Parasitology

Front 1

Types of intestinal nematodes

Meds:

Back 1

1. enterobius vermicularis
2. trichuris trichuria
3. ascaris lumbricoides
4. Hookworm - ancylostoma duodenalis/Necator americanus
5. Strongyloides stercoralis

Meds:
*first 4 - albendazole, mebendazole
*strongyloides - ivermectin, thiabendazole

Front 2

Types of tissue nematodes

Meds:

Back 2

1. A. braziliense, A. caninum
2. Toxocara catis and canis

Meds: Albendazole, mebendazole, topical thiabendazole

Front 3

Types of blood nematodes

Meds:

Back 3

1. Loa loa
2. Wucheria bancrofti and Brugia malayi
3. Onchocerca volvulus

Meds: Diethylcarbamezine, albendazole, ivermectin

Front 4

Types of Flukes or Trematodes

Meds:

Back 4

1. schistosoma mansoni
2. schistosoma hematobium
3. schistosoma japonicum
4. Fasciola hepatica

Meds: Triclabendazole, praziquantel

Front 5

Types of Cestodes

Meds:

Back 5

1. T. solium, T saginata
2. D. latum

Meds: Praziquantel

Front 6

Types of Larval forms

Meds:

Back 6

1. cysticercosis
2. echinococcus

Meds: albendazole

Front 7

Types of Protozoa

Back 7

1. entamoeba histolytica
2. giardia
3. cryptosporida spp.
4. cyclospora spp.
5. dientamoeba fragilis

Front 8

Nematodes =

Back 8

roundworms

Front 9

Cestodes =

Back 9

tape worms (flatworms)

Front 10

parasites always derive benefit (food and shelter) from the host, but they can either be

Back 10

pathogenic (causing harm) or commensal (giving benefit)

Front 11

eosinophilia (in general) results from

Back 11

stimulation of Th2 response (IL-3, IL-5, GM-CSF)

Front 12

eosinophilia seen in what disease

Back 12

NAACP

Neoplastic syndromes (lymphoma, leukemia)
Addison's (hypoadrenal)
Allergy
Collagen Vascular Disease
Parasites (usually helminths...nematodes, cestodes, trematodes...and specific fungal infections)*

*specifically when parasite is migrating through tissue

Front 13

what do nematodes have

Back 13

hypodermis
digestive system, pseudocoelum
nervous system

Front 14

Loeffler's syndrome

Back 14

fleeting infiltrate, peripheral eosinophilia

Front 15

which intestinal nematodes have Loeffler's?

Back 15

ascaris lumbricoides
n. americanus, a. duodenalis
strongyloides

Front 16

transmission of enterobias vermicularis

Back 16

oral-fecal

Front 17

transmission of trichuris trichuria

Back 17

oral-fecal

Front 18

transmission of ascaris lumbricoides

Back 18

oral-fecal, migration to lungs

Front 19

transmission of strongyloides

Back 19

soil - migration to lungs

Front 20

transmission of n. americanis/a. duodenales

Back 20

soil - migration to lungs

Front 21

enterobias vermicularis:

-aka
-typically seen in
-usually when
-transmission
-larvae hatch where
-egg is infective within what time
-egg is found where outside

Back 21

-aka pinworm
-school children (hand to mouth, oral-fecal), high pop density
-usually winter, but not exclusively
-aerosolized eggs or ingested...person-to-person
-larvae hatch in small intestine, gravid female migrates to perianal region to lay eggs (thousands of eggs)
-infective within 6 hours (stay that way for several days)
-found in dust

Front 22

enterobias vermicularis

-sx:
-dx:
-microscopic features:
-tx:
-complications
-prevention

Back 22

-kids: perianal itching and dermatitis, can get secondary bacterial infection; folliculitis in adults (pimple-like abscess)

-scotch tape test at night or early a.m.; DON'T do stool for o&p (only 5% of eggs deposited in bowel)

-albendazole, mebendazole -- RETREAT TWO WEEKS LATER; examine/treat family

-adult has alae, eggs look like coffebean
-rare, but can go into vagina/tubes/ovary/peritoneum (introduced by itching)
1. vulvovaginitis could look like sexual abuse
2. in peritoneum could form yellow nodule from granulomatous rxn
3. could migrate through perforated appendix
4. associated with d. fragilis!!!

-cleanliness, short fingernails, tight pajamas, bed clothes not shaken

Front 23

if you get a stool back that's positive for d. fragilis, you need to test for

Back 23

pinworm...strongly associated!

Front 24

albendazole/mebendazole contraindicated for

Back 24

pregnant women

Front 25

benzimidazoles (albendazole, mebendazole) MOA

practical difference between the two drugs

Back 25

-binds to helminthic tubulin
-inhibits glucose uptake

-mebendazole less well absorbed

Front 26

albendazole

1. increase levels with
2. toxicity

Back 26

1. fatty meal, steroids
2.
a. bone marrow suppression
b. hepatotoxicity (check LFT and CBC)
c. alopecia

*rapid hepatic first pass metabolism

Front 27

trichuris trichuria

1. aka
2. where
3. prevalence
4. transmission
5. microscopic features
6. how is infection established
7. how long to develop

Back 27

1. whipworm
2. SE, China, India, SA, subsaharan -- warm, damp soil that's fecally contaminated (esp. humid places, hyperendemic at higher temps, lower altitude)
3. a quarter of humanity (90% of a community infected, <10% intensely symptomatic)
4. oral-fecal (ingesting contaminated food...no autoinfection b/c they have to incubate in warm soil for 3-6 wks)
5. anterior whip, posterior genital tract = important part; egg is thick-walled, barrel-shaped, plug at each end
6. ingest embryonated egg, larvae migrates down and hatch in small intestine, eggs placed in bowel lumen
7. a while...not as quick as pinworm

Front 28

trichuris trichuria

1. dx:
2. what happens to body
3. clinical picture
4. complications
5. tx:
6. prevention

Back 28

1. stool for O&P (ova are thick walled, barrel shaped, plug at each end)
2. friable bowel, easily bleed; bowel edema, local eosinophilia infiltrate in mucosa
3.
a. chronic colitis with growth retardation
b. kids brought in with **short stature** and **pica** (eating soil because of iron deficiency)

4. trichuris dysentery syndrome:
a. prolapsed rectum (push it back in)
b. chronic diarrhea
c. anemia from the blood loss
d. increased TNF-alpha (low appetite, insulin, collagen)
...can also get clubbing of hands

5. albendazole (mebendazole)
6. community sanitation, handwashing, wash vegetables grown in contaminated soil; mass therapy with cyclic repetition for school aged children

Front 29

types of tissue nematodes

Back 29

a. braziliense, a. caninum (dog and cat hookworm) - cutaneous larvae migrans

toxocara catis and canis (dog and cat roundworm) - visceral larvae migrans

Front 30

types of cutaneous larvae migrans

aka

most common

Back 30

a. braziliense, a. caninum

(dog and cat hookworm)

a. braziliense

Front 31

CLM (cutaneous larvae migrans, creeping eruptions):

1. life cycle
2. human is __ host
3. where
4. who

Back 31

1. dog poops on beach, kid walks on it, larvae goes through foot...penetrates like human hookworm, but wanders around thinking, i'm in the wrong host
2. intermediate host (dead end)
3. SE u.s., warm regions
4. children more likely

Front 32

CLM

1. clinical presentation
2. tx:

Back 32

1. dermatitis - invasion of skin by hookworm (no deeper than epidermis)
2. albendazole, ivermectin, topical thiabendazole -- good outcome

Front 33

types of visceral larvae migrans

aka

Back 33

toxocara catis and canis

dog and cat roundworm

Front 34

toxocara catis and canis

1. life cycle
2. risk factors
3. human is __ host

Back 34

1. roundworm eggs in cat/dog stool, kid ingests it, they migrate through tissue
2. pets, are a child, pica (could also be in someone like sewer worker)
3. intermediate

Front 35

toxocara catis and canis (VLM)

1. clinical presentation
2. complications
3. tx:

Back 35

1. fever, *Loeffler's* eosinophilia (wheezing, bronchospasm), hepatomegaly
2. in adults who ingest low dose of eggs (like sewage worker), it can go to the eye after never being VLM...*RETINAL GRANULOMA* --> ocular larvae migrans...visual defects, ocular pain; seizure, myelitis are rare possibilities; note: kids need higher inoculum
3. albendazole (maybe thiabendazole) + steroids!!! if they have OLM, inflammation can lead to blindness

Front 36

what causes ocular larva migrans

leads to

tx:

Back 36

toxocara canis

eosinophilic inflammatory mass; visual defects, ocular pain...mimics retinoblastoma

albendazole, steroids!!!, surgery/laser therapy?

Front 37

mimics retinoblastoma

Back 37

ocular larvae migrans (dog/cat roundworm...toxocara)

Front 38

clinical differences between VLM and OLM

Back 38

OLM has no eosinophilia, no systemic signs

VLM won't have ocular lesion

Front 39

dx of larva migrans

Back 39

-clinical suspicion
-ELISA

*do not get stool for O&P...we are intermediate host*

Front 40

prevention of toxocariasis

Back 40

-laws to prohibit dogs on beach
-periodic tx of dogs/cats with anti-helminthic
-not letting kids play unattended outdoors

Front 41

blood nematodes associated with

types of blood nematodes

Back 41

human filariasis (microfilaria are particular to these)

loa loa
w. bancrofti, b. malayi
onchocerca volvulus

Front 42

loa loa

1. aka
2. where
3. life cycle
4. size
5. microfilaria features

Back 42

1. eye worm
2. west africa - really have to have been there for a while
3. red fly injects microfilaria, adults develop, release microfilaria as they migrate, leading to hypersensitivity reaction, **can live up to 17 years**; in eye, they migrate BENEATH conjunctiva
4. can be 5-7 cm
5. sheath and 3+ terminal nuclei

Front 43

loa loa

1. clinical presentation
2. complications
3. dx
4. tx (and duration)

Back 43

1. calabar swelling, urticaria, ADULTS in eye as opposed to ocular larva migrans; migratory angioedematous swelling; when migrating beneath conjunctiva, they're usually benign -- rare cases of retinal occlusion...usually just irritating; elevated eosinophils
2. renal = hematuria, proteinuria (mechanical trauma from filtering microfilaria; immune complexes?)
-endomyocardial fibrosis (high levels of Ab)
-retinal artery occlusion
-meningoencephalitis if high levels of microfilaria (HA, irritability, insomnia, coma, death) - could happen if you give ivermectin

3. NOONTIME SMEAR (you'll see sheathed microfilaria)
*extraction* of adult worm;
*serology* (helpful in visitors)

4. DEC - diethylcarbamazine fixed dose for 21 days, can give steroids or antihistamines (this is for amicrofilaremic pts); may need to retreat
*in microfilaremic patients, pretreat with steroids/antihistamines and CYTOPHARESIS, give DEC in gradually incr. dose, follow up with *ivermectin to kill microfilaria, *albendazole to kill adults;

DON'T give ivermectin or else you could get meningoencephalitis

Front 44

calabar swelling =

Back 44

loa loa (eye worm)

Front 45

difference between infected native and expatriots in loa loa

Back 45

natives - 90% have microfilaremia, 15% calabar swelling; lower eosinophils, parasite specific IgG and lymph proliferation

expatriot - 10% have microfilaremia, 95% have calabar swelling

Front 46

meningoencephalitis in loa loa associated with

Back 46

high levels of microfilaria (can find in CSF)

Front 47

The patient is a 42 year old female who was born in the Cameroon with a past medical history of HTN. She immigrated to the United States in January of 1982. She last traveled to the Cameroon for 3 weeks in 1999 and also visited there for greater than a month in 1996. She presented in February of 2000 with complaints of “sand in her eyes eyes”
since 1997. She also reported seeing a worm move across her eyes and across the bridge of her nose which was very painful. She noted swelling in her left hand which came and went.

19% eosinophils

Back 47

loa loa (blood nematode)

Front 48

onchocerca volvulus:

1. aka
2. where
3. life cycle

Back 48

1. river blindness
2. West Africa, Latin america (96% of Africa at risk)
3. black fly near river injects larva, larvae develop into adults in SC tissue, go to NODULES in pelvic brim or back of the head, produce microfilaria, another mosquito picks them up there

Front 49

onchocerca volvulus:

1. clinical manifestations

Back 49

1. dermal microfilaria > **pruritis so bad they just want to die** > less have blindness...punctate keratitis, uveitis, optic neuritis/atrophy (blindness)

NODULES contain adults, skin contains microfilaria

skin gets itchy; lichenification (skin gets thick), atrophy, DEPIGMENTATION (leopard skin); loss of elasticity

Front 50

onchocerca

1. dx
2. tx
3. tx contraindications

Back 50

1. skin snip
biopsy nodule
(serology is so-so...can't distinguish old from new)

2. ivermectin

3. don't give to children < 5
careful not to give in areas where loasis is endemic (do blood smear to rule out loa loa)

otherwise, little or no adverse reaction

Front 51

nodules and itching =

what do the nodules contain?

Back 51

onchocerca - nodules contain adults, skin contain microfilaria?

Front 52

hanging groin

Back 52

onchocerca - river blindness

Front 53

W. bancrofti filariasis

1. life cycle
2. who

Back 53

1. night-biting mosquito (incubation 1 yr); larvae migrate to lymphatics where they mature into adults; filariae go through lymph and blood; filaria have night periodicity (lie in deep vascular beds of lungs and other organs...lower pH in pulmonary vasculature during sleep)
-adult females have reproductive cycle of 5-10 years

microfilaria reach a plateau in number at 20-30 years old, that's when they come in sx...this is all a very LONG process

2. not travelers; greater in men

Front 54

adults in lymphatics

Back 54

w. bancrofti

Front 55

where is w. bancrofti vs. b. malayi

reservoirs?

Back 55

w. bancrofti = subsaharan, caribbean, Guyana, SE asia

b. malayi - india, china, malaysia only (feline/primate reservoirs)

bancrofti more prevalent

Front 56

w. bancrofti

1. clinical manifestations

Back 56

1. lymphangitis, elephantiasis, *hydrocele*, hyperkarytotic changes; retrograde lymphangitis/lymphadenitis appears in adolescence, after 6 wks hard work; genital involvement; sudden onset of high FEVER; can have the wood-looking skin

many have hematuria/proteinuria from damage of microfilaria, (similar to loa loa); chyluria; lymphoscintigraphy shows abnormal lymphatics (dilated, tortuous); regional LN often enlarged

can also be asx with abnormal lymphs

Front 57

always do a genital exam for people from endemic regions of ___

Back 57

bancrofti

can have hydrocele (accumulation of fluid in tunica vaginalis...+/- microfilaria; 40-50% of males affected; usually in adolescence

usually not painful! straw-colored fluid, thickening of scrotum (peau d'orange) and spermatic cord may occur

Front 58

bancrofti

1. dx
2. tx

Back 58

1. night-time smear, serology
2. DEC 10-14 days -- 90% reduction in 1 month...malayi is a little slower

Front 59

adults in loa loa found
microfilia in

Back 59

adults in SC tissue
microfiliar in blood

Front 60

tropical pulmonary eosinophilia

1. what parasite
2. who/where
3. sx
4. dx
5. tx
6. untreated...

Back 60

1. w. bancrofti or brugia malayi
2. males 4:1...often during 30's...india
3. nocturnal cough/wheezing; immunologic hypersensitivity to microfilaria; peripheral eosinophilia...LOEFFLER'S!
4. serology
-NOT smear b/c the microfiliaria aren't in circulation; in lungs, come out to play at night
5. DEC
6. can lead to chronic restrictive lung disease

Front 61

brugia malayi

1. clinical presentation

2. vector

Back 61

1. same as bancrofti but MINUS GENITAL INVOLVEMENT (i.e. no hydrocele)

lymphadenitis, lymphangitis, fever, elephantiasis

2. mosquito transmits both

Front 62

where are microfilaria in onchocerca

Back 62

skin

Front 63

site of infection for loa loa and onchocerca

site of infection for w. bancrofti, b. malayi

Back 63

SC tissue and eye for both

lymphatics for both (not genital for malayi)

Front 64

Fluke = Trematode = Platyhelminth = ?

all have these features:

Back 64

flatworm

anterior sucker (oral), ventral sucker (acetabulum)

all use snail as first INTERMEDIATE HOST

Front 65

snails are the ___ host for ___

Back 65

1st intermediate

flukes/trematodes/flatworms

Front 66

schistosomiasis:

1. life cycle
2. are we the intermediate or definitive host?
3. where?
4. which veins does each live in
5. who?
6. morbidity rates

Back 66

1. egg goes into water, goes through snail intermediate host, goes into feet/legs of person standing in water, lead to kabure itch; live in BLOOD VESSELS but don't cause pathology there; female lays eggs in blood, they go to organs and cause damage via host response
-once offspring get out, they NEED TO FIND ANOTHER SNAIL (thus an infected kid sharing a bath will not infect relative)
2. definitive
3.
haematobium = africa, arabia
mansoni = africa, arabia, eastern SA
japonicum = SE asia only
4.
haematobium = vesical plexus
mansoni = superior mesenteric
japonicum = inferior mesenteric
5. acquired in childhood, incr. in frequency and intensity with age...peak at 15-20 y.o.; elderly has same incidence but less intensity (not sure why)
6. most show low egg count; life span of worm is 3-7 years; 5% have extremely severe infections (exposure patterns? genetic?)

Front 67

schistosoma --> renal and bladder dysfxn

Back 67

s. haematobium

Front 68

schistosoma --> liver and intestinal disease

Back 68

s. mansoni, s. japonicum

Front 69

kabure itch =

Back 69

schistosomiasis

Front 70

schistosomiasis

1. clinical manifestations

Back 70

1.
-pruritic papular rash @ penetration site; within 24 hours, common in s.h. and s.m.
-katayama fever syndrome 4-8 weeks later (deposition of eggs in tissue...fever, sweats, chills, cough, diarrhea, headache)...lab findings: lymphadenopathy, hepatosplenomegaly, uritcaria, PERIPHERAL EOSINOPHILIA = LOEFFLER'S; 2/3 have respiratory sx (usually haematobium); hyperglobulinemia
--first infection or heavy reinfection
--sx secondary to immune complex disease
--this katayama syndrome most likely in TRAVELERS...can be brief exposure

Front 71

swimmer's itch

Back 71

abortive penetration of bird schistosome in places like Lake Michigan...usually on legs

Front 72

which parasite has the female nestled in the male thing

Back 72

schistosomiasis

Front 73

katayama syndrome

Back 73

schistosomiasis - late phase 4-8 weeks - fever, sweats, chills, cough, diarrhea, headaches - lymphadenopathy, hepatosplenomegaly, urticarial lesions, peripheral eosinophilia, 2/3 have respiratory sx (more in haematobium)

CAN HAPPEN IN FIRST INFECTION OR HEAVY REINFECTION

mostly japonicum and mansoni

Front 74

schistosomiasis

1. dx
2. tx

Back 74

1. serology! (eggs may not be present)
2. praziquantel - only kills adults...need to retreat

Front 75

schistosomiasis

1. what actually causes disease

Back 75

1. egg granuloma formation (fibrosis)

Front 76

s. japonicum and s. mansoni:

1. later clinical manifestations
2. dx
3. prognosis

Back 76

1.
INTESTINAL:
microabscess in intestinal wall, polyposis (actually has eggs in it); diarrhea, LLQ pain; occult blood in stool...can become chronic colonic stenosis (from all that fibrosis)

HEPATIC
-eggs can embolize to liver
-hepatomegaly early on
-**PREsinusoidal** inflammation, periportal fibrosis --> clay pipe stem fibrosis...5-8% of infected
-periportal collagen deposits --> obstruction of blood flow, portal hypertension, varices/bleeding, SPLENOMEGALY, hypersplenism

portal hypertension can lead to PULMONARY HYPERTENSION

dissemination to CNS
egg embolizes to cranial (japonicum) and spinal cord vasculature (mansoni) --> seizures, transverse myelitis respectively
-can embolize to brain cause paralysis

2. -for intestinal/hepatic, look for eggs in stool (viability testing - flame cells, hatching test); biopsy of those tissues; serology, but can't distinguish past and present...negative result is useful...traveler
-dx of CNS is difficult...

3. fibrosis will get better, pulmonary htn is irreversible

Front 77

presinusoidal inflammation

Back 77

s. mansoni, s. japonicum

clay-pipe-stem fibrosis

Front 78

in what parasites do you see splenomegaly

Back 78

chronic malaria, schisto, leishmania

Front 79

co-infection of HCV or HBV with ___ makes liver function worse and HCC more likely

THM:

Back 79

s. mansoni only; often in children

screen for hepatitis

(think of egypt's campaign to treat schisto...stopped b/c of needle re-use, coinfecting people with hep c)

Front 80

s. haematobium

1. where do the eggs reside
2. who
3. when do you see hematuria
4. later manifestations/complications
5. dx
6. after dx

Back 80

1. bladder wall and lower end of ureters...lots of inflammation, lots of blood, so most with this are sx...this chronic inflammation can predispose to cancer (carcinoma of bladder -- well differentiated, spread locally)
2. children (rite of passage)
3. 10-12 wks after exposure (dysuria early)
4. proteinuria, calcifications in bladder, obstruction of ureter, renal colic, renal failure; secondary bacterial infection, especially with SALMONELLA

bladder cancer

GENITAL schisto - ovaries, tubes, vaginga, cervix--> bleeding, abdominal pain, ectopic pregnancy; increased risk of STD acquisition, including HIV; 41% with genital dz were not shedding eggs (sceen!)

5. eggs in urine (viability test - hatch test; flame tells you if it's viable); eggs in bladder biopsy; ELISA - helpful if low egg burden

6. evaluate ureters, biopsy for squamous cell carcinoma

Front 81

praziquantel

1. cures __%
2. MOA
3. how many treatments

Back 81

1. 60-90%
2. unknown (tetanic contractures, vacuoles); incr. permability to calcium; paralyzes schistosomes; sequestered antigens are exposed (facilitating destruction by host)
3. 2-3 doses

Front 82

screening of travelers for schisto encouraged b/c

Back 82

1/3 asymptomatic
those seen early - pulmonary sx
missionary, volunteer, expatriates more likely to be dx (83% acquired in africa)

63% present within 6 months of travel

Front 83

fasciola hepatic

1. aka
2. get it from
3. where
4. __ is __ host
5. life cycle
6. acute phase =

Back 83

1. sheep liver fluke
2. eating watercress
3. mostly in sheep-raising areas - Bolivia, Peru, Iran, Egypt, Portugal, France; oooor people in PR, DR eating watercress
4. sheep is reservoir host
5. eat the watercress, ingesting metacecariae hatch in small intestine, make way to biliary tree, sit in biliary tree acting like gall stones; eggs go into small intestine and are pooped out
6. hepatic damage

Front 84

fasciola hepatica

1. dx
2. when do you see acute sx
3. what are acute sx
4. pathology
5. rare ectopic foci
6. chronic stage

Back 84

1. acute: serology
chronic: stool for O&P
2. 6-12 weeks, sx reflect migration of metacecariae through small intestine, peritoneum, liver capsule; can LAST FOR 2-4 months
3. eosinophilia, RUQ pain, fever, malaise, URTICARIA; hepatomegaly - liver may be tender to palpation
4. extensive hepatic necrosis (early); bile duct hyperplasia; periductal **fibrosis, cholangitis, stones** (cirrhosis is rare)
gall bladder often involved
liver seeded with ova
5. lung, SC tissue, brain, orbit
6. chronic obstructive stage: sit in biliary duct, appear in stool after 3-4 months; no longer eosinophilia; acute sx resolve, so pt may be asymptomatic; ascending cholangitis (fever, jaundice, UQ pain)

lithiasis of common bile duct/gall bladder is common sequelue

Front 85

watercress =

Back 85

fasciola hepatica

Front 86

fasciola hepatica

1. tx

Back 86

1. triclabendazole (only through CDC) -- once!

Front 87

cestode

1. aka
2. morphology

Back 87

1. tape worm
2. anterior scolex with suckers, metabolic neck, *segmented* proglottids (more distal ones = more mature, thus filled with eggs)
-longitudinal and ciruclar muscle, primitive nervous system, complex reproductive organs, primitive excretory system
3000-4000 proglottids

Front 88

d. latum

1. aka
2. size
3. where in body
4. how do you get it
5. prevalence
6. where
7. life cycle
8. we are the __ host

Back 88

1. broad or fish tapeworm
2. 3-12 m
3. ileum and jejunum
4. eating undercooked fish
5. 9-10 million worldwide
6. native americans in alaska/canada; lakes of MN, MI, CA, FL; freshwater lakes in africa; China, Taiwan, Japan, Turkey, Ireland (or, in NYC, people who eat freshwater fish on ice)
7. fish #2 (e.g. gefilte fish) eats fish #2, we eat it, larvae develop in small intestines
8. definitive; first intermediate host is crustacean, second intermediate host is fish #1

Front 89

D. latum

1. sx
2. lab findings
3. complications
4. dx
5. tx

Back 89

1. few, if any - vague abdominal pain (sensation of something moving), diarrhea, dx when stool done for another reason (**proglottids do not crawl out of anus**)
2. B12 deficiency anemia (hook worm is iron deficiency anemia)
3. the B12 deficiency can lead to neurologic sequelae (degeneration of dorsal and ventral columns)
4. eggs in stool
5. praziquantel

Front 90

Taeniasis

1. kinds
2. we are the __ host
3. how do you get it?
4. life cycle

Back 90

1. t. solium (pork), t. saginata (beef)
2. definitive (for pig we can also be intermediate)
3. ingesting raw beef or pork
4. pig or cow eats the egg (from soil contaminated with human poop); embryos encyst in the animal's muscle; develop into larvae there, which are called the CYSTICERCUS; we eat the animal and the cysticercus is activated

Front 91

taenia solium and saginata

1. where?
2. which is bigger
3. taeniasis sx and signs
4. dx
5. tx

Back 91

1. both - mexico, africa, latin america
saginata - europe, russia, japan
solium ("armed")- spain, slavic, india, china
2. t. saginata - 25 m (solium up to 8 m)...each about 1000 proglottids
3. intestinal obstruction, intussusception, appendicitis, toxemia, EOSINOPHILIA, nausea, abdominal pain
***proglottids migrate out of anus in 98% of cases***
4. must differentiate proglottids...eggs look identical
5. praziquantel

Front 92

which proglottids migrate out of anus

Back 92

taenia...NOT d. latum

Front 93

Cysticercosis (neurocysticercosis)

1. parasite
2. dx
3. stages
4. sx
5. tx

Back 93

1. larvae of t. solium (pork tape worm)
2. CT/MRI would show hole in brain and nodule which is the scolex (vesicular stage)...
-serology more sensitive than CSF
-antigen detection
-eye exam** they can get in eye...important
-stool will show you nothing


3.
1) vesicular stage - fluid; scolex
2) colloidal stage - turbid fluid, intense inflammation (give steroids); degenerating scolex
3) granular stage - wall, scar formation, scolex degenerated
4) calcified stage - intense gliosis (scar), giant cells

4. all from intracranial hypertension - seizures common (gray-white jct), meningeal signs, nausea, vomiting, headache, dementia, psychosis (big cause of Mexican psych hospitalization

cysticercal encephalitis mostly affects women and children; AMS, seizures, HA, vomiting, decreased visual acuity

5. albendazole (kills larvae), steroids to control for the ensuing edema (except do not give albendazole for the encephalitis...will make that worse)

Front 94

case of the c. america immigrant workers passing on disease was

Back 94

cysticercosis (to jews who didn't eat pork, mind you)

Front 95

is calcified cysticerci an inactive disease

tx

Back 95

no! can cause seizures, edema (edema comes and goes, esp. if you give steroids; calcification is permanent)

edema associated with ongoing seizures

DO NOT TREAT WITH ANTI-HELMINTHICS...steroids

Front 96

racemose neurocysticercosis

1. what is it
2. prognosis
3. tx

Back 96

1. ventricles, subarachnoid space cysts, or basilar cisterns; abnormal growth of cystic membranes, degeneration of scolex; cyst obstructs flow, leads to back up in ventricles

2. grim...progressive course; mass effect, stroke (cerebral arteritis) - present with headache, dizziness, AMS

3. albendazole + steroids, ventricular shunting, methotrexate as steroid sparing agent??

surgical removal of the cyst obstructing flow (endoscopic, but cysts can move...don't do if sig. ependymal enhancement...no shunting needed afterwards)

medical therapy usually reserved for those with no/mild dilation of ventricles

Front 97

neurocysticerocosis spinal disease

Back 97

extramedullary (downward migration from cisterns

intramedullary (hematological in origin and solitary)

epidural

Front 98

cystic hydatid disease

1. pathogen:
2. human is __ host
3. pathogenesis
4. endocyst =
5. pericyst =
6. ages
7. liver and __

Back 98

1. echinococcus granulosus
2. accidental
3. metacestode forms rind in liver; laminated layer --> germinal layer (both parasite derived --> stalk --> Brood's capsule
4. germinal + laminated layers
5. CTissue, granulomatous reaction
6. 20s/30s/40s
7. lungs

Front 99

cystic hydatid disease

1. tx
2. problems
3. who gets it?
4. dx

Back 99

1. albendazole + surgery or PAIR (latter if CE1 or CE2 with only one or two daughter cysts..aspirate and inject scolocidal agent --EtOH, hypertonic saline)...albendazole before and after surgery; ruel out obstructure prior to PAIR; wait and watch?

PAIR is really the way to go unless you can't (complicated cyst, proximity to major vasculature, biliary tree, leakage of contrast medium to any space, bile staining of drained cyst fluid)

2. portal hypertension (ascites), rupture into peritoneum (anaphylaxis), hepatomegaly, RUQ pain, cholangitis, up to diaphragm (referred pain)
but 75% asymptomatic

3. only those living in sheep herding region

4. imaging, epi, western blot/ELISA (cysts in brain/bone/eye may not produce antibodies);

Front 100

Sx of pulmonary hydatid disease

tx

Back 100

cough up cysts, tastes salty, looks like grape skin

hemoptysis, cough, dyspnea; pleural effusion; infection of ruptured cyst

68% asymptomatic

surgery

Front 101

CNS cysts in hydatid disease - tx

bone involvement?

Back 101

surgery - large cysts but little inflammation -- the cyst fluid is just CSF (maybe long term albendazole in inoperable cases

path fractures, pain swelling; vertebrae > pelvis > long bones
-tx: surgery + albendazole...relapse common

Front 102

alveolar hydatid disease (e. multilocularis)

dx

Back 102

cold places like russia, siberia, MN

fox

30 years before sx...RUQ pain, malaise

dx: MRI/CT, serology (only done in switzerland)

tx: surgery, albendazole for 2 years; liver transplant

Front 103

malaria (plasmodium)

1. life cycle
2. most important part of life cycle occurs in
3. in hyperendemic regions, __% might have malaria in blood

Back 103

1. sporogonic cycle in arthropod, exo-erythrocytic and erythrocytic in vertebrate host; mosquito injects sporozoites, which become merozoites and do stuff in RBC...some become gametocytes, but don't combine; vector sucks that, zygote forms, inject sporozoites
3. >75%
2. RBCs

Front 104

malaria

1. paroxysm
2. sx

Back 104

1. "malaria paroxysm"
prodromal - aches/fatigue 2-3 days prior
cold stage - shivering for 1 hr
hot stage - intense heat, dry burning skin, HA
sweating stage - profuse, declining temp 2-4 hours; exhausted and weak --> sleep
fever synchronized with merozoite release
----falciparum: 2 days on, 1 day off
----ovale/vivax: every 48 hours (tertian)
----malariae: every 72 hours (quartan)

2. only common thing is fever, and headache to large extent...otherwise can have diarrhea, cough, vomiting, abdominal pain...need high clinical suspicion

Front 105

where is p. vivax

need __ receptor

sx

tx

Back 105

SE asia, americas (pretty much never africa)

duffy

acute febrile illness, but almost no fatalities

artemisinins (resistant to chloroquine in New Guinea)

Front 106

P. ovale

1. features
2. where?

Back 106

1. oval RBCs with fimbriated edges; younger RBCs, fewer merozoites (smaller RBCs), lower parasitemia, stippling
2. subsaharan Africa, Western Pacific islands

Front 107

P. malariae

1. where
2. features

Back 107

1. Greece/S. Europe, but eradicated in 1950s (case of woman who had it for a long time, and when given methotrexate, spiked a quartan fever/headache)...blood smears were negative (not enough bugs)...need PCR
2. chronic stage: very low parasitemia, no evidence of persistent liver stages, nephrotic syndrome (due to immune complexes)

*never really seen on it's own, but FOLLOWS P. FALCIPARUM

Front 108

P. falciparum = severe malaria

1. features

Back 108

1. anemia (reduced RBC production, increased destruction)
cerebral malaria
ARDS
lactic acidosis
Blackwater fever
hypoglycemia
hyperparasitemia

Front 109

name motility and location of each in malaria

ookinete
sporozoite
merozoite

Back 109

ookinete - motile - vector gut
sporozoite - motile - vector saliva, human liver
merozoite - NONmotile - RBC

Front 110

exo-erythrocyte schizogony

hepatic invasion -->

Back 110

asexual replication
6-15 days
1000-10,000 merozoites
no overt pathology (small destruction of liver cells, but no overt problem)

Front 111

hypnozoite forms (malaria)

see in which ones?

Back 111

typical drugs do not kill this form!
dormant in hepatocytes...delayed

before merozoite...see this in *******p. vivax and p. ovale only*********

Front 112

only __ malaria can have RBCs that cytoadhere

Back 112

P. falciparum

it's the schizont that can adhere and invade

merozoite can become gametocyte, or they can continue on to be trophozoites and burst

Front 113

p. knowlesi needs what receptor

p. falciparum needs what receptor

Back 113

Duffy - DBP binds

sialic acid - EBA-175 binds

Front 114

__ forms knobs on RBC!!!

Back 114

p. falciparum

all forms make RBC more leaky; take up its hemoglobin

Front 115

talk about PfEMP1

what are the domains and receptors

Back 115

plasmodium falciparum erythrocyte membrane protein 1

-falciparum puts it on surface...it mediates:
1. cytoadherence
2. rosette formation
3. sequestration

it's a target for antibodies --> strain-specific immunity

waves of parasitemia, coincident with antigen switching

CIDR binds CD36 (cytoadherence
DBL-beta binds ICAM in BRAIN ENDOTHELIAL CELLS
DBL-gamma binds chondroitin sulfate A

Front 116

what will CSF and CT look like in cerebral malaria

Back 116

-normal

Front 117

malaria pathogenesis

Back 117

non-specific infiltration (spleen)
RBC rupture --> Mac and cytokines --> fever
-specific immunity evolves, but develops by age 5, controls sx but not the parasitemia, not protective during pregnancy, can be lost after a while

problems with immunity -- lack of MHC-II on RBC, very little antigen being presented (most of the time malaria is hiding in a cell), huge antigenic strain diversity

Front 118

sickle cell reduces risk by

Back 118

6-fold...impaired parasite growth at lower oxygen tension...shape of the cell resistant to entry

Front 119

malaria incubation times

Back 119

<10 days - falciparum
10-60 days - any
> 60 days - not falciparum
> 3 years - malariae

Front 120

stippling associated with

Back 120

p. vivax (bigger RBC), p. ovale (smaller RBC than vivax, but still enlarged)

Front 121

which malaria don't enlarge the RBC

Back 121

falciparum, malariae

malariae has no stippling unless with intense staining

Front 122

malariae can have __ complications

Back 122

renal

Front 123

vivax can last __

Back 123

8 years (others are like 2 years max, except malariae)

though symptoms rarely last longer than a few weeks for any of them

Front 124

ovale is pretty ___

Back 124

mild, smallest anemia, shortest course except for falciparum

Front 125

"atypical malaria"

1. pathogen
2. time course
3. course
4. dx

Back 125

1. p. knowlesi -- macaques -- Phillipines/Asia
2. 24 hr. cycle
3. severe disease - fever, abdominal pain, renal failure, jaundice, thrombocytopenia
4. hard because it resembles early falciparum and late malariae...use symptoms, Asia travel, high parasitemia, diverse pathologies

Front 126

what if you do not get treated for falciparum?

vivax?

Back 126

will probably die

will probably live

Front 127

talk about all these drugs (all of which kill pretty rapidly)
1. chloroquine
2. quinine
3. mefloquine
4. sulfadoxine-pyrimethamine
5. artemisinins
6. primaquine

Back 127

all are schizonticides, except primaquine -- most drugs act on the digestive vacuole which digests hemoglobin

1. was first choice for decades, but now resistance is a problem
2. no resistance really - use for severe malaria IV/oral/IM; doesn't work on falciparum gametocytes, some toxicities
3. expensive, resistance developing in SE Asia
4. highly effective, but resistance develops quickly
5. used in combo therapy - schizonticides and inhibits gametocytes

6.*primaquine - only one that kills hypozoites

Front 128

a lot of antibiotics act on the __ of malaria

Back 128

apicoplast
e.g. doxy, clindamycin, azithromycin

Front 129

chloroquine

1. tolerated?
2. toxicity
3. resistance
4. MOResistance

Back 129

1. tolerated well, cheap, available, effective -- kills early trophozoites
2. retinopathy
3. resistance in falciparum, now vivax in Asia...spread far east to west to east
4. mutations in receptor on digestive vacuole...probably interferes

Front 130

quinine

1. comes from
2. works on what stages
3. toxicity

Back 130

1. some tree
2. trophozoites + gametocytes of all but falciparum
3. narrow therapeutic range -- can worsen hypoglycemia, prolong QT, hypotension, hearing loss

Front 131

mefloquine

1. tolerated
2. downside
3. use
4. toxicity

Back 131

1. safe, effective
2. expensive ($3-4), resistance developing in SE asia
3. used in combination with artemisinins
LARIUM for traveler's prophylaxis
4. GI, neuropsychiatric

Front 132

primaquine

1. use
2. length
3. toxicity

Back 132

1. broad spectrum, affects a lot of stages
2. treatment or prevention of relapse -- long regimen of 2 weeks
3. massive hemolysis in GP6D deficiency

Front 133

artemisinins

1. use
2. where'd it come from
3. downsides

Back 133

1. might be the new CQ! - most potent, fastest, kills gametocytes, reduces transmission, no resistance yet! -- wonderful!
2. chinese plant used for a while
3. 2.40 per tx vs 0.20 for CQ (WHO is subsidizing cost), and more pills
must be used -- combo therapy
NOTHING SHOULD BE MONOTHERAPY ANYMORE
-combined with mefloquine can even be effective in areas of resistance

in Zanzibar (Tanzania), malaria has plummeted since ACT (combination therapy) and sprayed bednets

Front 134

problems in developing a malarial vaccine

Back 134

1. huge antigenic repertoire
2. logistical complexity of making radiation-attenuated sporozoites

might be feasible to block transmission to mosquito host, or to target placental infection

Front 135

riskiest places for malaria

Back 135

Sub-Saharan
Oceania
South Asia
Central America
SE Asia

Front 136

traveler's prophylaxis for malaria

Back 136

atovaquone-proguanil...best tolerated, but costly...daily dosing, ineffective against hypnozoites...ideal for 2-3 week travel, too expensive if longer

mefloquine - resistance in SE asia - side effects more in women, low BMI - only weekly dosing - effective though

doxycycline - pretty good stuff...just that you have to take it daily, can't use in children, might get GI upset, yeast infection, DDIs

*mefloquine, doxycycline, and chloroquine would not prevent initial infection, so you continue for 4 weeks after
*atovaquone-proguanil pretty good, so only continue for 1 week

Front 137

babesios (b. microti)

1. features
2. transmission
3. reservoir
4. where
5. we are the __ host
6. clinical
7. complications
8. Dx
9. differential
10. tx

Back 137

1. maltese cross - lack of pigment
2. ticks (also transfusion or vertical)
3. wild and domestic animals (mouse= larvae, big animals = nymph, we = adult)
4. NE, CT, NY, PA
5. accidental -- thus, you SHOULDN'T SEE DRUG RESISTANCE
6. mild, flu-like symptoms in young, life-threatening malarial like in elderly, immunocompromised, asplenic; mild hepatosplenomegaly
7. respiratory failure, CHF, renal failure, anemia, parasitemia...fatal in 5-10%
8. IFA, PCR (quicker)
9. Lyme, HGA
10. usually none...if mild case atovaquone plus azithromycin...if more severe, clindamycin + quinine...treatment is prolonged