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Week 5 of Micro TA presentation > Parasites pre-ASM week > Flashcards

Parasites pre-ASM week Flashcards

1
Q

List of helminths

A

Helminths –> multicellular
Nematodes (round worms)
- Intestinal: Ascaris
- Tissue: Filariasis

Platyhelminths

  • Cestodes (Flatworms): Taenia
  • Trematodes (Flukes): Schistosomes
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2
Q

List of protazoa

A

Protazoa –> unicellular
Intestinal
- Entamoeba, Giardia, etc.

Apicomplexa
- Plasmodia, Toxoplasma, Cryptosporidia, etc.

Kinetoplastids
- Leishmania, Trypanosomes

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3
Q

Plasmodium morphology

A

Intra-erythrocytic parasite. Type of apicomplexa protazoa.

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4
Q

Plasmodium Diagnosis

A

Visualization of parasites on peripheral blood smear – Trophozoite Ring in RBC or Schizonts full of Merozoites

Also DFA testing

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5
Q

Plasmodium clinical presentation

A

Malaria!

Fever, chills, joint pain, headache, vomiting; cyclical fevers; can get hemoglobinuria (black water fever),

Severe progression: anemia, organ failure, death.

Cyclical disease – for example, with P. vivax/ovale, fever recurs every OTHER day.

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6
Q

Plasmodium epidemiology

A

Endemic P. falciparum, P. vivax malaria occur in Africa, Asia, Central and S. America
P. Ovale found mainly in Sub-Saharan Africa
P. Malariae occurs in isolated pockets in Sub-Saharan Africa, SE Asia, Amazon

Most severe cases of Malaria are due to P. falciparum (risk of seizures)

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7
Q

Plasmodium treatment

A

Depends on species and region

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8
Q

Plasmodium pathogenesis

A

Transmitted via Anopheles mosquito;
inoculated sporozoites go to liver to form schizonts –> asymptomatic period –> rupture and release of merozoites that infect red cells and mature to trophozoite and into schizonts or gametocytes

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9
Q

schizonts

A

After infecting a host cell, a trophozoite (intracellular parasite in feeding stage) that increases in size while repeatedly replicating its nucleus and other organelles.

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10
Q

merozoites

A

Cytokinesis subdivides the multinucleated schizont into numerous identical daughter cells called merozoites.

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11
Q

Life cycle of plasmodium

A

Mosquito takes blood meal and injects Sporozoite –> Travel to liver to make Schizont (bag of infectious parasites ) –> Release Merozoites infect RBCs –> Mature to Trophozoite (ring form) in RBC –> EITHER develops to a gamete to be taken up by another mosquito OR forms a Schizont in RBC which will lyse and release more Merozoites or form a Hypnozoite in Ovale and Vivax types which is latent in the liver

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12
Q

plasmodium vector

A

Anopheles mosquito

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13
Q

Identifying factors for each type of malaria

A

Falciparum - Most pathogenic – high-level parasitemia, end-organ damage (cerebral malaria)
Vivax - Duffy blood group antigen needed for invasion, rare in Africa because many people lack the Duffy antigen
Ovale - Sub-Saharan Africa
Malariae - Can persist in blood 20-30yrs after infection

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14
Q

Each type of plasmodium invades what types of cells

A

Falciparum - RBCs of any age
Vivax - Reticulocytes only
Ovale - Reticulocytes only
Malariae - Aging RBCs

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15
Q

Each type of plasmodium wrt hypnozoites

What are hypnozoites?

A

Hypnozoites are the latent stage of the plasmoidum parasite, seen in the liver.

Falciparum - none
Vivax - hypnozoites lead to relapse.
Ovale - hypnozoites lead to relapse.
Malariae - no known hypnozoites

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16
Q

Type of infection seen in blood smear with each type of plasmodium

A

Falciparum - Only early trophozoites (rings) and gametocytes in peripheral blood, accole form, multiple infections of single RBC, can see “banana shaped” gametocytes in the blood
Vivax - All stages in peripheral blood, multiple infections, also can see Schuffner’s dots/ Schizonts have 12-24 merozoites around pigment mass
Ovale - All stages in peripheral blood, single infection, also can see Schuffner’s dots (brick red)/ Schizonts have 6-12 merozoites
Malariae - All stages in peripheral blood, single infection, band forms, Schizonts have 6-12 merozoites around pigment mass

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17
Q

Infected cell size with each plasmoidum

A

Falciparum - infected cells normal size
Vivax - infected cell greatly enlarged
Ovale - infected cell slightly enlarged with oval shape
Malariae - infected cell normal size

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18
Q

What is schizogeny?

Schizogeny with each plasmodium type

A

Schizogeny - asexual reproduction of protozoans etc characterized by multiple divisions of the nucleus and cell

Falciparum - Schizogony lasts 36-48 hours (irregular)
Vivax -Schizogony lasts 48 hours
Ovale - Schizogony lasts 48 hours
Malariae - Schizogony lasts 72 hours

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19
Q

Types of trophozoites seen with p. falciparum

A

Trophozoites of P. falciparum can be found on the edge of the red blood cells. These are known as accole forms and are found as three distinct types:

  1. Common: The single chromatin bead lies on the edge of the cell with most of the cytoplasm extended along the edge on both sides of the bead.
  2. Rim: The complete parasite lies in a thickened line along the edge of the cell with no evidence of ring formation.
  3. Displaced: The parasites are displaced beyond the edge of the host cell. All degrees of displacement may occur, from partial to marked displacement with most of the parasite lying beyond the cell margin.
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20
Q

Each type of plasmoidum wrt chloroquinone resistance

A

P. Falciparum – chloroquine resistant in most parts of the world
P. Vivax – some chloroquine resistance reported
P. Ovale – no chloroquine resistance; treat with chloroquine
P. Malariae – no chloroquine resistance; treat with chloroquine

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21
Q

Treatment hypnozoite stage of P. vivax and P. ovale

A

Treat hypnozoite stage of P. vivax and P. ovale with Primaquine/ contraindicated in patients with G6PD deficiency (can cause hemolytic anemia)

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22
Q

Prophylaxis of malaria

A

Oral doxycycline, mefloquine, or atovaquone-proguanil can be used as prophylaxis (primaquine prophylaxis in Vivax/Ovale areas)

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23
Q

Treatment of uncomplicated malaria

A

If chloroquine-resistant or sensitivity is not known, can use atovaquone-proguanil, oral quinine plus doxycycline, mefloquine, or artemisin combination therapy for uncomplicated malaria.

Need to know overview: *****
Begin with chloroquine (blocks plasmodium heme polymerase). If resistant, use mefloquine. If life-threatening, use IV quinidine (test G6PD deficiency before use). With P. Vivax/Ovale, add primoquine for hyponozoite (dormant) form – also test for G6PD deficiency (can lead to hemolysis if (+) deficiency)

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24
Q

Treatment of severe malaria

A

For severe malaria use IV quinidine plus doxycycline, tetracycline, or clindamycin.

Need to know overview: *****
Begin with chloroquine (blocks plasmodium heme polymerase). If resistant, use mefloquine. If life-threatening, use IV quinidine (test G6PD deficiency before use). With P. Vivax/Ovale, add primoquine for hyponozoite (dormant) form – also test for G6PD deficiency. (can lead to hemolysis if (+) deficiency)

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25
Q

Quinine vs Quinidine

Indications and formulations

A
  • IV quinine (is available in oral form) is not available in US/ Quinidine is used instead, but need to monitor for cardiotoxicity

mild malaria - oral quinine (+ oral doxycycline)
severe malaria - IV quinidine (+ IV doxycycline)

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26
Q

Adverse effects of quinine

A
  • most of these side effects are reversible once medicine is stopped
    1. Cinchonism –hearing loss, headache, nausea, vomiting, mild visual disturbances
    2. Rash, urticaria
    3. Rarely can cause agranulocytosis
    4. Nocturnal leg cramps
    5. Hemolysis in G6PD deficiency (many anti-malarials can cause increase in free radicals so patients with G6PD deficiency can have problems due to increased free radicals/ can try spreading out dose to deal with G6PD deficiency)
    6. Hypoglycemia –stimulates insulin secretion by pancreas
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27
Q

areas of world with chloroquine –sensitive plasmodium species

A

(Central America west of Panama canal, Caribbean, Dominican Republic, and a few countries in Middle East)

Resistance in South America, Africa, India, and Asia

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28
Q

Doxycycline indications for malaria treatment

A

–useful for treatment when combined with quinine

-inexpensive and useful prophylaxis but requires daily dosing

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29
Q

Adverse effects doxycycline

A

Side effects –photosensitivity

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30
Q

Chloroquinine indications for malaria treatment

A

treatment drug of choice for areas of world with chloroquine –sensitive plasmodium species (Central America west of Panama canal, Caribbean, Dominican Republic, and a few countries in Middle East)
-may use as prophylaxis in these areas as well

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31
Q

Dosing of Chloroquinine

A

-weekly dosing

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32
Q

Chloroquinine coverage

A

-effective against blood schizonts (schizontizide) but no activity against liver phase

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33
Q

Side effects of chloroquinine

A

Bitter taste, headache, nausea, blurred vision, dizziness/ relatively contraindicated in patients with psoriasis, retinal disease, porphyria.

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34
Q

Melofloquine dosing and indications

A
  • useful for treatment and prophylaxis of uncomplicated malaria, esp with chloroquinine resistance
  • convenient weekly dosing
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35
Q

Side effects for melofloquine

A

–psychosis, vivid dreams, EKG abnormalities, Stevens-Johnson Syndrome, insomnia

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36
Q

Melofloquine resistance

A

-there is some mefloquine resistance along the Thai-Burmese border

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37
Q

Primaquine indications

A

tissue schizontocide that treats liver hyponozoite stage of P. vivax and P. ovale malaria
-contraindicated in G6PD deficiency patients because can cause hemolytic anemia

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38
Q

Primaquine coverage

A

tissue schizontocide that treats liver hyponozoite stage of P. vivax and P. ovale malaria
-not effective against erythrocytic forms

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39
Q

Atovaquone/proguanil indications

A

–combination of 2 antimalarials

  • available in pediatric tablets
  • effective as prophylaxis, but is expensive so not useful for extended trips
  • some tissue schizontocidal activity
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40
Q

Atovaquone/proguanil side effects

A

-few side effects (mainly GI intolerance)

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41
Q

Artemesinin formulation/resistance

A

–powerful antimalarial available in parenteral forms (rectal suppository)
-no resistance reported but not available in US

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42
Q

Babesia microti morphology

A

Intra-erythrocytic parasite (almost impossible to distinguish from Plasmodium!)

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43
Q

Babesia microti diagnosis

A

Peripheral blood smear –> MALTESE CROSS (merozoite form creates that cross) and ring form in RBC

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44
Q

Babesia microti pathogenesis

A

Invasion of RBCs

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45
Q

Babesia microti clinical presentation

A

Asymptomatic infection – Incubation lasts weeks to months
Mild viral-like illness – Fever, chills, malaise, fatigue, depression
Severe fulminant disease – Acute respiratory failure, DIC, CHF, liver/renal failure. Seen in asplenics, immunosuppressed

Can be very similar to malaria

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46
Q

Babesia microti epidemiology

A

Transmitted by the Ixodes tick (Lyme Disease, Anaplasmosis – co-infection possible), reservoir in white-footed mice.
Most people do not remember tick bite.
Islands of the Northeast.
Can be transmitted through transfusion.

Seen in asplenics, immunosuppressed

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47
Q

Babesia microti treatment

A

Atovaquone+azithromycin is favored over clindamycin+quinine because of fewer side effects

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48
Q

Babesia microti vector

A

Transmitted by the Ixodes tick (Lyme Disease, Anaplasmosis – co-infection with all three at once possible)

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49
Q

Ascaris lumbricoides morphology

A

Helminth (largest one!)-Pearl white worm

50
Q

Ascaris lumbricoides pathogenesis

A

Fecal-oral transmission –> eggs ingested –> hatch in Small Intestine –> larvae invade intestinal wall (bloodstream, lymphatics) –> bloodstream to lungs –> grows in pulmonary capillaries (10-14 days) –> coughed-up –> swallowed –> mature into adults in SI –> eat host food and lay eggs in duodenum that pass in stool

51
Q

Ascaris lumbricoides diagnosis

A

Visualize eggs in stool, eosinophilia

52
Q

Ascaris lumbricoides clinical presentation

A

Asymptomatic (most),
eosinophlic pneumonitis (Loeffler’s syndrome),
malnutrition and weight loss;
bowel obstruction (possibly biliary and pancreatic tree obstructions which would cause jaundice)

53
Q

Ascaris lumbricoides epidemiology

A

¼ of world population infected; distribution is worldwide
Especially in impoverished areas, KIDS (lumen Is narrower, more likely to cause bowel obstruction)!

This worm is a huge public problem world wide because of malnutrition and subsequent developmental delay
-in many 3rd world countries there is annual treatment of school children as part of health care

54
Q

Ascaris lumbricoides treatment

A

Albendazole or mebendazole

55
Q

What is Loeffler’s syndrome

A

ascaris pneumonitis = hypersensitivity rxn to migrating ascaris lumbricoides larvae in lung (productive cough, dyspnea, wheezing, fever, angioedema, urticaria, pulmonary infiltrates, eosinophilia)

56
Q

Indication for albendazole/mebendazole:

A

Ascaris Lumbricoides treatment
Ancylostoma duodenale, Necator americanus treatment
Strongyloides Stercoralis

57
Q

Mechanism of action of albendazole/mebendazole:

A

inhibits assembly of microtubules and inhibits uptake of glucose –> parasite immobilization and death; also larvicidal

58
Q

Scientific names of human hookworms

A

Ancylostoma duodenale, Necator americanus

59
Q

Morphology of Ancylostoma duodenale, Necator americanus

A

Helminth. Warm temperate climates. NO reservoir host.

60
Q

pathogenesis of Ancylostoma duodenale, Necator americanus

A

Larvae penetrate INTACT skin on bare feet –> bloodstream to lungs –> swallowed –> larvae grow to adults in SI –> use cutting plates to attach to mucosal wall –> suck blood –> eggs passed in feces –> mature to infectious larvae in soil

61
Q

clinical presentation of Ancylostoma duodenale, Necator americanus

A
  • Gastroenteritis (abdominal pain)
  • Anemia (#1 cause in kids in developing nations) –> mental and physical growth retardation,
  • pneumonitis,
  • intense peripheral eosinophilia,
  • intense pruritis, edema, erythema, muacular papular eruption at entry
62
Q

Diagnosis of Ancylostoma duodenale, Necator americanus

A

Detect eggs in stool

63
Q

epidemiology of Ancylostoma duodenale, Necator americanus

A

Worldwide, up to 1.3 billion people infected

Africa, Asia, and South America.

64
Q

treatment of Ancylostoma duodenale, Necator americanus

A

Albendazole or mebendazole

65
Q

Anemia #1 cause in kids in developing nations

A

Ancylostoma duodenale, Necator americanus (hookworm)

66
Q

N.B. Ancytostoma braziliense pathogenesis

A

dog hookworm, so unable to be invasive in human hosts

can cause cutaneous eruption as the larvae wanders beneath surface of skin. “Creeping eruption” that leaves itchy, serpiginous tracks.

67
Q

Strongyloides Stercoralis morphology

A

Helminth.

68
Q

Strongyloides Stercoralis pathogenesis

A

Larvae penetrate intact skin (bare feet) –> bloodstream to lungs –> swallowed –> larvae grow to adults in SI and mate –> female lays eggs in mucosa –> leads to inflammation, pain, and diarrhea –> larvae can exit in stool or re-penetrate host: Lungs, CSF, other.

  • Motility and invasion are the main virulence factors
  • Only organism that can complete life cycle in single host (us)  auto-infection.
69
Q

Strongyloides Stercoralis clinical presentation

A

PNA from dragging GI bacteria into lungs (GNs, enterococcus); bacteremia (high parasite load – hyperinfection syndrome) and G(-) sepsis in immunocomp. N/V/D, GI pain.

See gut bacteria in lung pneumonia, associated with strongyloides

Most important: Can cause superinfections (especially in immunocompromised hosts), also don’t give steroids

70
Q

Strongyloides Stercoralis diagnosis

A

Detect larvae (not eggs) in stool, eosinophilia

71
Q

Strongyloides Stercoralis epidemiology

A

Worldwide, including southeastern USA
Predisposition with STEROID use

Steroids act as sex hormone on female and cause her to produce more eggs, making disease worse. Also predisposes to hyperinfection syndrome.

72
Q

Strongyloides Stercoralis treatment

A

Ivermectin, Albendazole, Thiobendazole.

Like the other nematodes treat with bendazoles but since it’s strong, add ivermectin. Mechanism of action of ivermectin = nervous system paralysis.

73
Q

*Only organism that can complete life cycle in single host (us) –> auto-infection.

A

Strongyloides Stercoralis

74
Q

Indications for Ivermectin

A

Strongyloides Stercoralis

Mechanism of action of ivermectin = nervous system paralysis.

75
Q

Mode of Entry

Ascaris
Ancylostoma and Necator
Strongyloides

A

Ascaris - Fecal-oral – consume eggs
Ancylostoma and Necator - Penetrate Intact Skin
Strongyloides - Penetrate Intact Skin

76
Q

Lungs

Ascaris
Ancylostoma and Necator
Strongyloides

A

Ascaris - Develop for 10-14 days – coughed up and swallowed
Ancylostoma and Necator - Coughed up and swallowed to enter GI
Strongyloides - Also occupies the lungs

77
Q

GI

Ascaris
Ancylostoma and Necator
Strongyloides

A

Ascaris - Unattached, Swims against the fecal stream
Ancylostoma and Necator - Attaches with cutting plates and sucks blood
Strongyloides - Adult form in Small Intestines. Lays eggs which hatch into larva and can be excreted in stool or AUTOINFECT

78
Q

Clinical Presentation

Ascaris
Ancylostoma and Necator
Strongyloides

A

Ascaris - 1. Asymptomatic

  1. Obstruction
  2. Nutrient Impairment (kids)
  3. Loeffler’s Syndrome

Ancylostoma and Necator - Anemia (childhood

Strongyloides - 
Obstruction
Nutritional deficiencies
Pulm Infiltrates
Hyperinfection Syndrome (sepsis, PNA, bacteremia)
79
Q

Treatment

Ascaris
Ancylostoma and Necator
Strongyloides

A

Ascaris - Albendazole, mebendazole
Ancylostoma and Necator - Albendazole, mebendazole
Strongyloides - Albendazole, mebendazole, ivermectin

80
Q

scientific name for pinworm

A

Enterobius Vermicularis

81
Q

Enterobius Vermicularis morphology

A

Helminth, nematode – small white worm

82
Q

Enterobius Vermicularis Pathogenesis

A

Fecal-oral transmission –> eggs ingested –> hatch in duodenum and jejunum and mature in ileum and LI –> mate in colon –> at night females migrate out to lay eggs in perianal skin –> scratch –> autoinoculation and fecal-oral

*Humans are the only host (no reservoir)

83
Q

Enterobius Vermicularis clinical presentation

A 
Perianal itchiness (or vaginal), many asymptomatic
*Most common intestinal Helminth in the USA*
84
Q

Enterobius Vermicularis diagnosis

A

Scotch tape test at night to look for eggs

85
Q

Enterobius Vermicularis epidemiology

A

Worldwide including USA, very prevalent-

20-40 million cases, common in school age children

86
Q

Enterobius Vermicularis treatment

A

Mebendazole, albendazole, pyrantel pamoate

87
Q

Pyrantel pamoate indication

A

Enterobius Vermicularis

Pyrantel pamoate is a depolarizing blocker of their NMJ

88
Q

most common GI nematode

A

Enterobius Vermicularis

89
Q

whipworm scientific name

A

Trichurius Trichura

90
Q

Trichurius Trichura morphology

A

Helminth, nematode.

91
Q

Trichurius Trichura clinical presentation

A

Diarrhea, abdominal pain. Rectal Prolapse from severe tenesmus

92
Q

Trichurius Trichura diagnosis

A

In stool, detect eggs: barrel shaped with polar plugs

93
Q

Trichurius Trichura epidemiology

A

Southeast Asia, sub-Saharan Africa, Caribbean islands. KIDS. Low SES. Human feces used as fertilizer (night soil).

Often see Polyparisitism with Ascaris, hookworm, malaria.

94
Q

Trichurius Trichura treatment

A

Mebendazole, Albendazole

95
Q

Trichurius Trichura pathogenesis

A

Fecal-oral –> ingest eggs –> go to colon –> Attach to mucosa of cecum with long tail –> mature into adult –> Tail embeds in epithelial mucosa while the Head remains in the lumen

NO tissue phase, stays in gut lumen

96
Q

Dog Helminth

A

Toxocara Canis

97
Q

Toxocara Canis morphology

A

nematode normally infecting dogs

98
Q

Toxocara Canis clinical presentation/pathogenesis

A

in humans can disseminate and cause visceral larvae migrans, retinal larvae migrans

99
Q

Toxocara Canis epidemiology

A

in sandboxes (reason for covers) – fecal oral transmission

100
Q

Wuchereria Bancrofti morphology

A

Helminth - nematode

101
Q

Wuchereria Bancrofti clinical presentation

A

Chronic lymphadema leads to elephantiasis, cannot be corrected even with treatment that kills larvae. Worse in legs and scrotum.

102
Q

Wuchereria Bancrofti diagnosis

A

Detect microfilariae in blood AT NIGHT

Diagnostic test is done at night because the life cycle of the nematode is timed to that of mosquito  mosquitoes tend to bite more at night so that is when microfilariae are released by adults into bloodstream

103
Q

Wuchereria Bancrofti pathogenesis

A

Infected mosquitoes (Culex) introduce larvae –> penetrate skin and go to lymphatics –> in lymphatics mature into adults (lives for up to 7 yrs) –> adults produce microfilariae, which move actively b/t blood (transmissable) and lymphatics

104
Q

Wuchereria Bancrofti epidemiology

A

Tropical areas worldwide. Culex mosquito vector.

105
Q

Wuchereria Bancrofti treatment

A

Diethylcarbamazine

Once lymphedema sets in, you can’t help it, thus important to prevent

106
Q

Wuchereria Bancrofti vector

A

Culex mosquito

107
Q

Onchocerca Volvulus morphology

A

Helminth, nematode

108
Q

Onchocerca Volvulus pathogenesis

A

Black fly that lives near river bites –> releases larvae into skin –> larvae move to subcutaneous tissue, where adults live –> microfilariae can migrate to eyes –> microfilariae can also by ingested by mosquitoes, who lay their eggs on the flies

109
Q

Onchocerca Volvulus clinical presentation

A

Blindness (‘River blindness’) if migrate to eyes. Hyper-pigmentation and pruritus if migrate to skin.

Black flies, black skin nodules, “black sight”

110
Q

Onchocerca Volvulus diagnosis

A

Skin biopsy (skin snips) to look for microfilariae

111
Q

Onchocerca Volvulus epidemiology

A

Africa mostly, with some foci in Latin America and Middle East. Blackfly vector.

112
Q

Onchocerca Volvulus treatment

A

Treat rIVER blindness with IVERmectin

113
Q

Onchocerca Volvulus vector

A

Blackfly

114
Q

guinea worm scientific name

A

Dracunculiasis Medinsis

115
Q

Dracunculiasis Medinsis morphology

A

Helminth – Nematode

116
Q

Dracunculiasis Medinsis pathogenesis life-cycle

A

Drink water with copepods that contain larvae –> larvae penetrate host stomach and intestinal wall –> enter abdominal cavity and retroperitoneal space –> females go to skin surface and form blister –> foot itches –> larvae released into water (upon contact)

117
Q

Dracunculiasis Medinsis clinical presentation

A

Foot pain and itchiness, bacterial superinfection possible.

118
Q

Dracunculiasis Medinsis diagnosis

A

Detect larvae (not eggs) in stool, eosinophilia

119
Q

Dracunculiasis Medinsis treatment

A

No antihelminthic tx available

Mechanical, progressive extraction of worm over period of days. Treat site with Abx to avoid bacterial infection

120
Q

Dracunculiasis Medinsis epidemiology

A

Africa and India, can help interrupt cycle

by filtering water through Nylon mesh or cloth.

121
Q

Intestinal nematodes

A 
Enterobius Vernicularis
Strongyloides
Necator Americanus
Ascaris Lumbricoides
Trichurius Trichura
122
Q

Tissue Nematodes

A 
Dracunculiasis Medinsis
Onchocerca Vulvulus
Wucheria Bancrofti
Toxocara Canis
Loa Loa

Week 5 of Micro TA presentation (4 decks)

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