Parasites and Fungi Flashcards
What are examples of endoparasites?
Protozoa (one cell)
Helminths (worms - many cells)
What are examples of ectoparasites?
Lice
Bedbugs
Scabies
Mites
What are the different parasite types?
Obligate - cannot survive without a host
Facultative - able to survive outside a host (ex. Acanthamoeba)
What are the different types of parasite hosts?
Definitive - parasite reaches reproductive form
Intermediate - parasite grows but doesn’t reach reproductive form
Reservoir - can harbor parasite without showing ill effects
How are Protozoa acquired by people?
Fecal oral
Ingestion of contaminated food or water
How can Protozoa live inside humans?
Extracellular in blood (filariasis), intestine, urogenital system (schistoma)
Intracellular in tissue macrophages (leishmania) or RBCs (plasmodium)
How are Protozoa differentiated?
Size
Nucleus - clumped or dispersed, Maryland
Cytoplasm appearance
Organs of motility
What are the stages of Protozoa?
Trophozoite - actively feeding organisms in host niche - assimilation of organic nutrients using pseudopods, simple diffusion or active transport - various metabolic pathways
Cyst - metabolically inactive, able to survive under unfavorable conditions, resistant to chlorination and drying, integral for most
What is the spectrum of disease in giardia?
Asymptomatic carriage
Mild diarrhea
Severe malabsorption
Incubation period is 10 days
What are the possible organs of motility for Protozoa?
Simple cytoplasmic extrusions (pseudopods) - amoebae
Flagellates - giardia
Ciliates
Undulating membrane - sporozoa - obligate intracellular
How does protozoan reproduction work?
Asexual in humans
Sexual absent or restricted to insect vector
What is neurocysticercosis and what organism can cause it?
Cysts with organisms in it in brain
Taenia solium = pork tapeworm
What is a proglottid?
Tapeworm segment with male and female reproductive organs
Uterine branches fill with ova (eggs)
What is the basic life cycle of taenia coli or t. Saginata (beef)?
Pigs or cows (intermediate hosts) ingest proglottid
Eggs hatch in intestine and form cysts
Humans eat animal and then tapeworm develops and start to reproduce (humans are definitive host)
Human can become intermediate host if they eat proglottid instead of animal –> inf in brain
How does nutrition work in helminths?
Some have rudimentary digestive apparatuses, others directly absorb host nutrients
Most lack TCA cycle
Unable to use FFA or AA for energy
Fermentative
What is the only helminth that multiplies inside human host?
*s. stercoralis
What are the three broad categories of worms?
Nematodes - roundworms (intestinal or extraintestinal)
Platyhelminthes - flatworms (Cestodes - tapeworm, Trematode/flukes)
What medications can interfere with a stool sample?
Anti diarrheal
Antacids
Barium or bismuth
Oily laxatives
What do giardia trophozoites and cysts look like histologically?
Trophozoites - teardrop shape, two nuclei, suckers on bottom, picked up on trichrome stain, flagella, normally stay attached to intestine
Cysts - two trophozoites per, so four nuclei
What is a dfa test for giardia?
Direct fluorescent antibody
AB reagent specific for giardia with fluorescent tag - fluorescence indicates presence of giardia
Also detects cryptosporidium
What are other diagnostic methods for parasites?
Serology - limited use in patients from endemic areas
Blood smears - plasmodium
Tissue biopsy - trichinella
Molecular testing
T. Cruzi
Hemoflagellate
Causes Chagas’ disease
Acute disease - no focal febrile syndrome
Late disease - cardiomyopathy, arrhythmia, death, mega colon, mega esophagus
*trypomastigote = infective in blood
*Amastigote = tissue form, binary fission
*epimastigote = binary fission
T. Cruzi Intermediate host Infection via... Vector Key terms
Bug
Bug poop
Yes
Cardiomyopathy, mud huts
Toxoplasma gondii
Sporozoan Acute disease - similar to mono Congenital Re activation - multifocal lesions Cysts are full of bradyzoites Oocyst - full of sporozoites
T. Gondii Intermediate host Infection via... Vector Key terms
Everything including humans
Multiple routes
No
HIV, pregnancy
Filariasis
W. bancrofti - near equator, most common, humans are definitive hosts, mosquito is intermediate, no reservoir
B. malayi - Asia and Indonesia, less common, humans are definitive hosts, mosquitoes are intermediate, has reservoirs
Mosquitos are also vectors
Helminths
Fasciola hepatica
Sheep liver fluke
Acute - larval fluke travel from intestines to bile duct and cause inflammation, reactions, bleeding, hives and cough, can kill sheep
Chronic - larva mature into adults in bile ducts and pass eggs into feces, may be asymptomatic, may cause obstruction
F. Hepatica Intermediate host Infection via... Vector Key terms
Snail
Watercress
No vector
Rancher, watercress
What are some common features of fungal infections?
*Most are chronic (indolent)
Most are exogenous
Few are communicable
Several have characteristic ecological niche - *clue is patient exposure to these habitats
What are some differences between fungi and bacteria?
*Fungi are eukaryotes
*cell wall has glucans and chitin instead of peptidoglycan
Most in nature live on decaying material
Do not need to colonize or infect tissues to perpetuate species
How does the fungal cell wall interact with drugs?
*beta 1,3-D-glucan is the target of echinocandins which inhibit glucan synthase and it is useful in diagnosis
What is the structure of fungal cell membrane?
Lipid bilateral
Phospholipids
*ergosterol - site of action of amphotericin b and azoles
Functions to protect, regulate intake and secretion and cell wall synthesis
What is the fungal physiology?
Respire aerobically
Metabolism is heterotrophic
Slow growing
What are different fungal growth patterns?
Yeast - *single celled forms, reproduce by budding(bud=blastospore), pseudohyphae, colonies reaemble bacteria, candida and cryptococcus
Molds - *grow as filamentous structures, *opportunists like aspergillus are monomorphic, hyphae, velvety granular appearance with pigment
What are dimorphic fungi?
Yeast form in mammalian host
Filamentous mold form in soil or environment
Perfect fungi have known sexual forms - s. cerevisiae, c. Neoformans
Imperfect have no known sexual forms
Reproduction of fungi: conidiogenesis
Arthroconidia -
Result from preexisting entire hyphae
*break loose and initiate another cycle of reproduction by germination
Reproduction of fungi: blastoconidiogenesis
Most fungi especially yeasts
Blastoconidia of yeast may continue to grow and elongate into *pseudohyphae
Others may develop into *true hyphae that do not separate at maturity
Reproduction of fungi: macro/microconidia and sporangiopore
Some form large *macroconidia and/or small microconidia
Others reproduce by cytoplasmic cleavage within structure called *sporangium
Hyphae of the fungi are aseptate
Mycoses (fungal disease)
Ubiquitious
Superficial and cutaneous grow on epidermis at 25 deg c and metabolize keratin - *caused by dermatohytes
Rarely invade deeper that outer layers of skin, nail, or hair
Subcutaneous Form deep, ulcerated, skin lesions involving extremities, caused by soil saprophytes and intro through trauma to hand, feet, or legs
Endemic mycoses
Systemic mycoses -
*characteristic endemicity of fungi in certain geographic regions of the world
*illness may occur in healthy individuals (primary infection)
Portal of entry is lungs
*endemic fungal pathogens all dimorphic
Include histoplasmosis, blastomycosis, and coccidioidomycosis
What is an important risk factor for opportunistic mycoses?
*certain host gene defects
Cryptococcus neoformans
Encapsulated yeast
Pneumonia
*meningitis in AIDs if cd4<100
Pneumocystis jiroveci
*pneumonia in AIDs if cd4<200
Adhesion by surface glycoproteins
Aspergillus
Ubiquitous environmental mold
Inhale spores
Causes pneumonia
Extra pulmonary spread
Bone marrow transplant, liver transplant, chemotherapy patients, CGD
Adhesion by complement receptors and hydrophobins
What is the pathogenesis of fungal infections?
Neutrophils actively recruited and destroy fungal hyphaes
*invasive fungal diseases like aspergillosis and candidemia develop in patients with severe neutropenia
What modifications do cryptococcus and histoplasma show during invasion process?
Increased metabolic rate
Modified metabolic pathways
Modified cell wall structure
How are macrophages involved in the pathogenesis of fungal infections?
Activated ones control multiplication of intracellular yeast
Granulomatous inflammation which can lead to calcified fibrinous granulomas, a characteristic pathology
Cytokine response lead to clinical manifestations - fever, fatigue, weight loss
What stains fungal cell walls?
Giemsa
Silver stain reveals organisms when giemsa not optimal
What is am common mycological agar?
*sabouraud dextrose
Ph less than 6
C-source
Inhibitory agents are cycloheximide, penicillin, streptomycin
What can be detected using direct antigen detection in blood and CSF?
Galactomannan - component of aspergillus cell wall
Beta 1,3 D glucan
How are intracellular parasites controlled?
By macrophages activated by parasite specific th1 cells
How does immunity to schistosomes work?
Dominant mechanism involves th2 cells, IgE, mast cells and eosinophils
Directed to prevention of reinfection - Adult worms reside in blood vessel lumen and resist immunologic mechanisms
Concomitant immunity - cercariae is form that penetrates skin - turns into schistosomula which is the stage vulnerable to attack (must happen within 48-72 hrs!) –> ADCC
What is concommitant immunity?
Mammalian host resists reinfection with skin stage worms yet is incapable of eradicating adult worm
ADCC is primary mechanism
How does immunity to toxoplasma work?
Obligate intracellular - sequestered from immune elements Dormancy and latent infections in immunocompromised Primary mechanism involves phagocytic killing by activated macrophages Sterile immunity rare - brain and eye cells lacking class 1 MHC hold latent inf
How does immunity to malaria at sporozoite stage work?
Sporozoites enter liver cells
AB promotes opsonization and complement mediated lysis, blocks binding and penetration of liver cells
Extracellular - ignored by CTL
How does immunity to malaria in liver stage work?
Intracellular - hidden from antibody
Express antigens on MHC 1
CTL kills and produce IFNgamma which promotes NO
How does immunity to malaria in the erythrocytic stage work?
No MHC - escape CTL
AB opsonizes and promotes removal by RES, also prevent binding and penetration by extracellularly merozoites
How does immunity to trichinella work?
Gut phase –> tissue migratory phase –> intramuscular
Adult worms in GI lumen is stage most vulnerable to attack
Rapid expulsion - IgE leads to growth of gut mast cells, goblet cells, prevents re-infection without affecting muscle larvae
More mucus increases gut motility and hampers parasite foothold
Parenteral involves ADCC of larvae
Intramuscular in larvae capsules - eventually calcify and die
What is an example of a parasite that uses antigenic variation to avoid immune system?
Trypanosomes
Where is antigenic mimicry best developed?
Schistosomes
How are different Th cells active in infections?
1 - protozoan, protect against leishmaniasis
2 - helminth, leads to lethal leishmaniasis
3 - bacteria
How does immunity to leishmania work?
Obligate intracellular parasite
Resides in RES
utilizes complement receptor on macrophages to gain entry - inhibits ROS
thrives in acid of lysosome
Infected macrophages become resistant to activation
What is the hygiene hypothesis?
Parasitic infections especially worms induce generation of t reg cells that down regulate allergic diseases
Not a result of a th1 response that cross regulates th2 response
How does immunity to schistosomiasis work?
Eggs in liver invoke immune response and cause pathology
Early th1 response followed by late th2 response to egg antigens in liver cause granuloma formation and eventual liver fibrosis
Culminates in ascites
How does immunity to onchocerciasis work?
Nematode infection
Th2 response to larval antigen creates chronic inflammation of ocular surface
Eosinophils and neutrophil infiltration
Leads no river blindness
