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SBM: ID > Parasitology I: Worms > Flashcards

Parasitology I: Worms Flashcards

1
Q

Definitive host vs. intermediate host:

A

Definitive host - host in which the organism reaches sexual maturity.
Intermediate host - host which supports growth of intermediate stages.

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2
Q

This immune cell is stimulated when worms are found in the tissues, but is usually not stimulated when worms are found in the intestines or by infections with protozoa:

A

Eosinophil

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3
Q

Causes of mild eosinophilia:

A 
Inhalant allergies
Some worms
Radiation
Drug allergies
Splenectomy
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4
Q

Causes of moderate eosinophilia:

A

Visceral larva migrans
Trichinosis
Tropical eosinophilia

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5
Q

Causes of severe eosinophilia:

A

Visceral larva migrans
Tropical eosinophilia
Eosinophilic leukemia

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6
Q

Enterobius vermicularis life cycle:

A

WORLDWIDE DISTRIBUTION
Humans ingest infectious EGG.
Eggs hatch in small intestine and mature in the cecum.
The mature female crawls through the anus and deposits eggs on the perianal skin and dies.
The eggs become infectious within six hours.
These eggs may re-infect the individual or infect others in the vicinity (family, friends, etc.).

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7
Q

Enterobius vermicularis treatment:

A

Mebendazole (repeated treatments are necessary)

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8
Q

Ascaris lumbricoides life cycle:

A

Humans ingest infectious EGGS from fecal contamination.
Larvae hatch in small intestine, penetrate portal circulation.
Larvae migrate to lung capillaries, break into alveoli, and partially mature.
Larvae make their way up respiratory tree and are swallowed. They mature in the small intestine and begin producing eggs, which are excreted and become infectious in about 3 weeks.

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9
Q

Ascaris lumbricoides diagnostic stage:

A

Egg in feces.

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10
Q

Ascaris lumbricoides signs/symptoms:

A

Mild infections are usually asymptomatic.
Heavy infections present with malabsorption, intestinal obstruction, BILIARY obstruction, pancreatic obstruction, and hemorrhagic pneumonitis. EOSINOPHILIA may occur during migration through lung.

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11
Q

Ascaris lumbricoides in the US:

A

May be seen in the southwest. In New England, pig ascaris is most common, from pig contamination. It is generally asymptomatic and transient, but finding adult worms in the feces is alarming.

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12
Q

Ascaris lumbricoides treatment:

A

Mebendazole

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13
Q

*Ancylostoma duodenale and necator americanus (hookworms) life cycle:

A

Infectious larvae in soil or vegetation penetrate skin and enter blood.
Larvae exit from alveolar capillaries and partially mature in the alveoli.
The larvae migrate from the alveoli and travel to the GI tract, where they mature.
Adults release eggs, which hatch into infectious larvae in the environment.

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14
Q

*Ancylostoma duodenale and necator americanus (hookworms) diagnostic stage:

A

EGG in the feces

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15
Q

*Ancylostoma duodenale and necator americanus (hookworms) signs and symptoms:

A

Papule and erythema at site of entry (ground itch/dew itch).
May produce pulmonary symptoms with eosinophilia.
Chronic heavy infection may cause ANEMIA, which may lead to mental retardation in children.

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16
Q

*Ancylostoma duodenale and necator americanus (hookworms) treatment:

A

Mebendazole. Iron or transfusions for the anemia.

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17
Q

Strongyloides stercoralis PARASITIC life cycle:

A

WORLDWIDE DISTRIBUTION
Infectious larvae penetrate skin and enter bloodstream.
Larvae exit the bloodstream in the alveoli, and partially mature there.
The partially mature larvae ascend the respiratory tree and are swallowed.
Larvae mature into HERMAPHRODITIC adults.
Adults burrow into intestinal mucosa and begin laying eggs, which HATCH IN THE INTESTINE and are excretes in the feces.
The excreted larvae mature into infectious larvae.

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18
Q

Strongyloides stercoralis FREE-LIVING life cycle:

A

Excreted larvae mature into non-parasitic males and females, which mate and lay eggs. These eggs mature into non-infectious males and females, etc.
Larvae may become infectious and initiate human infection again.

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19
Q

Strongyloides stercoralis AUTOINFECTION life cycle:

A

Newly hatched larvae in the GI tract penetrate the intestinal wall or perianal skin and thus enter the bloodstream, travel to the lungs, etc.

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20
Q

Strongyloides stercoralis diagnostic stage:

A

Larva in the feces.

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21
Q

Strongyloides stercoralis signs and symptoms:

A

Many infections are asymptomatic.
With heavy infection, symptoms include skin and pulmonary problems, diarrhea, nausea, abdominal pain, and eosinophilia.
Patients with autoinfection have recurrent Gram-negative bacteremia resulting from E. coli or other enterics during penetration of intestinal mucosa (HYPERINFECTION).
STEROID THERAPY may produce hyperinfection.

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22
Q

Strongyloides stercoralis treatment:

A

IVERMECTIN is best (all infectious must be treated due to possibility of hyperinfection).
THIABENDAZOLE is also useful.

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23
Q

Visceral larva migrans life cycle:

A

Humans are ACCIDENTAL HOST.
Children consume embryonated dog or cat round worm eggs. Larvae penetrate the intestinal mucosa and enter the portal circulation.
The larvae exit at the liver and begin wandering through the tissues.

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24
Q

Visceral larva migrans signs and symptoms:

A

Many infections are asymptomatic.
Some present with eosinophilia, fever, and hepatomegaly.
Various organs have eosinophilic granulomata that surroun dead larvae. RETINAL INVOLVEMENT MAY MIMIC RETINOBLASTOMA. No eggs are present in the stool (life cycle is not completed).

25
Q

Visceral larva migrans treatment:

A

Albendazole (or diethylcarbamazine)

26
Q

Cutaneous larva migrans signs and symptoms:

A

Organisms form intracutaneous tunnels, with itching and inflammation. The larvae die within 2 months.

27
Q

Cutaneous larva migrans treatment:

A

Thiabendazole

28
Q

*Trichinella spiralis life cycle:

A

Humans eat undercooked pork (or bear) with encysted T. spiralis larvae in the muscle cells.
The larvae are released in the small intestine, invade the mucosa, and mature. The male fertilizes the females, who begins to release live larvae which enter the blood and are disseminated throughout the body.
Larvae enter cells of striated muscle and grow over 3 weeks.
Larvae are enclosed in a fibrous capsule of host cell origin. They die and are calcified within the next 2 years.

29
Q

*Trichinella spiralis diagnostic stage:

A

Larval form in muscle.

30
Q

*Trichinella spiralis signs and symptoms:

A

Mucosal invasion may produce diarrhea and gastroenteritis. Light infection may be mild or asymptomatic. Death results from invasion into tissues that do not produce encystment (heart and brain). Signs and symptoms include eosinophilia, periorbital edema, diplopia, muscle pain, headache, and fever.

31
Q

*Trichinella spiralis treatment:

A

Albendazole. Steroids may be useful.

32
Q

Wuchereria bancrofti life cycle:

A 
Intermediate host is the MOSQUITO. Infective larvae are injected into the mosquite bite wound, and travel to the LYMPHATICS, where they mature and release microfilariae.
Harmless microfilariae (first-stage larvae) circulate in the blood and infect biting mosquitos.
33
Q

Wuchereria bancrofti signs and symptoms:

A 
Causes ELEPHANTITIS (adult worms, not microfilariae). Light infection may be asymptomatic or cause rash.
TROPICAL PULMONARY EOSINOPHILIA is a rare, potentially fatal consequence (presents with pulmonary infiltrates).
34
Q

Wuchereria bancrofti treatment:

A

IVERMECTIN, diethylcarbamazine, or albendazole.

35
Q

Onchocerca volvulus life cycle:

A

Intermediate host is the BLACK FLY. Infective larvae are injected into the mosquite bite wound, and travel to the SUBCUTANEOUS TISSUES, where they mature and release microfilariae, which travel to the skin. Microfilariae are responsible for much of the pathology.

36
Q

Onchocerca volvulus signs and symptoms:

A

BLINDNESS, subcutaneous nodules at site of black fly bite, dermatitis and itching (microfilariae), eosinophilia.

37
Q

Onchocerca volvulus treatment:

A

Once-a-year ivermectin. Kills microfilariae, but not adult worms.

38
Q

Schistosome (blood flukes) life cycle:

A

Human skin is penetrated by free-swimming freshwater CERCARIAE.
Cercariae transform into larval worms, migrate to the lungs, and then to the hepatoportal system, where they further mature.
Finally, the enter the mesenteric venules (S. mansoni and S. japonicum) or bladder venules (S. haematobium) as MATED PAIRS and females lay eggs in the venules.
Some of the eggs make their way to the intestines, and are excreted in the feces (S. mansoni and S. japonicum) or urine (S. haematobium).
In fresh water, eggs hatch to yield a ciliated stage which infect snails and multiply extensively to yield many cercariae.

39
Q

Schistosome diagnostic stage:

A

EGG in feces, urine, or rectal biopsy. EGG is also pathogenic stage in tissue.

40
Q

Schistosome signs and symptoms:

A

KATAYAMA FEVER 3-6 weeks after exposure, presenting with fever, flu-like symptoms, hepatosplenomegaly, lymphadenopathy, and eosinophilia. Granulomas form around eggs that do not make it from the portal veins to the GI tract. Eggs trapped in the liver produce PIPESTEM fibrosis.
S. haematobium can lead to hydronephrosis (bladder obstruction) and SQUAMOUS CELL CARCINOMA of the bladder.
Most pathology is due to eggs, as the adult worms cloak themselves in normal human antigen.

41
Q

Schistosome treatment:

A

Praziquantel

42
Q

Schistosome dermatitis:

A

Caused by cercariae that cannot mature in humans. Cercariae die in the skin and cause itchy dermatitis. May be associated with salt water or fresh water exposure.

43
Q

*Tapeworm anatomy:

A

Scolex (head) - with site for attachment to mucosa
Neck - growth results in new reproductive segments (proglottids).
Proglottids - hermaphroditic. Mature along the length of the tapeworm (ones at end are most mature). Involved in egg production.

44
Q

*Tapeworm treatment:

A

Praziquantel

45
Q

*Taenia saginata (beef tapeworm) life cycle:

A

Humans ingest encysted larvae (cysticerci) undercooked beef. Larvae attach to intestinal wall and mature into 12 to 30 foot hermaphroditic adults.
Mature proglottids containing 50,000 - 100,000 eggs are passed in the feces.
The intermediate host (cow) ingests the eggs. The larvae hatch, penetrate the intestinal wall, and become encysted in MUSCLE as larvae (cysticerci).

46
Q

*Taenia saginata (beef tapeworm) diagnostic stage:

A

Mature proglottid in the feces.

47
Q

*Taenia saginata (beef tapeworm) signs and symptoms:

A

None. Patients may notice passage of a proglottid in the feces or feel the movement of a multi-proglottid segment.

48
Q

*Taenia solium (pork tapeworm) life cycle:

A

Humans ingest encysted larvae (cysticerci) undercooked pork. Larvae attach to intestinal wall and mature into 12 to 30 foot hermaphroditic adults.
Mature proglottids containing 50,000 - 100,000 eggs are passed in the feces.
The intermediate host (pig) ingests the eggs. The larvae hatch, penetrate the intestinal wall, and become encysted in MUSCLE as larvae (cysticerci).
IF HUMANS INGEST THE EGGS, CYSTICERCI FORM IN THE TISSUES (CYSTICERCOSIS), WHICH CAN BE LIFE-THREATENING.

49
Q

*Taenia solium (pork tapeworm) diagnostic stage:

A

Mature proglottid in the feces. Free eggs may also be seen.

50
Q

*Taenia solium (pork tapeworm) signs and symptoms:

A

Usually none, unless cysticercosis develops. Cysticercosis can damage the brain (causing epilepsy), heart, or eye. Presents as calcified cysts on radiologic imaging of the brain.

51
Q

*Taenia solium (pork tapeworm) treatment:

A

Praziquantel. Treatment is mandatory, due to possibility of cysticercosis.

52
Q

*Diphyllobothrium latum (fish tapeworm) life cycle:

A

Humans ingest raw freshwater fish containing encysted larvae.
Larvae attach to small intestine and grow to maturity.
Mature proglottids release eggs that are excreted in the feces.
In fresh water, the egg hatches into a ciliated stage.
The ciliated stage is eaten by a copepod (small crustacean), which is eaten by a fish. The fish is then consumed by a human.

53
Q

*Diphyllobothrium latum (fish tapeworm) diagnostic stage:

A

Egg in the feces.

54
Q

*Diphyllobothrium latum (fish tapeworm) signs and symptoms:

A

B12 deficiency and diarrhea.

55
Q

*Echinococcus granulosus (dog tapeworm) life cycle:

A

Humans are accidental hosts.
Humans ingest eggs from contamination with dog feces, and early stage larvae form slowly-growing cysts containing many larval scolices (asexual multiplication).
The cysts are called HYDATID CYSTS, and scolices are called HYDATID SAND.

56
Q

*Echinococcus granulosus (dog tapeworm) signs and symptoms:

A

Usually asymptomatic. Calcified cysts (usually in liver or lung) are visible on X-ray. Enlargement of cysts in the liver can cause pain. Pulmonary cysts may cause cough and dyspnea. A RUPTURED CYST MAY PRECIPITATE ANAPHYLACTIC SHOCK.

57
Q

*Echinococcus granulosus (dog tapeworm) treatment:

A

Excision of cysts followed by sterilization with ethanol to prevent initiation of new cysts by scolices that happen to be released.

58
Q

*Echinococcus multilocularis (dog/fox tapeworm) signs and symptoms:

A

Cysts are multi-compartment alveolar cysts that give rise to metastatic growth at distant sites in the body (lung and brain).

SBM: ID (27 decks)

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