and water.

Also the infectious and invasive form.

2) flagellate trophozoites

Biflagellate.

Occurs within a minute of trophozoites being transferred to distilled water.

Can revert back to ameoboid form and hence Naegleria Fowltis classified as ameoboflagellate

3) cystic form

-Resting and dormant form
-enchantment when conditions are harsh
-can resist harsh conditions such as drying and chlorine up to 0.5ppm (dies at 2ppm)

Cyst and flagellate have never been found in tissues of CSF

27
Q

Life cycle of NF

A

Multiplies via binary fission

Flagellate helps spread NF to new water bodies

Completion of life cycle occurs in the external environment

28
Q

Pathogenesis and clinical features of NF

A

Invades the nasal mucosa, passes through olfactory branches in the cribriform plate and into meninges and brain

initiates an acute purulent meningitis and encephalitis (together, makes PAM)

CN palsies of CN 3,4,6

Fatal end within a week despite treatment

29
Q

Incubation period NF

A

2 days to 2 weeks

During which there is anosmia

30
Q

NF lab diagnosis

A

Microscopically:

Presence of motile NF trophozoites in wet mounts of freshly-obtained CSF

CSF picture resembles hat of bacterial meningitis: cloudy, pruluent appearance. Prominent neutrophilic leukocytosis, elevated protein levels, low glucose.

Autopsy: trophozoites demonstrated in the brain histologically with the aid of immunofluoroscent straining

31
Q

NF culture

A

Can grow in many kinds of liquid axenic media

Or

Non-nutrient agar plate coated with Escherichia coli

Both trophozoites and cysts occur in the culture

32
Q

Molecular diagnosis NF

A

New methods based on PCR technology are being developed

33
Q

NF treatment

A

Amphotericin-B is the drug of choice
Administered via IV or intrathecally (directly into the spinal canal or subarachnoid space)

Combination of miconazole and sulfadiazine
Limited success when administered early

34
Q

Acanthamoeba

A

A. Culbertsoni - most common cause of human infection out of all the Acanthamoeba.

A. Castalleni, A. Astromyx, A. Apolyphagia may also cause infection

35
Q

Morphology of Acanthamoeba

A

Two forms, both are infective

1) Highly active trophozoites, with spine-like pesudopodia (acanthopodia)

Trophozoites are large in size

No flagellate form.

2) Cystic form - highly resistant and double walled.

Present in all types of environment

Encystment occurs in tissue

36
Q

Acanthamoeba pathogenesis

A

Infections occur by:

inhalation of cysts or trophozoites
Ingestion of cysts
Contact of traumatised skin or eyes with cysts

After inhalation, cysts find themselves in the lungs.
Spread to the CNS hematogenously producing Granulomatous Amoebic Encephalitis (GAE)

They invade connective tissue leading to pro-inflammatory responses that cause neuronal damage

37
Q

Clinical features Acanthamoeba

A

Infection usually seen in patients with immunodeficiency, diabetes, malnutrition, systemic lupus erythematosus, malignancies

38
Q

Post-mortem biopsy Acanthamoeba

A

Shows severe edema and haemorrhagic necrosis

39
Q

Acanthamoeba disease

A

CAK and GAE

40
Q

CAK

A

Infection of eye mostly in healthy persons.
Cyst enters through abrasions on the cornea
Associated with use of contact lenses
Picture resembles herpetic keratitis

Unilateral photophobia, execessive tearing, redness and foreign body sensations
May lead to permanent visual impairment or blindness

41
Q

Laboratory diagnosis of Acanthamoeba

A

• Diagnosis of amoebic keratitis is by demonstration of the cyst in corneal scrapings on wet mount, histology and culture. Growth can be obtained from corneal scrapings inoculated on nutrient agar, overlaid with live or dead Escherichia coli and incubated at 30°C.

• Diagnosis of GAE is made by demonstration of trophozoites and cysts in brain biopsy, culture & immofluroscence microscopy using monoclonal antibodies.

• CSF shows lymphocytic pleocytosis, slightly elevated protein levels, and normal or slightly decreased glucose levels.

• CT scan of brain provides is inconclusive.

42
Q

Treating Acanthamoeba infrction

A

• In acantamoeba keratitis, current therapy involves topical administration of biguanide or chlorhexadine with or without diamidine agent.
• In severe cases, where vision is threatened, penetrating keratoplasty can be done.
• No effective treatment is available for GAE. Multidrug combinations including pentamidine, sulfadiazine, rifampicin, and fluconazole are being used with limited success.

PTM4310 (2 decks)

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