Amoeba Flashcards
Types of amoeba
Intestinal and free living
Intestinal ones are
E.Histolytica
E.Dispar
E.Coli
E.Gingivalis
E.Polecki
Endolimax Nana
Only E.Histolytica is pathogenic
Free living ones
Balamuthia Mandrillaris
Acanthamoeba spp
Naegleria Fowleri
All are opportunistic pathogens
E.Histolytica geographic distribution
Worldwide.
Especially is tropics and developing countries due to poor sanitation
E.Histolytica life cycle
Direct lifecycle, needs only a single human host
Habitat of E.Histolytica
The large intestines
Mode of transmission of E.Histolytica
Fecal oral route
Source of infection of E.Histolytica
Contaminated food and water (with cysts)
Means of diagnosis E.Histolytica
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.
Treating amoebiasis
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
Pleural amoebiasis
-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
Hepatic amoebiasis
-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
Preventing amoebiasis
Improve sanitation
Improve personal habits and hygiene
Health education
Detection and control of carriers. They should a wood handling food.
Amoeboma
Tumour-like masses of granulation tissue on the intestinal wall as a result of a chronic ulcer.
Other virulence factors for E.Histolytica
Amoebic lectin, cystine proteanise: inhibits complement factor C3 and ionophore
Colonic mucus glycoprotein
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.
Perforation and perinitis
May occur if ulcer involves the muscle and series layers of the colon
Clinical features of intestinal amoebiasis
Charcot-Leyden crystals present
Amoebic dysentery (but mostly just diarrhoea and vague abdominal symptoms)
Chronic involvement of caecum causes a condition that stimulate appendicitis.
What are pathogenic free living amoeba?
Amphizoic - can multiply both in the body of the host and in the free environment
What does NF cause
Primary amoebic Meningoencephalitis (PAM) by amoeboflagellate Naegleria (brain eating amoeba)
What does acantamoeba cause?
Granulomous amoebic encephalitis (GAE) and Chronic amoebic keratitis (CAK)
Balamuthia mandrillaris
Can also cause GAE
Free living amoeba infections are mostly seen in…?
PAM and CAK: seen in healthy individuals.
GAE - in immunodeficiency
Infectious species of the genus Naegleria
Naegleria Fowleri
PAM - brain infection that leads to destruction of brain tissue.
NF global distribution
Worldwide, found in soil and water.
Thermophilic so it strives in warm freshwater bodies (such as rivers, lakes and springs) at low oxygen tension
Morphology of NF
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
Life cycle of NF
Multiplies via binary fission
Flagellate helps spread NF to new water bodies
Completion of life cycle occurs in the external environment
Pathogenesis and clinical features of NF
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
Incubation period NF
2 days to 2 weeks
During which there is anosmia
NF lab diagnosis
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
NF culture
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
Molecular diagnosis NF
New methods based on PCR technology are being developed
NF treatment
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
Acanthamoeba
A. Culbertsoni - most common cause of human infection out of all the Acanthamoeba.
A. Castalleni, A. Astromyx, A. Apolyphagia may also cause infection
Morphology of Acanthamoeba
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
Acanthamoeba pathogenesis
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
Clinical features Acanthamoeba
Infection usually seen in patients with immunodeficiency, diabetes, malnutrition, systemic lupus erythematosus, malignancies
Post-mortem biopsy Acanthamoeba
Shows severe edema and haemorrhagic necrosis
Acanthamoeba disease
CAK and GAE
CAK
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
Laboratory diagnosis of Acanthamoeba
• 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.
Treating Acanthamoeba infrction
• 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.
