Parasitology Flashcards
What two forms can parasites occur in?
single celled – protozoa
- multicellular – metazoan - helminths or worms
What is the definitive host?
One in which the sexual cycle occurs or the adult is present
What is the immediate host?
One in which the asexual system occurs or the larva is present
How many species of plasmodium parasite are there?
5
What do the life cycles of all plasmodia consist of?
A sexual phase and an asexual phase
Where does the sexual phase mainly occur?
Mosquito vectors
Where does the asexual phase mainly occur?
Humans
Where can the life cycle be said to begin?
When the mosquito acts as a vector and transmits the plasmodium parasite in the sporozite stage into the host during a blood meal
What happens after the sporozoites enter the body?
They go to the liver and hepatocytes → they invade the hepatocytes by forming a parasitophorous vacuole where they differentiate into many thousands of merozoites
What happens after the sporozoites have become merozoites?
The infected heptocyte ruptures and merozoites are released into the blood → invade RBCs and begin the ASEXUAL reproductive phase
What does asexual reproduction involve?
Merozoites multiply → differentiae into ring-shaped trophozoites → these then mature into schizonts → these rupture, release merozoites that can infect other RBCs
What can a small number of merozoites differentiate into?
into male (microgamete) and female (macrogamete) gametocytes
What can happen to the gametocytes?
Taken up by the mosquito in her blood meal
What happens to the gametocytes once they are ingested?
Migrate to the midgut of the mosquito → pass through the wall of the midgut to form oocysts
What happens to the oocysts in the midgut?
They divide meiotically to form the sporozoites, which further move to the salivary glands and they are ready to restart the cycle of transmission - this is the sexual cycle
Summarise the asexual cycle
sporozoite → hepatocyte → merozoite → RBC → trophozoite -→ schizonts → merozoites → gametocytes
Summarise the sexual cycle
In mosquito stomach, microgametes penetrate macrogamates → zygotes → become motile ookinetes → invade midgut wall + form oocysts → sporozoites in salivary glands
Which stage accounts for malaria symtpoms?
Erythrocytic phase
Describe pathogenesis
haemolysis of the infected RBCs, releasing the parasites as well as malaria endotoxin
These trigger TLR9 and this leads to high levels of TNF production and clinical symtpoms, such as fever, heache, myalgia, arthralgia and chills
These symptoms recur every third day, due to the fact that the P. faliciparum asexual erythrocytic phase takes 48h to complete, hence there is periodic erythrocyte bursting and release of merozoites
Furthermore, the membrane of the infected RBC stiffens, and this can lead to capillary obstruction, which can affect vital organs in severe malaria
Anaemia is another common feature, due to erythrocyte loss and hence loss of oxygen-carrying capaciy
P. falciparum has an incubation period of about 2 weeks - this is the period it spends replicating in the liver before it invades erythrocytes
What is chloroquine resistance mediated by?
Mutation in the gene encoding chloroquine transport in the cell membrane of the organism
Mechanism of chloroquine
Caps the hemozoin to prevent biocrystallisation of heme - leads to heme build up - chloroquine binds to heme which is very toxic to the cell
What are trypanosomes characterised by?
Unicellular parasitic flagellate protozoa
What is T.brucei responsible for?
African trypanosomiasis (also known as sleeping sickness) in humans and the wasting disease nagana in livestock ONLY in sub-Saharan Africa
What is T.cruzi responsible for?
Chagas’ disease, most prominent in Central and South America
What three components is the disease caused by T.brucei composed of?
- the trypanosome, the tsetse fly and the host
Describe T.brucei life cycle
injected metacyclic trypomastigotes → bloodstream trypomastigotes → proliferate in bloodstream as slender forms which are replaced by non-proliferative stumpy forms when numbers increase (increases chances of host survival) → blood meal by tsetse fly → transformation into procyclic trypomastigotes in midgut (kinetoplast repositioning, surface coat changes, metabolism changes) → they arrest division and migrate to tsetse salivary gland → attach as epimastigotes (elaborationof flagellum) → generation of non-proliferative metacyclic forms (new coat)
How is the T.brucei able to survive in the bloodstream?
Evading immune system w antigenic variation → sequential expression of antigenically distinct variable surface glycoproteisn
How do trypomastigotes replicate?
Binary fission
Pathogenes of T.brucei
Stage 1 → haemolymphatic (fever, headaches, joint pains)
Stage 2 → meningoencephalitic → pass BBB neurological complication (disruption of sleep cycle)
What are the hosts of T.cruzi?
Humans (or some animals) and the triatomine bug as a vector
Life cycle of T.cruzi?
Triatomine blood meal → ingests trypomastigotes form blood → epimastigotes in midgut → trpomastigotes in hindgut → during meal, trypanomastigotes enter wound or mucosal membrane → penetrate varios cells at the bite wound → transformation into non-flagellated amastigotes which multiply by binary fission in cells of infected tissues → differentiate into trypomastigotes which burst out of cells and enter blood → taken up by bug
What are the most frequent cells infected by T cruzi?
Glial, myocaridal and reticuloendothelial
Pathogenesis of T. cruzi?
Acute phase of infection (both trpomastigotes in blood and amastigotes in cells) → local inflammation → mengingoencephalitis, hepatosplenomegaly etc
Cardiac muscle targetted → arrhythmias
What happens after acute T. cruzi infection?
Most people aymptomatic → some porgress to chronic
Nerve damage, cardiomyopathy, megacolon Death
What is leishmaniasis?
vector-borne disease that is transmitted by sandflies and caused by
obligate intracellular protozoa of the genus Leishmania.
Life cycle of Leishmania
Sandfly take blood meal, injects promastigote into skin → promastigotes are phagocytosed by macrophages → promastigotes transform into amastigotes inside macrophages → amastigotes multiply in cells of various tissues → sandfly takes blood meal and ingests macrphages with amastigotes → amastigotes transform into promastgote stage in midgut → divide in midgut and migrate to proboscis → blood meal
Clinical features of Leishmaniasis
- In cutaneous forms, skin ulcers usually form on exposed areas, such as the face, arms
and legs. These usually heal within a few months, leaving scars - In mucocutaneous forms, the lesions can partially or totally destroy the mucous
membranes of the nose, mouth and throat cavities and surrounding tissues. - Visceral leishmaniasis, also known as kala azar, is characterized by high fever,
substantial weight loss, swelling of the spleen and liver, and anaemia. If left
untreated, the disease can have a fatality rate as high as 100% within two years.
