15 Protozoa Flashcards
Apicomplexa components
Polar ring complex at apical end with conoid, structure of microtubules for invasion of host cell
Rhoptries with lytic enzymes e.g. disruption of RBCs
Micronemes with enzyme
Subpellicular membranes
Apicomplexa life cycle
5 steps
Zygote to Sporpzoites (cysts) via Sporogony
Sporozoites to Merozoites
Merozoites asexual replication (Merogony -> Shizont body)
Merozoites to gametes via Gametogony
Gamates to Zygotes (sexual reproduction)
Malaria
species
Disease
Species
Plasmodium falciparum (Africa), vivax, ovale, malariae
Transmission
bite from infected mosquito, detect humans via smelling: different receptor develop a molecule into a nerv signal via opening of ion channels
Life cycle
1. bite host and release sporozoites
- Sporozoites into liver
- Hypnozoites stay in liver cells (latency)
- Merozoites enter bloodstream
- Erythrocyte cycle -> RBC infection, Trophozoites, Shizont body, then ruptureed RBC to enter new RBC
- Can develop into gametes
- Mosquito takes blood meal to get infected by gametocytes
- Into stomach and develop into gametes
- Oocysts formation
- Sporozoite formation and migration to salivary gland
Disease
Incubation 1-4 weeks, flu like symtoms, but attack results in more severe symtoms and also complication can occur:
Hepatosplenomegaly, Anemia, delirious conditions
Malaria tropica incubation time 1-2 weeks, irregular fever, massive parasitemia and more severe conditions especially without treatment
Blackwater fever, Dark blood through release of hemoglobin
Plasmodium - Liver cycle
Sporozoites enter Kupfer cells that are attached to endothelial hepatozytes
Then infection of hepatocytes and replication via Shizogony
Rupture and then entering blood cell to infect RBCs
Plasmodium erythrocyte cycle
and result in symptoms
Merozoites actively invade RBCs after 5min
Formation of throphoblast (1day) that prepares different intracellular structures to facilitate Shizogony
Shizont with centered Merozoites: Merozoites detach from center and rupture RBCs to infect new ones (2-3 days)
symptoms
synchronized developement, therefore fever stages every 2-3 days, except for most dangerous Malaria tropica
Diagnosis of Malaria
classical
most rapid/common
classical
microscopic sample makes it easy to identify because RBCs do not habe nucleus/DNA, therefore staining for DNA is enough, you can even distinguish between species (e.g. bean form gametocates from P. falciparum)
common
Antigen test: Lysing agent and labelled Ab,
antigen will bind to labelled Ab after lysis of RBC and then bind to another bound antibody,
antibody antibody binding serves as control
Malaria Prophylaxis
Avoid exposure
Taking prophylactic anti-malarial drugs e.g. Chloroquin, Mefloquin
Cryptomsporidium parvum
Family
Transmission
Diagnostics
Disease
Life cycle
Family
Apicomplexa
Transmission
mostly animal, fecal-oral transmission, obligate intracellular pathogen
Diagnostics
Microscopic acid fast staining
direct/indirect fluorescence in stool
stool-ELISA to find proteins
Disease
obligate intracellular pathogen causing diarrhea, obligate pathogen, often associated with HIV
Life cycle
in one host but with enviromental stage
Oocysts ingested and sporozoites infect small intestine epithelial cells
Merozoites released and can develop into gametes; Microgametes penetrate macrogametes to form zygote
Oocysts formation and exit into enviroment
Life cycle inside host on one filae
Pathogenicity
mostly immunosufficient patients:
cant control infection, Enterotoxin release, cell apoptosis
Therapy
no efficient therapy
Toxoplasmosis
Family
Species
Life cycle
Family
Apicomplexa
Species
Toxoplasma gondii
Life cycle
Uptake of cysts, Tachyzoites infect liver cells, in infected macrophages axsexual reproduction via Shizogony
Pseudocysts in response to aquired immunity (latency)
Only harmful for immunocompromised patients and pregnancy (especially early): cross blood-brain barrier and blood-retina barrier and lead to severe symtoms up to death
Toxoplasma diagnosis
Treatment
Pathogen via histology or PCR
Antibodies IgG (mostly->longer in body), igM (current or fresh infection)
several options to treat, for pregnant women but also infants e.g. Spiramycin, Sulfadiazin for infants
Toxoplasma prophylaxis
meat, feces from cats
Antibody tests available
Other embryo damaging infections
STORCH
Syphillis
Toxoplasmosis
Others (Listeria)
Rubella
Cytomegaly
Herpes
Amoeba
Family and species
Rhizopoda
Entamoeba histolytica (Amoebiasis)
Acanthamoeba (Ceratitis)
Negleria fowleri (meningoencephalitis)
Amoeba histolytica
life cycle
Pathology
Life cycle
Eat/drink cysts with 4 nuclei, throhozytes in small intestine, invade colon tissue, throphocytes will develop cysts passed with feces
Pathology
Liver/brain abscess, Inflammation of intestine, colitis, diarrhea
but opportunistic
Diagnostics
Microscopy, Ag, PCR
Serology
Therapy
Metronidazol to remove abscess
Acanthamoeba ceratitis
transmission
Diagnostics
Transmission
free living trophozoites, can live in water, cysts stage most probably, not well known
Diagnostics
Direct preperation of cornea scraping for microscopy, Ag, PCR
Therapy
Miconazol (topical), cornea transplantation
