ACANTAMOEBA

POLYPHAGA
Name :- Dasu Giri Naga Sai ram
Group :-37 ,sem :-. 1
Subject :- biology
Classification
 Morphology
 Virions of Acanthamoeba polyphaga mimivirus (APMV) are 400 nm
in diameter, spherical in shape and surrounded by an icosahedral
capsid. They are not filterable through 0.2 μm pore size filters. No
envelope has been observed. Fibrils 80 nm in length can be seen
attached to the capsid. Virions resemble small Gram-positive cocci
when Gram stained and was therefore named “mimivirus” (for
mimicking microbe).
PHYSICAL PROPERTIES :-
 Nucleic acid :- double standard DNA
 PROTEINS :- not present
 Lipids – not present
 Carbohydrateses -not present
BIOLOGICAL PROPERTIES :-
 HOST RANG -Acanthamoebaa polyphaga mimivirus was isolated
from the water of a coolingtower .
 TRANSMISSION-Unknown.
 GEOGRAPHICAL DISTRIBUTION -ndirectct evidences (serology)
indicated human infection in England, Canada and France.
Life cycle
 TYPES
 Acanthamoeba are among the most prevalent environmental protozoa
and have been classified by 18s rDNA sequencing into at least 20
genotypes, designated T1-T20. The most common environmental and
human pathogens belong to the T4 genotype. The following species
of Acanthamoeba have been associated with human disease:
 Acanthamoeba castellanii (T4)
 Acanthamoeba polyphaga (T4)
 Acanthamoeba culbertsoni (T10)
 Acanthamoeba palestinensis (T2)
 Acanthamoeba astronyxis (T7)
 Acanthamoeba hatchetti (T11)
 Acanthamoeba rhysodes (T4)
 Acanthamoeba byersi (T18)
 Acanthamoeba divionensis (T4)

TRANSMISSION :-
 A. polyphaga is a direct pathogen when it enters the respiratory tract and
causes GAE or when contact lens wearers come in direct contact and
contract Acanthamoeba keratitis. However, the amoeba can serve as an
indirect pathogen as it becomes a host to other pathogenic organisms
 DISEASE CAUSED
 A. polyphaga can be pathogenic to humans with compromised immune
systems and cause a rare but fatal nervous system disease called
Granulomatous Amebic Encephalitis (GAE) . The amoeba enters the body
through the respiratory tract and invades the alveolar blood vessels,
ultimately passing through the blood-brain barrier and entering the central
nervous system (CNS)
 Granulomatous amoebic encephalitis (GAE)is a rare, usually fatal, subacute-to-
chronic central nervous system disease caused by certain species of free-living
amoebaeof the genera Acanthamoeba, Balamuthia and Sappinia pedata.
 The term is most commonly used with Acanthamoeba. In more modern references,
the term "balamuthia amoebic encephalitis" (BAE) is commonly used
when Balamuthia mandrillaris is the cause
MRI showing result
of GAE caused by an
infection of
Acanthamoeba,
• granulomatous amoebic
encephalitis (GAE), which
occurs most commonly in
humans with compromised
immune systems in the
setting of advanced human
immunodeficiency virus
(HIV) infection, organ
transplant, or chronic
debilitating illness.
 CLINICAL SYMPTOMS
 GAE starts slowly, with symptoms like headache, nausea, dizziness, irritability
and a low-grade fever. The CNS symptoms depend on the part of the brain that is
infected. Changes in behavior are an important sign. Other CNS signs may
include seizures, focal neurologic signs, diplopia (double vision),
cranial nerve palsies, ataxia, confusion, and personality changes.
 Some of the symptoms may mimic glioma (especially brainstem glioma), or other
brain diseases, which may hamper timely diagnosis. The symptoms are caused by
inflammatory necrosis of brain tissue brought on by compounds released from the
organisms
 TREATMENT
 Treatment of granulomatous amebic encephalitis rarely is successful, probably
because of a combination of late diagnosis and antimicrobial failure. Although no
standard regimen exists, anecdotally successful regimens have involved
combination therapy including pentamidine, sulfadiazine,
trimethoprim-sulfamethoxazole, flucytosine, and fluconazole, ketoconazole, or
itraconazole.
 Treatment of granulomatous amebic encephalitis in immunocompromised hosts
can be particularly challenging; however, treatment success has been reported
with combination therapy using fluconazole, pyrimethamine, and sulfadiazine
along with surgical resection of the CNS lesion.Oral regimens including a
combination of trimethoprim-sulfamethoxazole, rifampin, and ketoconazole have
been used successfully to treat children with chronic Acanthamoeba meningitis.
 A small retrospective analysis suggested that adding miltefosine to treatment
regimen may increase survival, but more data are needed to make definitive
conclusions. Miltefosine is currently available through the Centers for Disease
Control and Prevention as an investigational drug to treat free-living
ameba infections.
THANK YOU