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Fungi, Parasites & Vector-borne infections > Parasitology > Flashcards

Parasitology Flashcards

1
Q

Tx for Strongyloides

A

Ivermectin

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2
Q

Tx for parasitic worms (except Strongyloides)

A

Albendazole

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3
Q

Dx of chronic Strongyloides (asymptomatic)

A

Serology

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4
Q

What are the main components of the Th2 immune profile?

A

IL-4, IL-5, Eosinophils, IgE

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5
Q

Which virus is associated with hyperinfection (reactivation) of latent Strongyloides?

A

HTLV-1

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6
Q

What is the organism commonly known as Pinworm ?

A

Enterobius vermicularis

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7
Q

What is the life cycle of Enterobius vermicularis ?

A

Ingest eggs. Eggs hatch in proximal duodenum. Larvae migrate to ileum to become adults and copulate. Gravid (pregnant) females migrate to the rectum. At night, females exit through the anus and induce pruritus (itching). Host’s nails tear the female apart, liberating eggs which are ingested and the cycle repeats.

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8
Q

What is the classic diagnosis of Enterobius vermicularis?

A

Scotch tape test (scotch tape on the anus in the morning or at night to reveal adult female worms).

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9
Q

Tx for Enterobius vermicularis (pinworm)?

A

Albendazole

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10
Q

What is the nematode commonly known as whipworm?

A

Trichuris trichuria

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11
Q

What is the life cycle of Trichuris trichuria (whipworm)?

A

Eggs are ingested from contaminated soil. Eggs hatch, larvae mature in GI tract. Anterior portion of nematode embeds itself in an epithelial syncytium and releases eggs into the lumen. Eggs are shed in the feces to incubate in soil for 2 weeks. Adult worms may persist in intestines for years.

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12
Q

Symptoms of Trichuris whipworm ?

A

GI mucosal inflammation (local eosinophilia). Mucosal bleeding. Heavy infection can cause prolapse, at which point worms can be visible.
Heavy infection is associated with dysentery and low iron anemia. Also clubbing of fingers.

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13
Q

Trichuris trichuria (whipworm) diagnosis ?

A

Stoof for ova and parasites

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14
Q

What is the largest intestinal nematode ?

A

Ascaris lumbricoides. Females up to 40 cm long.

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15
Q

What causes asthma-like symptoms in Ascaris infection?

A

Larvae migrating through the lungs cause eosinophilic inflammation and hypersecretion of mucous. Infiltrates on CXR.

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16
Q

What is the most serious complication of Ascaris infection?

A

Bowel obstruction from a bolus of adult worms. Children are especially at risk. Other obstructions are possible (e.g. bile duct, pancreatic duct, appendicitis, bile duct perforation with peritonitis).

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17
Q

Diagnosis for Ascaris lumbricoides?

A

Stool for ova and parasites reveals characteristic ova.

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18
Q

Tx for Ascaris lumbricoides?

A

Albendazole

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19
Q

What are the two species known as Hookworm?

A

Necator americanus and Ancylostoma

duodenale.

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20
Q

What is the lifecycle of Hookworms?

A

Eggs are passed in feces into soil.
They hatch to liberate larvae which infect host through skin of barefeet.
Migration from skin to bloodstream to lungs (perforate alveoli) through respiratory tract up trachea, down esophagus into GI tract where they attach to mucosa, suck blood, and mature to adults and lay eggs.

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21
Q

Clinical manifestation of Hookworm infection?

A 
Local dermatitis (under feet).
Asthma like symptoms when larvae pass through lungs.
Peptid-ulcer like symptoms when larvae attach to GI mucosa.
Hallmark of chronic hookworm infection is iron deficiency anemia, which results in chronic fatigue, lassitude, apathy.
Cardiac symptoms (palpitations, sinus tachycardia) are common.
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22
Q

Diagnosis and treatment for Hookworm?

A

Stool for ova and parasites reveals characteristic ova.

Tx is albendazole (how to treat pregnant women?)

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23
Q

What is the life cycle of Ascaris lumbricoides?

A

Eggs are ingested and hatch in the Jejunum. Larvae pierce through the intestinal wall, and migrate via the hepatic venules to the right side of the heart where they enter pulmonary circulation. They perforate the alveoli and climb up the respiratory tract to be swallowed down into the esophagus and into the intestine where they become adults. From ingested eggs to egg producing adults takes 10-12 weeks.

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24
Q

What is the life cycle of Strongyloides stercoralis?

A

Filariform (infectious) larvae from contaminated soil pierce host skin and enter the bloodstream until they reach the lungs which they perforate. They ascend the respiratory tract, are swallowed and descend into the GI tract. In the intestines, they mature to adults which produce rhabditiform (non-infectious) larvae which are excreted in the feces. The transition from rhabditiform to filariform (non-infectious to infectious) larvae usually occurs in the soil but auto-infection in humans can occur when rhabditiform larvae manage to transform rapidly into filariform larvae. The process repeats ad nauseam and the infection lasts the lifetime of the host.

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25
Q

Clinical manifestation of acute strongyloides infection?

A

1) Dermatitis at site of skin perforation and initial migration (larva currens)
2) Epigastric abdominal pain / diarrhea when adults perforate the intestine.
3) Respiratory symptoms when larvae pierce through alveoli.

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26
Q

Describe chronic persistent Strongyloidiasis in immunocompetent individuals?

A

Chronic persistent strongyloidiasis is generally asymptomatic. Patients have high peripheral eosinophilia (> 250 IU/ml).

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27
Q

Who is at risk for Strongyloides hyperinfection syndrome?

A

HTLV-1 infected patients (#1), immunocompromised patients, patients using steroids. Generally, inactivation of the Th2 immune profile results in hyperinfection.

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28
Q

What is the pathophysiology of Strongyloides hyperinfection syndrome?

A

Loss of immune function leads to uncontrolled conversion of Rhabditiform larvae to Filariform (infectious) larvae which disseminate widely to any organ. Penetration of large numbers of larvae through the intestinal wall may result in bacterial sepsis.
Extensive lung damage is also common (bronchospasm, cavitation, alveolar hemorrhage).

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29
Q

Is strongyloides hyperinfection syndrome dangerous?

A

86% mortality rate.

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30
Q

Diagnosis of Strongyloidiasis ?

A

Acute:
Stool for ova and parasites. Or serology.

Chronic persistent:
Serology (due to low egg count).

Hyperinfection:
Stool or sputum show large numbers of ova and parasites.

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31
Q

Who should be screened for asymptomatic chronic strongyloides?

A

Patients at-risk (geographically) for Strongyloides infection who are:

1) newly diagnosed with HTLV-1
2) about to begin steroids
3) transplant candidates

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32
Q

Tx for strongyloides?

A

Ivermectin

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33
Q

What is cutaneous larva migrans?

A

Cutaneous larva migrans is the dermatitis caused by the migration of nematode larvae.

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34
Q

Which nematode species accounts for the majority of cutaneous larva migrans cases?

A

Anyclostoma braziliense and caninum (hookworms) account for most cases of larva migrans.

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35
Q

What is the life cycle of Ancylostoma braziliense and caninum (cutaneous larva migrans hookworms)?

A

The life cycle plays out in the dog or cat. Eggs are released in the feces which hatch into rhabditiform larvae and can become filariform (infective) larvae which penetrate the human epidermis but don’t move to deeper tissues. Humans are an aberrant host.

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36
Q

What is a definitive host?

A

A definitive host is a host in which the parasite matures and reproduces.

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37
Q

Clinical manifestation of Cutaneous Larva Migrans?

A

Inflammation and pruritus. Tracks of larva migrans are visible as encrusted and scarred tissue.

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38
Q

Diagnosis of larva migrans caused by cat/dog hookworm?

A

Clinical presentation and history.

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39
Q

Tx of larva migrans?

A

Albendazole (or ivermectin).

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40
Q

What nematode species cause Visceral Larva Migrans (VLM) and Ocular Larva Migrans (OLM)?

A

Toxocara caniis (toxocariasis) and Toxocara cati.

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41
Q

How is Toxocara transmitted from cats and dogs to humans?

A

Toxocara eggs are shed in the feces and ingested by humans. The eggs hatch in the host intestine and migrate to the liver. They can travel to numerous organs, including the lung.

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42
Q

What disease manifestation is most common in young children with Toxocariasis?

A

Hepatitis as larvae migrate through liver, with hepatomegaly.
Pneumonitis as larvae migrate through lungs, with pulmonary infiltrates.
Lymphadenopathy, fever, and eosinophilia are present.

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43
Q

Diagnosis of Toxocariasis?

A

Serology (ELISA)

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44
Q

Treatment of Toxocariasis?

A

Most commonly Albendazole.

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45
Q

What is the primary target organ of Baylisascaris procyonis (Baylisascariasis)?

A

Baylisascaris primarily targets the CNS and eye.

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46
Q

What animal sheds Baylisascaris in its feces?

A

The raccoon.

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47
Q

What is the serious complication associated with Baylisascariasis?

A

Eosinophili Meningoencephalitis (>50% of cases).

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48
Q

Diagnosis of Baylisascariasis?

A

Serology performed by CDC, and detection of typical larvae in tissues.

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49
Q

What is the treatment for Baylisascariasis?

A

There is no current treatment.

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50
Q

What region is Loa loa endemic to?

A

West and Central African rainforests.

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51
Q

In what tissues does Loa loa migrate?

A

In subcutaenous tissues and across the eye (eye worm).

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52
Q

At what time are microfilaria larvae found in the peripheral blood?

A

At noon.

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53
Q

How is Loa loa transmitted?

A

The Chrysops fly picks up the larvae from human peripheral blood (fly feeds at noon). The larvae become infective in the fly and are transmitted to a new host to become adults.

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54
Q

What is the most serious complication of Loiasis?

A

High numbers of microfilaria in peripheral blood may lead to eosinophilic meningoencelephalitis, especially following treatment with DEC (Diethylcarbamazine).

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55
Q

Treatment of Loa loa?

A

DEC (Diethylcarbamazine). Be careful not to cause meningoencephalitis.

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56
Q

Diagnosis of Loaisis?

A

Microscopic examination revealing microfilaria, or identification of the adult worm removed from subcutaneous tissue / eye.

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57
Q

What nematode causes “river blindness”?

A

The nematode Onchocerca volvulus causes onchocerciasis or river blindness.

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58
Q

How is Onchocerca transmitted?

A

By the bite of a black fly (Simulium).

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59
Q

Where is Onchocerciasis found?

A

Worldwide distribution including Central

Africa, the northern part of South America, and the Arabian Peninsula.

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60
Q

What is the life cycle of Onchocerca volvulus?

A

Black fly bite transmits larvae to host skin. Larvae mature to adults inside of subcutaneous nodules. Gravid females produce thousands of tissue-invading microfilariae daily which invade skin, eyes and subcutaneous tissues.

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61
Q

What are some classic clinical manifestations?

A

Itching and dermatitis. Potentially palpable nodules over bony prominences (e.g. iliac crests).
Inguinal lymphadenopathy which progresses to fibrosis of lymph nodes, lymphedema and genital elephantiasis.

62
Q

Diagnosis of Onchocerciasis?

A 
Skin-snip (gold standard).
Slit-lamp examination of the eye
Ultrasound of nodules
Antigen testing (serology)
PCR (not widely available)
63
Q

Tx of Onchocerciasis?

A

Ivermectin for microfilariae

+ Doxycycline for Wolbachia symbiotic bacteria.

64
Q

What nematode causes Bancroftian filariasis?

A

Wuchereria bancrofti

65
Q

What is the life cycle of W. bancrofti?

A

Mosquito bite transmits infective larvae, which develop into adults in lymph vessels and release microfilariae which enter the bloodstream and are picked up by mosquitoes.

66
Q

What is the clinical manifestation of Bancroftian filariasis?

A

Early on, acute episodes of (retrograde) lymphangitis.

This results in lymphatic insufficiency, lymphedema and elephantiasis. Hydrocele.

67
Q

Dx of Bancroftian filariasis?

A

Immigrants in US: Serology (because adults died off, no longer producing microfilariae).
Endemic area: Presence of microfilaria on blood smear at night (since mosquito born).

68
Q

1) Tx of Bancroftian filariasis?

2) Special consideration for Tx?

A

1) DEC

2) Suspected co-infection with Onchocerca (in parts of Africa).

69
Q

Which nematode is ingested through undercooked pork meat?

A

Trichinella spiralis (Trichiniasis).

70
Q

What is the clinical manifestation of Trichiniasis?

A

Phase 1: Enteric symptoms (1 wk).

Phase 2: Parenteral (systemic) (fever, myalgia, periorbital edema, eosinophilia).

71
Q

Dx of Trichiniasis?

A

Serology

72
Q

Tx of Trichiniasis?

A

Albendazole

73
Q

What is the main symptom of D. latum (tapeworm)?

A

Most infected hosts are asymptomatic but some may develop megaloblastic anemia (lack of B12 absorption). Other symptoms result from the anemia.

74
Q

How is D. latum transmitted to the host?

A

Via ingestion of contaminated shellfish and fish (freshwater).
Thorough cooking of fish eliminates all risk of contamination.

75
Q

Dx and Tx of D. latum?

A

Stool for Ova and Parasites.

Praziquantel.

76
Q

What is the pork tapeworm?

A

Taenia solium

77
Q

What is the beef tapeworm?

A

Taenia saginata

78
Q

What is the life cycle of Taenia tapeworms?

A

Cattle/pigs ingest eggs from human feces while grazing. Eggs hatch larvae which penetrate into muscle tissue (cysticercus). Humans ingest the larvae and constitute the definitive host. In host, larvae attach to intestinal mucosa and mature into adult tapeworm, releasing eggs.

79
Q

What are symptoms of regular (adult) tapeworm infection?

A

Most infections are asymptomatic except for psychological impact of visualizing proglottids in feces, feeling tapeworm move in anus, or witnessing the tapeworm exit the anus momentarily.

80
Q

What is a serious complication of tapeworm infection?

A

(Neuro)-cysticercosis infection with larvae (from eggs) migrating to the CNS.

81
Q

When can neurocysticercosis fatal?

A

When the extraparenchymal tissue is involved (subarachnoid and ventricular spaces), resulting in hydrocephalus.

82
Q

Dx and Tx of cysticercosis?

A

History, CAT, MRI, serology. Albendazole +/- Praziquantel.

83
Q

When do you do a serology rather than use another diagnostic?

A

1) Chronic infection (strongyloides)
2) Intermediate host (Trichinella)
3) Can’t access the parasite (CNS - Baylisascaris)

84
Q

What is Tropical Pulmonary Eosinophilia?

A

Immunological hyperresponse to W. bancrofti microfilariae.

85
Q

Dx of Tropical Pulmonary Eosinophilia?

A

Serology (microfilariae not seen in circulation, not accessible). (Bancrofti).

86
Q

What species of Schistosome causes blood in urine?

A

S. haematobium

87
Q

What causes pathology in schistosomiosis?

A

The host immune response to the eggs which become granulomas.

88
Q

Where do S. japonicum and S. mansoni eggs accumulate?

A

In the intestines (superior mesenteric veins for S. mansoni) and liver (inferior mesenteric and superior hemorrhoidal veins for S. japonicum).

89
Q

How does one get infected with Schistosomes?

A

By wading in contaminated water. The larvae penetrate the host skin.

90
Q

Where do the Schistosome larvae mature into adults and pair up as sexual couples?

A

In the hepatic portal venous system.

91
Q

How long do adult schistosomes live attached to blood vessels?

A

3-5 years.

92
Q

Signs and symptoms of acute schistosomiasis?

A

Phase 1: “Swimmer’s itch” - a pruritic urticaria (hives).
A particularly strong rash follows infection with avian schistosomes which don’t penetrate past the skin (larvae die in human skin, activating a strong inflammatory response).
Phase 2: Katayama fever syndrome, when adults mature and begin laying eggs (1-3 months post infection)

93
Q

What is the pathophyisiology of chronic schistosomiasis?

A

Granuloma formation and fibrosis around the eggs.
Inflammation can cause blood in stool or urine.
Complications follow.

94
Q

1) Describe the liver damage seen in chronic schisto with eggs embolized to the liver.
2) Do patients have jaundice ? Icteric sclera or nailbeds?

A

1) Eggs in liver -> Granuloma / fibrosis -> obstruction of blood flow -> peri-portal HTN -> varices / variceal bleeding.
2) No. LFTs are normal. The liver function is maintained (no damage to hepatocytes).

95
Q

What are some of the common varices (or sites of anastomoses) that result from portal HTN ?

A

Esophageal varices, rectal varices (hemmorhoids), paraumbilical (caput medusa), retroperitoneal (ascites).

96
Q

1) Dx of schistosomiasis?

2) Dx of Acute schisto?

A

1)
- Stool / Urine for Ova.
- Biopsy (if signs and symptoms but no eggs in stool / urine).
- Fast Elisa from CDC (but can’t distinguish between past and present infection.
2) Serology

97
Q

Tx of Schistosomiasis?

A

Praziquantel

98
Q

What is the Dx for acute phase Fasciolitis?

A

Serology (no eggs present yet since larvae have not matured).
Chronic fascioloitis can be diagnosed with Stool for O&P.

99
Q

Symptoms of acute (invasive) fasciolitis?

A

Abdominal pain, malaise, hepatomegaly, high eosinophilia, fever, urticaria. Lasts 2-4 months.

100
Q

Tx for Fasciolitis?

A

Triclabendazole

101
Q

How does one contract a Fasciola hepatica infection?

A

Ingestion of water plants (watercress).

102
Q

Is abnormal LFTs (and jaundice) common for acute or chronic Fasciolitis?

A

Chronic.

103
Q

What do pseudo-polyps in intestine suggest?

A

Schisto egg granuloma and fibrosis in intestine.

104
Q

Complication of S. haematobium?

A

Renal failure. Squamous cell carcinoma (controversial association).

105
Q

How do you get paragonomiasis?

A

Undercooked crustacean (infective larvae).

106
Q

Where do paragonimus larvae migrate to? What disease does it mimic?

A

The lung. It mimics TB (bloody sputum, cavitary lesions).

107
Q

Dx of paragonomiasis?

A

Sputum for O&P

108
Q

Tx of paragonomiasis?

A

Praziquantel (for flukes, except Fasciola h.)

109
Q

When do you ask for a sputum for O&P?

A

Strongyloides hyperinfection or paragonomiasis.

110
Q

How do you get echinococcus?

A

Sheep eating dog poop.

111
Q

What do you use PAIRS (liver aspiration) for?

A

echinococcal infection: cyst with no daughter cysts (CE1 stage or CE3a stage). This is aspiration.

112
Q

What are complicated cysts (daughter cysts inside of cysts)? How do you treat?

A

Echinococcus.

Treat with surgery.

113
Q
  1. What is the vector for Chagas?

2. What is the name of the protozoa that causes Chagas disease?

A
  1. Redjuviid bug. It bites, then poops in the bite.

2. Trypanosoma cruzi.

114
Q

Early signs of Chagas?

A

Chagoma (lesion at skin bite) or Romana’s sign (unilateral eye edema)

115
Q

Dx of acute chagas?

A

Blood smear with trypanosomes.

116
Q

Dx of chronic chagas?

A

Serology.

117
Q

How do you treat chagas?

A

Nifurtimox, Benzidazole. Bad side effects (Neuropathy, Bone marrow suppression…)

118
Q

Other modes of transmission for Chagas?

A

Congenital
Blood transfusion
Organ transplantation

119
Q

What are organ specific terminal complications of Chagas?

A

Chagas cardiomyopathy.

Megacolon.

120
Q

What are the two types of Leishmaniasis?

A

Cutaneous and Visceral.

121
Q

What differentiates the types?

A

The species (and to some extent the Cell Mediated Immunity of the patient).

122
Q

Dx of visceral leishmaniasis ?

A

Special media culture at CDC of bone marrow biopsy, or liver aspirate.

123
Q

Which kind of cutaneous leishmaniasis can metastasize?

A

New world species.

124
Q

Tx of leishmaniasis?

A

New world: amphotericin B

Old world: topical paromomycin

125
Q

Vector for leishmaniasis?

A

Sand fly

126
Q

What are the specific characteristics of the cutaenous lesion of Leishmaniasis?

A

Painless,

127
Q

Acute toxoplasmosis Dx?

A

IgM serology

128
Q

Describe the serology of chronic toxoplasmosis in immunocompetent hosts?

A

IgG serology (no IgM)

129
Q

Differential diagnosis for a ring enhancing lesion and encephalopathy?

A

Toxoplasmosis or Lymphoma.

Lymphoma usually has a single ring enhancing lesion, Toxoplasmosis can have multiple.

130
Q

Main symptom of Giardia lambila?

A

Chronic non bloody diarrhea

131
Q

Dx of Giardia?

A

Stool for O&P

132
Q

What causes an intermittent diarrhea (with constipations) and extreme fatigue?

A

Cyclospora

133
Q

What is the Tx for Cyclospora?

A

Trimethoprim-sulfamethoxazole

134
Q

How do you get Cyclospora?

A

Ingestion of (fecally) contaminated produce.

135
Q

What is the name of the invasive intestinal ameba?

What differentiates it from non-invasive species (e.g. E. dispar)?

A

Entameba hystolytica (lysis) has a Lectin that allows attachment and invasion of host cells.

136
Q

How does one get infected with E. hystolytica?

A

Ingestion of (fecally) contaminated water/food. The contagious form of E. hystolytica is in cysts.

137
Q

What is the name of the invasive form of E. hystolytica?

A

The trophozoite form.

138
Q

What is the pathophysiology of E. hystolytica?

A

Trophozoite form can phagocytose RBCs, releases proteolytic enzymes and selectively lyses WBCs.
This causes necrosis, ulcer formation,

139
Q

What is the treatment for E. hystolytica ? (distinguish Tx against cysts and trophozoites).

A

Trophozoite: Metronidazole
Cyst: Paromomycin

140
Q

What parasitic infection is Dientameba fragilis associated with?

A

Pinworm (Enterobius vermicularis), so perform scotch-tape test after D. fragilis Dx.

141
Q

What is the Dx of D. fragilis?

A

Stool for O&P

142
Q

What are symptoms of D. fragilis?

A

Mostly asymptomatic. GI upset, diarrhea, abd. pain, fatigue.

143
Q

What is the transmissible form of Giardia?

A

The cyst form.

144
Q

What is the pathogenesis of Giardia?

A

Trophozoite form attaches to brush border cell, results in malabsorption and diarrhea. Eventually, foul-smelling, fatty diarrhea.

145
Q

Tx for Giardia lambila?

A

Most infections are self-limited. If persisting, treat with metronidazole.

146
Q

Which parasite was responsible for the Milwaukee outbreak due to poor water supply sanitation (fecally contaminated drinkinng water)?

A

Cryptosporidium parvum

147
Q

Dx and Tx for Cryptosporidium?

A

Acid-Fast stain of Stool.

Tx: Selt-limited or Nitazoxanide

148
Q

Dx and Tx for Cyclospora?

A

Acid-Fast stain of Stool.

Tx: Trimethoprim-sulfamethoxazole

149
Q

Tx for uncomplicated malaria in the US (CDC) ?

A

Artemisin Combination Therapy

150
Q

Tx for severe malaria (falciparum) in the US (CDC)?

A

Quinidine + Quinolone

151
Q

WHO Tx guidelines for uncomplicated malaria ?

A

Artemisin Combination Therapy

152
Q

WHO Tx guidelines for severe malaria ?

A

Artesunate (IV or IM)

Fungi, Parasites & Vector-borne infections (6 decks)

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