Parasites Flashcards
definitive host
the host in which the parasite reaches SEXUAL MATURITY (usually where gametocytes fuse and form a complete zygote)
intermediate host
a host that is required for parasite development but in which the parasite does NOT reach sexual maturity
malaria - definitive and intermediate hosts
definitive = mosquito
intermediate = humans
schistosoma - definitive and intermediate hosts
definitive = human
intermediate = snail
“dead end” or accidental host
when a helminth that usually infects another animal attempts to invade or infect a human but cannot complete the necessary stage of its lifecycle (not the correct host)
when is eosinophilia seen with parasitic infections
ONLY in TISSUE INVASIVE or migratory portions of the parasite’s life cycle
do you see eosinophilia with protozoal infections
NO
do you see eosinophilia with adult worms in the intestinal lumen
NO
are parasites prokaryotes or eukaryotes
EUKARYOTES
*can be one-celled or multi-cellular
protozoa
simple, unicellular parasites
*can be in blood, tissue, gut, and/or genital system
helminths
multicellular, complex organisms
(worms)
*covered by a cuticle or tegument that protects them from digestion and environmental stresses
do you have eosinophilia with malaria
NO
entamoeba - 2 species
1) entamoeba histolytica (pathogenic)
2) entamoeba dispar (non-pathogenic)
entamoeba histolytica - transmission
fecal-oral (through contaminated food and water)
person-to-person spread may occur
entamoeba histolytica - 2 forms
- trophozoite
- cyst
entamoeba histolytica - life cycle
- ingest cysts
- cysts transform to trophozoite upon exposure to stomach acid
- trophozoites colonize and subsequently invade intestinal mucosa
- invasion causes COLITIS
- some of the trophozoites transform into infective cysts and are released in stool, allowing for spread
entamoeba histolytica - disease
DYSENTERY (bloody, mucous-y diarrhea)
complications = liver abscesses and intestinal perforation
entamoeba histolytica - virulence factors
- galactosamine adherence lectin
- proteinases
- lysis of WBCs
entamoeba histolytica - 3 stages for infection
- attachment to host mucosal colonic epithelium through receptors
- contact-dependent killing
- ingestion of the killed host cell
entamoeba histolytica - host defense
cell-mediated immunity (T cells)
giardia lamblia - transmission
WATER, predominantly
giardia lamblia - epidemiology/risks
WATER
examples:
1) backpackers drinking from a stream
2) go to water park and swallow a lot of water
3) daycare
giardia lamblia - life cycle
- ingest cysts
- cysts transform to trophozoite upon exposure to stomach acid
- trophozoites colonize and subsequently ATTACH TO SMALL INTESTINAL VILLI
- some of the trophozoites transform into infective cysts and are released in stool, allowing for spread
compare and contrast - giardia vs. amoeba
*amoeba goes to COLON and invades; causes dysentery
*giardia goes to small intestine and attaches to villi; causes watery diarrhea
giardia lamblia - host defense
IgA immunoglobulin
(so IgA deficiency people are at high risk)
giardia lamblia - disease
WATERY diarrhea
cryptosporidium - characteristics
INTRACELLULAR pathogen
cryptosporidium - transmission
water > fecal-oral > person-to-person
cryptosporidium - problem with oocysts
resistant to disinfection, including chloride
cryptosporidium - epidemiology
day care
swimming pools/water parks
food-borne (especially CALVES)
cryptosporidium - staining
ACID FAST STAINING ORGANISM
high risk populations for malaria
*children less than 5 yo
*pregnant women
*non-immune travelers
4 malaria-causing species
- Plasmodium falciparum (most dangerous)
- / 3. P. vivax & ovale (can RELAPSE because of “hidden liver” stage that can persist)
- P. malariae (rare)
what species of mosquito transmits malaria
Anopheline mosquito (females only; night biters)
malaria life cycle
- anopholene mosquito inoculates SPOROZOITES into human
- sporozoites infect LIVER CELLS
- sporozoites MATURE INTO SCHIZONTS
- schizonts rupture and release MEROZOITES
- merozoites infect RED BLOOD CELLS
- merozoites mature into TROPHOZOITES
- trophozoites mature into schizonts
- schizonts rupture and release merozoites
- cycle continues
important difference in P. vivax and P. ovale life cycle (compared to falciparum)
have a dormant stage (hypnozoites) in liver and can persist for years, causing RELAPSES when they invade the bloodstream
primary vaccine approach for malaria
form immunity to the SPOROZOITE (because that is what infects us)
pathogenesis of P falciparum malaria disease
*causes MICROVASCULAR DISEASE
*adherence to endothelial receptors
*infect RBCs clogging up capillaries, leading to cytokine release and reduced blood flow, and hypoglycemia in tissues
host factors against malaria
*normal spleen function is important (removes parasitized RBCs from circulation)
*G6PD deficiency and sickle cell anemia may be protective against malaria transmission
malaria clinical presentation
fever, headache, myalgias
malaria prevention
vector control
bednetting
mosquito avoidance
antimalarial prophylaxis
malaria diagnosis
blood smear (Giemsa or wright staining)
antigen detection
PCR
babesiosis - 2 species
- B. microti (most common in USA, esp Connecticut and New England)
- B divergens
babesiosis tick vector
Ixodes tick (same as Lyme disease and ehrlichiosis)
babesiosis life cycle
requires tick, mouse, AND deer
*humans are a dead-end host
trypanosomiasis brucei
*found in Africa
*causes sleeping sickness (encephalitis brain infection)
*vector = tsetse fly, through its bite
trypanosomiasis cruzi
*found in South America
*causes Chagas disease (infection of GI tract and heart)
*vector = reduvid bug, through its defecation
trypanosomiasis - life cycle
1) promastigote (insect stage in GI tract)
2) amastigote (tissue infective stage)
*promastigote enters human blood stream where it is distributed to tropic tissues
trypanosomiasis - host immunity
*main immunity is HUMERAL (immunoglobulin)
trypanosomiasis - how do parasites avoid immunity
*periodically change its glycoprotein coat through antigenic variation
*occurs through movement of genetic “cassettes” that code glycoprotein into portion of active genome that is being expressed
toxoplasma - definitive and intermediate hosts
definitive = cats
intermediate = humans
toxoplasma transmission
*ingestion of a small amount of cat feces (cats get infection from eating a mouse)
OR
*ingestion of under-cooked meat
toxoplasma - disease
*reactivation of LATENT INFECTION in AIDS PATIENTS, causing toxoplasma ENCEPHALITIS
toxoplasma - congenital infection
*in first trimester of pregnancy, can cause chorioretinitis, cerebral calcifications, disseminated disease in fetus
hookworms - 2 species
- ancylostoma duodenale (middle east)
- NECANTOR AMERICANUS = USA, etc
risk for hookworm infection
SKIN EXPOSURES TO FECALLY CONTAMINATED SOIL in endemic areas
*especially seen in people walking BAREFOOT
*also seen in troops
hookworm life cycle
- infective larva penetrate SKIN that contacts soil
- migrates through systemic venous circulation to LUNG
- matures in lung, migrates up trachea, and SWALLOWED
- matures further in small intestine; attaches to mucosa
- causes IRON DEFICIENCY ANEMIA due to slow, chronic blood loss
- eggs passed into stool and hatch in soil
- cycle repeats
hookworm - disease presentations
*eosinophilic pneumonia
*iron deficiency anemia
cutaneous larva migrans (creeping eruption)
*HOOKWORM example of humans as a dead-end host
*worm crawling around under skin, causing a rash
schistosomiasis - exposure
FRESH WATER
schistosomiasis - 3 species
- schistosoma mansoni
- schistosoma japonicum
- schistosoma hematobium
schistosoma mansoni and japonicum
*reside in the venous plexuses of the GI TRACT
*cause portal hypertension and cirrhosis in liver (after 20 years)
schistosoma hematobium
*resides in venous plexuses of the URINARY TRACT
*high risk of bladder cancer
schistosomiasis - evasion of immune response
*absorb host proteins onto their own tegument surfaces, thus masquerading as the host by displaying the host’s antigens
schistosomiasis - life cycle
*eggs get into SNAIL and mature, forming a CERCARIAE
*CERCARIAE penetrates skin and enters circulation
*goes to its tissue (GI or bladder)
3 tapeworms
- saginata (beef tapeworm)
- solium (pork tapeworm)
- diphyllobothriasis (FISH; causes vitamin B12 deficiency)
cysticercosis - disease of tapeworms
*occurs when humans are the INTERMEDIATE host of a cestode (tapeworm)
*humans infected when eggs make it into the stomach, then the intestine
*eggs hatch in the intestine and then enter the blood
*most serious infections include the brain and eyes
*you DO see eosinophilia when humans are the intermediate host