Protozoology
Protozoa & Protozoology – General Overview
Protozoology: a sub-discipline of Parasitology that studies protists commonly called “protozoa.”
“the kingdom of misfit phyla”: basically everything that couldn’t be classified gets shoved into this category (thus many are not genetically related)
thus, classified based on behavioral or morphological traits instead of true phylogenetic relatedness.
Characteristics of Protozoa:
all: high moisture environment for active growth, unicellular eukaryotes
varies: habitat- most are free-living aquatic organisms, will inhabit guts of animals, found in soil
most have 2 life stages: both forms can be infectious just depends on the protist
trophozoite: feeding & growing, multiplying
cyst: dormant & infectious (lives longer in harsh cond.)
Classification
bc not related, classified by behavior (*= contains human pathogens)
Plant-like groups (photosynthetic, unicellular)
• Euglenoids
• Diatoms
• Dinoflagellates*Animal-like groups* (motile, heterotrophic)
• Mastigophora (flagellates)
• Amebozoa (amoebae)
• Apicomplexa
• Ciliophora (ciliates)Fungus-like groups (switch bet. independendent unicellular life and organized multicellular behavior)
• Slime molds
• Water molds (Oomycetes)
Protozoan Parasites
Phylum Mastigophora
all have flagella
some perform cytoplasmic streaming… basically moving their cytoskeleton to transport nutrients w/i cell (moves ameoba)
they are free living! they prefer not to live w/i us but if entered there are some that can cause diseases
pathogens:
1. Giardia lamblia
🧠 Structure: 1 cell, 2 nuclei
❌ Lacks mitochondria → can’t make its own energy
🧪 Disease: Giardiasis (Traveler’s diarrhea)
Mild, often self-limited (goes away on its own)
If not → intestinal malabsorption → treatment needed
lifecycle: Giardia cysts ingested (food, water, soil) → binary fission in small intestine → new trophozoites will attach to intestinal wall → exit body in their cyst form in poop
2. Trichomonas vaginalis
⚠ Only sexually transmitted protozoan (cannot live outside host, no cyst stage)
often asymptomatic → may change urinary discharge
Disease: Trichomoniasis (replicate in urogenital tract)
Phylum Amoeboid
movement: cytoplasmic streaming via pseudopodia which are basically “false feet”
cell structure: unicellular, no mitochondria, heterotrophic
will secret digestive enzymes to break food down externally and then phago their nutrients
habitat: normally free living in water and soil
Entamoeba histolytica: causes Amebiasis
1. non-invasive colonization- after swallowed will become trophozoites and latch onto intestinal lining and start to feed on mucus and bacteria
2. invasive colonization- penetrate into intestinal mucosa and start to dmg tissue → enter blood → travel to liver, lungs & brain (in order of severity & chance of recovery)
Acanthamoeba: causes Keratitis → Amoebic encephalitis
entry: example given was gets trapped between your contact lens and your sclera so must decides to enter through pupil
can worsen & enter NS causing rare and fatal death but typically have warning signs
Naegleria fowleri: causes Primary Amoebic Encephalitis
“brain eating amoeba” → from contaminated still water
enters thru nose → directly to the brain.
no warning, rapid onset, usually fatal
Characterized by an apical complex of organelles adapted for host cell penetration.
All members are obligate intracellular parasites with complex life cycles that commonly alternate between sexual and asexual stages.
Phylum Ciliophora
movement: cilia
cell structure: unicellular, no mitochondria, heterotrophic
will secret digestive enzymes to break food down externally and then phago their nutrients
habitat: free living
sexual reproduction: unique! keeps 2 copies of their genome at all times
macronucleus → actively transcribed DNA. controls day-to-day functions
micronucleus → transcriptionally silent “germ line” copy held in reserve (doesn’t use)
conjugation
Two genetically compatible ciliophorans est. a mating bridge → the entire macronuclear genome is exchanged (whole-genome swap, not just fragments) → Bridge dissolves → each cell now carries a foreign micronucleus alongside its original macronucleus
why is this so unique and important for us to understand?
they exchange and then undergo meiosis (vs the standard of meiosis and then exchange) → allowing for complete genetic blending (half them, half other)
Phylum Apicomplexa
Immotile → thus obligate parasites (so many are pathogens!)
b/c obligate parasite… requires a host:
definitive host: only one host that the organism can undergo sexual reproduction in
developed a commensal rlshp with their host (no symptomology for illness)
intermediate host: organism is restricted to asexual reproduction
host will show signs of illness
Evolutionary & ecological riddles
Why a species selects a definitive host and loses sexual competence elsewhere is unknown (“got comfy & never left”)
host specificity can narrow to single vector species
Cryptosporidium
mammalian parasite
Unique life-history twist
evidence suggests their definitive host died→ thus only has asexual cycles
never undergoes sexual reproduction
Environmental resilience
their cysts (oocysts) are large (so can be filtered) but are very resistant to chlorination and are difficult to destroy!
Filtration usually removes them, but filter failure causes outbreaks (pooped in pool)
outbreaks typically → many people will come in with diarrhea, leading to significant public health concerns and potential strain on healthcare resources.
Outbreak archetype described
Recreational water (public pool, FDR Park) contaminated by child or wildlife feces → filter broken → mass exposure event
Clinical picture: sudden cluster (≈100–125 cases) of explosive watery diarrhea; ERs rapidly overwhelmed (run out of bedpans)
Infection control quandary: large-scale containment without infringing human rights (no “hose-down in parking lot” allowed)
Plasmodium (causes Malaria)
most relevant pathogen → 50% pop. at risk based on equatorial belt so affects worldwide. 400k deaths/year. disease of the RBC
Anopheles mosquitoes- Definitive host
all warm, coastal areas stretching from the Indian sub-continent to the Philippines (Himalayan highlands excluded → vector cannot survive altitude/temperature) and extends to the southern US
Sporogonic Cycle:
mosquito bites human → trophozoite enters → senses their back in definitive host → break into gametes → move to mosquito gut for sexual reproduction → move to their saliva glands
the only way mosquito get malaria is if they bite someone with maraia… “no vertical transfer”
plasmodium will sexually reproduce in salivary glands of mosquito → 1st nose blow has analgesic → pierce skin and feast blood →2nd nose blow while inserted allows for the plasmodium to enter blood stream and evade normal immune defenses/surface barriers
Exo-erythrocytic: starts by attacking liver
sporozoite enters hepatocyte (liver cells) → it is undetectable and can even go dormant in this phase
the parasite asexually reproduces and creates a bunch of nuclei within the cell → as leaving the liver when matured … schizogony: forcing the host liver cell to help form cell membranes, proteins, etc and begins sectioning themselves into a bunch of functional plasmodiums → cell shatters →
Erythrocytic Cycle
Synchronous invasion of RBCs.
Detectable stages
• “Ring stage” (early trophozoite) — tiny chromatin “dot” inside RBCs; asymptomatic
• “Schizont stage” (mature, multi-nucleated) — looks like “chocolate-chip cookie” RBCs; symptomatic cold phase.
Paroxysm: Cyclic Symptomatology that repeats every 24–72 h in accordance the stages of the plasmodium infection; severity amplifies each round.
Cold Phase - Infected RBCs lose hemoglobin bc the schnizont phase ⇒ ↓ O_2 delivery to muscles/skin (so spasm and shake/ chills)
Hot Phase - Mass rupture of schizont-loaded RBCs → massive immune response → cytokine storm (high fever, headache, myalgias, nausea, vomiting all trying to fight)
Wet Phase - Body attempts to cool from hot phase + trying to get rid of excess hemoglobin fluids from their rupture (profuse sweating, exhaustion)
Asymptomatic Interval - New ring-stage; patient feels briefly normal before next cold phase repeats and worsens
Treatments / Prevention
prophylaxis: dates back to 1800’s… now we have pills too
quinine slightly toxifies blood so makes u not ‘tasty’
not good at treating, great at preventing
Mosquirix: first vaccine for fungal and protists… only 50% efficacy and life for 12mths… best option we have for treatment rn even tho it’s shit (hard to make vaccine for non-virus)
Aedes ("aegis") mosquitoes instead transmit many arboviruses (dengue, yellow fever, West Nile); Aedes range is narrower ⇒ explains why viral diseases do not spread as widely as malaria.
“Toxo” (Toxoplasma Gondii)
Cat = definitive host; present on all 7 continents ⇒ worldwide distribution.
\approx 50\% of humans have been exposed/seroconverted.
will target the epithelial cells in humans
asymptomatic unless:
• Severely immunocompromised (AIDS, leukemia) → flu, joint pain, aches
• Pregnant women (asymptomatic BUT)➜ trans-placental infection causes congenital toxoplasmosis (birth deformities!!!)in rats or other animals will cause them to get very angry and will attack cat → cat eats mouse → toxoplasmosis is back in the original host
Phylum Mastigophora
adult ≠ microscopic (1mm-25m), but larva and eggs are
NOT annelids (earthworms)! all helminths are obligate parasitic
Round worms: extremely pathogenic and life threatening
ex: nematodes (lung worms, 🖤 worms.. mainly infects animals)
Flat worms: almost exclusively gut pathogens → not pathogenic / infectious
ex: tapeworm (use to lose weight), flukes