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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
Quinine vs Quinidine | Indications and formulations
- 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)
26
Adverse effects of quinine
- 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
27
areas of world with chloroquine –sensitive plasmodium species
(Central America west of Panama canal, Caribbean, Dominican Republic, and a few countries in Middle East) Resistance in South America, Africa, India, and Asia
28
Doxycycline indications for malaria treatment
–useful for treatment when combined with quinine | -inexpensive and useful prophylaxis but requires daily dosing
29
Adverse effects doxycycline
Side effects –photosensitivity
30
Chloroquinine indications for malaria treatment
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
31
Dosing of Chloroquinine
-weekly dosing
32
Chloroquinine coverage
-effective against blood schizonts (schizontizide) but no activity against liver phase
33
Side effects of chloroquinine
Bitter taste, headache, nausea, blurred vision, dizziness/ relatively contraindicated in patients with psoriasis, retinal disease, porphyria.
34
Melofloquine dosing and indications
- useful for treatment and prophylaxis of uncomplicated malaria, esp with chloroquinine resistance - convenient weekly dosing
35
Side effects for melofloquine
–psychosis, vivid dreams, EKG abnormalities, Stevens-Johnson Syndrome, insomnia
36
Melofloquine resistance
-there is some mefloquine resistance along the Thai-Burmese border
37
Primaquine indications
tissue schizontocide that treats liver hyponozoite stage of P. vivax and P. ovale malaria -contraindicated in G6PD deficiency patients because can cause hemolytic anemia
38
Primaquine coverage
tissue schizontocide that treats liver hyponozoite stage of P. vivax and P. ovale malaria -not effective against erythrocytic forms
39
Atovaquone/proguanil indications
–combination of 2 antimalarials - available in pediatric tablets - effective as prophylaxis, but is expensive so not useful for extended trips - some tissue schizontocidal activity
40
Atovaquone/proguanil side effects
-few side effects (mainly GI intolerance)
41
Artemesinin formulation/resistance
–powerful antimalarial available in parenteral forms (rectal suppository) -no resistance reported but not available in US
42
Babesia microti morphology
Intra-erythrocytic parasite (almost impossible to distinguish from Plasmodium!)
43
Babesia microti diagnosis
Peripheral blood smear --> MALTESE CROSS (merozoite form creates that cross) and ring form in RBC
44
Babesia microti pathogenesis
Invasion of RBCs
45
Babesia microti clinical presentation
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
46
Babesia microti epidemiology
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
47
Babesia microti treatment
Atovaquone+azithromycin is favored over clindamycin+quinine because of fewer side effects
48
Babesia microti vector
Transmitted by the Ixodes tick (Lyme Disease, Anaplasmosis – co-infection with all three at once possible)
49
Ascaris lumbricoides morphology
Helminth (largest one!)-Pearl white worm
50
Ascaris lumbricoides pathogenesis
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
Ascaris lumbricoides diagnosis
Visualize eggs in stool, eosinophilia
52
Ascaris lumbricoides clinical presentation
Asymptomatic (most), eosinophlic pneumonitis (Loeffler’s syndrome), malnutrition and weight loss; bowel obstruction (possibly biliary and pancreatic tree obstructions which would cause jaundice)
53
Ascaris lumbricoides epidemiology
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
Ascaris lumbricoides treatment
Albendazole or mebendazole
55
What is Loeffler’s syndrome
ascaris pneumonitis = hypersensitivity rxn to migrating ascaris lumbricoides larvae in lung (productive cough, dyspnea, wheezing, fever, angioedema, urticaria, pulmonary infiltrates, eosinophilia)
56
Indication for albendazole/mebendazole:
Ascaris Lumbricoides treatment Ancylostoma duodenale, Necator americanus treatment Strongyloides Stercoralis
57
Mechanism of action of albendazole/mebendazole:
inhibits assembly of microtubules and inhibits uptake of glucose --> parasite immobilization and death; also larvicidal
58
Scientific names of human hookworms
Ancylostoma duodenale, Necator americanus
59
Morphology of Ancylostoma duodenale, Necator americanus
Helminth. Warm temperate climates. NO reservoir host.
60
pathogenesis of Ancylostoma duodenale, Necator americanus
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
clinical presentation of Ancylostoma duodenale, Necator americanus
- 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
Diagnosis of Ancylostoma duodenale, Necator americanus
Detect eggs in stool
63
epidemiology of Ancylostoma duodenale, Necator americanus
Worldwide, up to 1.3 billion people infected | Africa, Asia, and South America.
64
treatment of Ancylostoma duodenale, Necator americanus
Albendazole or mebendazole
65
Anemia #1 cause in kids in developing nations
Ancylostoma duodenale, Necator americanus (hookworm)
66
N.B. Ancytostoma braziliense pathogenesis
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
Strongyloides Stercoralis morphology
Helminth.
68
Strongyloides Stercoralis pathogenesis
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
Strongyloides Stercoralis clinical presentation
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
Strongyloides Stercoralis diagnosis
Detect larvae (not eggs) in stool, eosinophilia
71
Strongyloides Stercoralis epidemiology
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
Strongyloides Stercoralis treatment
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
*Only organism that can complete life cycle in single host (us) --> auto-infection.
Strongyloides Stercoralis
74
Indications for Ivermectin
Strongyloides Stercoralis | Mechanism of action of ivermectin = nervous system paralysis.
75
Mode of Entry Ascaris Ancylostoma and Necator Strongyloides
Ascaris - Fecal-oral – consume eggs Ancylostoma and Necator - Penetrate Intact Skin Strongyloides - Penetrate Intact Skin
76
Lungs Ascaris Ancylostoma and Necator Strongyloides
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
GI Ascaris Ancylostoma and Necator Strongyloides
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
Clinical Presentation Ascaris Ancylostoma and Necator Strongyloides
Ascaris - 1. Asymptomatic 2. Obstruction 3. Nutrient Impairment (kids) 4. Loeffler’s Syndrome Ancylostoma and Necator - Anemia (childhood ``` Strongyloides - Obstruction Nutritional deficiencies Pulm Infiltrates Hyperinfection Syndrome (sepsis, PNA, bacteremia) ```
79
Treatment Ascaris Ancylostoma and Necator Strongyloides
Ascaris - Albendazole, mebendazole Ancylostoma and Necator - Albendazole, mebendazole Strongyloides - Albendazole, mebendazole, ivermectin
80
scientific name for pinworm
Enterobius Vermicularis
81
Enterobius Vermicularis morphology
Helminth, nematode – small white worm
82
Enterobius Vermicularis Pathogenesis
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
Enterobius Vermicularis clinical presentation
``` Perianal itchiness (or vaginal), many asymptomatic *Most common intestinal Helminth in the USA* ```
84
Enterobius Vermicularis diagnosis
Scotch tape test at night to look for eggs
85
Enterobius Vermicularis epidemiology
Worldwide including USA, very prevalent- | 20-40 million cases, common in school age children
86
Enterobius Vermicularis treatment
Mebendazole, albendazole, pyrantel pamoate
87
Pyrantel pamoate indication
Enterobius Vermicularis Pyrantel pamoate is a depolarizing blocker of their NMJ
88
most common GI nematode
Enterobius Vermicularis
89
whipworm scientific name
Trichurius Trichura
90
Trichurius Trichura morphology
Helminth, nematode.
91
Trichurius Trichura clinical presentation
Diarrhea, abdominal pain. Rectal Prolapse from severe tenesmus
92
Trichurius Trichura diagnosis
In stool, detect eggs: barrel shaped with polar plugs
93
Trichurius Trichura epidemiology
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
Trichurius Trichura treatment
Mebendazole, Albendazole
95
Trichurius Trichura pathogenesis
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
Dog Helminth
Toxocara Canis
97
Toxocara Canis morphology
nematode normally infecting dogs
98
Toxocara Canis clinical presentation/pathogenesis
in humans can disseminate and cause visceral larvae migrans, retinal larvae migrans
99
Toxocara Canis epidemiology
in sandboxes (reason for covers) – fecal oral transmission
100
Wuchereria Bancrofti morphology
Helminth - nematode
101
Wuchereria Bancrofti clinical presentation
Chronic lymphadema leads to elephantiasis, cannot be corrected even with treatment that kills larvae. Worse in legs and scrotum.
102
Wuchereria Bancrofti diagnosis
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
Wuchereria Bancrofti pathogenesis
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
Wuchereria Bancrofti epidemiology
Tropical areas worldwide. Culex mosquito vector.
105
Wuchereria Bancrofti treatment
Diethylcarbamazine Once lymphedema sets in, you can’t help it, thus important to prevent
106
Wuchereria Bancrofti vector
Culex mosquito
107
Onchocerca Volvulus morphology
Helminth, nematode
108
Onchocerca Volvulus pathogenesis
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
Onchocerca Volvulus clinical presentation
Blindness (‘River blindness’) if migrate to eyes. Hyper-pigmentation and pruritus if migrate to skin. Black flies, black skin nodules, “black sight”
110
Onchocerca Volvulus diagnosis
Skin biopsy (skin snips) to look for microfilariae
111
Onchocerca Volvulus epidemiology
Africa mostly, with some foci in Latin America and Middle East. Blackfly vector.
112
Onchocerca Volvulus treatment
Treat rIVER blindness with IVERmectin
113
Onchocerca Volvulus vector
Blackfly
114
guinea worm scientific name
Dracunculiasis Medinsis
115
Dracunculiasis Medinsis morphology
Helminth – Nematode
116
Dracunculiasis Medinsis pathogenesis life-cycle
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
Dracunculiasis Medinsis clinical presentation
Foot pain and itchiness, bacterial superinfection possible.
118
Dracunculiasis Medinsis diagnosis
Detect larvae (not eggs) in stool, eosinophilia
119
Dracunculiasis Medinsis treatment
No antihelminthic tx available Mechanical, progressive extraction of worm over period of days. Treat site with Abx to avoid bacterial infection
120
Dracunculiasis Medinsis epidemiology
Africa and India, can help interrupt cycle | by filtering water through Nylon mesh or cloth.
121
Intestinal nematodes
``` Enterobius Vernicularis Strongyloides Necator Americanus Ascaris Lumbricoides Trichurius Trichura ```
122
Tissue Nematodes
``` Dracunculiasis Medinsis Onchocerca Vulvulus Wucheria Bancrofti Toxocara Canis Loa Loa ```

Week 5 of Micro TA presentation (4 decks)

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