Parasite Conference – Worms

Case 1: Toxacara cati

-Pet cat  possible taxacara cati, but would have to contact feces 2-3 weeks after
-some respiratory issues  develop in lung then move elsewhere
-pica  gives route for fecal contact
-pork sausage  taenia solium possible
-eosinophilia = parasitic infection
-hepatosplenomegaly – possible parasitic infection causing portal issues
-No stool sample  Visceral Larvae MIGRANS = not necessarily in GI tract and contributing
to stool

1. Parasitic infection , Other DDx – Trichinella spiralis, taneia solium (but NO

eosinophilia)

a. eosinophilia, pet cat, undercooked pork consumption, pica,

hepatosplenomegaly,

2. Serology, could also maybe do eye exam if ocular migrans has occurred
a. This worm does NOT leave reminants behind (eggs) or other items other
than just humoral immunity against it.

Toxacara  kitten/puppy roundworms,

Lifestyle like ascaris: 3-4 week maturation in the soil before ingestion of eggs,
bloodstream  lungs  Migrate due to NO clues
-key symptoms  eosinophilia, fever, hepatosplenomegaly

In this case  kid is sick so use anti-helminth – albendazole, possibly also immune
suppress if organ damage from inflammatory resonse is a concern

Notes:
**Eosinophilia  worms as they MIGRATE/TRAVEL through your body, not when they sit
in the gut.
Case 2: schistosomiasis

1. schistosoma japonicum  endemic in area (asia/philippines)

a. though endemic in history-related region  mansoni is everywhere so
cannot be excluded

2. Eggs could be depositied causing continued inflammatory responses

(granulamata) without a current infection (current parasites producing eggs into
the stool)
a. Immunological disease to the EGGS deposited in portal circulation NOT to
current worm infection.

3. Jejunum (japonicum = jejunum)  serotype possible

a. Blood sample looking for organism (can live in vessels for decades)
b. Since they lay eggs into the venules  either go into venous plexus of
target organ area, or swept up by portal circulation
c. Serologic testing, but problem – doesn’t tell us when or where or if still
infectious  only timing clue is Ig type
d. HIGHEST YEILD  rectal test – essentially a rectal biopsy

4. Hepatic artery gives adequate perfusion of sinusoids. Egg deposition in portal

circulation causes granuloma like inflammatory reactions in the portal tracts
that cause portal hypertension and back up into collateral circulations. (drainage
routes into portal system)

5. See # 2  no curret infection, manifestations of portal hypertension due to

previous deposition of eggs and inflammatory rxns. This confirms that a former
infection was the original insult and this is resulting form continual immune
disease against the eggs depositied then.

6. Yes  japonicum egg is smaller and rounded  allows more frequent eptopic
localization of egg (brain/lungs, etc) neurological sequelae more common
a. Small, round and NO SPINE = more likely to embolise
b. Mansoni- lateral spine, Haematobium – terminal spine, Japonicum – None

Case 3: Ascarius

1. “warty” surfaced eggs = ascarius lumbricoides

2. albendazole – inhibitor of b-tubulin polymerization
3. History – treated symptomatically  progressed w/ abdominal issues a stool
sent. The pneumonitis would have been earlier and may be mentioned in an
earlier visit
4. Kind of a TRICK  actually normal is NO symptoms, you would expect no
symptoms
 4. warty looking egg = ascarius
5. albendazole treatment
6. Brother had it, and even with NO symptoms it might be important to check
7. worm made its way out  stimulated by fever bacterial infection  also
peritonitis may have been stimulated by worm migration and subsequent bacterial
infection

Case 4: Enterobius

1. ? Ascarius? Warty outer edge of egg?  NOPE - Plant material

2. Scotch tape
3. First thing in the morning
4. Enterobius vermicularis – “pinworm” nematode
5. Standard  pyrantel, mebendazole or albendazole
a. In practice  antihelminthic is often not enough so how else do you
break the cycle? - hygiene , clean all bed linens and clothing etc
6. Treat or at least watch entire family

Case 5: schistasomiasis

1. schistasoma haematobium
a. history/story, and image = schistasoma eggs with miracidium inside and
egg shape with TERMINAL spine
2. Nigerian immigrant, urinary issues (masses/lesions= calcified eggs), hematouria
3. ? read about a rare bug?
4. Fresh water exposure – especially SNAIL infested waters, other endemic area
experiences?
5. Prazequantal
6. Calcified eggs in urine?

Case 6: cysticercosis  from taeina solium tapeworm  Neurocystocercosis

1. Cysticercosis

2. Columbia endemic, various CNS symptoms, Vessel-free area = not tumor

3. CSF – eosinophillia
a.  won’t always see it – depends upon location of infection (sub-
arachnoid vs other)
b. serology – “menu” by WHO has been developed

4. Rule out enterobius, or enterobius co-infection – multiple infections common

 a. Also MIGHT pick up a tanea solium egg, maybe, doubtful

5. Three circumstance?
a. You can have cysts without eggs in stool  if you eat egg get cysticerus
(cysts) and NO adults, thus no egg-laying
b. You can also have both – cysts and adults  then the adults are killed off,
and cysts remain after
c. Or adults just die off (not treated like above)

Cycle  we have worm – pass egg in feces, eaten by intermediate host – cysts form in
intermediate host – we eat cysts within underpreserved or uncooked meat.

Case 7: Long-standing strongyloides stercoralis infection with acute hookworm

1. Long standing, sometime over 20 years ago when he lived in Vietnam

a. Enters skin  blood  lungs  adults move into GI, pass larvae which
may re-infect  AUTOINFECTION
2. Immunosupression therapy  downplays the Th2 response to helminthes
a. Steroid therapy is THE RISK FACTOR for hyperinfection of strongyloides
3. Acute infection exacerbates previous stronglyoides infection 
pneumonitis/additional respiratory issues, rash
a. Hookworm EGGS should be in stool but in TIME for specimen to be
analyzed  hookworm incubation finishes and eggs HATCH

4. Yes, if other family immigrated from Vietnam? Any current unsanitary practices
(hookworm?) Is he anemic?
a. Anwer  this is essentially an opportunistic infection, so ensure that he
has no OTHER opportunistic infections, especially since this was brought
on by asthma treatment, he will continue asthma treatment which could
be risky.

Roundworms
Inside gut  mebendazole, pyrantal
Outside  albendazole, ivermectin

Flat worms
Inside gut  Niclosamide
Outside gut  Albendazole

Flukes
In general  Praziquantel