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IBI Test 2 > B3-090 Protozoal Infections > Flashcards

B3-090 Protozoal Infections Flashcards

1
Q

main species causing 95% of malaria

A

plasmodium faciparum
plasmodium vivax

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2
Q

a majority of malaria in the US comes from

A

imported from visiting friends and relatives

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3
Q

risk factors for malaria

A

living in an endemic area

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4
Q

why are VFRs the highest risk causing malaria?

A

travel to more rural areas

poor adherence to propyhlaxis

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5
Q

how is malaria most often transmitted?

A

anopheles mosquito bite

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6
Q

less common transmissions of malara

A

blood transfusion
transplacental
needlestick

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7
Q

incubation time of malaria

A

2 ish weeks

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8
Q

which strains of malaria become hypnozoities and remain in the liver?

A

P. ovale
P. vivax

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9
Q

sporozoites penetrate the hepatocyte via attachment of the sporozoitie surface protein coat to the hepatocyte heparan sulfate glycoproteins and LDL receptor

A

malaria

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10
Q

diagnosis is really in thinking about it and having a low threshold of suspicion

A

malaria

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11
Q

clinical presentation of malaria

A

fever, chills, headache, splenomegaly

**almost any symptom has been reported.

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12
Q

3 stages of malarial paroxysm

A
  1. cold or chilling stage
  2. hot stage
  3. sweating stage
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13
Q

cyclic fevers are a hallmark of ________ caused by ___________

A

malaria; lysis of RBCs

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14
Q

tertian malaria is caused by what organisms?

A

P. vivax, P. ovale

Fevers occur every 48 hours

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15
Q

Quartan malaria is caused by what organisms?

A

P. malariae

fevers occur every 72 hours

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16
Q

P. falciparum causes _________ fevers

A

continuous

w/ intermittent irregular spikes
**on 48 hour cycle

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17
Q

laboratory findings: malaria

A

anemia
WBC fluctuation
thrombocytopenia
evidence of hemolysis

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18
Q

Sequestration is caused by __________ and results in ___________

A

P. faciparum; endothelial margination and stickiness

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19
Q

why is P. falciparum the most virulent strain of malaria?

A

infects all RBCs
sequestration

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20
Q

cerebral malaria
hypoglycemia
lactic acidosis
severe anemia
pulmonary edema
tropical splenomegaly
blackwater fever

are complications of which malarial organism

A

P. falciparum

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21
Q

late splenic rupture is a complication of which malarial organism

A

P. vivax

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22
Q

immune complex glomerulonephritis is a complication of which malarial organism

A

P. malariae

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23
Q

a parasitemia >5% indicates

A

severe malaria

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24
Q

risk factors for severe malaria

A

children 6 months-3 years
children and traveler’s who are not immune

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25
Q

malaria immunity requires

A

repeated exposure
**wanes with lack of exposure

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26
Q

in endemic areas, children are usually protected from malaria after ________ years

A

three

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27
Q

gold standard for diagnosis of malaria

A

parasites in RBC on peripheral blood smear

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28
Q

what kind of stain do you use to visualize malaria parasites in RBCs?

A

Giemsa stain

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29
Q

disadvantage: giema stain

A

requires expertise and can’t be done STAT

patient deteriorate rapidly

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30
Q

antigen detection has _________ sensitivity for non-falciparum species

A

decreased

**always back up with smear

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31
Q

a PCR test can be performed for suspected malaria but

A

not commercially available, and not run STAT

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32
Q

the thick portion of a peripheral blood smear is for

A

a screening test

**sensitive

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33
Q

the thin portion of a peripheral blood smear is for

A

species identification and %parisitemia

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34
Q

how should you draw peripheral blood smears for optimal sensitivity?

A

3 spaced draws over 12-24 hours

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35
Q

a lateral flow assay done for malaria is detecting

A

HRP-1

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36
Q

con of lateral flow assay for malaria

A

less sensitive, must be backed up by thick smear

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37
Q

what drug is tissue schizonticidal for malaria?

A

primaquine

**P. ovale, P. vivax

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38
Q

what drug is the best choice for blood schizonticidal for malaria?

A

atovaqunone/proguanil

**resistance to chloroquine and mefloquine is growing

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39
Q

if you have clinical suspicion of malaria

A

perform thick and thin blood smears AND read them within hours (STAT)

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40
Q

if quindine is unavailable, contact CDC malaria hotline for

A

artesunate

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41
Q

what is malaria related mortality so high?

A

lack of prevention
diagnostic failure
management failure

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42
Q

“looks like malaria, acts like Lyme disease”

A

babesia

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43
Q

most common babesia species

A

B. microti

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44
Q

babesia is usually transmitted by

A

ixodes tick (NE, MN, WI)

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45
Q

rare routes of transmission for babesia

A

blood transfusion
transplacental

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46
Q

pathogenesis: malaria and babesia

A

invade RBCs
cytokine and TNF-a release
fever

causing anemia, thrombocytopenia, splenomegaly

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47
Q

incubation period: babesia

A

1-4 weeks

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48
Q

may-september seasonality
(75% June-August)

A

babesia

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49
Q

most babesia infections are

A

asymptomatic

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50
Q

symptoms of babesia

A

febrile illness with anemia

shaking, chills, fever, headache, myalgia

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51
Q

what patient population are we concerned about with a babesia infection?

A

asplenics

also elderly and immunocompromised

52
Q

on physical examination of babesia infection, what would be noted?

A

fever, splenomegaly, hepatomegaly

53
Q

babesia is often seen as a coinfection with

A

Lyme disease

54
Q

diagnosis of babesia on blood smear is indicated by

A

ring forms and maltese crosses

55
Q

treatment of mild to moderate babesia (<4% parisitemia)

A

atovoquone and azithromycin

56
Q

treatment of severe babesia (>4% parasitemia)

A

IV azithromycin + atovoquone

IV clindamycin + quinine

57
Q

hemoflagellates

A

trypanosoma and leishmania

58
Q

two clinically important species of trypanosom

A

T. brucei
T. cruzi

59
Q

epimastigote of trypansoma

A

found in vector

60
Q

amastigote of trypansoma

A

non motile, dividing, found in tissues

61
Q

trypomastigote

A

motile, non-dividing, found in blood

62
Q

identify nucleus, flagellum, undulating membrane, and kinetoplast

A
63
Q

T. brucei is transmitted by

A

tsetse fly

64
Q

african sleeping sickness is caused by

A

T brucei

65
Q

T. brucei gambiense is endemic to _______ Africa

A

western

66
Q

T. brucei rhodesiense is endemic to ______ Africa

A

east

67
Q

the primary reservoir for T. brucei is

A

animals

68
Q

Stage I of a T brucei infection is characterized by

A

intermittent fever, headache, rash, posterior cervical lymphadenopathy, chancre at bite site

69
Q

stage 2 of a T. brucei infection is characterized by

A

wasting, meningoencephalitis
headaches, phychosis, ataxia, tremor, difficulty concentrating, altered sleep cycle, convulsions

70
Q

Which T. brucei species is the most severe, charactereized by rapid progression from stage 1 to stage 2?

A

T. brucei rhodesiense

71
Q

diagnosis of T. brucei is

A

limited

can develop over years, so hard to get a good hx
labs are nonspecific
can see trypomatigotes in blood smear

72
Q

chagas disease

A

T. cruzi (american trypanosomiasis)

73
Q

T. cruzi is most commonly transmitted by

A

Kissing Bug (reduviid/triatome)

74
Q

5-20% of T cruzi infections are transmitted via

A

blood transfusion

75
Q

less common transmission of T cruzi

A

transplacental
transplantation
oral transmission
accidental-laboratory

76
Q

T cruzi: slyvatic cycle exists in

A

US-west and South

77
Q

T. cruzi is most prevalent in

A

Central and South America

**blood donors and individuals from these areas are classical presentation

78
Q

wild and domestic animals around ________ are reservoirs of T. cruzi

A

rural mud/thatch homes

79
Q

contaminative transmission

A

bug bites, turns around and poops into the conjunctive or it it itches and the host scratches the poop into the wound

80
Q

T. cruzi spreads via

A

contaminative transmission

81
Q

Acute chagas symptoms:

A

chagoma-followed by malaise and fever
romana’s sign- painless unilateral edema of both eyelids

**mostly occurs in children under 15. highest 1-5

82
Q

chronic chagas symptoms

A

most are indeterminate/latent phase with minimal symptoms

some progress to cardiomyopathy, GI involvement, megaesophagus, megacolon

83
Q

T. cruzi diagnosis

A

clinical
acute disease: blood smears
chronic: histopath biopsy

84
Q

the kinectoplast on T. brucei is _________ compared to T. cruzi

A

much larger

85
Q

treatment T cruzi

A

nifurtimox
benznidazole

86
Q

intracellular pathogens that live in the macrophage

A

leishmania

87
Q

leishmania is transmitted by

A

sand fly

88
Q

Old World Leishmania (mediterranean, africa, asia)

A

L. donovani
L. infantum
L. tropica

89
Q

New World Leishmania (latin America)

A

L. chagasi
L. mexicana
L. braziliensis

90
Q

reservoirs of Leishmania

A

dogs, rodents, etc

91
Q

wet, dry, pizza-like chronic ulcer with raised borders. sporotrichoid

(variable lesions at site of inoculation)

A

cutaneous leishmaniasis

92
Q

dissemination of skin to naso-oropharyngeal mucosa
erosive mucosal regions in nose, mouth, pharynx, larynx

A

mucocutaneous leishmaniasis

93
Q

mucocutaneous leishmaniasis is caused by

A

L. braziliensis

New World

94
Q

L. tropica associated with Gulf War

A

viscerotropic leishmaniasis

95
Q

insidious onset of malaise, fever, weight loss, splenomegaly, hepatomegaly, pancytopenia

A

visceral leishmaniasis

caused by L donovani, L infantum

96
Q

most severe form of visceral leishmaniasis

A

kala azar (black fever)

97
Q

diagnosis Leishmania

A

clinical/epidemiological

aspirate spleen or bone marrow
amastigotes on slide in macrophages

98
Q

leishmania treatment requires

A

expert consulations

99
Q

is treatment required for cutaneous leishmaniasis?

A

no, self limited

100
Q

definitive host for toxoplasma gondii

A

cats

101
Q

intermediate host for toxoplasma gondii are infected by

A

fecal contamination

102
Q

toxoplasma gondii can be transmitted to humans via

A

undercooked meat (tissue cyst)
contaminated food/water
transplacental
blood transfusion
organ transplant

103
Q

toxoplasma gondii presentation in immunocompetent host

A

mostly asymptomatic

may be mono like-mono spot neg

104
Q

toxoplasma gondii presentation in immunocompromised host

A

febrile illness with CNS symptoms, pneumonitis, chorioretinitis

**can be primary or reactivate

105
Q

congenital toxoplasma gondii is from a _______________ infection in mother

A

acute primary

106
Q

classic triad for congenital toxoplasmosis:

A

chorioretinitis, intracranial calcifications, hydrocephalus

107
Q

AIDS defining illness [from this lecture]

A

toxoplasma gondii

108
Q

toxoplasma gondii: diagnosis

A

compatible clinical syndrome
imaging
brain biopsy
IgM, IgG

109
Q

toxoplasmosis on CNS imaging will show

A

multiple ring enhancing lesions

110
Q

what would you see on tissue histopath of toxoplasma gondii?

A

tissue cysts- bradyzoites
free tachyzoites (cresent shaped)

111
Q

treatment of toxoplasma gondii in newly infected women

A

spiramycin

112
Q

treatment of toxoplasma gondii in immunocompromised

A

pyrimethamine+sulfadiazine+folinic acid

**maintenance for life

113
Q

feeding and dividing form of amoeba

A

ameboid trophozoite

114
Q

environmentally resistant form of amoeba

A

cyst

115
Q

mobile form of amoeba

A

flagellate

116
Q

free living means

A

humans play no part in life cycle

117
Q

where are free-living amebae found

A

everywhere

118
Q

Naegleria fowleri is an amoeba causing

A

primary amebic meningoencephalitis

119
Q

rapid onset
severe headache
vomiting
stiff neck rapidly progresses to coma
seen in healthy children, sometimes adults

A

naegleria fowleri

120
Q

Acanthamoeba and Balamuthia cause

A

granulomatous amebic encephalitis

121
Q

prolonged onset
headache
low-grade fever
focal neurological deficits
seen in immunocompromised adults

A

Acanthamoeba (and Balamuthia)

122
Q

acanthamoeba causes

A

amebic keratinitis in cornea

123
Q

diagnosis PAM

A

wet mount or Giemsa of CSF
brain biopsy

124
Q

male 18-28, contact lense wearer may be at risk for

A

amebic keratinitis

125
Q

Diagnosis: GAE

A

brain or skin biopsy

126
Q

diagnosis: AK

A

culture corneal scraping or contacts
giemsa stain

127
Q

treatment AK

A

prescription eye medication
debridement
corneal transplant, enucleation

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