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GI- Week 5 > Zimmer: GI parasites > Flashcards

Zimmer: GI parasites Flashcards

1
Q

What are common features of GI parasites?

A

Infections are commonly long lasting or chronic (or have the potential to become so)

Malnutrition a common feature of chronic parasitic GI infections–>Childhood malnutrition

Infected individuals are often asymptomatic

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2
Q

GI parasite related morbidity and mortality depend on:

A

parasite burden
species
preexisting community
pt comorbidities

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3
Q

Why is the rate of parasitic infection increasing in the US?

A

international travel
immigration
children in day care
AIDS and the immunocompromised

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4
Q

What is a key way to prevent parasites?

A

Adequate disposal and treatment of human waste
Adequate treatment of drinking water
Hand washing, food washing

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5
Q

What are the three most prevalent GI protozoan parasites in the US?

A

Giardia- Giardiasis
Cryptosporidium – “Crypo”
Entamoeba – Amebiasis

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6
Q

How are protozoan GI parasites transmitted?

A

Water-borne

Ingesting cysts or oocysts

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7
Q

How do protozoan GI parasites affect individuals?

A

Usually NOT serious for healthy individuals

  • do not tx w/ drugs
  • some ppl may be assymptomatic
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8
Q

What is the most common intestinal parasite in the US?

A

Giardia lamblia (foe of backpackers and hikers)

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9
Q

What are the sxs of giardia lamblia?

A

sxs for 1-2 weeks or more>

resolve then come back

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10
Q

What is the mechanism for giardia lamblia?

A

presence of parasite>

loss of epithelial absorptive surface area

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11
Q

How can you positively dx giardia lamblia?

A

Trophozites and cysts in fecal matter

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12
Q

A pt presents w/ FOUL SMELLING diarrhea, flatulence, greasy/floaty/fatty stools and malabsorption of lipids and vitamins.

A

Giardia Lamblia

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13
Q

How do you prevent giardia lamblia?

A

filter water in areas where giardia cysts are likely to exist

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14
Q

When do you often see cystosporidium parvum?

A

When a sanitation system fails

  • pool/waterpark chlorination/UV tx
  • storms or issues w/ drinking water
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15
Q

What sxs are associated w/ cryptosporidium parvum?

A

diarrhea sxs for 1-2 wks but up to 30 days!

Sxs will resolve then come back.

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16
Q

How does c. parvum cause illness?

A

Epithelial cells infected by cryptosporidium>

impaired absorption and enhanced secretion

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17
Q

What type of infection is c. parvum?

A

opportunistic

HIV/Immunocompromised individuals
Chronic Diarrhea/fluid loss
Can be fatal

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18
Q

What is the diff dx for c. parvum?

A

WATERY, non bloody stool

sometimes fever

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19
Q

Describe the life cycle of c. parvum.

A

Disrupts epithelial microvilli>
slides into host cells>
envelopes itself in the host cell membrane

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20
Q

How do you dx c. parvum?

A

Acid fast stained oocycts in feces

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21
Q

What subclass does c. parvum belong to?

A

coccidia

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22
Q

What two other coccidia also cause human GI infection?

A 
Cystoisospora belli (formerly Isospora belli)
Cyclospora cayetanensis
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23
Q

Cyclospora caytetanesis

A

?

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24
Q

What does e. histolytica cuase?

A

amebiasis

AKA Amebic Dysentery, Amebic liver abscesses

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25
Q

Where is e. histolytica most prevalent?

A

tropical/subtropical climates

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26
Q

What percent of individuals infected w/ e. histolytica become ill?

A

10-20%

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27
Q

Of the US population, who is most vulnerable to e. histolytica ?

A

male homosexuals

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28
Q

What is the diff dx for e. histolytica ?

A

BLOODY MUCUSEY loose stool

relatively mild sxs BUT can invade liver and form an abscess (xray/ultrasound to detect damage)

*MUST DIFFERENTIATE SXS FROM BACILLARY DYSENTERY

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29
Q

How do you dx e. histolytica?

A

Cysts in stool sample.

Must differentiate from non-pathogenic entamoeba, takes a specialist.

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30
Q

Describe the life cycle of e. histolytica.

A

Cysts in water>
cysts become trophozoites (excystation) in sml intestines>
trophozoites migrate to the colon>
cysts and trophozoites found in fecal matter

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31
Q

How does e. histolytica do in the large intestine?

A

Cytotoxic! Maximally tissue-invasive
Adhere and kill
Phagocytose

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32
Q

What happens when e. histolytica invades mucosal cells?

A

mucosal cell invastion: results in replication> cysts in feces

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33
Q

What happens when mucosal cell invastion: results in replication> cysts in feces invades blood vessels?

A

Amebic hepatitis= single abscess in right lobe; should present w/ right upper quadrant pain, fever, weight loss

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34
Q

What class do metronidazole and tinidazole belong to?

A

nitroimidazoles

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35
Q

What is the spectrum of metronidazole and tinidazole?

A

Effective against Giardiasis, Amebic dysentery, also anaerobic GI bacteria, NOT Cryptosporidium

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36
Q

How are Metronidazole and Tinidazole distributed?

A

TISSUE antiparasitic- low concentration in intestine, oral dose almost completely absorbed with high bioavailability

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37
Q

What is hte MOA of nitroimidzoles?

A

drug breakdown>
toxic metabolites generate free radicals>
induce DNA strand breakage

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38
Q

What is the toxicity of nitromidazoles?

A

Disulfiram reaction, avoid alcohol

Nausea, diarrhea, metallic taste common

Disturb normal GI flora!

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39
Q

What is the spectrum of nitazoxanide?

A

Giardiasis and Cryptosporidosis

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40
Q

How is nitazoxanide used in immunocompromised pts?

A

Crypto often not treated in immunocompetent hosts, but Nitazoxanide effectiveness goes down in this pop

If AIDS pt has crypto- used in combination with retroviral therapy for AIDS patients if at all, because of ineffectiveness

Anti-peristaltic agents (Loperamide) and oral rehydration is important

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41
Q

How is nitazoxanide distributed?

A

Rapidly metabolized to tizoxanide. Parent compound is not detected in plasma. Moderately absorbed (33%), primarily luminal

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42
Q

What is the toxicity of iodoquinol?

A

loss of visual acuity, use caution in patients with thyroid disease

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43
Q

What is the distribution of iodoquinol?

A

only 10% of the drug is absorbed so it works locally on the protozoa including cysts in the GI tract, luminal antiparasitic (amebicide)

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44
Q

What is the spectrum of iodoquinol?

A

Amebic dysentery

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45
Q

What is the mechanism of paromomycin?

A

Aminoglycoside- targets 30S subunit ribosome

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46
Q

What is the toxicity of paromomycin?

A

Diarrhea, other GI effects including issues with intestinal flora because it has activity against some bacteria.

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47
Q

What is hte distribution of paromomycin?

A

Luminal antiparasitic- Minimal absorption after oral administration

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48
Q

What is the spectrum of paromomycin?

A

Intestinal protozoa, but only partially effective against Cryptosporidium.

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49
Q

Why do we need to consider absorption and tissue distribution?

A

Entamoeba histolytica destroys tissue

A symptomatic infection means organism has invaded tissue, but also still at lumen

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50
Q

What are luminal amebicides?

A

iodoquinol or paromomycin

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51
Q

What are tissue amebicides?

A

metronidazole

tinidazole

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52
Q

What is TMP-SMX used for?

A

Broad spectrum, many bacteria, but also effective against apicomplexans including Toxoplasma and Cystoisospora (formerly Isospora), and Cyclospora

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53
Q

What is the mechanism of TMP-SMX?

A

Synergistic action

??

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54
Q

What is the selectivity of TMP-SMX?

A

differential action of Trimethoprim action on protozoan/bacterial dihydrofolate reductase vs human isozyme

55
Q

What is the toxicity of TMP-SMX?

A

Well-tolerated by many patients
Crosses blood-brain barrier, neurological side effects are possible
High potential to interfere with intestinal flora
Rapid cell growth during pregnancy potentiates the drug’s antifolate effect in humans

56
Q

What helminths cause intestinal sxs?

A

nematodes- round worms

cestodes- tapeworms

57
Q

What is enterobius vermicularis?

A

A round worm that is staple size and causes enterobiasis (pinworm infection)

58
Q

What is the MC helminth infection in the US?

A

E. vermicularis

59
Q

What causes PERIANAL PRURITIS, insomnia, abbdominal pain, anorexia and irritabiilty?

A

e. vermicularis

60
Q

How do you acquire e. vermicularis?

A

ingestion of pinworm eggs (can remain viable on surfaces for 2-3 wks)

*day cares

61
Q

Describe the life cycle of e. vermicularis.

A

Embryonated eggs ingested by a human>
larvae hatch in sml intestine>
adults enter lumen of cecum>
gravid F migrates to perianal region at nigh to lay eggs>
eggs on perianal folds>
larvae mature w/in 4-6 hrs>
eggs are released into environment OR retroinfection occurs after anal eggs hatch and larvae crawl back in

62
Q

How long does it take from egg ingestion of e. vermicularis to adult males and females?

A

1-2 mos

Adults live about 2 mos

63
Q

What is the diff dx for e. vermicularis?

A

anal itching

64
Q

How do you confirm e. vermicularis?

A

Appearance of worms 2-3 hrs after person is asleep

A.M. Scotch tape method to pick up eggs from perianal region
Sample from under fingernails

Eggs will likely NOT be found in stool sample!

65
Q

What is a pinworm paddle?

A

A way to obtain eggs from e. vermicularis

66
Q

What soil transmitted roundworms are found in the southern US?

A

Hookworms (Necator)

Whipworms (Trichuris)

67
Q

Where are giant roundworms (ascaris) found?

A

rarely in the US

68
Q

What soil transmitted roundworms are found in large north american cities and the southern US?

A

strongyloides

69
Q

What environment do soil transmitted round worms like?

A

places where human feces is used as fertilizer

warm, humid climates

70
Q

What soil transmitted roundworms enter the human body by skin pennetration?

A

Necator – Skin penetration
9-11 mm (small staple size)

Strongyloides – Skin penetration
a few mm

71
Q

What soil transmitted roundworms enter the human body by egg ingestion?

A

Trichuris – Egg ingestion
3-5 cm

Ascaris – Egg ingestion
15-40 mm (spaghetti, a ruler)

72
Q

What causes hookworm and strongyloidiasis?

A

Necator americanus/Ancylostoma duodenale and Strongolides stercoralis

73
Q

How do you dx Necator americanus/Ancylostoma duodenale and Strongolides stercoralis
?

A

stool sample

Necator- eggs

Strongolides- larvae

74
Q

Describe the life cycle of Necator americanus/Ancylostoma duodenale and Strongolides stercoralis.

A 
Larvae in soil>
skin penetration> 
circulatory system (respiratory sxs)>
coughing and swallowing>
intestines (GI systems)
75
Q

What causes a pruritic papular erythematous rash?

A

Necator americanus/Ancylostoma duodenale

76
Q

What is the major symptoms of the blood sucking hookwoms: Necator americanus/Ancylostoma duodenale
?

A

iron def. anemia–> 1/4 ml/day/worm

77
Q

A pt presents w/
an itchy, red rash that occurs where the worm entered the skin
recurrent raised red rash typically along the thighs and buttocks.

They also have:
Stomach and GI complaints

dry cough
throat irritation

A

strongolides stercoralis

78
Q

What makes strongolides stercoralis different?

A

Autoinfection possible, especially with Immunosuppressed individuals

79
Q

What causes whipworm or trichuriasis?

A

Trichuris trichiura (one of the roundworms

80
Q

How do you dx Trichuris trichiura? What is hte best indicator of severity of infestation?

A

Eggs in feces have a characteristic barrel-shaped appearance

Finger clubbing best indicator of
severity of infestation

Bloody diarrhea = iron deficiency anemia

81
Q

What is seen in heavy cases of Trichuris trichiura ?

A

Frequent, painful stools with mucus, water and blood, tenesmus
Rectal prolapse

82
Q

What infect about half of the pop in tropical and subtropical areas?

A

Ascaris lumbricoides (giant roundworm)

83
Q

What sxs are associated w/ ascaris lumbricoides?

A

IF symptoms are experienced, abdominal discomfort

If a severe case, intestinal blockages
Ultrasonography and radiology to determine

has a lung stage life cycle> cough (infiltrate and charoct leyden crystals)

84
Q

HOw do you dx ascaris lumbricoides?

A

eggs w/ thick shells

85
Q

What are the general goals for antiparasitic tx of GI helminths (round and tape worms)

A

Treatment goal: remove adult worms from the GI tract

Usually can be accomplished with drugs

In the case of severe blockages, imaging and surgery may be required

Multiple-helminth infections common

Mass drug administrations of albendazole and ivermectin to school children in developing nations

No vaccines

86
Q

What selective toxicity strategies are used to exploit the GI roundworm?

A

Differentially distribute the drug.
The parasite is exposed to high concentrations of the drug in its intestinal habitat by the use of orally administered non-absorbable drugs.

87
Q

What are the mechanisms of GI roundworm?

A

target worm motor activity or reactions that generate metabolic energy

88
Q

What are broad-spectrum benzimidazole drugs used for?

A

roundworms and tapeworms

89
Q

How are albendazole and mebendazole distributed?

A

Limited oral absorption, albendazole is better absorbed if targeting tissue-migrating larvae is important

90
Q

What is the mechanism of albendazole and mebendazole?

A

Binds to parasite β-tubulin and inhibits the formation of microtubules

e

91
Q

What is hte specificity of albendazole and mebendazole?

A

diff in tubulin

92
Q

What is the toxicity of albendazole and mebendazole?

A

Systemic toxic affects on liver/bone marrow rare

Abdominal pain, nausea, dizziness, headache

Embryotoxic and teratogenic in pregnant rats

Evidence suggests safe for use in children when warranted

93
Q

What is mechanism of levamisole?

A

Selectively opens a restricted subgroup of nematode acetylcholine receptor (AChR) ion channels in nematode nerve and muscle. depolarization entry of calcium through the opened channels, and an increase in sarcoplasmic calcium, producing spastic muscle contraction the parasite is then unable to maintain its location (often in the intestine) and is then swept away, effecting the cure.

94
Q

What is the toxicity of Pyrantel pamoate and Levamisole?

A

nausea, vomiting, diarrhea

95
Q

How is Pyrantel pamoate and Levamisole

distributed?

A

poorly absorbed

96
Q

What is the spectrum of Pyrantel pamoate and Levamisole

?

A

Pyrantel for roundworms except whipworm, Lavamisole for roundworms

97
Q

What is the mechanism of ivermectin?

A

Binds to glutamate-gated chloride channels in invertebrate nerve and muscle cells, causing deactivation of channel: worm paralysis and death by starvation

98
Q

What is the resistance of ivermectin?

A

efflux transporters

99
Q

What is the toxicity of ivermectin?

A

Generally well-tolerated
Itching, swollen lymph glands and rarely dizziness
Inflammatory reaction due to death of adult worms

100
Q

What is the specificity of ivermectin?

A

This type of channel restricted to phyla Nematoda and Arthropoda. in humans are only in the CNS , Doesn’t cross blood-brain barrier

101
Q

What is the spectrum of ivermectin?

A

Nematodes- Ascaris, Strongyloides and Onchocerca

102
Q

What is a proglottid?

A

a segment of a tapeworm (which are all segmented)

103
Q

What is taenia?

A

Your typical human tapeworm, beef or pork tapeworm

3 – 10M in length!

104
Q

How big is a diphyllobothrium fish tapeworm?

A

The monster: up to 30 ft in length

105
Q

How big are Echinococcus and what do they cause?

A

Causes echinococcocis, a disease of liver, lungs, brain, and other organs

Tiny, a few mm in length

106
Q

What are zoonotic diseases?

A

tapeworms

107
Q

How are taenia and diphyllobothrium obtained?

A

improperly cooked meat/fish

108
Q

What is the life cycle of Diphyllobothrium: Fish tapeworm?

A

Acquired by eating the musculature of fish where larvae have migrated
Adheres to mucosa of small intestine

109
Q

How do you dx Diphyllobothrium: Fish tapeworm?

A

The standard intestinal “problems”
Anemia due to competition for B12 in intestine
Stool contains eggs and/or proglottids

110
Q

Describe the life cycle of taenia: beef/pork tapeworm.

A

acquired by human when meat containing cysticerci is consumed>
cysticercus grow into tapeworm>
eggs or gravid in feces are passed into environment

111
Q

How do you dx taenia?

A

The standard intestinal “problems”
Stool contains eggs and/or proglottids
Cysticercosis possible if cysticerci migrate to muscle, brain, or other tissue

112
Q

Describe the life cycle of echinococcus.

A

eggs in feces (dog)>
oncosphere hatches and penetrates inestinal lining>
circulatory system>
slow growing cysts in organs

113
Q

How do you dx echinococcus?

A

Not really a GI illness at all
Pain or discomfort in the upper abdominal region or chest

Sheep farming + uncontrolled living with canines; trappers

114
Q

What antiparasitics target tapeworms?

A

Benzimadazoles: albendazole and mebendazole (also target GI roundworms)

115
Q

What is the mechanism of praziquantel?

A

increased permeability of the parasite to divalent cations leading to contraction of the worm’s musculature

116
Q

What is the toxicity of praziquantel?

A

Generally well-tolerated, but dizziness and nausea are side effects

117
Q

What is hte spectrum of praziquantel?

A

Cestodes (tapeworms) and TREMATODES (flukes)

118
Q

WHAT CAUSES SCHISTOSOMIASIS?

A

Schistosoma mansoni, and S. japonicum

two forms: intestinal and urogenital

119
Q

What is hte most devastating parasitic disease?

A

Schistosoma mansoni, and S. japonicum

120
Q

What is an intermediate host for s. mansoni?

A

biomphalaria glabrata

121
Q

What is a definitive host for schistosoma?

A

humans (reproduction can occur)

122
Q

What causes sxs related to schistosomiasis?

A

Symptoms are caused by immune response to egg stage of Schistosoma

123
Q

What is the mechanism of schistosomiasis?

A

Eggs shed by the adult worms become lodged in the intestine or bladder, causing inflammation, scarring.

After years, this damages the liver, intestine, spleen, lungs, and bladder

Repeatedly-infected children can develop anemia, malnutrition, and learning difficulties

124
Q

What sxs are associated w/ schistosomiasis w/in days and months of an infection?

A

Within days of infection: rash or itchy skin

1-2 months of infection: fever, chills, cough, and muscle aches

125
Q

What are hte sxs of chronic schistosomiasis?

A

Chronic: abdominal pain, enlarged liver, blood in the stool or urine, and problems passing urine.
Chronic infection can also lead to increased risk of bladder cancer.

126
Q

Describe the life cycle of schistosomiasis?

A
  1. eggs hatch and release miracidia
  2. miracidia penetrate snail tissue
  3. sporocysts in snail
  4. cercariae released by snail into water and free swimming
  5. penetrate skin
  6. cercariae lose tails during penetration and become schistosomulae
  7. circulation
  8. migrate to portal blood in liver and mature into adults
  9. paired adult worms migrate to mesenteric venules of bowel/rectum (lay eggs that circulate to the liver and shed in stools) and venous plexus of bladder
127
Q

Where do shistosomulae go after skin penetration?

A

find capillaries and migrate first to LUNGS second to HEART and third to LIVER

128
Q

What is the avearge life span of adult worms

A

5-20 yrs

*adult F release 300 eggs/day into the bloodstream

129
Q

How do you dx shistosomiasis?

A

Stool or urine samples can be examined microscopically for parasite eggs

Eggs are passed in small amounts intermittently, it may be necessary to perform a blood (serologic) test.

130
Q

How do you tx schistosomiasis?

A

praziquantel

steroid medication to control allergic rxn to eggs responsible for sxs

131
Q

What should you keep in mind when treating schistosomiasis w/ praziaquantel?

A

Low efficacy against immature worms, so may need to give a second dose if eggs still present in stool or urine 2-3 months later

In acute cases, treatment with praziquantel is usually delayed until three months after infection as this is when it is most effective

132
Q

How do you prevent schistosomiasis?

A

Superior sanitation
Do not swim in freshwater that may be contaminated
Mass Drug Administration (MDA) of Praziquantel in endemic areas has reduced disease burden and eliminated Schistosomiasis in some disease foci

133
Q

What are you likely to see in the US?

A

Giardiasis
“Crypto”
Pinworm

GI- Week 5 (9 decks)

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