Microbiology 51 Introduction to Parasitology
Key Concepts:
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Ecology and socioeconomic factors determine type
Symptoms from high burden or prolonged duration of infection (except malaria)
Diagnosis depends on direct sample
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Common parasitic infections often have no symptoms
Infection v. Disease
o Many infected with Toxoplasma gondii but not many are ill
o Small hookworm infection (consume blood) insignificant
o Depend on host to survive
o Disease associated with prolonged, repeated or unusually burdensome infection
 Subacute or chronic
o Malaria (Plasmodium falciparum) may be rapidly fatal
Parasitic Infections as Zoonoses
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Zoonoses = caused by agents that infect animals (require both human and nonhuman host to
complete life cycle)
o ex. Beef tapeworm goes from human to cattle (cysticercosis) and infects if undercooked
beef eaten
o Others can start in animals -> humans = dead-end hosts
 Ex. Blood fluke (schistosome) of birds causes “swimmer’s itch” after death in
human
Types of Parasites and Modes of Transmission
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Protozoa
o One-cell eukaryotes
o Plasmodium (malaria), Giardia, Cryptosporidium, Leishmania, and trypanosomes
o Replicate intracellularly (plasmodia in RBCs and Leishmania in macrophage) or
extracellulary (lumen of GI tract for amebas and Giardia)
o Transmission depends on arthropod vectors or two forms (active trophozoite in host
and dormant cyst surviving in environment)
 Plasmodia use mosquitoes
 Protozoa of GI tract use 2 form strategy
o Locomotion:
 Amebas -> use pseudopods towards stimulus and streaming cytoplasm
 Intestinal parasites (2 form strategy)
 Flagellates -> use flagellae
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 If intestinal, 2 form strategy. If tissue or blood, arthropods
Ciliates -> covered in cilia; unusual
Apicomplexans (sporozoa) -> use “tractor-tread” gliding motility
 malaria, toxoplasmosis
 Intracellular replication
Helminths
o Worms are multicellular animals (metazoa)
o Reproduce sexually (male and female worms)
 Some are hermaphroditic
o Roundworms -> circular; no visible body segmentation
 Ex. Ascaris lumbricoides
o Flatworms -> asymmetric
 Flukes (Schistosoma, Fasciola): short and nonsegmented
 Tapeworms: segmented, generate from worm head that makes chain (each seg
w/ own organs)
o Typically extracellular and have cuticle
 Larvae of Trichinella spiralis (trichinosis) and tapeworms are dormant cyts
o No helminth completes life cycle in single human
 Parasitic burden causes disease
Vectors
o Transmitters of disease (parasites, bacteria, and viruses)
o Most are arthropods
 Ex. Anopheles mosquito (transmits malaria), tsetse flies (sleeping sickness),
black flies (river blindness), reduviid bugs (Chagas disease), ticks (babesiosis)
o May determine what parasite can survive where
Reservoirs
o Sources of parasites that do not participate directly in transmission to humans
 Ex. Other humans (malaria and amebas), animals and environment
Parasitic Infections and Disease
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Entry
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Fecal-oral route = amebiasis, ascariasi; penetration = hookworm, schistosomiasis
 Contaminated food or water; inadequate control of human waste
o bite of arthropod = malaria, filariasis
 very efficient
Spread and multiplication
o Inoculum size
 Large inocula for amebiasis
 Small for cryptosporidiosis
 Helminthic infections -> severity proportional to inoculum size
o Parasite Survival mechanisms in Immunologically normal hosts
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Antibody and cell-mediated responses evaded
 Shistosomes (blood flukes) coat with host plasma proteins
 Trypanosomes vary surface antigens
 Leishmania (in macrophages) secrete superoxide dismutase protecting
them from phagolysosome; direct lymphocytes to Th2 pathway
Antigenic variation
Intracellullar infection
Encystation
Camouflage
Cleavage of antibodies/complement
components
Suppression or redirection of cellular immune
response
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Trypanosomes, Plasmodium and Giardia
Plasmodia, Toxoplasma
Amebas, cestodes
Schistosomes
Amebas, Leishmania
Plasmodia, Leishmania, schistosomes
Species and Tissue Tropisms
 Tropisms define host and tissue parasite can infect
 Strongyloides species invade intestinal wall
 Hookworms remain in GI lumen
 Pork tapeworm causes cysticercosis (deep tissue) but beef can’t
 Some tropism depend on receptor
 Duffy factor antigen on RBC necessary for Plasmodium vivax
o Black Africans don’t have so uninfected
 Temperature plays role for tropism and induce change in parasite
 Leishmania donovani replicates at 37°C in BM, liver, and spleen ->
visceral leishmaniasis
 L. tropica grows 25-30°C in skin
 Promastigote to amastigote form from cooler insect to warmer host
Damage
o Amebas cause damage by direct cytolytic effect
o Chronic inflammation is hallmark of schistosomiasis and cutaneous filariasis
 Adult parasite innocuous. Progeny induce response
o Host inflammatory response may cause persistent disease
 Ex. Trichinosis
o Cysticercosis may be asymptomatic until death of parasite -> triggers hypersensitivity
rxn
o Eosinophilia
 Occurs in response to surface glycoproteins and polysaccharides
 Increased IgE driven by elevated levels of interleukin-5
o Timing of Clinical cmplications
 Schistosoma mansoni -> GI bleed continues, portal hypertension with
esophageal varices
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Schistosoma haematobium -> urinary tract bleed continues, obstructions/cancer
of UT
 Complications at distant sites
 Pork tapeworm (Taenia solium) asymptomatic by larvae encyst deep
tissues = cysticerci (asymptomatic if in muscle or CNS but may cause
seizure or hydrocephalus)
 Chagas disease (American trypanosomiasis) -> heart block, impaired
swallowing/defecation years after infection
o Environmental constraints
 Shcistosomiasis depends on snail not in N. America/Europe
 Anopheles mosquitoes transmit malaria in US
Diagnosis
o ID parasite or progency
 Hookwarms have eggs in stool
 Strongyloides species larvae are in stool
 Wuchereria bancrofti release microfilaria into bloodstream at night (so draw
blood at midnight)
Treatment and prevention
o Chemoprophylaxis (inhibit replication) or drug treatment (prevent morbidity),
immunization and control measures (inhibit extrahuman stage)
 Eradication with 2 simultaneous strategies
o Different drugs for different stage
 Ec. T. solium in intestine (taeniasis) use niclosamide or in tissue (cysticercosis)
use praziquantel
o Sanitation and wearing shoes reduce hookworm infection, ascariasis, strongyloidiasis
o Drugs
 Chemoprophylaxis -> chloroquine prevents malaria (all Plasmodium)
 Some strains can become resistant
 Treatment -> good for human reservoir diseases
 Must be given to all infectious persons (symptomatic and
asymptomatic)
 Albendazole -> cysticercosis
 Praziquantel -> schistosomiasis
 Ivermectin -> onchocerciasis
 Difluoromethylornithine (DFMO) -> African sleeping sickness
o Immunity and Immunization
 Circulating antibodies against parasite antigens may be ineffective if parasite
uses host as cover (schistosomes) or alter surface antigens (trypanosomes)
 Different proteins at different stages of life cycle
 Malaria mosquito stage immunization (sporozoite) suscpetile to
infection by RBC stage (merozoite)
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 Need antigens from each stage in effective vaccine
Control measures
 Insecticides (DDT) reduce malaria transmission
 Potable water low