Toxoplasma Flashcards
a protozoan parasite, phylum Apicomplexan and often referred to as a coccidian
Toxoplasma
who does Toxoplasma infect?
infects most species of warm-blooded animals, including humans, but only multiply sexually in cats
- infect 1/3 of world popl’n = mostly asymptomatic
Toxoplasma lives an obligate intracell lifestyle and has a unique ability to…
invade host cells and evade immune system
two basic morphologies of toxoplasma
trophozoites and cysts
both extraintestinal and seen in several tissues
toxoplasma trophozoites
two gens: tachyzoites (fast multiplying), bradyzoites (inert or slow multiplying = at this point, huddle together to form cysts)
shape: crescentic, single nucleus; asexual multiplication via endodyogeny (internal budding)
T. gondii lytic cycle
process of invasion and destruction of host cell by indiv Toxoplasma trophozoites
- tachyzoite = initial invader = parasitophorous vacuole is thin membrane that protects it
- keep multiplying until host cell lysis
- parasite egress = frees out daughter trophozoites to start new cycle of destruction in neighbouring host cells
toxoplasma cysts
- also extraintestinal AK tissue cyst)
- resting/chronic/diagnostic stage
- thick wall (protection from immune system, digestive enzymes, inflammatory rxn)
- result of asexual multiplication
intestinal form of toxoplasma parasite
seen in cats only due to sexual repro (gamogony = jejunal epithelium of cats)
oocyst with two sporocysts containing 4 sporozoites; each protected with tough but flexible wall
pathogenesis of toxoplasmosis
- intracellular parasite of both phagocytic & non-phagocytic cell, characteristically invading only nucleated cells !!!!
- cell invasion facilitated by the apical complex/drill- like conoid, micronemes, rhoptries, and dense granules
- survival assured by creation of protective parasitophorous vacuole (comes from repurposing host membrane) inside host cell
conoid
- central part of apical complex
- hundreds of fibers in a spiral; like drill
- can retract, extend, rotate
- can secrete compounds that aid in attachment and penetration of host cell
main secretory organelles that participate in cell entry for toxoplasma
micronemes, thoptries, and dense granules
micronemes
- apical complex; toxoplasma
- release very early in
- host cell binding and gliding motility
T or F. Apicala complexes are unique to Toxoplasma gondii
F! seen in apicomplexans
rhoptries proteins
- Toxoplasma
- released early during invasion
- can be detected in lumen of newly generated paratoph vacuole
dense granules
- Toxoplasma
- released after during/after formation of paratoph vacuoles
- often modify vacuoles environment
= aiding intracell survival and replication of parasite
organs affected by toxoplasma
retina (eyes)
brain
lymph nodes
liver
T or F. Transmission across placenta in a pregnant woman to fetus can only occur if toxoplasma was ingested after conception
T!
sites of invasion of Toxoplasma
- brain = behavioural changes
- eye (immunologically sequestered site, just like brain)
- lymph nodes
- cardiac or skeletal muscle
Two phases of Toxoplasma during human stage
Early (acute) phase: - tachyzoites invading cells
- cell destruction/necrosis
- mononuclear cell inflammation
- blood vessel blockage
Late (chronic) phase:
- bradyzoites/tissue cysts
- latency/immunological evasion
- hypersensitivity
Reactivation of chronic infection after being latent
clinical picture of toxoplasmosis
- acute:
asymptomatic = 90%
lymphadenopathy
infectious mono-like
hepatitis with jaundice
splenomegaly
rash
RARE: involvement on CNs and eye - chronic: ALWAYS asymptomatic (unless of course blind = residual effect)
ocular toxoplasmosis
can be seen during ophthalmoscopic eye exam = dull area where hemorrhage occurred
Neonatal Toxoplasmosis (2)
Transplacental transmission: acute toxoplasmosis in pregnancy
Congenital toxoplasmosis:
* abortion or stillbirth * CNS lesions = mental retardation
* eye involvement: blindness
toxoplasmosis in pregnancy:risk of congenital infection
first trimester = 5%, 60% of offsprings show clinical signs
2nd trimester = 40%, and 25% of offsprings show clinical signs
third trimester = 70%, 10% of offsprings show clinical signs
principal reservoir of toxoplasma
rodents