Flatworms- Cestodes And Trematodes

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What are the different kinds of flatworms?

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What is taeniasis?
-Most important 3?

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-GI tapeworm infection
-of these 3, the pork tapeworm can cause human tissue invasion --> cysticercosis
-From the dog tapeworm, humans can't get a GI tapeworm; we can only get tissue invasion.

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Life cycle of tapeworms in humans:

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-From contaminated, undercooked meat.
-Eggs (proglottids) look distinct for each kind of tapeworm.

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In tapeworms, which host is the "definitive" host?

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The host in which the tapeworm reproduces.

The other one is the "intermediate host" -- no sexual reproduction occurs.

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Where is the invasive stage in tapeworms?

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-In the intermediate host.

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Who are the definitive and intermediate hosts for taenia saginata and taenia solium?

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*In taenia solium, we can be intermediate hosts --> we can get cysticercosis.

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-tapeworms!
-we don't need to distinguish between different ones by appearance.

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Left: Beef tapeworm larvae/cysts
Right: "Measly" pork with tapeworm larvae/cysts

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-Tapeworm
-solium has really effective hooks, helping them to latch onto the intestinal mucosa.

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-Thick outer layer with striations are indicative of taenia eggs.

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Diagnosis of tapeworms:

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-we don't have to know how to distinguish b/t species.

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Treatment for tapeworms:

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*This is the best drug for ALL THE CESTODES

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Cestodes in Cows-- prevention & control:

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Cestodes: Pigs-- prevention & control:

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Life cycle in Cysticercosis:
-what are cysticerci?
-What kind of lesions are there in this infection?

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-ONLY in taenia solium.
-Pigs eat human poop; that completes the cycle.
-WE BECOME the intermediate hosts

1) brain --> seizures (space occupying lesion &/or inflammatory response)
2) eye
3) subcutaneous

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Transmission of Cysticercosis:

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-ingestion of T. solium eggs (not T. saginata) from someone else’s or ones own (autoinfection) tapeworm infection i.e. not from eating infected pork!

-people who don’t eat pork can get cysticercosis by ingesting food or water contaminated by an infected food preparer (e.g. orthodox Jews in NY outbreak)

-YOU DON'T HAVE TO EAT PORK!

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-Head imaging of cysticercosis.
-No real issue when they're alive.
-Edema and inflammation is what causes seizures.
-Can be focal or diffuse.
-Calcifies in late stage, after cysts die.

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-alien appearance is a cross section of a cysticercus

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-What is this and what's dangerous about it?

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-Indicates that the cysticerci could be ANYWHERE in the body.

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Distro of cysticercosis?

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-Pretty global. Anywhere there are pigs.
-Most cases in U.S. appear in immigrants.

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Cysticercosis: clinical epidemiology:

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Can the definitive and intermediate organisms ever be the same organism?

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NO NO NO NO NO.

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Clinical features of Cysticercosis: 4

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-asymptomatic
-CNS: headaches, seizures*, hydrocephalus, paralysis
-visual disturbance
-lumps under the skin

*major cause of adult onset seizures in low-income countries (caused by dying and calcified cysts)

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Diagnosis of Cysticercosis:

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-serology: blood, CSF (EIA or immunoblot)
-brain imaging: CT, MRI
-ophthalmology: eye exam

-*stool: Taenia solium eggs and proglottids in the feces diagnoses taeniasis and not cysticercosis.*

-serology screening: persons who are found to have eggs or proglottids in their feces should be evaluated serologically since autoinfection, resulting in cysticercosis, can occur.

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-Describe autoinfection in cysticercosis:

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-Carriers of T. solium carry a substantial risk of acquiring cysticercosis by fecal-oral autoinfection and members of their households are also at risk.
-BABIES ARE DUMB AND EAT THEIR OWN POO.

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Treatment guidelines for Cysticercosis:

*What do you definitely want to examine before starting treatment?

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-depends on number of cysts, location and stage of infection (viable, degenerating, or calcified/dead)
-no anti-parasitic treatment for dead cysts
-treat viable cysts with ALBENDAZOLE x 15-30 days (or praziquantel) plus STEROIDS x few days (dexamethasone) to counteract the inflammatory edema induced by dying cysticerci (controversial)

-anticonvulsants if needed

-eye examine before starting therapy

-surgery (eye, brain) in some settings

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Why are steroids important in treating cysticercosis?

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-Because when albendazole starts to kill the cysticerci, it causes inflammation. That inflammation can lead to BLINDNESS or other negative effects.

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What is Echinococcus granulosis?

What does it cause?

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-the dog tapeworm

echinococcosis=hydatid disease (in humans)
*we don't ever get tapeworm, just the invasive disease*

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Life cycle of echinococcus granulosus:

Where does the parasite's replication occur?

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-Replication occurs in the dog.
-We interject ourselves into this life cycle (think about sheepdogs)

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How exactly are dogs involved in the life cycle of echinococcus granulosus? What do they eat?

How are we involved? What do we eat?

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-They are fed the offal of slaughtered sheep.
-They eat the cysts in the process.

-We get the eggs from dog feces; they invade, form cysts, and migrate anywhere and everywhere in us.

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Where do the cysts in Echinococcus granulosis go inside of humans and in what order?

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gut --> liver --> everywhere.
*lungs are 2nd most common site after liver.

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Distribution of Echinococcus granulosis by species:

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X= alveolar echinococcosis (E. multilocularis); much more dangerous--multiple cysts.

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Distro of Hydatid cysts in the human body:

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*Lungs and Liver are most important.

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What would the differential be for this?

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-It IS Hydatid cysts in liver.

∆= abscesses, ascaris, e. histolytica (amebiasis)

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Hydatid cyst being removed from the liver.

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Structure of a Hydatid cyst:

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-Hydatid cyst with daughter cysts
-Remember, inside the daughter cysts are protoscolices.

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-Daughter cysts of Hydatid cysts.

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-Hydatid sand.
-Contains hooks, protoscolices; these are what spread

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Describe the clinical presentation of Hydatid Disease:
-in liver?
-in other organs?
-dangers?

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*Rupture & anaphylaxis is fatal.

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Diagnosis of Hydatid Disease:
-Direct
-and Indirect

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What's the treatment for Hydatid disease:

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-Inject hypertonic saline or ethanol before cyst removal in PAIR technique.

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What drug do you use for Hydatid Disease?

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Hydatid disease: prevention-

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Diphyllobothrium latum:

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-the fish tapeworm

-ingestion of eggs from raw freshwater fish in northern hemisphere

-can cause vitamin B12 deficiency anemia

-treat with praziquantel

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Diphyllobothrium latum: the fish tapeworm

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Schistosomiasis:
-what's the cycle triad? who is the definitive host?

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-blood fluke

-fresh water snails are the intermediate hosts

-humans are definitive hosts

-clinical disease related to parasitemia, location of eggs in various organs, and to adult worms in ectopic sites.

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Schistosomiasis: distribution

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-japonicum= japan, china, indonesia
-mansoni= most common one

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Life cycle of Schistosomiasis:
-what's unique about the relationship b/t male and female?

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-Male lives "in the embrace" of the female.

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-schistosoma mansoni - hook on side, infects GI/Liver
-schistosoma haemaToBium - hook at tip, infects bladder

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-infects GI/liver (less important and common than mansoni and haematobium)

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-There's a special name for this.

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-Lateral spine of the schistosome causes granuloma formation --> cirrhotic symptoms.

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Clinical presentation of Schistosomiasis:

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*Chronic phase is most important.
-esophageal varices leads to coughing up blood.

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-Complications of Bladder Schistosomiasis: 3

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*Squamous cell carcinoma

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Diagnosis of Schistosomiasis: 3

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Treatment of Schistosomiasis:

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Schistosomiasis transmission is encouraged by: 3

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Prevention of Schistosomiasis:

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-mass drug administration with praziquantel in high risk groups, but re-infection happens quickly, unless:

-snail control and environmental management

-health education

-sanitation

-safe water

-economic development

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What is this?
How do you get it?
What does it cause? 3

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-Clonorchis sinensis--Chinese liver fluke

-eating raw/undercooked infected fish

-biliary tract inflammation --> pigmented
gallstones

-associated with cholangiocarcinoma

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Paragonimus westermani:
what is it?
how do you get it?
what does it mimic?
treatment?

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-Oriental lung fluke

-ingestion of raw/pickled/undercooked infected freshwater crab or crayfish

-chronic infection may mimic pneumonia or TB with hemoptysis, chest pain, lung cyst/cavity

-Rx: praziquantel

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What's the ∆ ? 2

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Paragonimus westermani
OR
TB

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Summary of Clinical Findings:
Hookworm (Ancylostoma/Necator)
Clonorchis sinensis
Diphyllobothrium latum
Echinococcus granulosus
Enterobius vermicularis
Paragonimus westermani
Schistosoma mansoni
Schistosoma hematobium
Taenia solium (cysticercosis)

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microcytic anemia hookworm (Ancylostoma/Necator)
cholangiocarcinoma Clonorchis sinensis
vitamin B12 deficiency Diphyllobothrium latum
liver cyst Echinococcus granulosus
perianal pruritis Enterobius vermicularis
hemoptysis Paragonimus westermani
portal hypertension Schistosoma mansoni
hematuria, bladder Ca Schistosoma hematobium
brain cyst, seizures Taenia solium (cysticercosis)

**Make an extended list**

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Summary of Medications:

Protozoa-
flagellates:
amoeba:

Nematodes (roundworms)-
luminal:
blood and tissue:

Trematodes (flukes):

Cestodes (tapeworms)-
luminal:
tissue:

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Protozoa-
*flagellates: metronidazole, tinidazole (exceptions: trypanosomiasis; leishmaniasis)
*amoeba: metronidazole, tinidazole

Nematodes (roundworms)-
*luminal: albendazole, mebendazole (ivermectin: Strongyloides)
*blood and tissue: DEC, albendazole (certain species), ivermectin: onchocerciasis (River Blindness- NO DEC)

Trematodes (flukes): praziquantel (triclabendazole)

Cestodes (tapeworms)-
*luminal: praziquantel (niclosamide)
*tissue: albendazole

**NOTE THERE ARE EXCEPTIONS**

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What is the "Rapid Impact Package"?

cost?

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“Rapid impact package” of 4 drugs:

1) albendazole or mebendazole
2) DEC or ivermectin
3) praziquantel
4) azithromycin

-Would cost 50 cents / person / year
-Would cover 5, 6, or even 7 endemic diseases.

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Summary of the Big 7 NTDs in the Rapid Impact Package by category and treatments:
-luminal nematodes
-tissue nematodes
-flukes
-bacteria

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