FINAL Flashcards
protozoa
- single celled, animal-like
- amoeba, ciliates, flagellates, sporozoans
- structures: cytoplasmic membrane, cytoplasm, usually with flagellum
- aquatic, obligate parasites
- chronic or acute diseases: amerbiasis, sleeping sickness, chagas disease, STD
entamoeba histolytica
- cause of amoebiasis (intestinal disease)
- mostly mild diarrhea; dysentery, abdominal pain, fever fatigue, weight loss
- ## tissue damage and in severe cases can lead to extra-intestinal infections
treatment of amoebiasis
- drugs that target parasites both in the feces and the tissues
- iodoquinol, metronizadole, dehydroemetine, chloroquine
naegleria fowleri
- common, free living protozoans, accidental parasites
- live in lakes, hot springs, swimming pools, hot tubs, moist soil
- cause of primary amoebic meningoencephalitis (brain infection)
- invades nasal mucosa
- has cyst and trophozoite stages and can grow into flagellates as well
acanthamoeba
- common, free living protozoans, accidental parasites
- live in lakes, hot springs, swimming pools, hot tubs, moist soil
- cause of granulomatous amoeba encephalitis (brain infection)
- invades through broken skin, conjunctiva, lung, and eyes
- course of infection lengthier than naegleria
treatment for naegleria meningoencephalitis
- advances too fast to have an effective treatment
- amphotericin B, sulfadiazine, tetracycline, and ampicillin can be of some benefit if treated early in the infection
ciliates characteristics
- has cilia for movement
- two nuclei: macro and micro
- undergo sexual and asexual production
- life cycle includes trophozoites and mature cysts
- natural habitats: large intestines of pigs and other domestic animals, primates: cysts in feces
- causes balantidiosis
balantidium coli
- infection of intestinal mucosa (ciliate protozoa)
- symptoms: irritation, injury, nausea, vomiting, diarrhea, dysentery, and abdominal colic
- healthy individuals are resistant
- prevention: prevent food or drink contamination with pig manure
treatment of balantdium coli
oral tetracycline
- if this fails, dodoquinol, nitrimidazine or metronidazole
flagellates
- mastigophorans
- common feature: long, filamentous flagella
- diseases:
- trichomononiasis and giardiasis (mild)
- trypanosomiasis and leishmaniasis (debilitating)
trichomonads
- small, pear-shaped protozoa, with four flagella and an undulating membrane (flagellate)
- does not produce cysts
- reservoir: human urogenital tract: 50% asymptomatic
- mode of transmission: sexual contact, communal bath, public facilities, mother to child
trichonomoniasis
- 2nd most prevalent STD
- symptoms:
- females: foul smell, green to yellow vaginal discharge, vulvitis, cervicitis, urinary frequency and pain
- males: urethritis, milky discharge, prostate infection
treatment of trichomoniasis
oral and vaginal metronidazole; both sexual partners have to be treated
Giardia lamblia
- flagellate protozoa
- causes giardiasis
- most common flagellate isolated in clinical specimens
- prominent cause of diarrhea
giardiasis
- infection caused by giardia lamblia - prominent cause of diarrhea
- outbreaks: traveler’s diarrhea, hikers, campers drinking from fresh mountain streams, children in day care centers
treatment of giardiasis
quinacrine or metronidazole
hemoflagellates
- vector-borne blood parasites (in blood and tissues)
- two major species:
- trypanosoma
- leishmania
- life-threatening diseases
- spread by blood-sucking insects
- complicated life cycles
amastigote
round cells lacking a free flagellum
- development stage of hemoflagellates
promastigote
cell with single, free, anterior flagellum
- development stage of hemoflagellate
epimastigote
- flagellate stage, with both flagellum and an undulating membrane
- development stage of hemoflagellates
trypomastigote
the large, fully formed stage of trypanosoma
leishmania development stages
- amastigote - intracellular in human macrophages
- promastigote - found in sand fly gut; infective to humans
trypanosoma brucei development stages
- epimastigote - present in salivary glands of tsetse fly
- trypomastigote - in biting mouthparts of tstete fly; infective to humans
trypanosoma cruzi development stages
- ALL STAGES OCCUR
- amastigote: intracellular in human macrophages, liver, heart, spleen
- promastigote: occurs
- epimastigote: present in gut of reduviid
- trypomastigote: in feces of reduvid big; transferred to humans
trypanosoma brucei
- one of the two major trypanosoma species
- cause of african sleeping sickness
- two subspecies: T.b. gambiense (west africa) T.b. rhodesiense (east africa)
- principle vector: tsetse flies
trypanosoma cruzi
- cause of chagas disease
- insect host: kissing bug
sleeping sickness
- caused by trypanoma brucei
- intermittent fever, enlarged spleen, swollen lymph nodes, joint pain
- personality change, sleep disturbances (sleepiness in the day and sleeplessness at night)
- advanced neuromuscular disorders:
- muscular tremors, shuffling gait, slurred speech, epileptic seizures, paralysis
- death: coma, secondary infections, heart damage
treatment of sleeping sickness
- chemotherapy: successful if administered prior to brain damage
- treatment of brain infections: expensive
- melarsoprol - toxic arsenic-based drug
- difluoromethylornithine (DFMO): less toxic
why can’t the immune system defeat the trypanosome?
- trypanosomes produce a large number of surface antigen in succession (>100 antigenic variations)
- antibodies produced by the host fail to stop bugs with new antigen
- host becomes overwhelmed
- difficult to immunize
chagas disease
- fever, swelling lymph nodes, spleen and liver
- favored targets are heart muscle and large intestine
- heart enlargemnt and death in 2 years
treatment of chagas disease
- nifurtimox and benzonidazole for early treatment
- side-effects are damaging (humans cells similar to protozoans - cross-reactivity)
leishmaniasis
- capillary infection of leishmania (gets into capillaries and causes tissue damage)
- transmitted among mammals by phlebotomine flies (sand flies)
- endemic to equatorial regions
- special risks: travelers and immigrants
- death by destruction of tissues
apicomplexan parasites
- sporozoan protozoas
- lack locomotor organelles in the mature stage
- sexual and asexual reproduction
- most important human pathogens
- plasmodium - malaria
- toxoplasma - toxoplasmosis
malaria
- caused by plasmodium (apicomplexan parasite)
- symptoms:
- chills and fever at regular intervals, followed by sweating, due to synchronous rupturing of RBCs
- anemia in young children; organ rupture from accumulated cell debris (spleen, liver and kidneys)
- long recovery: up to 5 years
plasmodium
- cause of malaria
- obligate intracellular sporozoan
- four species: P. malariae; p. vivax, P. falciparum, P. ovale
- transmission
- mostly by female anopheles mosquitoes
- occasionally sharing needles
- blood transfusions
- mother to child
P. falciparum
- causes the most severe cases of malaria
- persistent fever, rapid pulse, cough, weakness for weeks without relief, high death rate in acute phase
diagnosis of malaria
- stained blood smear
- antibodies
- DNA-PCR analysis
treatment of malaria
- chloroquine, less toxic side effects for non-resistant strains
- for resistant strains - mefloquine or quinine
- for eliminating the parasites from the liver: use primaquine or proguenil
toxoplasma gondii
- cause of toxoplasmosis
- exposure rate: 90%
toxoplasmosis
- caused by toxoplasma gondii
- most cases: mild, sore throat, lymph node enlargement, low grade fever
- immunodeficient patients: brain lesions, fetal disruption of the the heart and lungs
- infection in pregnant women (33% chance transmission to fetus) -> leads to still birth, liver failure, hydrocephalus, convulsions, and retina damage and blindness
Helminth Life Cycle A
- route of infection: oral
- source: water and food contaminated with mature eggs
- larvae hatches in tissues and then migrates into the intestine to mature and mate
- embryonic eggs are then released back into the environment
Helminth Life Cycle B
- route of entry: skin penetration
- source: contaminated soil
- eggs develop into the larvae to allow skin penetration in the environment
- larvae migrates into the intestine to mature and mate
- embryonic eggs are then released back into the environment
Helminth Life Cycle C
- route of entry: oral
- source: contaminated meat with encystment in the muscle
- larvae migrate into the intestines to mature and mate
- embryonic eggs are then released back into the environment to be taken up by livestock again
Helminth Life Cycle D
- two routes of infection: direct skin penetration or contaminated meat
- larvae migrate to intestine or bladder to mature or mate
- embryonic eggs are then released back into the environment
- eggs develop into the first larval stage then infect intermediate host then, enter larval stage
- second larval stage can be taken in through skin penetration of contaminated meat
Helminth Cycle E
- parasite transferred through insect bites
- infective larvae get lodged in tissues and new larvae are released into circulation and ready to be transferred into new insects and hosts
pathology of helminth infection
- symptoms: enlargement of organs, hemorrhage, weight loss, anemia
- ## worms migrate with enzymes to liquefy and penetrate tissues -> tissue damage, blocked ducts and organs, toxic secretions, pressure
methods for diagnosis of helminths
- eosinophilia (increase in eosinophils)
- travel history
- detection of eggs in stools, urine or blood
Ascaris Lumbricoides
- intestinal nematodes
- cycle A
- causes ascariasis
- retain motility (do not attach)
- severe inflammatory reactions mark the migratory route
- allergic reactions can occur
- heavy worm loads can retard physical and mental development
Hookworms
- intestinal nematode
- cycle B
- larbae burrow into the skin -> circulation -> lungs –> throat –> small intestine
- symptoms:
- dermatitis
- pneumonia
- nausea, vomiting, pain, bloody diarrhea
- chronic fatigue, anemia
Strongyloidiasis
- intestinal nematode
- cycle B
- threadworm (also called pinworm) infections
- 100 to 200 million patients worldwide
- symptoms:
- bloody diarrhea
- liver enlargement
- bowel obstruction
- malabsorption
trichinella spiralis
- intestinal nematode
- cycle C
- mammalian hosts
- encysted larval form in muscles
- humans infections from raw meat from swine or bear
trichinosis
- caused by trichinella spiralis
- symptoms:
- initially: fever, diarrhea, nausea, abdominal pains, and sweating.
- Second phase: intense muscle and joint pain, shortness of breath, and eosinophilias –> heart and brain damage –> death
- prevention: cook meat well. freezing also kills the worm larvae
filarial nematodes
- tissue nematode
- cycle E
- long, threadlike worms
- biphasic life cycle: alternating between humans and mosquitoes or flies
- two major species: wuchereria bancrofti and oncocerca volvulus
bancroftian filariasis
- wuchereria bancrofti
- affects 120 million people
- symptoms: elephantiasis
- inflammation and blockage of main lymphatic channels –> accumulation of fluid
onchocerca volvulus
- tissue nematode
- causes river blindness/ onchocerciasis
- inflammation, and granulomatous lesions
- river blindness: invasion of eyes
- transmitted by black flies that breed along rivers in west Africa
Loa Loa
- tissue nematode
- cycle E
- the African eye worm
- transmitted by a fly
- treatment: pull worm out; diethylcarbamazine
Dracunculus medinensis
- tissue nematode
- cycle D
- dragon worm
- found in india, middle east, and central Africa
- parasite first infects cyclops (arthropod found in still water
- infection cycle: ingestion of larva in cyclops -> intestine -> subcutaneous tissue -> irritants -> itching blisters (fireworm) -> eruption in water -> cyclops
blood flukes/ schistosomes
- trematode
- cycle D
- causes schistosomiasis
- life cycle: infected humans -> eggs -> ciliated larva (mircadium) -> snails (host) -> forked larva (cercaria) -> human skin -> circulation -> liver -> intestine -> feces
schistosomiasis
- caused by schistosomes/ blood flukes
- symptoms: fevers, chills, diarrhea, and cough
- chronic infections: hepatomegaly, splenomegaly, bladder obstruction, kidney damage, blood in urine, brain damage
- control: snail-eating fish
cercaria
capable of penetrating exposed human skin
liver and lung flukes
- trematode/fluke
- cycle D
- develop in liver or lung
- sexual development in humans
- intermediate hosts: snails
- infection by ingesting inadequately cooked or raw freshwater fish and crustaceans
- larvae hatch and crawl into the bile duct -> matures -> shed eggs into the intestinal tract -> feces into standing water -> snails -
Cestode/ Tapeworm
- cycle C
- morphology:
- scolex: head - sucker, no mouth
- neck
- strobila: ribbon composed of reproductive segments (proglottids)
taenia saginata
- beef tapeworm
- cause of taeniasis
- 2000 proglottids anchored by a scolex with suckers
- worldwide
- cows infected by ingesting in fields with proglottids or eggs contamination
- humans infected by eating raw beef
- symptoms: mild abdominal pain and nausea
taenia solium
- swine tapeworm
- T. solium is smaller than T. saginata
- endemic in areas consumin raw or partially cooked pork
cysticercosis
a severe form of Taenia solium infection
- tapeworm larvae migrate to different tissues
- form peculiar cysticerci
- tissue damage - heart, eye, brain
anisakis
- fish helminths
- cause of anisakiasis
- tingling sensation in the throat a few hours after eating sushi or sashimi
- anisakis larvae will try to burrow into the tissue causing irritation and vomiting but usually gets expelled without further symptoms
- can cause acute GI pain, cramping and vomiting
diphyllobothrium latum
- tapeworm/cestode
- found in the great lakes region, Canada, and Alaska
- humans are definitive hosts
control of helminth infections
- sewage treatment
- now use of human feces as fertilizer
- water treatment
- no raw meat
- chemotherapy: paralyze worms and interfere with worm metabolism
Ivanovski and Beijernick
identified tobacco mosaic virus causing a tobacco disease (1890)
Louis Pasteur
- postulated that rabies was caused by “living things” smaller than bacteria
- in 1884, developed the first vaccine for rabies
- proposed the term virus
Loeffler and Frosch
identified foot-and-mouth virus
size of viruses
- animal viruses 20 nm to 450 nm
- electron microscope needed to observe viruses (up to 5,000,000x magnification)
negative staining
use thin layers of an opaque salt to outline the shape of the virus against a dark background and to enhance the texture of the viral surface
positive staining
detects internal details of proteins and nucleic acids
shadowcasting
spread metallic vapor from a certain angle. the metallic coating over the surface approximates the viral contours and a shadow is cast on the unexposed side
capsid
a protein shell that surround the nucleic acid in the central core
- made up of identical subunits called capsomers
nucleocapsid
capsid + nucleic acid
envelope
some possess modified host cell membrane that wraps outside of the nucleocapsid
Icosahedron
- 3D, 20 sided object, with 12 evenly spaced corners
- constructed from single or multiple types of capsomers
- variations in the number of capsomer in each virus
- with or without envelop
papillomaviruses
icosahedral virus with no envelope
herpes virus
enveloped icosahedron
functions of viral capsid/ envelope
protection of nucleic acids:
- capsids of enteric (intestinal) viruses such as polio and hepatitis A are resistant to the acid and protein- digesting enzymes of the GI tract
- host cell invasion (adsorption; introduction of viral DNA or RNA)
- contain antigenic elements for immune responses
poxviruses
- complex virus
- very large
- DNA
- lack regular capsid, but have several layers of lipoproteins, and coarse surface fibrils
- cause smallpox
bacteriophage
- complex virus
- DNA
- polyhedral head
- helical tail
- fibers for attachment to the host cells
Mumps
- enveloped virus
- helical nucleocapsid
- RNA
Herpes virus
- enveloped virus
- DNA
rhabdovirus
- enveloped virus
- RNA
HIV
- enveloped viruses
- RNA
adenovirus
- Naked viruses
- DNA
multiplication cycle in bacteriophages
- (adsorption: tail fibers bind to specific bacterial surface receptors
- injection of phage DNA into the bacteria by pushing the inner tube through the bacteria wall into the bacteria
- phage DNA: direct synthesis of phage parts: capsid heads, parts of the tail, new genome, and enzyme that weakens the cell wall in preparation of phage release
- spontaneous assembly to generate progeny phages
penetration of animal viruses
- via endocytosis: entry into cells in a vacuole or vesicle
- enzymes in the vesicle digest away the envelope and capsid: uncoating to release viral nucleic acid into the cytoplasm (ex: herpes virus)
- membrane fusion between viral envelope and the cytoplasmic membrane, releasing nucleic acid into the cytoplasm (ex: mumps)
plaques
develop when the viruses released by an infected cell radiate out to adjacent cells
- as new cells become infected and they die and release more viruses and result in more cell lysis
- lysed cells give rise to a clear area
