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MICRO II > parisitology review > Flashcards

parisitology review Flashcards

1
Q

what are parasites?

A

eukaryotic pathogens that lack a cell wall (unlike fungi)

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2
Q

what are single cell parasites?

A

protozoa

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3
Q

what are multi-cellular parasites?

A

helminths and arthropods

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4
Q

parasites are separated into what 2 groups?

A

GI and blood/tissue depending on the usual site of the pathology

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5
Q

what is a definitive host?

A

the site of sexual reproduction of a parasite

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6
Q

what is an intermediate host?

A

the site of non-sexual dvpmt of a parasite (ie it matures, but doesn’t reproduce)

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7
Q

what is a dead end host?

A

a host that doesn’t transmit the parasite– that said, the host can become sick and die from the parasite

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8
Q

can vectors be hosts?

A

yes

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9
Q

the human is a definitive host for which 3 parasites?

A
  1. Filaria
  2. GI Helminths
  3. Taenia Solium
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10
Q

Humans are intermediate hosts for which parasites?

A

Plasmodium species

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11
Q

Humans are a dead end host for which parasites

A

Echinococcus granulosus

Taenia Solium

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12
Q

which parasite can use the human as a definitive host or a dead end host depending on the route of ifxn?

A

Taenia Solium

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13
Q

what is a vector?

A

an arthropod that transmits an ifxn– it can double as a host (ie it is a definitive host for malaria)

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14
Q

anopheles mosquito is the vector for which parasite?

A

plasmodium species

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15
Q

plasmodium species are transmitted by what vector?

A

anopheles mosquito

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16
Q

triatomine bug is teh vector for which parasite?

A

trypanosoma cruzi

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17
Q

trypanosoma cruzi is transmitted by which vector?

A

Triatomine bug

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18
Q

Tsetse fly is the vector for which parasite?

A

Trypanosoma brucei

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19
Q

Trypanosoma brucei is transmitted by which vector?

A

Tsetse fly

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20
Q

the sandfly transmits which parasite?

A

Leishmania species

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21
Q

Leishmania species are transmitted by which vector?

A

the sandfly

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22
Q

Simulium blackflies transmit which parasite?

A

onchocerca volvulus

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23
Q

onchocerca volvulus are transmitted by which vector?

A

simulium blackflies

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24
Q

what is a reservoir?

A

a non-human site where a pathogen survives

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25
Q

reservoir control is critical for…

A

ifxn control

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26
Q

4 mechanisms of damage by parasites

A

1) mechanism impairment
2) kills cells (invasion or cytolysis)
3. competition for nutrients
4) inflammation —> tissue damage

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27
Q

which 3 parasites damage their hosts via mechanical damage? where is this damage?

A
  1. Echinococcus granulosus - liver
  2. Ascaris lumbricoides - intestine
  3. Plasmodium falciparum- capillaries, PCV
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28
Q

where does echniococcus granulosus cause mechanical damage, and how does it do it?

A

in the liver via the formation of hepatic cysts

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29
Q

where does ascaris lumbricoides cause mechanical damage and how does it do it?

A

intestine, via obstruction

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30
Q

where does plasmodium falciparum cause mechanical damage and how does it do it?

A

in the capillaries and PCV, via obstruction (by binding RBCs to the endothelium) which causes hypoxia (esp in the brain)

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31
Q

which 3 parasites kill host cells? and where do they do this?

A
  1. Entamoeba histolytica- liver
  2. trypanosoma cruzi - heart
  3. Leishmania species - macrophages (spleen/liver)
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32
Q

Where does Entamoeba histolytica kill host cells, and what is the resultant damage?

A

liver —> necrosis that’s like anchovy paste

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33
Q

Where does Trypanosoma cruzi kill host cells, and what is the resultant damage?

A

heart —> myocarditis, enlargement

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34
Q

Where do Leishmania species kill host cells, and what is the resultant damage?

A

macrophages (liver/spleen) —> splenomegaly and hepatic failure

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35
Q

what are two parasites that compete for nutrients, and where are they located?

A
  1. Hookworms in the GI tract

2. Diphyllobothrium latum in the GI tract

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36
Q

where do Hookworms compete for nutrients and what damage does it cause the host?

A

in the GI tract– the worm sucks out blood leading to blood loss —> anemia

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37
Q

where do Diphyllobothrium latum (tapeworms) compete for nutrients and what damage does it cause the host?

A

In the GI tract. They adsorb vitamin B12 through their skin —-> anemia

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38
Q

2 parasites that cause damage by inflammation, and where the inflammation is located

A
  1. Onchocerca volulus - in the eye

2. Trypasnosoma cruzi - nerves

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39
Q

Where does Onchocerca volvulus cause inflammation, and what damage results?

A

in the eye —> blindness

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40
Q

where does Trypanosoma cruzi cause inflammation and what damage results?

A

in the nerves —> megasophagus, megacolon, heart (arrhythmia)

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41
Q

how are protozoa classified?

A

by motility

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42
Q

3 groups of motility by which protozoa are classified

A

1) flagella – can swim
2) pseudopods
3) often non-motile

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43
Q

3 groups of protozoa and their motility

A
  1. flagellates- flagella
  2. amebas- pseudopods
  3. apicomplexans (coccida) - often non-motile
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44
Q

flagellates
motility:
other features (2):

A

flagellates
motility: flagella
other features (2): asexual, trophozoite and cyst

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45
Q

amebas
motility:
other features (1):

A 
amebas
motility: pseudopods
other features (1): asexual
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46
Q

Apicomplexans (Coccidia)
motility:
other features (3):

A

Apicomplexans (Coccidia)
motility: often non-motile
other features (3): asexual and sexual. apical complex organelle, intracellular replication

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47
Q

which Apicomplexan protozoan parasites are GI parasites?

A

none

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48
Q

which Apicomplexan protozoan parasites are Blood/Tissue parasites? (2)

A
  1. Plasmodium species

2. Toxoplasma gondii

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49
Q

which flagellate protozoan parasites are GI parasites? (1)

A

Giardia lamblia

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50
Q

which flagellate protozoan parasites are blood/tissue parasites? (2)

A
  1. Trypanosoma species

2. Leishmania species

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51
Q

Which ameba protozoan parasites are GI parasites? (1)

A
  1. Entamoeba histolytica (but it also spreads from there)
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52
Q

Which ameba protozoan parasites are blood/tissue parasites?

A

none– although entamoeba histolytica does spread from the GI to other areas

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53
Q

Giardia Lamblia spreads to the host from? via? in what form?

A

animals and people via fecal oral transmission in cyst form

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54
Q

Giardia Lamblia is what type of protozoa?

A

flagellate

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55
Q

pathogenesis of the flagellate Giardia Lamblia? (4)

A
  1. cyst consumed via fecal oral route from people or animals
  2. replication in GI tract
  3. Giardia adheres to the mucosa of the small intestine
  4. maladsorption
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56
Q

symptoms of giardia?

A
  1. asymptomatic

2. symptmatic: diarrhea, flatus (gas), cramping

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57
Q

entamoeba histolytica is what type of protazoa?

A

ameba

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58
Q

how is entamoeba histolytica spread?

A

fecal-oral consumption of cysts- spread from person to person

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59
Q

pathogenesis of entamoeba histolytica

A
  1. fecal-oral transmission of cysts
  2. replication in the GI tract
  3. adheres to colonic mucosa
  4. It kills cells with contact
  5. it invades and spreads locally
  6. causes colonic ulceration and hepatic abscesses (anchovy paste)
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60
Q

Plasmodium species and toxoplasma gondii are what type of protozoa and where do they attack?

A

they’re apicomplexans and they attack blood/tissue

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61
Q

how do you acquire Toxoplasma Gondii? (3)

A
  1. Primary route: ingestion of oocysts from rare meat
  2. ingestion of oocysts from cat feces
  3. vertical transmission (newly infected mother)
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62
Q

How does Adult (aka post natal) toxoplasmosis gondii spread in the the body?

A

through the blood

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63
Q

adult toxoplasmosis gondii spreads in the blood, encysts and…

A

is generally controlled by the immune response

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64
Q

manifestations of Primary infection with toxoplasmosis gondii

A

asymptomatic or mononucleosis like

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65
Q

what things have mononucleosis like symptoms?

A

EBV- mononucleosis
CMV- non-heterophile mono
Toxoplasmosis gondii
Acute HIV ifxn

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66
Q

when immunocompromised people with T cell defects (like HIV pts) get toxoplasmosis gondii, what happens?

A

reactivation/proliferation of toxoplasmosis —> severe ifxn with encephalitis

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67
Q

What is congenital toxoplasmosis?

A

when toxoplasmosis gondii spreads in the blood of the mother, crosses the placenta and infects the fetus

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68
Q

why are pregnant women instructed to avoid raw meats and cats?

A

to avoid Toxoplasmosis gondii

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69
Q

3 different outcomes of congenital toxoplasmosis gondii

A
  1. stillbirth/spontaneous abortion
  2. illness at birth with jaundice and hepatosplenamegaly
  3. unapparent ifxn at birth
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70
Q

babies with congenital toxoplasmosis who are ill at birth have…

A

jaundice and hepatosplenomegaly —> chorioretinitis and CNS abnormalities (calcifications, hydrocephalus and microcephaly)

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71
Q

babies with congenital toxoplasmosis that is unapparent at birth will still get (3)

A
  1. chorioretinitis
    2, hearing loss
  2. developmental delay
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72
Q

plasmodium species are transmitted by which vector?

A

anopheles mosquitos

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73
Q

3 modes of transmission of plasmodium species?

A
  1. anopheles mosquito
  2. vertical transmission
  3. transfusion
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74
Q

why do they ask you about travel when you’re giving blood

A

to screen you for malaria

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75
Q

pathogenesis of plasmodium species

A
  1. transmitted via anopheles mosquito, vertical transmission or blood tranfusion
  2. travels in the blood to the liver
  3. either becomes latent hynozoites (dormant protozoa) (P. vivax or P ovale) or go into RBCs
  4. Once in the RBCs they replicate and dvp gametocytes
  5. the gametocytes are picked up by mosquitoes where they sexually reproduce
  6. the mosquito bites a new host…
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76
Q

3 different malaria species. Which is the most severe?

A

Plasmodium ovale
plasmodium vivax
plasmodium falciparum – most severe!!

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77
Q

manifestations of all 3 malaria species (vivax, ovale and falciparum)

A
  1. constitutional symp: fever, headache nausea
  2. fever can become cyclical (every 2-3 days)
  3. anemia and splenomegaly is variable
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78
Q

severe manifestations of malaria caused by plasmodium falciparum

A

cerebral malaria: encephalopathy and coma
severe anemia, hypoglycemia, acidosis (bc of damage to kidneys/lysis of RBCs) and renal impairment (bc of damage to kidneys/lysis of RBCs)

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79
Q

2 reasons why Plasmodium falciparum is more virulent than plasmodium vivax/ovale?

A
  1. P falciparum infects RBC of any age (unlike others that only infect really young or really old RBCs) —> high parasitemia and more severe anemia
  2. P falciparum-infected RBCs stick to vascular endothelial cells —> poor perfusion and hypoxia
80
Q

what is Pfemp?

A

the protein that causes Plasmodium falciparum-infected RBCs to bind to endothelium, block blood flow and cause hypoxia

81
Q

what do early plasmodium Trophozoites look like?

A

Purple rings inside of RBCs with 1 or 2 darker stained purple dots on them

82
Q

What to P falciparum gametocytes look like?

A

bananas or sausages in an RBC with a large, dark granular stain near its middle

83
Q

trypanosoma and Leishmania species are what type of protozoa and they affect what part of the body?

A

they’re flagellates that infect the blood/tissue

84
Q

African Trypanosomiasis (trypanosoma brucei) is transmitted by what?

A

the Tstetse fly

85
Q

pathogenesis of African Trypanosomiasis (trypanosoma brucei)

A
  1. Tsetse fly bites human
  2. replication of trypanosoma brucei in the blood
  3. spread to lymph nodes
  4. spread to CNS
86
Q

african trypanosomiasis is aka

A

trypanosoma brucei

87
Q

Trypanosoma brucei (African Trypanosomiasis ) replication in the skin causes

88
Q

trypanosoma brucei (African Trypanosomiasis) spread/replication in the blood/lymph causes

A

fever, sweats, headache, winterbottom’s sign

89
Q

what is winterbottom’s sign iand which parasite species is it associated with?

A

it’s swelling of the lymphnodes along the back of the neck on the posterior cervical chain that are evidence that trypanosomes have travelled to the lymph nodes and caused inflammation. it’s associated with Trypanosoma brucei (african trypanosomiasis)

90
Q

Trypanosoma brucei (African Trypanosomiasis) spread/replication in the CNS is associated with?

A

meningoencephalitis, confusion, somnolence, coma

91
Q

3 areas of the body often affected by Trypanosoma brucei (African Trypanosomiasis)

A
  1. skin- ulcers
  2. lymph/blood
  3. CNS
92
Q

2 subspecies of trypanosoma brucei

A
  1. Trypanosoma brucei gamiense - western africa

2. trypanosoma brucei rhodensiense - eastern

93
Q

Trypanosoma brucei gambiense
region of africa:
reservoir:
time to death if untreated:

A

Trypanosoma brucei gambiense
region of africa: western
reservoir: none– only humans
time to death if untreated: years

94
Q

why can you live for years with trypanosoma brucei gambiense, but only months with trypanosoma brucei rhodesiense?

A

gambiense only has human hosts, so it has to be less virulent so that it can continue to live. Rhodesiense has many, many hosts, so it can be more virulent and skip around

95
Q

trypanosoma brucei rhodesiense
region of africa:
reservoir:
time to death if untreated:

A

trypanosoma brucei rhodesiense
region of africa: eastern
reservoir: many mammals
time to death if untreated: < 9 months

96
Q

african sleeping sickness is associated with which species of parasite?

A

Trypanosoma brucei (African trypanosomiasis)

97
Q

what do trypanosomes look like in the blood?

A

longer, really swirly purple things outside of RBCs

98
Q

American Trypanosomiasis is aka

A

tropanosoma cruzi

99
Q

Trypanosoma cruzi is transmitted from a mammalian reservoir to a human via the

A

tritomine insect which bites at night and poos the parasite onto your arm. you then spread it into yourself through the eye, or by scratching the bite

100
Q

pathogenesis of trypanosoma cruzi (American trypanosomiasis)

A
  1. Tritomine insect bites a human and poos out the parasite
  2. humans either put the poo in their eyes, or scratch it into the wound
  3. replication at the site of entry —> skin or eye problems
  4. spread to the lymph nodes
  5. replication in RBCs
  6. spread and damage to peripheral nerves and heart
101
Q

trypanosoma cruzi (american trypanosomiasis) causes manifestations in what 3 places?

A
  1. skin/eye (place of entry)
  2. blood
  3. GI/Heart
102
Q

trypanosoma cruzi (american trypanosomiasis) causes what manifestations at the skin/eye

A

chagoma —> resolves

103
Q

trypanosoma cruzi (american trypanosomiasis) causes what manifestations in the blood

A

fever, malaise –> hepatosplenamegaly

104
Q

trypanosoma cruzi (american trypanosomiasis) causes what manifestations in the GI/heart

A

GI: megaesophagus, megacolon
heart: arrythmia, cardiomyopathy

105
Q

what is Chaga’s disease and what parasite is it associated with?

A

it includes Romana’s Sign (unilateral eye swelling from rubbing parasite latent feces into the eye) and megacolon due to nerve damage/abdominal obstruction and inability to pass stool (this had the picture of the intestine opened up filled with worms)

it’s caused by Trypanosoma cruzi (American Trypanosomiasis)

106
Q

how are Leishmania species transmitted from their mammalian reservoir?

A

via the sandfly

107
Q

where do Leishmania speceis replicate?

A

in Reticuloendothelial Cells (cells of macrophagic origin that are in solid organs)

108
Q

Pathogenesis of Leishmania species

A
  1. transmitted from mammalian reservoir to humans via the sandfly
  2. replicates in reticuloendothelial cells
  3. undergoes Disseminated replication (leading to visceral Leishmania) or replicates at the site of entry leading to Cutaneous Leishmania.
  4. cutaneous leishmania can either resolve or spread to skin and mucosa (mucocutaneous Leishmania)
109
Q

3 different manifestations of leishmania

A
  1. Disseminated replication —> visceral leishmaniasis
  2. replication at site of entry —> cutaneous leishmaniasis (ulcers that will resolve on their own over time due to TH1 response)
  3. spread from the site of entry to surrounding skin and mucosa —> mucocutaneous leishmaniasis crusty and bulbous scarring/inflammation all over due to a TH2 resp)
110
Q

visceral Leishmaniasis leads to what manifestations?

A

fever, weight loss (but big tummy/wasting of arms), anemia, thrombocytopenia, neutropenia

111
Q

the anemia, thrombocytopenia and neutropenia found in visceral leishmaniasis indicates…

A

that replication is occuring in the bone marrow —> hemoatopoiesis is affected

112
Q

how is the protozoa toxoplasma gondii transmitted?

A

ingestion of raw meat

113
Q

which 3 important protazoan species are transmitted by vectors?

A
  1. Plasmodium species
  2. Trypanosoma species
  3. Leishmania species
114
Q

Which 3 important protozoa are transmitted via the fecal-oral route (including non-human feces)

A
  1. Toxoplasma gondii
  2. Giardia lamblia
  3. Entamoeba histolytica
115
Q

how are helminths (worms) classified?

A

by shape in cross section

116
Q

what are the 2 major classes of worms?

A
  1. Roundworms (aka nematodes)

2. Flatworms

117
Q

what is another name for a roundworm?

118
Q

what are two types of flatworms?

A
  1. Tapeworms (aka cestodes) which are segmented

2. flukes (aka trematodes) which are leaf shaped and non-segmented

119
Q

tapeworms are aka

120
Q

flukes are aka

A

trematodes

121
Q

4 GI Roundworms that we studied?

A
  1. Trichuris trichura
  2. Ascaris lumbricoides
  3. Hookworms
  4. Strongyloides stercoralis
122
Q

3 Gi tapeworms

A
  1. Diphyllobothrium
  2. Taenia saginata
  3. Taenia solium
123
Q

4 Blood/Tissue Roundworms

A

Filaria:

  1. Loa Loa
  2. Lymphatic filaria
  3. Onchocerca volvulus
  4. Dracunculus medinensis
124
Q

2 GI Tapeworms

A
  1. Taenia solium

2. Echinococcus granulosus

125
Q

1 Tissue/Blood Fluke

A

Schistosomiosis species

126
Q

which parasite is aka the whipworm and why?

A

Trichuris Trichiura because it has a thick part (which stays in the lumen of the GI tract) and a skinny part (which goes into the mucosa)

127
Q

how is Trichuris trichuiura (whipworm) transmitted?

A

eggs mature in the soil and then they’re eaten —-> transmitted via fecal oral route, but the eggs have to be in the envt between cycles to mature

128
Q

pathogenesis of Trichuris trichiura (whipworm) (5)

A
  1. Person sheds eggs in stool
  2. eggs mature in the soil and then are eaten (fecal oral transmission)
  3. the eggs hatch in the stomach
  4. Trichuris trichiura matures and mates in the intestine
  5. this causes blood loss and inflammation
129
Q

How does a light infection of Trichuris Trichiura (whipworm) manifest?

A

it’s asymptomatic

130
Q

How does a heavy ifxn of Trichuris trichuira manifest? (3)

A

dysentary (bloody diarrhea), anemia and malnutrition

131
Q

how do you diagnose someone with Trichuris trichuira

A

by seeing the eggs in the stool

132
Q

What is a light manifestation of Ascaris lumbricoides?

A

asymptomatic, rarely clock biliary or pancreatic ducts

133
Q

what are the sx of a heavy ifxn of Ascaris lumbricoides?

A

pneumonitis and GI obstruction

134
Q

Ascaris lumbicoides is transmitted via:

A

fecal oralspread

135
Q

pathogenesis of Ascaris lumbricoides (9)

A
  1. Person poos out eggs which mature in the soil
  2. person eats the eggs
  3. eggs hatch in the duodenum
  4. larvae enter circulation
  5. Lodge in the lung
  6. Mature
  7. migrate up/get coughed up in into the trachea and swallowed
  8. Mature and mate in the intestine
  9. poop out the eggs…
136
Q

what type of host are humans for Ascaris lumbricoides?

A

definitive

137
Q

two types of hookworms?

A
  1. A duodenale

2. N. americanus

138
Q

How do hookworms spread?

A
  1. eggs are shed in species, the eggs hatch, mature and the larvae penetrate the skin
139
Q

pathogenesis of hookworms

A
  1. Larvae penetrate the skin and enter circulation
  2. the larvae lodge in the lung and they mature there
  3. migrate up, are swallowed
  4. mature, mate in the intestine
  5. attach and suck blood
  6. shed eggs in species which hatch, mature and the larvae penetrate the skin
140
Q

what are the manifestations of a skin ifxn with hookworms?

A
  1. Hypersensitivity to larva (“ground itch”)
141
Q

what are the manifestations of a heavy hookworm ifxn?

A
  1. pneumonitis
  2. blood loss —-> anemia
  3. malnutrition
142
Q

the image of the raised line of the worm on the foot that is really red/crusty is what?

A

“ground itch”– the linear pattern of larvae moving under the skin and the host response to the larva

143
Q

what’s unique about strongyloides stercoralis?

A

it can autoinfect the host– uncommonly, larvae mature in the GI —> autoinfection and superinfection

144
Q

how is a host infected with strongyloides stercoralis?

A

immature larvae in feces —> mature larvae penetrate skin. There are also free livin adults in the envt that produce eggs —> larvae penetrate skin

145
Q

pathogenesis of strongyloides stercoralis? (7)

A
  1. immature larvae are passed in stool
  2. mature larvae penetrate the skin
  3. larvae enter the circulation
  4. the larvae lodge in the lung and mature
  5. they migrate up and are swallowed
  6. they mature and mate in the intestine
  7. They produce immature larvae which are passed in the stool
146
Q

what is “superinfection” referring to in terms of strongyloides stercoralis?

A

when production of tons of parasites that drag in gram negative bacteria —> sepsis

147
Q

what increases the risk of autinfection/superinfection by strongyloides stercoralis

A

corticosteroids– they act as sex hormones for worm and drive them twd differentiation

148
Q

manifestations of strongyloides (3)

A
  1. Ground itch (worm passing around on the foot- like hookworms)
  2. GI Ifxn w/o hyperinfection is rarely symptomatic
  3. Hyperifxn: fever, abdo pain, diarrhea, dyspnea, wheezing, hemptysis, cough
149
Q

why does styongyloides stercoralis often leave to wheezing, hemoptysis and cough

A

because the larvae lodge themselves in the lung where they mature

150
Q

3 parasites that lead to auto ifxn

A
  1. stongyloides stercoralis (roundworm)
  2. pin worms
  3. Taenia solium (tapeworm)
151
Q

how are all filiarial Ifxns are acquired?

A

vector bites —> larvae penetrate the skin

152
Q

pathogenesis of filarial ifxns (5):

A
  1. vector bites —> larvae penetrates skin
  2. larvae mature to long-lived adults
  3. adults produce microfilaria
  4. microfilaria enter vector during bite
  5. vector bites host, larvae penetrates skin…
153
Q

are manifestations of filarial diseases caused by adults or microfilia?

A

they can be caused by both

154
Q

three types of filarial parasites

A
  1. Loa loa (the African eye worm)
  2. Lymphatic Filariasis
  3. Onchocerca volvulus (River blindness)
155
Q

the vector for the African Eye Worm: Loa loa (filarial parasite)

156
Q

pathogenesis of the African Eye Worm (Loa loa– filarial parasite)

A
  1. Tabanid bites, larvae penetrate skin
  2. larvae mature in subqutaneous tissue
  3. adults migrate in subQ tissue (inc eye)
  4. Microfilaria released into blood stream
  5. little host response or damage
157
Q

adults who are infected with Loa loa (The African Eye worm) get manifestations where? (2)

A
  1. Eye: local edema– can see the filaria crossing
  2. Skin: local edema —> “calabar swellings” (fugitive, swollen lumps of subcutaneous tissue caused by a parasitic filarial worm, that move with the worms)
158
Q

calabar swellings and a worm moving across the eye are associated with what parasite?

A

Loa loa (African Eye Worm)

159
Q

lymphatic filariasis are spread via

A

mosquitoes (many species) —> larvae injected

160
Q

pathogenesis of lymphatic filariasis

A
  1. mosquito bites —> larvae injected
  2. larvae enter circ
  3. larvae lodge in lymph and mature
  4. adults release microfilia
  5. microfilia in lymph and blood
161
Q

Early manifestations of lymphatic filariasis

A

lymphadenitis, fever

162
Q

manifestations of Chronic lymphatic filariasis

A

worms + scarring —> obstruction of lymph —> fluid accumulation/elephantiasis

163
Q

elephantiasis is associated with which parasite?

A

lymphatic filariasis

164
Q

pathogenesis of River blindness (Onchocerca volvulus)

A
  1. Simulium blackfly bites, larvae is injected
  2. Larvae mature in the skin
  3. Adults in skin
  4. release microfilariae
  5. microfilaria in lymph, blood, tissue (eye- conjunctiva)
  6. hypersensitivity
165
Q

how is River Blindness (Onchocerca volvulus) transmitted?

A

Simulium blackfly

166
Q

manifestations of River blindness (Onchocerca volvulus)

A
  1. Skin and connective tissue: atrophy, depigmentation

2. Eye: blindness due to ifxn of the conjunctiva

167
Q

Loiasis
Species that causes the disease:
Site and damage (2)

A 
Loiasis
Species that causes the disease: Loa loa (filarial parasite)
Site and damage (2): 
1. skin (adult) ---> calabar swelling
2. Eye (adult) ---> pain
168
Q

Lymphatic filariasis
species that causes disease (2):
Site and damage (1)

A

Lymphatic filariasis
species that causes disease: 1) W. bancrofti and 2)B. malayi
Site and damage (1): Lymphatics (adult) —> obstruction, lymphedema and elephatiasis

169
Q

River blindness
species that causes disease:
Site and damage (2)

A

River blindness
species that causes disease: onchocerca volvulus
Site and damage: 1) eye (microfilaria) —> blindness, 2) skin (microfilaria) —> pigmentation changes and loss of elasticity

170
Q

Intestinal tapeworms are all acquired from…

A

eating larvae in rare meat

171
Q

pathogenesis of intestinal tapeworms

A
  1. Larvae are ingested in rare meat
  2. eggs are passed in stool
  3. eggs or larvae are ingested by animals
  4. larvae are ingested in rare meat
172
Q

Tapeworm Taenia solium comes from

173
Q

tapeworm taenia saginata comes from

174
Q

tapeworm Diphyllobothrium latum comes from

A

freshwater fish

175
Q

Sx from Gi ifxn with tapeworm

A

rarely symptomatic. Diphyllobothrium latum —> B12 deficiency, anemia

176
Q

Two forms of Taenia solium- and how you get each

A
  1. GI tapeworm that you get from ingesting pig larvae

2. Cysticerosis– tissue ifxn caused by eating the eggs shed in human stool rather

177
Q

cysticercosis manifestations

A

T. solium larvae travel to muscles and brain. they die —> immune response —> seizures and hydrocephaly

178
Q

what is neurocysticercosis

A

cysts of T. Solium in the brain from ingesting eggs from human stool, rather than larvae from rare meat

179
Q

normal lifecycle for Echinococcus granulosus and how humans fit in

A

Normal:

  1. carnivore (like a dog) ingests animal with cyst (immature worm) in it —> GI parasite
  2. Carnivore poos out eggs in stool.
  3. sheep eats stool with egg in it —> tissue parasite
  4. Sheep gets eaten by dog…

Humans take over the sheep part and get the tissue parasite

180
Q

Hyatid disease pathogenesis

A

humans ingest E. granulosus eggs.

  1. embryonic worms penetrate intestinal wall and enter circulation
  2. they migrate to tissue, usually liver and lung
  3. slowly form large cysts full of protoscolices – asymp. except when they impinge on adjacent structure (bile duct)
  4. cysts can rupture —> anaphalyxes
181
Q

Schisto pathogenesis

A
  1. Cercarae mature
  2. reach hepatic portal vessels, mature
  3. paired adults migrate to veins of mesentary or bladder (no host response)
  4. release eggs
  5. hypersensitivity
182
Q

how is schisto transmitted?

A

cercariae penetrate the skin —-> eggs shed in urine/stool —> infect snails —> cercariae penetrate skin

183
Q

3 species of schisto

A

schistosoma mansoni
schistosoma japonicum
schistosoma haematobium

184
Q

which 2 types of schisto infect the GI mesenteric veins and shed eggs in the stool?

A

Schistosoma mansoni and japonicum

185
Q

which type of schisto infects th bladder veins and sheds eggs in the urine?

A

schistosoma haematobium

186
Q

manifestations of schisto

A
  1. “swimmer’s itch”- dermatitis caused by cercariae as they swim through
  2. febrile illness when flukes reach venules
  3. eggs —> granulomas (symp vary with tissue) (liver/spleen: enlarged, portal HTN, ascites, Intestine: colitis, cramps, pain, bleeding, Bladder: hematuria)
187
Q

how do schisto eggs —> granulomas in the liver manifest?

A

liver = enlarged, portal HTN, ascites

188
Q

how do schisto eggs —> granulomas in the intestine manifest?

A

colitis, cramps, pain, bleeding

189
Q

how do schisto eggs —> granulomas in the bladder manifest?

190
Q

What 3 helminths do we get from ingesting meat?

A 
Diphyllobothrium latum (fish)
Taenia saginata (beef)
Taenia solium (pig)
191
Q

what helminthe do we get via vectors?

A
  1. filaria

2. onchocerca

192
Q

which helminths do we get from fecal-oral transmission? (4)

A
  1. Taenia solium (cysticercosis)
  2. Trichuris (human feces)
  3. Ascaris (human feces)
  4. Echinococcus (dog feces)
193
Q

which helminths can we get from skin penetration? (3)

A
  1. hookworms
  2. strongyloides
  3. schistosomas
194
Q

fever with incubation period of under 14 days is most likely to be one of which 4 things?

A
  1. plasmodium falciparum
  2. typhoid fever
  3. dengue
  4. Campy, Sal, Shig
195
Q

fever with incubation period of 14 days-6wks is most likely to be

A

acute HIV or EBV

196
Q

Fever with incubation period of more than 6 weeks is most likely to be which 2 things

A

plasmodium vivax

Visceral Leishmaniasis

MICRO II (8 decks)

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