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DT4- Exam 2 > Walden- GI Parasites X4- Melissa** > Flashcards

Walden- GI Parasites X4- Melissa** Flashcards

1
Q

Naegleria:
Pathogenesis of infection?
Symptoms?
How is it diagnosed?

A

Swimming in stagnant fresh water/heated pool–>
Invades nasal mucosa–> cribriform plate–>
Ollfactory N.–> Brain + Meninges–>
Primary Amoebic Meningoencephalitis (PAM)

Sx: Severe Frontal HA, N/V, meningitis sx.–> FATAL coma within 1 week
Dx: Motile Amoebas on wet prep of CSF

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2
Q

Where is Naegleria found in the US?

A

-VA, GA, FL, TX, CA (warm/ costal US states)

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3
Q

Acanthamoeba: Two mechanisms of infection? What two infections does this cause?

Where is this amoeba found?
How is infection prevented?

A

1) Skin lesion, Eye infection, Inhalation–> Hematogenous spread–>
Granulomatous Amoeboid ENCEPHALITIS
Sx: FATAL progressive brain disease

2) Soft contacts/ corneal trauma/ contaminated water–>
** Chronic Amoebic KERATITIS**
Sx: Ocular pain + corneal lesions w diffuse, indolent, inflam.
Tx: Successful treatment with drugs

Note: both diseases found in US
Px: Avoid warm stagnant fresh water, especially around power plants…

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4
Q

Onchocerciasis:
What disease does this amoeba cause?
Vector?

A

River blindness, Simulium Fly (Black)

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5
Q

Onchocerciasis:
Describe the pathogenesis of river blindness.
What are 4 clinical manifestations of the disease?
(Remember: location of nodules in Africa vs Guatemala)

A

Simulium flies breed in riffles of rapid flowing streams–>
Female fly bites human–>
Inoculates larvae into skin–> mature–> adult worms form NODULES –>MICROFILARIAE released by female–>
Migrate to eye–> RIVER BLINDNESS

Clinical Manifestations:

  • Itching–> scratching–> depigmented lizard/ leopard skin
  • Lymphadenitis–> “Hanging groin”
  • pelvic (Africa) or head (Guatemala) nodules
  • Blindness
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6
Q

Onchocerciasis:
3 ways to dx?
Tx (DOCs and management)?
How is it prevented?

A

Dx:

1) Tenting (microfilarieae in skin)
2) Mazzotti Test (admin DEC, intense itching in 24 hours)
3) slit lamp exam of eye

Tx: 
-Surgical removal of nodules
-NO DRUG TO TREAT ADULT WORMS
Ivermectin= DOC for microfilariae
Doxy = Wolbach Bacteria* (endosymbiotic bacteria)

Px: Premetherin, Deet, avoid rapidly flowing streams in endemic areas I.e. Ferry crossings

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7
Q

What are wolbach bacteria?

A

Endosymbiotic bacteria that live in microfilariae of onchocerciasis; they are responsible for primary inflammatory response in the cornea that leads to river blindness **Tx w doxy

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8
Q

Bancroftian Filariasis:

3 worms and disease caused?

A

Wuchereria bancrofti
Brugia Malawi
Mansonella Filariasis **asx
**ELEPHANTITIS

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9
Q

Describe the pathogenesis of Bancroftian Filariasis induced elephantiasis. What are the early and late manifestations of disease?

A

Infected MOSQUITO bites human–>
Microfilariae transmitted into human–>
Migrate through lmyphatics–>
Immunologic Reaction–>

**Early: Inflammation
(fever, erythema, swelling, +/- lofflers in lung)

**Late: Elephantiasis w/ prolonged exposure + repeat infxn.
(Enlarged legs, arms, genetalia) +/- Chyluria (pee lymph)

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10
Q

3 ways to dx Bancroftian Filariasis?
DOC for treatment/ management procedures?
Prevention?

A

DX:

1) Microfilariae (+) in NIGHT-time blood draw (“Bancroft=elephants’ bedtime”)
2) Mazotti (DEC itch) test
3) antifilarial IgG4-ELISA in blood w active infection
* Lab tests ~ negative in patients with elephantitis

TX:
Ivermectin = DOC
Surgery for hydrocele in scrotum or breast, not effective for general elephantitis

Px: Prometherin soaked nets at night, deet, etc.

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11
Q

Mansonella Filariasis infections are typically…

A

asymptomatic

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12
Q

Loiasis: Microbe the pathogenesis and three manifestations of disease?

A

Day biting Chrysops fly bite–> hypersensitivity reaction–>
1) Calabar (Transient) swellings +/- pain and itching, arthritis

2) Migration to eye–> Ocular pain/ conjuncitivitis/ eyelid edema; noticed when looking in mirror
“‘Lo’ and behold you have a Loa Loa in your eye”

3) rarely CNS manifestations (encephalitis + seizure)

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13
Q

How do we diagnose Loiasis?

How do we treat it (DOC)?

A

Dx:
microfilariae (+) in DAYTIME (noon) blood draw
(Contrast with elephantitis = NIGHT)
“if you suspect Loa, draw blood in the ‘L’ight”

Tx:
DEC = DOC (can cause encephalopathy, Ivermectin») + Surgical removal of worms

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14
Q

Where is Loiasis endemic?

A

Rainforest of west and central Africa: Congo River Basin

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15
Q

Describe the lifecycle of Draculus medinensis–

With what is this infection associated?

A 
Lifecycle:
Human drinks Cyclops (STEP WELL**)--> 
Larvae freed from Cyclops in stomach--> 
Penetrate intestine--> 
Migrate in SQ tissue to legs--> 
Mature, copulate, males dies--> 
Females form blisters on skin--> 
Blister ruptures in water--> new larvae released--> 
Larvae ingested by Cyclops
**Infectious for 2-3 weeks inside Cyclops**
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16
Q

Symptoms of Dracunulus medinensis infection:

A
  • Red itchy blister + n/v/ fever; allergic rxn

- Ulceration–> possible cellulitis or septicemia if worm is broken during removal

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17
Q

Dracunulus medinensis: Dx/ Tx/ Px

A

Dx:
See worm coming out of blister; calcified worms on X-ray

Tx:
**Wrap worm around stick (+/- Metronidazole for inflam.)

Px:
Temphos in existing step wells (insecticide); eradicate step wells; boil step well water before drinking

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18
Q

Where is Dracunculiasis endemic?

A

Sudan; war-torn African countries

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19
Q

Toxoplasmosis: Which animal is the only living host?

A

Cats

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20
Q

What are 5 ways to get toxo?

To which two populations is this disease particularly relevant?

A 
Important infection for Preggos and AIDS 
5 ways to get it: 
1) Undercooked meat with cysts 
2) Fecal oral ingestion of cysts 
3) Blood transfusion/ organ transplant 
4)  Transplacentally
5) Lab accident
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21
Q

Describe:

  • congenital toxo
  • ocular toxo
  • AIDS toxo
  • How toxo can infect immunosuppressed patient
  • How does it present in healthy patients?

How does toxo infection typically manifest in otherwise healthy individuals?

A
  • Congenital Toxo: not apparent at birth; sequelae apparent as child grows (intellectual disability)
  • Ocular Toxo: chorioretinitis (congenital or after birth)
  • AIDS Toxo: ring enhancing lesions; encephalitis

Immunosuppressed: newly acquired OR reactivated latent infection

Typically asx in healthy people; possibly flu sx w cervical lymphadenopathy

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22
Q

How common is toxo in the US?

A

USA 23% population seropositive;

Most NOT symptomatic

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23
Q

Describe the lifecycle for fresh water shistosomas:

A

SNAIL –> MAN –> SNAIL

Cerariae in contaminated water–>
Penetrate skin–> Lung–> Liver–>
Mature + mate in liver–> portal circ–> mesenteric venules (can live here up to 30 yrs!)–>
Females lay eggs containing MIRACIDIUM–>
Miracidium eggs migrate to intestine–> Pooped out–>
Miracidium eggs hatch in fresh water–>
Free miracidium penetrates snail–>
Cerariae formed–> released to fresh water to go to humans again

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24
Q

What are the manifestations of shistosoma mansioni disease (2)?
How is infection diagnosed?
How is it treated?

A

Diseases: LIVER AND INTESTINE

  • Liver fibrosis, Portal HTN, chronic SALMONELLA infection
  • Katayama Fever (acute typhoid-like illness)

Dx: Oval eggs with prominent lateral spine in stool or intestine/ liver biopsy

Tx: Praziquantel (DOC for all GI/GU shistosomaisis)

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25
Q

Katayama Fever: what is it and what causes it?

A

Acute typhoid-like illness w ^ EOS

  • immune complex mediated
  • shistosoma mansioni or japonicum infection in patients without prior immunity
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26
Q

Schistosoma Mansoni: endemic areas

A

Classically: PUERTO RICO!
(But can appear in many other countries)
“MAN it’s SONI in puerto rico”

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27
Q

Where do shistosoma mansioni lay their eggs?

A

Inferior mesenteric vessels (large intestine)

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28
Q

Describe manifestations of shistosoma japonicum infection.
Where do these guys lay eggs?
Dx and Treatment?

A

Same as shistosoma mansioni, except lays eggs in superior mesenteric vessels (large and small intestine)!!

DX and TX the same way as well.

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29
Q

Shistosoma Haematobium:
Where do these guys lay eggs?
What are 3 sequelae of disease?
How is the disease diagnosed and treated?

A

Lays eggs in urinary bladder

Diseases:

  • Painful, frequent urination w/ terminal hematuria
  • Chronic obstructive disease + salmonellosis
  • ^^^ risk bladder ca.

Dx:
Oval eggs with terminal spine in urine or bladder mucosa

Tx: Praziquantel

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30
Q

Shistosoma Haematobium: Endemic areas?

A

Africa, Middle East

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31
Q

Salt water Avian Schistosomes:
Endemic areas and infection caused?
Pathogenesis and treatment?

A

Cape Cod
-Clam Digger’s Itch—transient dermatitis
-Does not mature in humans
-Cerariae in contaminated water penetrate skin
Tx: Antihistamine

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32
Q

Fresh Water Avian Schistosomes:
Endemic areas and infection caused?
Pathogenesis and treatment?

A

Great Lakes
**Worse w hydro-dams and agricultural irrigation
-Swimmer’s Itch—transient dermatitis
-Does not mature in humans
-Cerariae in contaminated water; ingested or penetrate skin
Tx: Antihistamine

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33
Q

Taenia Saginata: Animal Reservoir?

Taenia Solium?

A

Saginata: Cow Tapeworm (“SAGgy Utter’s”)
Solium: Pig

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34
Q

Tania Solium: Animal Reservoir?

A

Pig tapeworn

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35
Q

Lifecycle for Tanea Saginata and Solium?

A

(Humans = only definitive hosts)
Eggs (gravid proglottids) pooped out by human–>
Proglottid contaminated grain eaten by pig or cow–>
Infected Pig or cow meat ingested by humans

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36
Q

Clinical manifestation of Tanea Saginata infection?

Dx and Tx?

A

Typically asx; mild GI upset; eggs not directly infectious to humans; emotional trauma from shitting worms

Dx: Eggs in stool; not distinguishable from solium
Tx: Prazaquantel
(“if you see worms in your poop, prazaquantel will cure in one swoop”)

37
Q

Clinical manifestation of Tanea Solium infection?

A

Same as Saginata or Neurocysticercosis
Human ingests eggs shed from human feces–> Oncopsheres released in intestine–>
Penetrate intestinal wall–>
Cysts lodge in MSK + BRAIN–>
Mental disturbance, seizures

**Suspect infxn in Latin American migrant workers w/ new onset seuzures and strong bx!!!

38
Q

Dx and Tx for Tanda Solium Infection?

A

Dx:

  • Ab detection w immunoblot assay + purified T. sodium Ag
  • CT or MRI for brain cysts

Tx:
Prazaquantel or Albendazole +/- anticonvulsant, steroids

39
Q

Where are Tanea solium and saginata found?

A

worldwide

40
Q

Diphyllobothriasis: Réservoir?

A

Fish tapeworm of cold water

41
Q

Describe the Diphyllobothriasis Lifecycle

A

Eggs pooped out (human= definitive host)–>
Eggs in freshwater–>
Eggs hatch–> larvae eaten by water fleas–>
Waterfleas grow into crustadeans–>
Crustaceans w infectious larvae eaten by fish–>
Undercooked fish eaten by humans–>
Larvae grow into tapeworms in SMALL INTESTINE –> spread and create cysts (liver, lung, brain)

42
Q

Clinical manifestation, Dx + Tx for Dihyllobothriasis Infection

A

Clinical:
Asx.»>; Diarrhea + fatigue; B12 deficiency anemia
Dx:
Characteristic egg w/operculum ; Megaloblastic Anemia
Tx: Praziquantel

43
Q

Hymenolpiasis: Vector? Prevalence?

A

Fleas and Beetles in GRAIN: #1 HUMAN TAPEWORM WW

44
Q

Where is Hyminolpiasis found?

A

WW; mostly hot places like SE rural US

45
Q 
Hymenolpiasis Nana (dwarf tapeworm): 
Two modes of infection, clinical manifestations of infection, and how it's diagnosed?
A

Modes of transmission:

1) Human poops eggs eggs immediately infectious Fecal oral transmission
2) Human poops eggseggs ingested by flea or beetle insect consumed in contaminated grain

Clinical: Asx»; abdominal pain, diarrhea

Dx: Eggs in stool

46
Q

H. diminuta (rat tapeworm): Describe the route of infection.

A

Human infection swallowing infected insect in grains or flour; typically a rat infection

47
Q

Dipylidium Caninum: What are the reservoir and vector?

A

Dog Tapeworm; Flea = vector

48
Q

Dipylidium Caninum:
Describe the route of infection and its clinical manifestations.
How is it treated?

A

Dog infected –> passes to flea– > Flea bite–> Human infected

Clinical: Perianal itching, diarrhea/ belly pain/ restlessness CUCUMBER SEEDS (parglottids—pieces of worm) in poops

Tx: Prazaquantel

“Dogs and FLEAS and cucumber Seeds” (that rhymes, right?)

49
Q

Echinococcus granulosus:

Describe the lifecycle; what disease does the worm cause in humans?

A

Human CYSTIC ECHINOCOCCUS (more common version)

Lifecycle:
Dogs eat infected sheep viscera w heated cysts–>
Adult worms mature in dog intestine–> Eggs exit in dog poop–>
Humans somehow eat dog poop –> Larvae penetrate human intestinal wall–>
Travel to liver + brain + lung = hyatid cysts

(‘ECH= shEEp, Canine, human’- if you see this then pick ECHinococcus granulosus)

50
Q

Echinococcus granulosus:
What’s the disease?
How is the disease diagnosed (2)?
Treatment (2)?

A

**HYATID CYSTS OF LIVER + LUNGS (Cystic echinococcosis)

Dx:

  • Imaging + Hx
  • Serologocally: EIH/ IHA screen–> Echinococcal “Arc5”

Tx:

  • Surgery—careful removal of cysts to prevent ANAPHYLAXIS + seeding of more cysts
  • Albendazole or Prazaquantel
51
Q

Where is Echinococcus granulsus endemic?

A

Rural herding areas, classically Greece

52
Q

Echinococcus multilocuaris:

Disease caused in humans and route of infection

A

Human ALVEOLAR ECHINOCOCCUS
Eggs ingested by rodents–> larvae released in rodent stool & eaten by fox/dog –> Human ingests veggies/ raw fruit w/ dog or fox feces–> Larvae form vesicles that invade + destroy tissues–>
LIVER FAILURE

53
Q

Paragonimus westermani:
Where is it found and what kind of infection does it cause?
What do the eggs look like?

A

Found in asia; causes infection that mimics TB w/ “rustier” colored sputum

Like TB, can infect the lungs + brain (as well as GI tract)

Operculated eggs MINUS knob (compare to opisthorchiasis)

54
Q

Paragonimus westermani:

Describe the lifecycle

A

(MAN–> SNAIL–>CRAB–MAN)

Human eats raw/ undercooked crayfish/ crab w/ cercariae-->
Larvae penetrate intestinal wall-->
Migrate to lungs--> lay eggs--> 
Cough up, swallow eggs-->
Poop eggs out--> Eggs mature in FRESHWATER-->
LARVAE (miracidium) Penetrate SNAILS-->
CERCARIAE emerge from snail-->
Encyst in freshwater CRUSTACEANS
55
Q

***Clonorchiasis/ Opisthorchiasis: Describe the lifecycle

A

(MAN–> SNAIL–> FRESHWATER FISH–> MAN)

Human eats fish w encysted larvae–>
LARVAE Migrate to BILE DUCTS–>
Mature, lay EGGS containing MIRACIDIA–>
MIRACIDIA into bile–> pooped out in feces–>
Eaten by snails–> CERCARIAE released to water–>
Penetrate fish –> encyst in fish muscle

56
Q

***Clonorchiasis/ Opisthorchiasis:
Clinical presentation (acute vs. chronic)
Diagnosis
Prophylaxis

A

Clinical:
Acute–>epigastric pain, tenderness in RUQ
Chronic–> jaundice w/ diarrhea, fever, HSM, RUQ pain, cirrhosis, ^ risk CHOLANGIOSARCOMA*

Dx:
Tiny ovoid eggs w ‘knob’ in feces or duodenal asparate; ELISA

Px: 
Night soil (human waste) should not be used to fertilize fish ponds; cook fish well
57
Q

***Clonorchiasis/ Opisthorchiasis:
Where is this found?
What do the eggs look like?

A

Asia, especially SE—
US in refugees** from endemic areas
Operculated eggs + knobs

58
Q

Fascioliasis:
What kind of infection does this cause?
How does one get infected?
Where is it found?

A

-liver abscesses; chronic infection NOT Asstd. w cholangiosarcoma (liver rot!!) (Think of it as being named after “fasciitis” so its just causing rot but be careful not to confuse with fasciolopsiasis)

Infection caused by eating contaminated freshwater plants in areas where cattle and sheep herding is common

WATERCRESS!!!!=FASCIOLIASIS/LIVER ROT

59
Q 
Fasciolopsiasis
What kind of infection does this cause?
Basic life cycle? 
How does one get infected?
Where is it found?
A
  • Heavy infection will cause alternating diarrhea and constipation
  • Pig –> snail –> plant –> human

Associated with eating contaminated water chestnut/ bamboo shoots/caltrop in SE asia; look for giant worms in poops or vomit

“fascioloP(ig)S(nail)I(ngest chest…nut)A(human)sis”

60
Q

Entamoeba histolytica:
Where are entamoeba found?
What three infections do they cause?

A

Poor countries (Africa, C/S America, India) **Immigrants and travelers in US

Infections:
1) BLOODY MUCOID DYSENTARY DIARRHEA, +/- flu sx, necrotizing colitis

2) Liver abscesses = right elevated diaphragms
3) LUNG INFECTION (liver abscess rupture seed through diaphragm):pleuritic + RUQ pain, red-brown sputum, SOB

**Note: don’t typically see these conditions all together! May not even see worms in stool! (Only 20% + for worms!)

61
Q 
Entamoeba histolytica, dispar, or moshkovskii: 
Describe the organisms. 
How is it transmitted during epidemics? 
What is the natural reservoir? 
Which cause asx. colonization?
A

Pseudopod forming non-flagellate protozoan
Transmitted from fly feet (cysts) to water during epidemics
Humans are only significant reservoir

  • E. dispar & moshkovskii infection is asx even in immunocompromised
  • E. histolytica can be asx for years
62
Q

Etatmoeba histolytica, dispar, or moshkovskii:

Describe the life cycle

A

Ingestion of contaminated food, H2O/ Oral-anal sex–> Trophozoites multiply (binary fission), form cysts + invade (flask shaped large bowel)–>
Trophozoites migrate to liver, lung, brain via portal circ.

63
Q

What are the two ways we diagnose Entamoeba infection?

A

1) OPx3 (examine stool w/in 30 min, look for charcot-leyden crystals, gliding amoeba w pseudopods, not sensitive or specific)
2) Colonoscopy + Biopsy, Ag testing (15-30min; invasive trophozoites + cysts) + observe multiple flask shaped ulcerations

64
Q

How do we differentiate E. Histolytica from its non-infectious counterparts? (2)

A

E. histolytica:
- Cysts = 1-4 nuclei (more nuclei = noninfectious)

-Trophozoites = single nucleus, central karyosome, INGESTED RBCs, rounded chromatidal bars (frayed chromatin, eccentric karyosome = non infectious types)

65
Q

Blastocystis hominis

How common is this? What disease does it cause? Where is it found and how its it treated?

A
  • Over 50% MSM have this
  • Causes n/v/d abdominal pain, anorexia, malaise
  • WW esp in tropics
  • Treatment is typically supportive care
66
Q

What two diseases will have chariot-leyden crystals?

A
  • Enteric amoebiasis (E. Histolytica)

- Isospora Belli

67
Q 
Giardia Lamblia: 
Where is this found? 
Describe the organism.
Two commonly assc animal carriers?
Tx?
Px?
A

Worldwide; WV, CO, St Petersburg
Motile protozoan 4 flagella (trophozote pic)
Beavers, dogs
Tx: tinidazole (Metronidozole =disulfiram-like rxn)
Px: Chloride resistant (filtration is needed)

68
Q

Giardia Lamblia: Describe the transmission of infection

A

Waterborne», person-person contact, food–>
Ingest 10-20 cysts–>
Excyst in stomach acid–>
Trophozoite colonization of duodenum/ upper small intestine (form cysts as they move down the intestine)–>
Pass cysts + trophozoites in stool

69
Q

Describe the clinical manifestations of Giardia infection:

Wha tis the course like and what are three possible sequelae?

A

Clinical:
**1-2 wk incubation (Shorter think ETEC)–>
Bloating, cramping, yellow/frothy/floaty STANKY DIARRHEA–> ~Malabsorption (ADEK), B12 deficiency

Possible sequelae include LACTOSE INTOLERANCE, RECURRENT sx., REACTIVE ARTHRITIS, failure to thrive in kids

*B12 def also seen with Diphyllobothrium Latum (fish tapeworm)

70
Q

What is the #1 Human pathogenic protozoan in the developed world?
How does the infection present?

A

Trichomoniasis vaginalis

NOT AN INTESTINAL PROTOZOAN (STI)

  • Infects female lower GU and male urethra + prostate
  • Presents with itchy lady parts, frothy/ fishy/ STANKY yellow-green discharge, strawberry cervix
  • Girls symptomatic, boys not
  • TX with metronidazole
  • ^ risk HIV transmission, preterm birth
  • See motile trichomonads on saline slide; serious fishy stank w KOH prep (diff.from candida)
71
Q

Dientamoeba fragilis

Where is it located? describe the organism.

A

Worldwide; rare infection

HAS NO FLAGELLA BUT STILL CONSIDERED FLAGELLATE!!!

72
Q

Dientamoeba fragilis

Describe the pathogenesis.

A

Fecal oral transmission alone or within PINWORM and ASCARIS eggs–>
Trophozoites from ONLY (no cysts)–>
Diarrhea, farts, abdominal pain

73
Q

Balantidium Coli: Describe one important structural fact about the parasite + the infection.

A

LARGEST INTESTINAL PROTOZOAN IN HUMANS!

Incidental human infection–>
Intermittent diarrhea/ acute dysentery w crater like colon ulcers

” LARGEST GI protozoa, from LARGE bowels of pigs, causing LARGE amounts of diarrhea, LARGE crater ulcers”

74
Q

Balantidium Coli:

Where is it found? Describe the organism.

A

Tropics (large bowel of pigs)

CILIATE—only ciliate infectious to humans

75
Q

List the 4 intestinal coccoidal infections that can be stained w acid fast. What kind of infection do these organisms generally cause?

A
  • Cryptosporidium parvum
  • Isospora belli
  • Cyclospora cayetanensis
  • Sarcocystis

Cause severe protracted diarrhea in immunocompromised patients and travelers to the third world

76
Q

What are two factors that make Cryptosporidium parvum exceptionally infectious?

A
  • Chlorine resistant**

- Small oocysts= pass through H2O filters

77
Q

Describe the Cryptosporidium parvum mode of infection and three diseases caused:

A

Infection: waterborne (pools), animal –> person, person –> person, food borne all possible

1) Endemic childhood watery diarrhea (third world)
2) Traveler’s diarrhea (Immunocompetent= 2-3 days)
3) Protracted diarrhea in AIDS patients (cholera-like diarrhea for mos)

78
Q

How do we diagnose cryptosporidium parvo?

How do we treat it?**

A

Dx: Acid fast stain feces; EIA test more sensitive + specific

Tx:

  • REHYDRATION/SUPPORTIVE CARE ONLY for immunocompromised (RX QUESTION)
  • Immunocompetent patients get Nitazoxanide (classically but in real life walden says it isn’t effective)
79
Q

What random animal is associated with CRYptosporidium parvo infection? Where is this infection generally found?

A

pre-weened calves; infection is found ww

“the CRYing pre-weened cow”

80
Q 
Isospora belli: 
Where is infection found? 
Describe mode of transmission. 
What kind of infection does it cause? 
How is it diagnosed and treated?
A

Found in US; humans= only host

Fecal oral spread to immunocompromised patients–> Acute non-bloody diarrhea +/- EOSINOPHILIA, CHARCOT-LEYDEN CRYSTALS in stool

Dx: bright ted cysts on acid fast
Tx: TMP-SMX even for AIDS patients

81
Q

Cyclospora cayetanensis:
Where is this disease found?
Describe the infection caused–high yield mode of transmission?
How do we dx and treat it?

A

Found WW:
Ingest sporulated oocysts in water or food–>
N/V/ prolonged watery diarrhea +/-flu sx–>
Poop out unsporulated oocysts–> contaminate food

**Raspberries, mesclun lettuce, snow peas = commonly contaminated foods

Dx: UV microscopy of stool; PCR
Tx: TMP-SMX

82
Q

Sarcocystis: High yield points regarding lifecycle

A

Require 2 hosts for life cycle
Sexual dvlpmt/ definitive host: carnivore
Intermediate host: herbivore

83
Q

Sarcocystis: two infections caused?

A

Two manifestations of human disease:

1) Intestinal infection; human = definitive host
(Tx w TMP-SMX)

2)Muscle infection; human = intermediate host

84
Q

Microspora: what kind of organism is this?

A

Obligate intracellular parasitic fungus!

85
Q

Microspora:
Describe the lifecycle + 2 high yield infections caused.
Who does it typically infect?

A

Typically infects immunocompromised patients

Ingestion or Inhalation of infectious spores–>
Coiled polar filament extrudes infective spore into host cells–> Replication within host cell–>

Many systems affected…

1) Keratoconjunctivitis
2) Chronic diarrhea

86
Q

Microsporidia:

How is infection treated?

A

Fumagillin/ albendazole

87
Q

What 4 have snail interaction in their lifecycle?

A
  1. liver fluke (man-snail-freshwater fish-man)
  2. lung fluke (man-snail-crab-man)
  3. intestine fluke (pig-snail-plant/water chestnut-man)
  4. Schistosomiasis (man-snail-man)
88
Q

which two acid-fast staining parasites cause chronic diarrhea in immunocompromised?

A
  1. microsporidia

2. cryptosporidium parvum

DT4- Exam 2 (12 decks)

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