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Parasitic & Fungal Infections Flashcards

1
Q

Toxoplasmosis

caused by what?

parasite name

A

Toxoplasma gondii

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2
Q

Toxoplasmosis

transmission

3 modes, host species

A
  • fecal oral
  • transplacental transmission
  • inoculation via blood transfusion/organ transplantation

cats = hosts

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3
Q

Toxoplasmosis

Signs/sx in typical population

4 sx, 1 sign, 1 statement?

A
  • can be asx
  • fever, malaise, headache, sore throat
  • cervical lymphadenopathy
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4
Q

Toxoplasmosis

effects of congenital infections

in offspring

A

CNS abnormalities
retinochoroiditis
hydrocephalus
intracranial calcifications

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5
Q

Toxoplasmosis

infections reactivation can lead to?

4

A
  • reactivation leads to encephalitis, retinochoroiditis, pneumonitis, myocarditis
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6
Q

Toxoplasmosis

Dx

5 different things

A
  • serology (IgG or IgM)
  • PCR (amniotic fluid, blood, CSF)
  • observation of parasites in stained tissues (meh)
  • isolation from blood/other fluids (meh)
  • CT or MRI of brain
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7
Q

Toxoplasmosis

what will CT or MRI show?

A

multiple ring-enhancing lesions

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8
Q

Toxoplasmosis

IgG Serology
IgM Serology

general population vs immunocompromised

A
  1. IgG will be positive in all populations
  2. IgM will only be positive in the non-immunocompromised individuals
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9
Q

Toxoplasmosis- Congenital

when in pregnancy are infections more likely to have serious outcomes?

A

earlier infection

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10
Q

Toxoplasmosis- Congenital

outcomes from early infection

A
  1. spontaneous abortion
  2. stillbirth
  3. neurologic problems
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11
Q

Toxoplasmosis

Complications of infections in immunocompromised

AIDS/cancer

A
  1. encephalitis with necrotizing brain lesions
  2. chorioretinitis
  3. pneumonitis
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12
Q

Toxoplasmosis

how to treat general population vs immunocomp

A
  • self limiting
  • Immunodeficient: full therapy for 4-6 wks followed by maintenance therapy with lower dosese
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13
Q

Toxoplasmosis

what to treat in pregnancy

A

treat primary infection to reduce risk of fetal transmission

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14
Q

Toxoplasmosis

when to treat- retinochoroiditis

A

treatment ok if decrease in visual acuity, multiple/large lesions, macular lesions, inflammation, >1 mo in duration

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15
Q

Toxoplasmosis

Meds- general population

meds, freq

A
  • pyrimethamine (PO QD)
  • sulfadiazine (PO, QID hrs)
  • folinic acid/leucovorin QD
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16
Q

Toxoplasmosis

Meds- pregnancy

A
  • spiramycin PO Q8 hrs until delivery
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17
Q

Toxoplasmosis

Prophylaxis dose HIV+ pts

when/what to use

A
  • use in pts with low CD4 counts
  • Trimethoprim/sulfamethoxazle
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18
Q

Toxoplasmosis

Prevention

3 categories

A
  • fully cook meat
  • cat related care
  • hygiene when gardening
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19
Q

Amebiasis

parasites of concern

3: entamoeba……

A

Entamoeba dispar
Entamoeba moshkovskii
Entamoeba histolytica

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20
Q

Amebiasis

transmission

A

fecal oral
waterborne

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21
Q

Amebiasis

signs/sx

5- which is most common?

A
  • abd pain
  • diarrhea
  • severe infections
  • extraintestinal disease
  • liver abscess (MOST COMMON)
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22
Q

Amebiasis

dx

3 things

A
  • stool test
  • serologic testing
  • U/S, CT, MRI for liver abscess
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23
Q

Amebiasis

Tx

A

metronidazole or tinidazole

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24
Q

Malaria

mode of transmission

A

exposure to female anopheline mosquitoes in a malaria endemic country

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25
Q

Malaria

where is malaria endemic?

5 things

A
  • South America
  • Central America
  • Africa
  • Middle East
  • Southeast Asia
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26
Q

Malaria

parasite responsible

A

plasmodium falciparum

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27
Q

Malaria

Pathophys

A
  1. upon bite, mosquitoes inject sporozoites which infect hepatocytes
  2. Merozoites are released by liver and rapidly infect RBCs
  3. Mulitple rounds of reproduction = systemic infection (can spread to others if bitten by mosquito)
  4. infected cells lyse which dumps toxins into bloodstream
  5. infected RBCs adhere to vein walls
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28
Q

Malaria

“Classical” presentation (not usually how it is)

3 stages

A
  1. Cold Stage (chills)
  2. Hot Stage (fever, HA, v, seizures)
  3. Sweating Stage (sweats, fatigue)
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29
Q

Malaria

Common Sx

8

A
  • fever/chills/sweats
  • headaches
  • n/v
  • body aches, malaise
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30
Q

Malaria

Clinical Findings

7 things

A
  1. severe anemia
  2. hypotension
  3. pulmonary edema
  4. AKI
  5. hypoglycemia
  6. acidosis
  7. hemolysis
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31
Q

Malaria

why does severe anemia occur?

A

RBCs getting blasted apart by parasites

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32
Q

Malaria

why does hypoglycemia occur?

A

reduced gluconeogenesis

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33
Q

Malaria

why does acidosis occur?

A

microcirculatory flow affected, anaerobic glycolysis

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34
Q

Malaria

why does renal impairment occur?

A

infarcts, capillary leakage

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35
Q

Malaria

why does pulmonary edema occur?

A

sequestration of parasitized RBCs in lungs and/or cytokine-induced leakage from pulmonary vasculature

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36
Q

Malaria

Dx

A
  • parasite in peripheral blood smears
  • urine dipstick for antigen
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37
Q

Malaria

Tx

First Line

A

Chloroquine- use only when no suspected resistance

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38
Q

Malaria

Tx- chloroquine resistance

A

Artemisinin

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39
Q

Malaria

Tx- severe malaria

A
  • IV Artemisinin
  • Maintenance of fluids/electrolytes
  • resp/hemodynamic support
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40
Q

Malaria

prevention

A
  • bed nets/insecticides
  • travelers can take prophylactic abx
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41
Q

Malaria

which meds are used prophylactically in travelers?

A
  • chloroquine
  • malarone
  • mefloquine
  • doxycycline
  • primaquine
  • tafenoquine
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42
Q

what are helminthic infections?

A

worms :)

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43
Q

Enterobius (Pinworms)

caused by what worm?

A

Enterobius vernicularis

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44
Q

Enterobius (Pinworms)

who usually gets sick?

A

chilren under 18 or those in congregate settings

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45
Q

Enterobius (Pinworms)

mode of transmission

A

oral after scratching
exposure to eggs on contaminated food/fomites

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46
Q

Enterobius (Pinworms)

Pathophys

A
  1. eggs hatch in duodenum
  2. larvae migrate to cecum
  3. females mature after 1 mo, are viable for another mo after
  4. migrate through anus nocturnally to deposit eggs on perianal skin
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47
Q

Enterobius (Pinworms)

Key sign to watch for

PPP

A

perianal pruritus
particularly at night

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48
Q

Enterobius (Pinworms)

Dx

A

characteristic eggs on perianal skin using clear tape
worms seen in feces

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49
Q

Enterobius (Pinworms)

Tx

A
  1. Albendazole or mebendazole (paralyzes parasite)
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50
Q

Enterobius (Pinworms)

when to redose?

A

2 wks after tx because of frequent reinfection

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51
Q

ancylostoma duodenale and necator americanus (Hookworm)

what have patients usually have done prior to infection?

A

walked barefoot

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52
Q

ancylostoma duodenale and necator americanus (Hookworm)

Life Cycle

A
  1. eggs deposited via feces into warm moist soil
  2. eggs hatch into larvae that are infective for a week
  3. larvae contact skin and travel via bloodstream to pulmonary capillaries
  4. in lungs, larvae penetrate into alveoli and are carried via cillia into upper airway & then swallowed.
  5. Once in the GI tract, they attach to bowel mucosa & mature into adults where they suck blood
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53
Q

ancylostoma duodenale and necator americanus (Hookworm)

what is blood loss proportionate to?

A

worm burden

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54
Q

ancylostoma duodenale and necator americanus (Hookworm)

Signs/Sx

7 things

A
  • transient pruritic skin rash (can “see” worm through skin)
  • pulmonary sx
  • anorexia, diarrhea, abd discomfort
  • iron def anemia
  • blood/eggs in stool
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55
Q

ancylostoma duodenale and necator americanus (Hookworm)

Dx

A
  • characteristic eggs in stool
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56
Q

ancylostoma duodenale and necator americanus (Hookworm)

Tx

A
  • ivermectin PO
  • albendazole PO 3 days
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57
Q

Tapeworms

Taenia saginata

A

tapeworm from eating raw or undercooked beef

58
Q

Tapeworms

Taneia solium

A

tapeworm from eating undercooked pork

59
Q

Tapeworms

Diphyllobothrium latum

A

tapeworm from undercooked freshwater fish

60
Q

Tapeworms

hymenolpeis nana

A

tapeworm from food contaminated w/ human feces

61
Q

Tapeworms

signs/sx

3

A
  1. GI sx
  2. anorexia
  3. wt loss
62
Q

Tapeworms

Dx

A

eggs in stool

63
Q

Tapeworms

tx

A

praziquantel x1

64
Q

Ascariasis

what is the most common intestinal worm?

A

ascaris lumbricoides

65
Q

Ascariasis

mode of transmission?

A

ingestion of eggs in contaminated food

66
Q

Ascariasis

pathophys

A
  1. larvae hatch in small intestine
  2. penetrate the blood-stream
  3. migrate to lungs
  4. travel via airway back to GI tract
67
Q

Ascariasis

Dx

A
  • most are asx
  • dx made by ID of eggs in stool/worms
68
Q

Ascariasis

Tx

A
  • mebendazole
  • albendazole
  • pyrantel pamoate
69
Q

Fluke

caused by which 3 things?

A
  1. clonorchia sinensis
  2. opisthorchis viverrine
  3. fasicola hepatica
70
Q

Fluke

mode of transmission

A
  • humans get ill by eating undercooked fish, crabs, crayfish, water plants in endemic areas
71
Q

Fluke

sx

A

most are asx
mild GI complaints

72
Q

Fluke

dx

A
  • clinical findings
  • eggs in stool
73
Q

Fluke

tx

A

Praziquantel

74
Q

Trichinosis (Roundworm)

causative agent?

A

trichinella spiralis

75
Q

Trichinosis (Roundworm)

mode of transmission

A

ingestion of raw pork

76
Q

Trichinosis (Roundworm)

sx

7 sx

A
  • primarily asx
  • GI sx, fever, myalgias, periorbital edema, HA, cough, rash
77
Q

Trichinosis (Roundworm)

dx

A
  • elevated muscle enzymes
  • serological tests
  • muscle biopsy (last resort)
78
Q

Trichinosis (Roundworm)

tx

A

mebendazole
albendazole

79
Q

Filariasis

caused by what?

A

wuchereria bancrofti

80
Q

Filariasis

signs & sx

A
  • episodic attacks of lymphangitis
  • fever
  • chronic progressive swelling of extremities & genitals
81
Q

Loiasis

transmitted by?

A

chrysops flies

82
Q

Loiasis

when adults, migrate to where?

83
Q

Rocky Mountain Spotted Fever

causative agent

A

rickettsia rickettsii

84
Q

Rocky Mountain Spotted Fever

mode of transmission

85
Q

Rocky Mountain Spotted Fever

pathophys

A
  • R. rickettsii damanges vascular endothelial cells
  • endothelial cells produce prstaglandings that cause increased vascular permeability
  • hyponatremia from release of ADH as a response to hypovolemia/leaky vasculature
86
Q

Rocky Mountain Spotted Fever

signs & sx

A
  • classic: fever, HA, rash, hx of tick bite
  • general: malaise, myalgias, arthralgias
87
Q

Rocky Mountain Spotted Fever

describe rash

A
  • rash in approx 90% of pts
  • rash on palms, soles
88
Q

Rocky Mountain Spotted Fever

Lab results

initial vs more progressed

A
  1. normal WBC, maybe left shift
  2. thrombocytopenia becomes more severe
89
Q

Rocky Mountain Spotted Fever

lab testing

A
  • serial serologic examinations by indirect fluorescent antibody can retrospectively confirm diagnosis
90
Q

Rocky Mountain Spotted Fever

empirical abx therapy

A
  • doxycycline (100mg PO, QID, 5-7 days)
  • 10-14 days if case was severe
  • Chloramphenicol is second choice
91
Q

Rocky Mountain Spotted Fever

prevention

A
  • protective clothing
  • tick-repellent
  • prophylaxis is not recommended
92
Q

Lyme Disease

caused by?

A

borrelia burgdorferi

93
Q

Lyme Disease

location?
seasonality?

A
  • northeastern and north central US
  • late spring to summer
94
Q

Lyme Disease

Stages

A
  1. early localized
  2. early disseminated
  3. late
95
Q

Lyme Disease

describe the early localized stage

A
  • erythema migrans
  • bulls-eye rash w/ central clearing
  • non-specific flu like sx
96
Q

Lyme Disease

describe the early disseminated stage

A
  • weeks to several months after bite
  • acute neurologic sx (palsy, aseptic meningitis)
  • cardiac involvement (arrhythmias)
97
Q

Lyme Disease

describe the late stage

A
  • months to years after infection onset
  • arthritis
  • encephalopathy or polyneuropathy
98
Q

Lyme Disease

common sites of tick bites

A

thigh
groin
axilla

99
Q

Lyme Disease

Dx

3 criteria & 2 tests

A
  • exposure to tick habitats
  • erythema migrans
  • 1 late manifestation of disease
  • lab confirmation: ab testing, pos western blot test
100
Q

Lyme Disease

Tx

A
  1. Doxycycline (100mg PO, Q12 hrs, 10 days)
101
Q

Lyme Disease

prophylaxis tx

A

doxycycline 200mg PO

102
Q

Histoplasmosis

caused by what?

A

Histoplasma capsulatum

103
Q

Histoplasmosis

mode of transmission

A

exposure to bird and bat droppings (common along Ohio/Mississippi river valleys)

104
Q

Histoplasmosis

pathophys

A
  1. conversion into yeast cells
  2. engulfed by phagocytes in lungs
  3. organism proliferates and then lymphohematogenous spread to other organs
105
Q

Histoplasmosis

sx

A
  1. usually asx
  2. if sx, then respiratory & macular/papular rash
  3. can be mild to severe
106
Q

Histoplasmosis

what do severe infections usually have?

A

atypical pneumonia

107
Q

Histoplasmosis

Presentation when disseminated in immunocompromised pts

A
  • CNS lesions
  • adrenal lesions/insufficiency
  • pancytopenia
  • pulmonary: cavities, nodules, infiltrates

variable presentation

108
Q

Histoplasmosis

Dx

5 things

A
  • sputum culture (rarely pos)
  • Antigen testing
  • CXR
  • urine + serum antigen assays
  • blood/bone marrow cultures
109
Q

Histoplasmosis

Tx

immunocompetent pts

A
  • observation if mild sx and immunocompetent
  • most cases resolve in 4 wks
  • itraconazole (PO, 12 wks)
110
Q

Histoplasmosis

tx

immunodeficient/severe disease

A
  • hosp: amphotericin B IV (1-2 wks) followed by itraconazole (PO, 12 wks)
111
Q

Histoplasmosis

who might require lifelong suppressive therapy?

A

pts with AIDS related infection

112
Q

Cryptococcosis

mainly caused by

A

cryptococcus neofromans

113
Q

Cryptococcosis

risk factors

A
  • chemotherapy for hematologic malignancies
  • Hodgkin lymphoma
  • corticosteroid therapy
  • structural lung disease
  • transplant recipients
  • TNF-alpha inhibitor therapies
  • AIDS
114
Q

Cryptococcosis

approx 80% of Cryptococcal infections are ?

A

opportunistic infection in pts with AIDS

115
Q

Cryptococcosis

most common cause of fungal ____

type of infection

A

meningitis

116
Q

Cryptococcosis

mode of transmission

A
  • inhalation
  • no P2P transmission
117
Q

Cryptococcosis

pathophys

A
  • tissue destruction is through increasing fungal burden
118
Q

Cryptococcosis

outcomes of tissue desctruction

2 things

A
  1. pulmonary disease w/ pneumonia
  2. CNS disease
119
Q

Cryptococcosis

signs/sx

pulmonary, CNS, integum

A
  1. pulmonary: variable (mild/mod cough to ARDS)
  2. CNS: meningitis, encephalitis, delerium, ataxia, HA, coma, visual disturbance
  3. pustular skin rash
120
Q

Cryptococcosis

Dx

3 tests, 2 to do if sx dissemination to specific spots

A
  • lumbar puncture
  • antigen detection in blood
  • biopsy of lesions
  • MRI of brain if mass lesion is suspected
  • if pulm sx: sputa
121
Q

Cryptococcosis

tx in immunocompetent

med, freq, duration asx vs sx

A
  • fluconazole (PO, QD, 6-12 mo)
    asx: 6 mo
    sx: 12 mo
122
Q

Cryptococcosis

Tx in severe pulm or CNS disease

A

Amphotericin B IV QD
Flucytosine PO Q6 hrs
Fluconazole PO QD

123
Q

Pneumocystosis (PJP)

caused by?

A

pneumocystis jirovecii pneumonia

124
Q

Pneumocystosis (PJP)

mode of transmission

A

airborne transmission of spores

125
Q

Pneumocystosis (PJP)

who gets infected with this?

A
  • immunodeeficient pts (cancer, transplants, AIDS, corticosteroids)
126
Q

Pneumocystosis (PJP)

% of AIDS pts that this occurs in? criteria for it occuring?

A
  • 80%
  • in AIDS pts who are not receiving prophylaxis
127
Q

Pneumocystosis (PJP)

signs & sx

7 things

A
  • limited to pulm
  • dry cough, SOB
  • thick secretions
  • spontaneous pneumothorax
  • fever, fatigue, wt loss
128
Q

Pneumocystosis (PJP)

Dx

3 things

A
  • sputum cultures
  • pos beta-D-glucan
  • CXR and CT scan
129
Q

Pneumocystosis (PJP)

Tx

A

start empirically
trimethoprim-sulfamethoxazole (PO)

130
Q

Coccidioidomycosis (Valley Fever)

caused by?

A

coccidioides immitis
coccidioides posadasii

131
Q

Coccidioidomycosis (Valley Fever)

sx & signs of acute infection

7 things, mainly

A
  • ILI ( fever, myalgia, HA, fatigue, cough)
  • erythema nodosum
132
Q

Coccidioidomycosis (Valley Fever)

what can dissemination result in?

3 things

A

meningitis, bony lesions, skin/soft tissue abscesses

133
Q

Coccidioidomycosis (Valley Fever)

who has disseminated infections most often?

A

AIDS patients

134
Q

Coccidioidomycosis (Valley Fever)

Dx

A
  • chest imagin
  • serologic useful
  • supportive care/self-limited
135
Q

Aspergillosis

caused by?

A

aspergillus fumigatus

136
Q

Aspergillosis

mode of transmission

A
  • inhalation of spores of fungus
  • most common cause of non-candida invasive fungal infection in transplant recipients/pts with hematologic malignances
137
Q

Aspergillosis

risk factors

5 thigns

A
  • leukemia
  • bone marrow
  • organ transplant
  • corticosteroid use
  • advanced AIDS
138
Q

Aspergillosis

most common disease sites

3

A
  1. pulm
  2. sinus
  3. CNS
139
Q

Aspergillosis

Dx

A

detection of galactomannan in serum

140
Q

Aspergillosis

Tx

A

antifungal drugs

CMT (78 decks)

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