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145 Cards in this Set

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Enterobius Vermicularis (pinworm) Lifecycle?
- Eggs in environment become infectious w/in 4-6 hours
- eggs are eaten
- eggs hatch in intestine
- worms grow to adults in 6 wks
-Adult migrates to perianal skin and lays eggs
- if not eaten, eggs die in 2 weeks
Pinworm Infectious Form?
Egg w/ differentiated larva inside (gets ingested)
Pinworm Dx?
Egg which is flatter on one side than other
- Found @ perianal skin
- Scotch Tape Diagnosis
Pinworm Treatment?
MEBENDAZOLE--Must treat once then again later to treat infection that will have re-curred from swallowing eggs in environment from first infection
Ascaris Lumbricoides Infectious Form?
Egg w/ larva inside (gets ingested on plants)
Ascaris Dx?
Egg w/ characteristic bumpy shell and larva inside (found in feces?)
Ascaris Symptoms?
- Can cause intestinal or bile duct obstruction
- Malabsorption of Lactose
Hookworm infectious form / route of infection?
LARVA get in thru unbroken skin
Hookworm Disease Causing Form
Adult worm in small intestine
Hookworm Symptoms
Chronic blood loss
- (anemia, fatigue, SOB, developmental delay, edema)
Hookworm diagnostic stage
eggs found in stool
Strongyloides Infectious Form / Route of Infection
Filariform larvae
- Penetrate skin
Strongyloides Diagnostic Stage
Rhabditiform (1st stage) larvae in stool
Strongyloides Causes of Hyperinfection
-Steroids
-Bacterial Sepsis
Visceral Larva Migrans (Toxocara)
- Infectious Form / Route of infection?
(Kids) Ingest the eggs
Visceral Larva Migrans Disease Presentation
-Eosinophilia/Inflammation
- Altered LFTs
- Various Symptoms
- Invasion of retina resembling retinoblastoma
Visceral Larva Migrans Dx?
- Serology! (wont usually larva or egg)
Cutaneous Larva Migrans infectious form/ route of infection?
Filariform (3rd stage) Larvae
- Penetrate skin
Cutaneous Larva Migrans disease-causing form?
Larvae (can't mature to adults in humans!)
Cutaneous Larva migrans dx?
- Eosiniophillic inflammation on biopsy of serpiginous lesion
- (infrequently can see actual larva)
Trichinella Spiralis Infectious Form/ Route of Infection?
- Larva encysted in muscle of carnivore is eaten
Trichinella Spiralis Diagosis?
Finding encysted larva in muscle
- "Squash Test" on a piece of fresh muscle tissue shows encysted larvae
- Can also use serology if there is not a good place to biopsy
Trichinella Spiralis Life Cycle in humans?
Larva ingested, mature to adults in small bowel
- Adults mate and produce new larva (no eggs!)
- Larva migrate thru bowel->portal circulation-->muscle
Trichinella Spiralis disease mechanism?
Larva in muscle induce inflammation!
- Heavily used/ oxygenated muscles preferred (heart, diaphragm, peri-orbital)
Filaria (General) Life Cycle?
- Adults in SC nodules / lymphatics
- Produce larvae in blood stream
- Vector bites and gets infected w/ larvae thru blood
- Larvae matures thru several stages in vector
- Mature larvae passed back to human thru bite
Lymphatic Filariasis (Wucheria) Infectious form / Route of infection?
Mature larval form transmitted through mosquito bite
Lymphatic Filariasis (Wucheria) Disease causing form / Disease mechanism?
Adults in lymphatic system cause lymphatic obstruction-->elephantiasis
Lymphatic Filariasis (Wucheria) Diagnostic form?
Microfilaria (larva) in blood
- show distinct pattern of nuclei
- faintly staining sheath is present
Dirofilaria (Dog Heartworm) Manifestation in humans?
Larvae don't mature in humans but can be deposited in lung and form fibrotic lesion
Onchocerca Disease Causing form/ Disease Mechanism / Disease manifestations?
Microfilaria (larva) migrating through dermis and causing inflammation
- chronic, atrophic, dermatitis
- blindness (whole eye affected)
Onchocerca Infectious form / route of infection?
Infective Larva transmitted by BLACK FLY bite
Onchocerca Diagnosis?
Skin snip--ID microfilaria in dermis
Onchocerca Treatment?
Ivermectin administered 1X/year-- kills microfilaria in blood and prevents disease manifestations
- does NOT kill adults in SC nodules
Schistosomiasis Indermediate Host
SNAIL
Schistosomiasis Life Cycle
Ciliated larva hatches from egg--infects snail--cercariae larva (swimming form) breaks out of snail--penetrates human skin (loses tail)--portal system-->matures to adult-->paired adult worms in mesenteric v. or bladder--shed eggs into feces or urine-->hatch to ciliated form in water
Schistosomiasis Habitat
FRESH WATER
What causes Disease in Schistosomiasis?
Overactive immune response to Eggs trapped in organs
-TH2 response-->granuloma-->massive proliferation of fibrosis
Organs that Can be Damaged in Schistosomiasis
Liver--pipestem Fibrosis-->portal htn, ascites
Lung
Brain
Spinal Cord
Bladder--SCC
Species of Schistosomes / Characteristics
Mansoni: lateral spine--excreted in feces
Hematobium: spine at end--secreted in urine
Japonicum--no spine, rounder egg--secreted in feces--has zoonotic host
Diagnosis of Schistosomiasis
Look for eggs in stool/urine
Treatment of Schistosomiasis / What stage does it kill?
Praziquantel
- Kills adult forms only
Prevention of Schistosomiasis
Snail monitoring
Prevent human waste from reaching water
Schistosomiasis Infectious Form
Cercariae Larvae--penetrate skin
Taenia Saginata/Solium Infectious Form:
Encysted larva in meat of beef/pork
Taenia Saginata Intermediate Host
Cow
Taenia Solium Intermediate Host
Pig
Taenia Saginata / Solium Diagnostic Stage
Egg or Proglottid in Stool
Differences in appearance between Taenia Saginata & Solium
Saginata: uterus in the proglottids has smaller but more numerous branches

Solium: scolex has a "circle of hooklets" in addition to 4 suckers
- uterus in proglottids has larger but fewer branches

-Eggs are indistinguishable
Taenia Lifecycle
-Cow or pig eats egg or proglottid in human feces
- Larval form migrates to animal muscle
- Human eats encysted larva in undercooked meat
- Larva matures in s.intestine-->adult
- Adult produces eggs--shed in stool
Taenia Saginatum Clinical Sx
None
Taenia Solium Clinical Sx
Human can act also as intermediate host--larva encysts in muscle, brain, heart, bone, eye--"Cysticercosis"
- can cause epilepsy
Dx of Cysticercosis
When larvae die--cysts calcify and can be seen on xray
(cysts of trichinella are too small to be seen on xray)
Tx for Taenia
Praziquantal for adult worms +
Albendazole for larvae in t.solium
Diphyllobothrium Latum Diagnostic Stage?
(Freshwater fish tapeworm)
Egg in feces
Fish Tapeworm Intermediate Hosts
- Copepod crustacean
-Fish
Fish Tapeworm infectious stage
larva encysted in muscle of undercooked fish
Definative Hosts for Fish Tapeworms
Humans
Cats
Dogs
Pigs
Fish Tapeworm lifecycle
Eggs in human feces-->into water-->ciliated larva hatches-->infects copepod->eaten by fish-->larva encysted in fish muscle-->eaten by human
Diphyllobothrium Latum (Fish Tapeworm) Differences from other two tapeworms (taenia)
- Gets longer! (up to 75 ft)
- Shorter, broader proglottid
- Eggs have a small "hatch" at one end
- Release more eggs / day
Fish Tapeworm Clinical Symptoms
Adults in small bowel-->interfere w/ B12 absorption-->macrocytic anemia
Anisikiasis
Assoc. w. saltwater fish
- larvae encysted in fish muscle--eaten by humans (sushi!)
Larvae cause pain/eosinophilic inflammation ~72 hrs
-human=accidental host
Echinococcus Granulosus Hosts
Definitive: Dog (Dog Tapeworm)
Intermediate: Sheep
Accidental Intermediate: Human
Echinococus Granulosus Route of infection of humans
Eating eggs that were in dog feces
Echinococcus Granulosus Life Cycle in Humans
Ingest eggs--larva break out--migrate to liver/bone/brain--form Hydatid Cysts--asexual repro--production of protoscolices ("hydatid sand")
Echinococus Granulosus Clinical Manifestation
Leakage of cyst contents in response to trauma--acute allergic rxn (anaphylaxis) and seeding of new cysts
Echinococus Granulosis Tx
Surgery to remove cysts (careful not to rupture)
Echinococcus Mulitlocularis Hosts
Definitive= dog/fox
Indermediate=rodent
Accidental intermediate=human
Echinococcus Multilocularis Clinical Disease
Cysts w/ protoscolices can rupture SPONTANEOULY
- daughter cysts invade organs like malignant tumor (make surgical removal difficult)
Echinococcus Multilocularis Geographical Distribution
Alaska, Northern MN, Canada, Circumpolar
Entamoeba Histolytica Clinical Syndrome
Amebic Dysentary: Acute colitis w/ flask-shaped ulcer
- blood and mucus in stool
- abd pain
- fever
- steroid may activate disease-->perf. colon
-"STERILE ABSCESS" in liver, brain, lung, skin
Entamoeba Histolytica Virulence Factor
Amebic Surface Lectin--allows it to invade GI + Complement resistace
Entamoeba Histolytica Life Cycle
-Cyst in environment (v.stable--resist Cl-)
- Cyst swallowed (fecal/oral)--trophozoite breaks out--invades GI
-Trophozoite changes back to cyst--excreted in feces
Entamoeba Histolytica Diagnosis
Cysts (round w/ chroamotidal bars) and Trophozoite (single nucleus and occassionaly RBC inside) in feces
- difficult to ID the trophozoites b/c look like Macros

- Ag detection of surface lectin=best
Entamoeba Histolytica Tx
Metronidazole kills trophozoites
Entamoeba Coli
Not pathogenic, but used as marker of having been exposed to contaminated food/water--look for e.histolytica
Naegleria Fowleri Clinical Sx
Primary Amebic Encephalitis
- nasal passages exposed to amebae--they invade cribriform plate-->necrotic lesions of brain
- rapidly lethal (wks-days)
Naegleria Fowleri Geographic Distribution
Mid-atlantic states, southern US
- Warm ponds
Giardia Lamblia Life Cycle
- Cysts in environment (v. stable-resist Cl-)
- cyst ingested (contam food/water)
- trophozoite breaks out in s.bowl
- trophozoite multiplies w/in GI and adheres to epithelial cells
- Cysts and trophozoites Exreted in stool
Giardia Lamblia Clinical Sx
- trophozoite covers surface area for absorption-->MALABSORPTION
- Steatorrhea (floating stools)
- Diarrhea, abd discomfort, wt loss
- Chronic inf: may be asymptomatic
Giardia Lamblia Dx
Cyst and Trophozoite in Stool
Giardia Lamblia Tx
Metronidazole kills trophozoites
Giardia Lamblia Geographic Distribution
All over world!
Trichomonas Vaginalis Infectious Stage
Trophozoite in vagina or urethra
Trichomonas VAginalis Dx
Trophozoite in vaginal or prostatic secretions or urine
- wet mount to look for flagellated trophozoite
- rapid enzyme immuno assay will probably replace other techniques
Trichomonis Vaginalis Replication
- No cyst stage
- multiplies by binary fision
Trichomonas Vaginalis Clinical Syndrome
- vagintis w/ purulent discharge
- urethritis
- prostatitis
- often asymptomatic
- inflammation increases risk of HIV acquisition
Trichomonas Vaginalis Transmission
- Sex
- Wet towel/ bathing suit
Trichomonas Vaginalis Tx
- Metronidazole (both partners!)
Toxoplasma Gondii Definitive Host?
Any type of Cat
Toxoplasma Gondii Infectious form
Fecal cyst excreted by cat--infectious 2 days after excretion and remains infectious in soil for long time
Toxoplasma Gondii disease causing form
Trophozoite--rapidly dividing stage--invades tissue in muscle and brain
Toxoplama Gondii route of human infection?
Eating animal meat with tissue cyst OR ingesting fecal cyst from soil
(Dogs may roll in cat poop and human pats dog)
Toxoplasma Gondii primary infetion symptoms
Usually asymptomatic! Sometimes mono-like symptoms or more severe in immunocompromised only
Toxoplasma Gondii Reactivation disease?
Toxoplasma Encephalitis--AIDS defining lesion
Toxoplasma Gondii Congenital Disease?
CNS (encephalitis) and Ocular (retinitis) manifestations
Toxoplams Gondii Treatment?
Pyrimethamine-Sulfadiazine (Anti-folate)
Toxoplasma Gondii Diagnosis
Serology (IgG and IgM)
- dont ever really find the dividing stage in people
Cryptosporidium route of transmission
Usually contaminated water (cysts are resistant to chlorination--water must be filtered)
Cryptosporidium infectious form
Infectious cysts in feces-->contaminate water sources
Cryptosporidium life cycle in human
Infectious cyst ingested-->multplies intracellularly just under the plasma membrane in s.intestine epithelial cells-->excreted back out to environment
Cryptosporidium Clinical Manifestations
(normal vs. AIDS)
Normal: self-limited watery diarrhea
AIDS: protracted and debilitating diarrhea
Cryptosporidium Tx?
None---symptomatic for diarrhea
Cryptosporidium Diagnosis
Acid Fast Cysts in stool
Plasmodium Falciparum Life Cycle
Sporozoite injected by mosquito in to blood-->infects hepatocytes->matures to merozoite-->infects RBCs-->infects more RBCs-->gametocytes eventually form-->M and F gametocyte must be transferred back to mosqito
Plasmodium Falciparum Disease Causing Mechanism
Merozoite digests Hgb w/in feeding vacuole in red cell-->hepatosplenomegaly from malaria pigment
When it breaks out of RBC--cytokines released-->periodic fevers + ANEMIA
Parasitic proteins inserted in RBC membrane-->adhere to endothelial cells in small blood vessels-->ischemia (renal fail, cerebral dysfunction)
Plasmodium Falciparum Initial Clinical Presentation
Shaking chills X 1 hour + h/a--> fever, n/v-->drenching sweat
- fevers become periodic after several weeks
Plasmodium Flaciparum Dx
Blood smear (thin and thick film) too look for RING STAGE or BANANA SHAPED GAMETOCYTE in red cells

PCR is more sensitive--but only at ref. lab, results take several days
Plasmodium Vivax Differences from Falciparum
- Milder Clinical Course, lower parasitemia, fewer complications
- can be dormant up to 12 months and then RELAPSE (survives winters)
Plasmodium Vivax Diagnostic Features
- Infects Retics only so infected cells will larger than others
- Will likely see other forms besides ring stage
- Schuffner's Dots
Alternative Pathways of Malaria Transmission
- Transfusion
- Transplacental
Genetic Defects that confer resistance to Malaria
- G6PD
- Sickle Cells trait
- Duffy blood Ag
Malaria Tx (primary infection)
- Chloroquine (oft. resistant)
- Mefloquine
- Atoavaquone
- Artesunate
Malaria Tx for relapse prevention in plasmodium vivax
Primaquine
Babesia Microti Definitive Host
Ixodes Tick
Babesia Microti Life Cycle
Sporozoite injected into human by tick, has erythrocytic life cycle (merozoite) similar to that of p.falciparum
At-Risk patient population with Babesia Microti
Asplenic Patients
Geographic Distribution of Babesia Microti
NE, West Coast, Southern US, Europe
- Especially NE coastal islands--NANTUCKET/ MV
Babesia Microti Dx
Look at blood smear--can be difficult to distinguish from malaria, but difference is Babesia CAN be found extracellularly, malaria can not.
Babesia Microti Tx
Mild/Asymptomatic Disease: none

Symptomatic Disease: Combo tx
- atovaquone and azithromycin OR
- quinine and clindamycin
Babesia Microti commonly co-infected with?
-Borellia Burgdorferi (Lyme Dz)
- Anaplasma Phagocytophilum
Hemoflagellates
-Leishmaniasis
-Chagas (Trypanosoma Cruzi)
- Sleeping Sickness (Trypanosoma Brucii)

Common Characteristics?
- All have a blood stage
- All have flagella originating from a kinetoplast
- SOME have obligate intracellular stage AMASTIGOTE
- All have insect host/ vector
- Definitive host=u/k
Leishmaniais Insect Host
Sandfly "Phlebotomus"
Leishmaniasis Life Cycle
Sandfly injects flagellated form-->enters monocyte in skin-->loses flagella-->mult. intracellularly as amasticgote-->cell lysis-->more monos/macros infected-->uninfected fly ingests infected macros-->they become extracellular flagellated form and mult in insect GI-->infectious 1-2 wks later
Leishmaniasis Diagnositic Stage
Intracellular Amastigote on histology (see 2 dark staining bodies inside each parasite)
Leishmaniasis Clinical Syndromes
- Visceral (Kala Azar)
- Cutaneous
- Mucocutaneous
Visceral Leishmaniasis clinical manifestations
- wasting, hepatosplenoegaly, likely fatal
Visceral Leishmaniasis Dx
BMBx--original cutaneous lesion healed before visceral sx appear
(look for intracellular amastigote)
Cutaneous Leishmaniasis Clinical Appearance
Papule at site of bite that grows and becomes ulcer that last 6mos-->years
- heaped up edge, center clears first, wet or dry
Cutaneous LEishmaniasis Dx
- Biopsy along edge of ulcer
Mucocutaneous Leishmaniasis Clinical Presentation
STarts like cutaneous form, but weeks-years later it disseminates to produce massive necrotizing lesions at mucocutaneous junctions of mouth or nose
Leishmaniasis Tx
Difficult--available agents are toxic
- Amphotericin B for visceral
- Antimony compounds--very toxic
Trypanosoma Cruzi Insect Vector
Reduvid bug
T. Cruzi mode of transmission
Reduvid bug bites human and defecates, feces contain extracellular flagellated form--gets spread into bloodstream thru site of the bite
Trypanosoma Cruzi Geographic Distribution
S. America, Central America, Mexico
T. Cruzi Life Cycle
Flagellated form into blood via reduviid bug-->enters monos/skeletal& cardiac muscle-->becomes amastigote and multplies intracellularly-->flagellated forms break out of cells and infect others-->extracellular forms ingested by reduviid bug-->multiply in gut of bug and mature to infectious form in rectum
Trypansoma Cruzi Dx: (Acute Disease)
See extracellular flagellated forms in blood smear "C-shped" with kinetoplast at end
Trypanosoma Cruzi Dx (Chronic Disease)
Xenodiagnosis (b/c not high enough parasitemia to see it in blood smear)
Alternate Routes of T. Cruzi Transfer
- Reduviid feces contaminated food
- Blood transfusion (US blood supply monitored by PCR)
- Transplacental
T. Cruzi Clinical Manifestations (Acute)
- Often Asx
- Romanas sign-- painless swollen lesion near eye at site of bite
T. Cruzi Clinical Manifestations (Chronic)
- Dilated Cardiomyopathy (damage due to amastigotes dividing in muscles)
- Destruction of Autonomic ganglia-->megacolon or megaesophagus
T. cruzi prevention / treatment
Bug control, housing improvements

Bendazole--but only 50% effective in chronic disease
Trypanosoma Brucei Insect Host
Tsetse fly
Trypanosoma Brucei life cycle
infected fly bites and transmits trypanosome in saliva--multiplies in CSF,lymph, tissues--transmitted back to uninfected fly--multiplies in insect gut and salivary glands
Trypanosoma Brucei Clinical Syndrome
- Local nodule at bite site-->ulcer
- post. cervical adenopathy--winterbottom's sign
- disseminates to CSF-->lethargy, coma, death
Trypanosoma Brucii Diagnosis
See extracellular form in blood (THERE IS ONLY EXTRACELLULAR FORM)
- kinetoplast is not at then end, as in t.cruzi