Micro Flashcards
(110 cards)
1
Q
Enterobius vermicularis
A
Pin worm
2
Q
Enterobius vermicularis Epidemiology
A
most common helminth infection in US crowded conditions (i.e. daycare)
3
Q
E. vermicularis morphology
A
adults=small, non descript
eggs flattened on one side
4
Q
E. vermicularis presentation
A
perianal irritation, rarely GI probs
5
Q
E. vermicularis Dx
A
Find adults and/or eggs in perianal area (sticky tape test)
6
Q
E. vermicularis Rx
A
two doses of pyrental pamoate two wks apart
Rx whole family
sanitize bedclothes
Mebendazole=alternative
7
Q
E. vermicularis life-cycle
A
- eggs on perianal folds; larvae in eggs mature w/in 4-6 hrs
- embryonated eggs ingested by human
- Larvae hatch in SI
- adults in lumen of cecum
- gravid females migrate to perianal region AT NIGHT to lay eggs
8
Q
Host
A
organism in which parasite lives
9
Q
Reservoir
A
Host which maintains parasite in nature as a source for continued transmission
10
Q
definitive host
A
host in which sexual reproduction takes place
11
Q
Intermediate host
A
host in which development occurs, possibly asexual reproduction, but
NO SEXUAL REPRODUCTION
12
Q
Soil transmitted helminths
A
ascariasis (MC)
trichuriasis (whipworm)
Hookworm
conducive soil=warm, moist (i.e. tropical areas)
infection may last 1-5 yrs (lifespan of worm)
13
Q
Trichuriasis
A
whipworm
14
Q
whipworm life-cycle
A
only different from pin worm cycle by embryonation in soil
- eggs in soil/fecal matter
- swallowed
- hatch
- Attach to gut wall
- eggs excreted in feces (not infectious)
- embryonate in soil (become infectious)
15
Q
Embryonate
A
non-infective–>infective
16
Q
whipworm clinical presentation
A
Asymptomatic/nonspecific
diarrhea +/- blood
chronic blood loss/ IBD picture
17
Q
whipworm Rx
A
Mebendazole or albendazole
Resolves in ~2 yrs w/out Rx
Reinfection is very common
18
Q
Hookworm
A
Ancylostoma duodenale (old world…Mediterranean and northern Asia)
necator americanus (new World…Americas, Africa, southern Asia, Australia)
19
Q
Hookworm portal of entry
A
skin! (not gut like most things else)
20
Q
Hookworm life cycle
A
skin–>blood–>lungs–>coughed up and swallowed—-> SI
- eggs in feces
- Rhabdiform larva hatches
- Filariform larva
- Filariform larva penetrate skin
- Adults in SI
diagnositic form=eggs
infectious form=larva
21
Q
Hookworm dz
A
Hookworm Gastroenteritis
22
Q
Hookworm Gastroenteritis pathophys and clinical
A
hookworms grasp onto intestinal villi and eat tissue
produce anticoagulant, which facilitates bleeding –>(microcytic anemia!!!)
Larval stage is migratory… can produce eosinophilia and inflamation
23
Q
Hookworm morphology
A
adults have teeth or cutting places
eggs have clear outer shell
24
Q
Hookworm gastroenteritis Dx
A
eggs in feces
25
Hookworm Rx
mebendazole
26
Ascariasis lumbricoides morphology
females=30cm long
| eggs have characteristic irregular outer coating (makes harder to destroy)
27
Ascariasis presentation
degree of dz directly related to # organisms present (which depends on # of EGGS ingested)!!
large burdens can initially lead to pneumonitis, later intestinal obstruction, w/ occasional perforation
(Can cause pancreatitis (via mechanical obstruction of biliary tree) in adults)
ball of worms--> bowel obstruction--> ischemia and perforation
28
Ascarias Dx
signs and symptoms NOT useful
generally there is some suspicion of intestinal helminths based on Hx
Eggs in stool definitive
29
Ascarias Rx and prevention
```
Pyrantel pamoate (one dose)
mebendazole (3 doses)
```
Proper sewage disposal (although eggs are resistant to chemical disinfectants)
30
Ascaris life cycle
1. eggs embryonate in warm/humid environment soil
2. embryonated (now infectiou) eggs ingested
3. hatch in SI
4. Larvae enter venules or lymphatics--> pass thru heart and lung to reach alveoli
5. migrate up bronchi, ascend trachea, pass down esophagus to SI, where they mature into adults
6. females produce 200,000 eggs per day
7. eggs leave host thru feces
live for 1-2 yrs
31
Loeffler syndrome
Can be caused by any w/ a lung phase
Eosinophilic pneumonitis
ascariasis, strongyloidiasis,
32
Dx
adults in SI
33
Toxocara canis and T. cati
embryonation in soil (3-4 wks to develop)
eggs from dog or cat roundworm ingested
larvae penetrate mucosa, enter circulation, carried to liver, lungs, eyes--> inflammatory necrosis!! (eventually cleared)
visceral or ocular larval migrans
34
human hosts in Toxocara canis and T. cati
Humans=accidental hosts, so larvae DON'T develop into adults, but rather migrate into tissues--> provokes harmful inflammatory response! (b/c can't complete life cycle, so it causes problems)
Inflammatory response IN TISSUE is very high in eosinophils and IgE compared to when infection is in GI system... so Toxocara causes HUGE eosinophilia
35
Baylisacaris procyonis
raccoon roundworms
| uncommon but severe (eosinophilic meningitis or encephalitis)
36
Rx for visceral larval migrans
nothing or antiparasitic meds
MUST give steroids if eye involvement b/c dying worms cause a flare!!!
37
Cutaneous larval migrans
creeping eruption
Larva penetrates skin!!!
migrates in subcutaneous tissue and causes inflammation
Can see the worm in foot and eye???????
38
Strongyloides stercoralis life cycle
Same basic cycle: eggs--> rabditiform larva--> filariform larva-->penetrate-->circulatory system--> lungs-->coughed up and swallowed--> become adults in SI--> lay eggs in intestinal mucosa--> hatch and move to lumen--> excreted in stool as larvae!!
Key points:
Can be free-living worms in water and still mature, fertilize, and reproduce eggs
excreted in stool as larvae, so 3 choices--
1. free-living in water
2. develop into filaform and then penetrate skin (like hookworm)
3. develop into filaform and penetrate perianally AUTOINFECTION!!!!
self-perpetuating infection
39
Epidemiology
High prevalence b/c doesn't clear unless you Rx it
40
Strongyloidiasis
*frequently asymptomatic w/ eosinophilia
Problem in immunosuppressed pts! (may carry around silently for 50-60 yrs even until decr. immune system allows it to cause probs)
Symptoms related to 3 stages:
1. skin invasion (purpuric papule
2. lung migration (Loeffler's syndrome)
3. Intestinal phase (abdominal pain and diarrhea)
Chronic infection due to autoinfection
Hyperinfection syndrome
41
Hyperinfection syndrome of strongyloidiasis
disseminated strongyloidiasis in immunocompromised host
Massive parasite burden in lungs-->Respiratory failure
Acute abdomen and GNR sepsis also possible (b/c leakage from bowel walls)
Blood eosinophillia may be absent (b/c pt is immunosuppressed!!)
42
Strongyloidiasis Dx
larvae in stool or sputum
| serology
43
Strongyloidiasis Rx
Ivermectin oro albendazole
| empirically treat high-risk pts prior to immunosuppressive therapy!!!
44
Trichinella spiralis life cycle
1. Encysted larva in striated muscle
2. We eat the muscle (under-cooked meat, i.e. pork or bear!)
3. Larva released in SI
4. Adults in SI
5. Larva deposited in mucosa
6. enter circulation
7. encysted in striated muscle
can happen in human, pig, bear, etc.
We are eating larva!! not eggs this time
45
Trichinosis
caused by trichinella spiralis (tiny adults and larvae)
signs and sx depend on worm burden
(ranges from asymptomatic to serious)
initially gastroenteritis, followed by fever, muscle tenderness, inflammation, and weakness
***muscle pain, diarrhea, and facial (i.e. periorbital) swelling with marked eosinophilia!!
Elevated WBC and major eosinophilia!!
46
Trichinosis Dx
Hx of consumed meat
eosinophilia and positive serology by day 12
larvae in biopsy
47
Trichinosis Rx and control
supportive care for inflammation
Mebendazole eliminates adults but NOT larvae
cook meet well!
48
Lymphatic Filariasis
elephantiasis
Wuchereria banccrofti
tropical areas
transmitted via multiple mosquito species
49
Wuchereria bancrofti morphology
adults in lymphatics (10cm)
Microfilaria in blood stream (tiny)
cells of microfilaria contain multiple nuclei!!
50
Wuchereria bancrofti presentation
adults in lymphatic channel provokes inflammation
adults die after about 5 yrs, calcify, elicit additional inflammation--> blocks lymphatic channel!
fluid accumulates distal to blockages-->elephantitis
51
Elephantitis Dx
microfilaria in blood AT NIGHT!! (peripheral smear at night)
cells of microfilaria contain multiple nuclei, which helps w/ Dx
serology (IgG4)
Lab tests tend to be negative when lymphedema though, b/c blockage due to inflammation due dead and calcified worms
52
Elephantiasis Rx
Diethylcarbamazine kills adults
Steroids reduce inflammation
Prevention: avoid mosquitoes
53
True elephantiasis
manifestations of CHRONIC infection due to mechanical obstruction of lymphatics (adults die and calcify...etc.)
54
Tapeworm etiology, epidemiology, and morphology
```
Taenia saginata (beef)
T. solium (pork)
```
Epidemiology: cosmopolitan of developing world
morphology: HUGE (10 meters)
- -scolex (head w/ sucking/ grasping parts)
- -Proglottids (segments w/ branched uteri designed to produce thousands of eggs)
proglottids closest to scolex are immature.
terminal (gravid) proglottids break off and are released with numerous eggs
hermaphroditic w/ no digestive tract! (that's why they are flat... must absorb nutrients directly)
Larval stage of T. solium can produce cysts in various tissues--> symptomatic dz
55
Tapeworm life cycle
1. eggs or gravid proglottids are in feces in environment
2. cattle / pigs ingest (intermediate hosts!!)
3. oncospheres hatch, penetrate intestinal wall, and circulate to musculature
4. oncospheres develop into cysticerci in muscle 5. humans infected by ingesting raw/ under-cooked meat
6. scolex attaches to intestine
7. Adults in SI
Humans = definitive host!
Portal of entry= ingestion of animal muscle w/ cysts (causes GI stuff) or ingestion of eggs (causes cystercosis)
56
Tapeworm presentation
symptoms appear based on tissue location
Usually asymptomatic, b/c doesn't cause much problems when happy in gut (if not huge burden)
T. solium can cause cysticercosis after ingestion of eggs (neuro, ocular, muscular)
dying worms are the problem!
57
Tapeworm Dx
stool microscopy (eggs or proglottids), serologies and brain imaging for extraintestinal
58
How T. solium can cause neurocysicercosis
1. eggs ingested by human rather than intermediate host
2. go into and hatch in gut
3. encyst in muscle
4. since humans are outside food chain, problem isn't that human is then infectious, but rather that they go to other places and cause inflammation, including when larvae die. may have asymptomatic larval cysts in brain and elsewhere for many years, and not have symptoms until larva die and thus inflammatory rxn--> seizures
maybe only one cyst that causes problems even though there are many cysts at a time... all in different stages (alive, dead w/ inflammation, long dead) picture CT system
59
Neurocysticercosis Rx
antihelminths even though this will kill parasites still living, leading to inflammation and problems???
Or wait for them to do what they're going to do and then treat w/ steroids and support when they do start causing probs??
antihelminths and steroids simultaneously?
60
Tapeworm prevention
adequate cooking or freezing kill cysticerci
61
Why someone might choose to be infected w/ tapeworm...
weight loss or autoimmune prevention
62
Echinococcus granulosus life cycle
```
Humans = accidental host!!
dogs/wolves= definitive hosts
sheep= intermediate hosts
```
1. adults in GI tract of dogs
2. eggs shed into environment
3. ingestion of eggs by humans--> larvae released and spread hematogenously
4. secretes a membrane
5. inner part differentiates into germinal layer and produces protscolexes (hydatid cyst) in various tissues
6. Fully mature cysts contain thousands of protoscolexes
63
Hydatid Cyst dz
Ecchinococcus granulosus
smallest of all tapeworms!!
Scolex + 1 mature, 1 immature, and 1 gravid proglottid
Forms cysts in many tissues that grow slowly
presentation can be similar to slow growing tumor (liver cyst--> obstructive jaundice; brain cyst--> increased ICP, epilepsy, etc.)
BIG problems if cyst ruptures (anaphylaxis)
64
Hydatid cyst dz Dx
clinical picture + Hx (sheep dogs)
serology can be helpful
space occupying lesions w/ eosinophilia!
65
Hydatid cyst Rx
surgery for cyst (PAIR-puncture aspiration w/ injection/reaspiration- vs. cystectomy)
mebendazole in high doses
preventative measures for dogs
66
terminal hematuria
last drops of urine have blood
67
Schistosomiasis
blood fluke
Trematodes: S. mansoni, S. japonicum, S. haematobium (Africa&America, Asia, Africa)
complicated life cycle (fresh water snails and mammal host)
Adults live in blood vessels draining intestine/bladder, producing huge numbers of eggs
68
Schistosomiasis presentation
asymptomatic OR 3 phases: dermatitis, Katayama fever, Liver probs or bladder probs
dermatitis (swimmers itch) due to penetration of infectious forms (cercariae). Egg deposition is the major problem--> immune rxn
CHRONIC INFECTIONS:
S. haematobium--> bladder granulomas, hematuria, associated w/ bladder cancer!!
S. mansoni, S. japonicum--> periportal firbosis, portal HTN w/ hepatosplenomegaly
Hypersensitivity to eggs= major cause of pathology (causes probs in intestine rather than bladder)
Eosinophilia
Acute vs. Chronic infection (intercurrent flu-like illness in first or second month= Katayama fever/ liver dz late)
--another where sx may occur very late (early on may be asymptomatic w/ eosinophilia)
69
Schistosomiasis Dx
Hx confirmed by ID of eggs in stool (mansoni or japonicum) or urine (haematobium)
70
Schistosomiasis Rx and Prevention
Praziquantel
Snail control, proper sewage disposal, avoid exposure freshwater in endemic areas
71
Schistosomiasis Pathogenesis
inflammation:
if around liver-->portal HTN
if around bladder--> increased blood vessel formation, increased bleeding, increased fibrosis, increased risk of cancer
72
S. mansoni
Africa, middle east, americas
Dz= hepatosplenomegaly
Egg morphology= lateral spine on edge of egg "little hidenburg" (Middle spine)
73
S. japonicum
Asia
hepatosplenomegaly
round, spineless egg
74
S. haematobium
Africa, Middle East
Terminal haematuria
Terminal spine on egg
75
Schisto life cycle
1. eggs in urine or feces depending on type
2. eggs hatch miracidia
3. miracidia penetrate snails
4. sporocysts in snails
5. cercariae released by snail into water (free-swimming!)
6. Penetrate skin
7. lose tails, become something else, enter circulation
8. migrate to and mature in portal blood
9. paired adults migrate to where they cause probs (bladder or mesenteric venules/ plexi)
76
Intestinal Nematodes
```
Pinworm
Ascariasis
Hookworm
Whipworm
Strongyloides
```
77
Tissue Nematodes
Trichinella
Wuchereria bancrofti
Toxocara canis, T. cati
78
Flatworms (trematodes..flukes...)
Schistosoma
79
Flatworms (Cestodes...tapeworm...)
Taenia saginata or solium (intestinal or tissue!)
| Echinococcus granulosus
80
Entamoeba histolytica life cycle
1. mature cysts ingested in fecally contaminated food, H20, hands
2. excystation occurs in SI
3. Released trophozoites migrate to colon
4. Trphozoites produce cysts, passed in feces and can survive outside body
81
Entamoeba histolytica
major cause of amebic dysentery
trophozoite=active form (single nucleus, often contains ingested RBCs)
Cyst=excreted, durable form (may contain up to 4 nuclei)
82
Entamoeba histolytica presentation, pathology,, Dx, and Rx
1. asymptomatic
2. Intestinal dz (acute= dysentery w/ abd. pain; chronic= recurrent episodes w/ blood and mucus in feces)
3. extra-intestinal abscesses (disseminates to liver, lung, brain to form abscesses)
Flask-shaped ulcers in large intestine
no protective immunity
anchovy paste aspirate
Dx via sx, Hx, etc.; lab looks for cysts in stool; serology amoeba antigen and PCR tests
Rx w/ Metronidazole for symptomatic infection (doesn't fully clear infection, so...) Paromomycin for eradication of luminal carriage)
83
N. fowleri
amoeba
outbreaks associated w/ diving in fresh H2O and neti pots
Portal of entry= nose (crawls up cribiform plate into brain...)
meningitis/ encephalitis w/ poor Rx success
Amphotericin?
84
Trichomoniasis
tricomonas vaginalis (flagellated protozoan)
STD
Trophozoite, single nucleus, 4 anterior flagella, undulating membrane
NO CYST FORM (different from amoebas)
asymptomatic in men; women (with appropriate vaginal environment...i.e pH>4.5)=frothy discharge, contact-dependent vaginal epithelium damage, strawberry cervix
Dx clinical confirmed by trophozoites in discharge (PCR)
Metronidazole Rx
85
T. vaginalis life cycle
1. organism in female lower genital tract and male urethra
2. multiplies via binary fission; no cyst stage
3. transmitted by sex and urine; doesn't survive outside host and no reservoir
86
Giardiasis
Giardia lamblia
MC protozoan intestinal dz in US (water and daycare)
Flagellated protozoan
trophozoite w/ 2 nuclei and bilateral symmetry of axostyles and suction discs)
Cysts w/ 4 nuclei and well defined wall
Sx: uncontrollable flatulence; abd distension, foul-smelling bulky diarrhea
stool contains excess lipids, but usually not blood or necrotic tissue
trophozoites cover and flatten intestinal epithelium--> may lead to malabsorption of nutrients
Dx: clinical + cysts and trophs in stool
Metronidazole Rx
Dysentery very uncommon b/c not invasive usually
87
Giardia life-cycle
1. cysts in contaminated eating
2. ingested
3. trophozoites multiply by binary fission in SI
4. encystation occurs as parasites move toward colon
5. animals may be reservoir (think camping)
88
T. brucei life cycle
1. Tsetse fly bites human
2. injected trypomastigotes transform into bloodstream trypomastigotes
3. multiply via binary fission in body fluids (blood, spinal fluid, lymp, etc.)
4. Tsetse fly bites
(continues life cycle in tsetse fly)
89
T. brucei variant surface glycoprotein
VSGs/anitgenic variation
(immune evasion!)
minichromosomes w/ transcriptionally silent VSGs, which are switched (one active at a time)
90
African trypanosomiasis
sleeping sickness
gambiense in Wst Africa, rhodesiense in East Africa
Morphology: trypomastigote w/ kinetoplast and undulating membrane
Sx: bite rxn (chancre); parasitemia/LNs (fever)----> CNS (coma and death)
East Africa form rapidly progressive
Primarily immunologic pathology due to antigenic variation
Dx: card agglutination test (detection of parasite in blood or LN)
Rx: blood stage- pentamidine, suramin
CNS stage- Melarsoprol, nifurtimox/eflornithine
91
T. cruzi life cycle
1. Triatomine (kissing) bug bites and defecates
2. injected trypomastigotes transform in cells into amastigotes
3. multiply in cells via binary fission (meanwhile, can invade and multiply in other cells in other tissues)
4. intracellular amastigotes transform into trypomastigotes and burst out of cell--> enter bloodstream
5. Triatomine bug bites
lifecycle continues in bug
Non human reservoir hosts: oppossum, raccoon, rodent, dog, cat, armadillo, etc.
Largely a zoonosis, but can adapt to homes and floors!
Other transmission forms: blood transfusion, breast milk, organ transplant, contaminated foods
Trypomastigotes can liver for wks in refrigerated blood, so kill w/ gentian violet plus heat
92
Chagas dz
t. cruzi
central and south america
trypomastigote in blood, amastigote in tissue
```
Primary lesion= chagoma at site of infection (usually face... Romaña's sign)
Acute stage= nonspecific (fever, myalgia, rash), parasitemia and lymphocytosis
Chronic stage (many yrs later)= (10-20% of infected), involves heart, esophagus, colon
```
Direct damage to infected cells (i.e. cardiomyopathy)
destruction to autonomic nerve ganglia (mega-esophagus or mega-colon)
Dx: clinical + blood smear + tissue histology
Rx: complex; benznidazole, nifurtimox
93
Leishmaniasis
90% leishmaniasis occur in Bangladesh, Brazil, india, nepal, and sudan
Obligate intracellular!!!
Vector= phlebotamus, Lutzomyia (sandflies)
multiple species
promastigote taken up by macrophages, differentiate into amastigote, infection propagated by amastigote
Pathology: mainly immunologic; leukoenia, anemia, thrombocytopenia, elevated (unhelpful) immunoglobulins
Dx: Hx, blood, or tissue exam
Rx: sodium stibogluconate
milefosine
vector control
Prevent by sleeping off ground b/c sandflies don't fly high; permethrin-impregnated beds
94
Visceral (kala-azar) Leishmaniasis
L. donovani (Asia)
L. infantum/chagasi (Midle East, Asia, Africa, Latin America)
organisms multiply in phagocytes of spleen, liver, nodes, etc.
hyperpigmented skin
superinfections
95
Mucocutaneous Leishmaniasis
organisms in skin metastasize to mucoid tissue, leading to severe deformity
L. brazilliensis (Latin America)?
96
Cutaneous Leishmaniasis
L. major (middle East, asia, africa)
L. tropica (Old world)
*L. oethiopica (Diffuse... ethiopia, kenya)
L. mexicana (New World)
*L. amazonenisis (diffuse.. Amazon basin)
forms ulcer at site of lesion
*deficient cell-mediated immunity leads to diffuse cutaneous leishmaniasis
97
Toxoplasma gondii life cycle
Human infection through undercooked meat containing cysts or water contaminated with parasite oocyts
Parasite differentiation due to selective pressure (adaptive immune response) causes differentiation to bradyzoites (tissue forms as cysts)
Embryonation in cat litter, cat as definitive host
4 means of transfer:
1. cat liter
2. blood transfusion
3. undercooked meat
4. mother to fetus in pregnancy
98
Toxoplasmosis
Toxoplasma gondii
very common sero-positive (once infected, infected for life)
intracellular replication
cat=definitive host (must sit outside cat for 1-2 days, so cat litter, NOT fresh feces is infectious)
pseudocysts form in intermediate hosts
Rarely symptomatic in immunocompetent
Congenital infection= serious!!
(still mostly normal births, but rarely miscarriage, brain damage, or visual handicap)
REACTIVATION of latent infection or NEW infection in immunocompromised pt can be deadly
(cell mediated immunity controls acute infection, so only mild flu-like while tachyzoites disseminate)
```
vertical transmission (pregnancy)
brain mass in HIV
```
Pyrimethamine and sulfadiazine
Avoid cat litter and rare meat`
when dx in pregnancy: look for IgG and IgM (recent if both present; not recent if IgG only and extremely high affinity)... serology can be confusing
99
Cryptosporidium parvum life cycle
1. thick walled oocyst released (infectious)
2. recreational water source
3. oocyst ingested; sporozoites infect gastric epithelial cells... differentiate and grow asexually or into male and female--> zygote
4. oocyst containing sporozoites
100
Cryptosporidiosis
cryptosproidium parvum/ hominis
outbreaks of diarrhea due to contaminated water source (not killed by chlorine)
oocysts, sporozoites, merozoites
(oocysts contain 4sporozoites, which differentiate into merozoites in GI tract; some merozoites differentiate into gametocytes--> oocyst)
severity of diarrhea depends on dose ingested
Serious dz in immunocompromised (can disseminate to gall bladder, biliary tract, lung)
dehydration from chronic diarrhea
Dx: antigen testing, stool microscopy
Rx: Nitazoxanide
101
Malaria cycle
1. mosquito takes a bite (injects sporozoites)
2. infects liver cell
3. schizont
4. ruptured schizont... increases parasite burden
5. blood
6. trophozoite in RBC matures
7. schizont
8. ruptured schizont (hemolytic anemia sort of)... increases parasite burden
(meanwhile)
9. gametocytes form in RBCs
10. mosquito bites
11. forms oocyst in mosquito, which ruptures, releasing sporozoites... cycle starts again
P. vivax and P. ovale also form HYPNOZOITE (chronic infectious stage) in liver before forming schizont... malaria can return years later unless hypnozoitses specifically treated)
102
Malaria presentation
fever, chills, rigors (correspond w/ RBC rupture)
**cyclic if untreated (tertiary fever, occurs every 2 days)
HA, vomiting, diarrhea, malaise
Acute anemia (RBC rupture, incr. immune clearance)
Cerebral dz (decr. conscious state and seizures... related to sticky RBCs)
Pulmonary edema/respiratory distress
--ARDS like picture
Hypoglycemia
Lactic acidosis
Pregnancy: severe b/c hypoimmune state
103
P. falciparum
48hrs
Deadliest!!
Widespread (tropics/subtropics)
104
P. vivax
48 hrs
Hypnozoites--> relapse
Widespread, but extends to temperate zones and less in Africa
105
P. ovale
48 hrs
Hypnozoites--> relapse
tropical africa, particularly W. coast
106
P. malariae
72 hrs (quartan)
broad range, but lower incidence
107
malaria Dx
giemsa stained blood smear (thin/thick)
--identify parasites by morphology
Antigen detection by rapid antigen tests (control, falciparum, non falciparum... often mixed infection, so may need to treat hypno..)
108
Malaria morphology
ring form trophozoites of P. falci
109
sporozoea protozoan parasites
cryposporidium parvum
plasmodium
toxoplasma gondii
110
Flagellate protozoan parasites
leishmania
trypanosoma
giardia
trichomonas vaginalis
