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Clinical Micro > Cumulative Final Exam > Flashcards

Cumulative Final Exam Flashcards

1
Q

What is PK?

A

What our bodies do to the antimicrobrials

Absorbtion, Distribution, Metabolism, Excretion

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2
Q

What is PD?

in regards to microbiology

A

What the antimicrobrials do to the pathogen

links drug exposure to microbiological and/or clinical effect

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3
Q

Gram Positive

Staphylococcus Coagulase (-) Organisms

Catalase + “clusters”

A

S. Epidermis
S. Saprophyticus
S. lugdunesis
S. Haemolyticus
S. Hominis
S. Warneri

Commonly live on human skin

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4
Q

Gram Positive

Staphylcoccus Coagulase (+) Organisms

Catalase + “clusters”

A

S. Aureus

important

note: MRSA is methicillin-resistant staph aureus

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5
Q

Gram Positive

Streptococcus Hemolysis α Organisms

Catalase - “pairs/chains”

A

S. pneumoniae

there are others but we never rlly discussed

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6
Q

Gram Positive

Steptococcus Hemolysis γ Organisms

Catalase - “pairs/chains”

A

Enterococci:
- E. Faecalis
- E. Faecium
Group D Strep

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7
Q

Gram Positive

Streptococcus Hemolysis β Organisms

Catalase - “pairs/chains”

A

Group A Strep = S. pyogenes
Group B Strep: S. agalactiae
Group C/G Strep = S. Dysgalactiae

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8
Q

Gram Negative

Enterobacterales Organisms

A

Escherichia spp.
Klebsiella spp.
Plesiomonas spp.
Enterobacter spp.
Citrobacter spp.
Salmonella spp.
Shigella spp.
Proteus spp.
Providencia spp.
Serratia spp.
Edwardsiella spp.
Yersinia spp.
Morganella spp.
Hafnia spp.

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9
Q

Gram Negative

Lactose Fermenting Spot Indole (+) Organisms

A

Escherichia coli
Klebsiella oxytoca

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10
Q

Gram Negative

Lactose Fermenting Spot Indole (-) Organisms

A

Enterobacter cloacae
Citrobacter freundii
Klebsiella aerogenes
Klebsiella pneumoniae

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11
Q

Gram Negative

Non-Lactose Fermenting Oxidase (+) Organisms

A

Pseudomonas
Vibrio
Aeromonas
Flavobacterium
Alcaligenese
Plesiomonas
Chromobacterium

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12
Q

Gram Negative

Non-Lactose Fermenting Oxidase (-) Organisms

A

Acinetobacter
Salmonella
Shigella
Serratia
Edwardsiella
Yersinia
Morganella
Hafnia

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13
Q

Gram Stain Tells us

Determines Cell Wall Form

A

gram positive: stains purple
gram negative: stains pink/red
other: stains clear

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14
Q

Gram Stain Tells us

Determines morphology (shape)

A

cocci, bacilli, or other

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15
Q

Gram Stain tells us

Acceptability of specimen

A

If site is non-sterile than other organisms will likely present

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16
Q

Gram Stain Tells us

Quantification of Bacteria

A

is there a lot of bacteria? or not too much?

a lot of WBC= infection
a lot of epithelial cells= bad sample

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17
Q

What is Bactericidal?

A

Kills organism through the action of antimicrobrial

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18
Q

What is Bacteriostatic?

A

Halts organism growth through the action of the antimicrobrial

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19
Q

Is Bacterio- static or -cidal better?

A

Depends on the concentration!
- Low concentrations of -cidal drugs can be -static
- High concentrations of -static drugs can be -cidal

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20
Q

What is Broad Spectrum Activity?

A

Antimicrobrial targets many types of pathogens

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21
Q

What is Narrow Spectrum Activity?

A

Target only a few types of pathogens

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22
Q

What is Empiric Antimicrobrial therapy?

A

therapy that is started before pathogen and susceptibility are known because
- culture results are nto available/complete
- antimicrobrial susceptibility is not known

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23
Q

What is Definitive Antimicrobrial therapy?

A

Therapy that is started after pathogen and susceptibility is known. AKA “directed therapy” or “step-down therapy”

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24
Q

Frequent Blood Culture Contaminants

A

Staph Epidermis: skin cells
Corynebacterium spp.
Bacillus spp.
Cutibacterium acnes
Micrococcus spp.

Common skin cell contaminants when we see these we don’t always treat

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25
Q

NEVER Blood Culture Contaminants

always represent true infection

A

Staph aureus, Staph lugdunensis, Gram-negatives, some anaerobes, Yeast

ALWAYS TREAT THESE ORGANISMS

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26
Q

What to consider when there is a blood culture contaminant

A
  • What is the clinical status of patient? Do they seem sick?
  • Is this a common contanimant?
  • Do they have an indwelling medical device
  • Repeat the culture in another location - is the contaminant still there?
  • Is it taking a long time for the organisms to grow?
  • Are all the blood culture bottles positive?
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27
Q

What is Antimicrobrial Resistance?

A

The antimicrobiral concentration below that MIC at which a typical patient will usually respond given a typical dose

pathogens gain the ability to not be killed by drugs at safe doses

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28
Q

Intrinsic Resistance

A

Natural resistance of microbes to antimicrobrials

Resistance microbes are born with and is always expressed within species

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29
Q

Acquired Resistance

A

Obtained resistance of microbes to antimicrobrials -
Resistance microbes obtain to antimicrobials they were prevously susceptible to

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30
Q

big purple chart

Methicillin-resistant Staphylococcus Aureus Treatments

A

Vanc (+13), Dappin up Lids, Caroline D’alba, Teleports Over Prissy Tigers& Teachers, Temporarily Clinching Rifle Delays

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31
Q

big purple chart

Vancomycin-resistant Enterococci Treatment

A

Dappin up Lids Over Prissy TIgers& Frostbite Nights

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32
Q

big purple chart

Atypicals Treatment

A

Fuck My Teachers

lol not actually

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33
Q

big purple chart

P. Auruginosa Treatment

A

Piper Aztec Amber Loves Delays ,
Polly Cips Cefs & Carbs

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34
Q

big purple chart

Anaerobe Treatment

A

Piper Aims Amps ox&teet Carb Make Metro Tigers Delay

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35
Q

big purple chart

Carbapenem-resistant Enterobacterales Treatment

Only drug that treats this one and not others

A

Meropenem-vaborbactam

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36
Q

big purple chart

pAMPC- Type Cephalosporinase Producing Organisms Treatment

ones that only treat amp c

A

Cefepime and TMP-SMX

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37
Q

bIg purple chart

Extended Spectrum Beta Lactamase Producers Treatment

ones that only treat ESBL

A

Ceftolozane-tazobactam, Nitrofurantoin, Fosfomycin

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38
Q

big purple chart

Treats ESBL and AmpC

A

Carbapenems/BLI and Fluoroquinolones

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39
Q

big purple chart

Treats ESBL, AMPc, and CRE

only ones that treat all 3

A

Polly & Amber Cef Tigers

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40
Q

What is Zone of Inhibition?

A

qualitative way to measure the activity of drug. organism grows on top of media and antibiotic diffuses on plate for 18-24 hours
↑zone of clearance = ↑antimicrobial activity

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41
Q

What is MIC?

A

Lowest concentration of given antimicrobial that will inhibit the visual growth of an organism after 18-24h incubation.
↓ MIC = ↑ antimicrobial activity

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42
Q

4 Methods of Susceptibility Testing

A

Qualitative:
1. Disk Diffusion
**Quantitative: **
2. Broth Dilution
3. Etest (agar diffusion)
4. Automated susceptibility testing

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43
Q

What is the relationship between zone of inhibition and MIC

A

Inverse relationship
↓ MIC = ↑ zone of inhibition

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44
Q

Susceptibility

Susceptible Interpretation

A

antimicrobrial concentration is ABOVE the MIC

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45
Q

Susceptibility

Intermediate Interpretation

A

antimicrobrial concentration is close to the MIC

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46
Q

Susceptibility

Resistant Interpretation

A

antimicrobrial concentration BELOW the MIC

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47
Q

What are Local Antibiograms?

A

Overall antimicrobrial susceptibility profile of specific microorganisms to various antimicrobrials (typically at your hospital)

Informs the clinician of local institutional patterns and thus inform empiric antimicrobrial precribing patterns while we wait for culture results

↑ percentage = ↑ susceptible

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48
Q

What does MRSA mean?

A

Methicillin-resistant Staphylococcus Aureus
OR Nafcillin OR Oxacillin

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49
Q

What does MSSA mean?

A

Methicillin-susceptible Staphylococcus Aureus
OR Nafcillin OR Oxacillin

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50
Q

What does it mean if resistance report says: “S. aureus, mecA positive or PBP2a”

A

MRSA

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51
Q

Enterococcus Faecalis vs. Enterococcus Faecium

A

Faecalis is more common and less drug resitant
Faecium is less common and more drug resistant

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52
Q

Enterococcus Faecalis Treatment

A

Ampicillin

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53
Q

Streptococcus Pyogenes Treatment

A

Penicillin
has absolutely no resistance to penicillin

~gram positive~

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54
Q

Necrotizing Faciitis Treatment

A

Cell wall active agent (penicillin) plus toxin-inhibiting antibiotic (clindamycin)

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55
Q

Streptococcus Pneumoniae Treatment

A
  • Penicillin
  • 3rd Gen Cephalosporins: cefdinir, ceftriaxone, etc.
  • Fluoroquinolones
  • Vancomycin (highly resistant strains)
  • Vaccines: PCV13 (prevnar) and PPV23 (pneumovax)

~gram positive~

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56
Q

Clostridioides Difficile Treatment

A

Oral Vancomycin
and discontinue offending antibiotic
- fidaxomicin
- metronidazole
- fecal transplant

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57
Q

C. diff risk factors

A
  • exposure or previous history
  • older age
  • recent hospitalization
  • immunocompromising conditions
  • CLINDAMYCIN
  • fluoroquinolones, carbapenems, 3rd/4th gen cephalosporins

C. diff is gram positive

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58
Q

Enterobacterales Treatment

A

varies with type/severity of infection, patient history, abx susceptibility
- pipercillin/tazobactam
- ceftriaxone
- cefepime
- carbapenems
- fluoroquinolones
- nitrofurantoin

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59
Q

What is the most common Gram (-) Non-lactose fermenting organism?

A

Pseudomonas aeruginosa

found in skin/soft tissue, urinary tract, & eye/ear infections

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60
Q

Yeast is divided into:

A

Candida Species and Cryptococcus Species

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61
Q

What are the candida species?

A

C.:
albicans, glabrata, parapsilosis, tropicalis, krusei, lusitaniae

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62
Q

What are the cryptococcus species?

A

C. neoformans

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63
Q

What are the Dimorphics?

A

Coccidoides immitis, Blastomyces dermatidis, Histoplasma capsulatum

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64
Q

What are the Molds?

A

Aspergillus fumigatus, Zygomycetes (Mucor), Fusarium spp., Scedosporium spp.

Fuck (fusarium)
Zach’s (zygo)
Ass (asp) has
Skid marks (sced)

65
Q

What are primary yeast pathogens?

A

can infect otherwise normal and healthy hosts

66
Q

What are opportunistic yeast pathogens?

A

typically require “abnormal/immunocompromised” hosts to establish infection
ex: Candida spp. or Cryptococcus neoformans

67
Q

Which is the most prevalent fungal infection?

A

Candida albicans
- associated with UTI’s, candidemia, CNS candidiasis, endocarditis

68
Q

Risk factors for Invasive Candidiasis

A

immunosuppression, central venous catheters, surgery, paranteral nutrition, neutropenia, renal replacement therapy in ICU, implantable prosthetic devices, broad spectrum antibiotics

69
Q

Candida spp. Oropharyngeal Infections

A

AKA thrush
- typically caused by C. albicans
- Sx: white patches in mouth
- Tx: swish and swallow and rinse mouth after ICS

70
Q

Candida spp. Vulvovaginal Infections

A

AKA yeast infection
- Sx: itching, redness, irritation, cottage cheese discharge
- Tx: “One and done” dose of fluconazole!

we familiar unfortunately

71
Q

Candida spp. UTI

A

AKA Candiduria (rare compared to bacterial UTI)
- Sx: cystitis, blood in urine
- Dx: symptoms and urine culture
- must distinguish colonization vs. infection

72
Q

Candida spp. Bloodstream Infections

A

AKA candidemia
- more common in hospital
- Sx: high fever, chills, malaise, sepsis
- Dx: blood culture
- never a contaminant!!!

73
Q

Candida spp. Treatments

A

C. albicans (fluconazole-susc), C. lusitaniae, C. parapsilosis, C. tropicalis, C. glabrata (flu-susc) = fluconazole
C. albicans (fluconazole-res), C. glabrata or C. krusei (fluconazole-res) = Echinocandin or Amphotericin B

usually start more empiric & eventually move to fluconazole if possible

74
Q

Fluconazole-susceptible Treatment normal dosing

A

800 mg (or 12 mg/kg) loading dose
400 mg (6 mg/kg) once daily

75
Q

C. glabrata (fluconazole-susceptible dose dependent) dosing

A

800 mg (12 mg/kg) once daily

76
Q

Fluconazole PK/PD

A

The AUC and dose have a linear relationship, so when giving a dose you can assume the AUC is the same

77
Q

Cryptococcus neoformans

A

Opportunistic pathogen that affects the CNS and is typically acquired through inhalation of aerosolized cells from environment

Causes meningitis!

78
Q

Cryptococcus neoformans treatment

A

Induction: liposomal amphotericin B + flucytosine for 2 weeks
Consolidation: Fluconazole for 8 weeks
Maintenance: Fluconazole for 12 months

79
Q

More common opportunistic mold pathogens are?

A

Aspergillus spp. and Mucormycetes (zygo one)

80
Q

Aspergillus spp. concepts

A
  • opportunistic so host needs to be immunocompromised
  • primarily inhaled
  • aspergillosis is the fungal infection caused by pathogenand mortality is high!
81
Q

Examples of immunosuppression risk factors for invasive Aspergillosis

A
  • prolonged neutropenia
  • allogeneic hematopoietic stem cell transplant
  • solid organ transplant
  • inherited/acquired immunodeficiencies
  • immunosuppressie therapies (TNFalpha inhibitors and corticosteroids)
  • others
82
Q

Invasive Pulmonary Aspergillosis

A
  • Most common in neutropenia or those recieving cytotoxic chemotherapy
  • Sx: pulmonary infiltrates, pleuritic chest pain, hemoptysis, fever
  • can range from mild to destructive
  • Halo sign(early) and Air-crescent(late) sign can be seen on the computed tomography
83
Q

Invasive Aspergillosis treatment

A

VORICONAZOLE!

84
Q

Dimorphics Pathogenicity

A

Primary pathogens: Coccidoides immitis, Histoplasma dermatitidis, Blastomyces capsulatum
Endemic pathogens: cause disease via inhalation of spored from specific environmental/geographical locations

85
Q

Where is Coccidoides spp. found?

A

Highly endemic in southwestern US (Arizona, New Mexico, California, Nevada, Texas, Utah)

AKA “valley fever” or Coccidioidomycosis

86
Q

Coccidoidomycosis risk factors/treatment

A

Risk factors: ethnicity, 3rd trimester, males, cellular immunodeficiency, extremes of age
Treatment: mild forms may not need treatment but if needed fluconazole

87
Q

Where is Histoplasmosis found?

A

highly endemic in Ohio and Mississippi River valleys

88
Q

Where is Blastomycosis found?

A

highly endemic in Ohio, Mississippi River valleys, and Great Lakes

89
Q

Histoplasmosis and Blastomycosis treatments

A

mild forms may not need treatment
mild-moderate: itraconazole
severe/disseminated: liposomal amphotericin B or itraconazole

90
Q

What is a virus?

A

neither prokaryotic or eukaryotic
- non-living, intracellular parasites
- no organelles or ribosomes
- cannot make energy/proteins independently of a host cell
- genomes may consist of RNA or DNA (NEVER BOTH)
- morphology: naked capsid or envelope

91
Q

How are viruses classified?

A

structure, biochemical characteristics, disease, means of transmission, host range, tissue or organ

92
Q

Steps in Viral Infection of Host Cell

IN ORDER

A
  1. Recognition of target cell
  2. attachment
  3. penetration
  4. uncoating/release of genome
  5. transcription
  6. protein synthesis
  7. replication of genome
  8. assembly of virus
  9. lysis of naked capsid viruses or budding of enveloped viruses –> release
93
Q

What are the Nucleoside Analogs?

A
  • Acyclovir
  • Valacyclovir
  • Ganciclovir
  • Valganciclovir
94
Q

What is the Nucleotide Analog

A

Cidofovir

95
Q

What is the Pyrophosphate Analog?

A

Foscarnet

96
Q

What is the CMV DNA Terminase Complex Inhibitor

A

Letermovir

97
Q

What is the Neuraminidase Inhibitor?

A

Oseltamivir

98
Q

HSV-1 and HSV-2

A

Herpes Simplex Type 1 and 2
Spreads through close contact (STD)
Subfamilies: HHV-1 and HHV-2
Targets mucoepithelial cells

99
Q

VZV

A

Varicella-zoster virus
subfamily: HHV-3
spreads through respiratory and close contact
Targets mucoepithelial cells and T-cells

100
Q

EBV

A

Epstein-Barr virus
subfamily: HHV-4
spreads through saliva (its mono)
targets B-cells and epithelial cells

101
Q

Cytomegalovirus

A

subfamily: HHV-5
spreads through close contact (STD), transfusions, tissue transplants, and congenital
targets monocytes, granulocytes, lymphocytes, and epithelial cells

102
Q

HSV triggers

A
  • Ultraviolet B radiation (skiing, tanning)
  • Fever
  • Emotional stress
  • Physical stress
  • Menstruation
  • Foods (spicy, allergic, acidic)
  • Immunosuppression

basically body stresses

103
Q

Orolabial and Mucocutaneous HSV

A

Clear vesicles that rapidly ulcerate
Sx: soreness, burning sensation, tingling, blisters, rashes
Dx: PCR
Tx: topical meds, oral acyclovir or valacyclovir
recurrences are normal

104
Q

Genital HSV

A

Grouped 2-4 mm vesicles with underlying erythema that progress to ulcers
Sx: super painful ulcers/lesions, fevers, headache, myalgias
Dx: PCR
Treatment: oral acyclovir or valacyclovir

105
Q

Varicella (Chickenpox)

A

Caused by Varicella Zoster
-more common in children
Tx immunocompetent: supportive care
Tx immunosuppressed: acyclovir, valacyclovir

106
Q

Herpes Zoster (Shingles)

A

Results from reactivation of a patients latent virus acquired earlier in patients life
- severe pain precedes appearance of chicken pox-like lesions and can be fatal in immunocompromised
- Tx: Acyclovir or Valacyclovir and potentially analgesic for neuralgia
- Immunity wanes in elderly population so more common for them to get it
- lesions are viable virus so be careful around non-immune

107
Q

Varivax Vaccine treats

A

Chickenpox
live attenuated vaccines

108
Q

ProQuad Vaccine treats

A

Chickenpox
Live attenuated vaccine

109
Q

Shingrix treats

A

Shingles
Inactivated Vaccine

110
Q

Most novel coronavirus is?

A

SARS-CoV-2: virus name
COVID-19: disease name

111
Q

What are the 4 structural proteins of SARS-CoV-2?

A
  1. Spike protein: Vaccines work with this one. It mediates binding and fusion with host cell membrane. Forms the crown.
  2. Membrane protein: viral assembly
  3. Envelope protein: transmembrane protein
  4. Nucleocapsid protein: forms nucleocapsid
112
Q

COVID-19 Therapies

A
  • monoclonal antibodies
  • dexamethasone
  • remdesivir
  • paxlovid
  • molnupiravir
113
Q

COVID-19

Remdesivir indications

A

antiviral: nucleotide analog prodrug
IV only
use in hospitalized patients requiring oxygen

114
Q

COVID-19

Dexamethasone indications

A

corticosteroid
use in hospitalized patients requiring oxygen, mechanical ventilator support, or extracorporeal membrane oxygenation

115
Q

COVID-19 Tx WE DON’T USE

A

hydroxychloroquine and ivermectin

116
Q

COVID-19

Pfizer-BioNTech Vaccine

A

mRNA
MOA: encodes the prefusion spike glycoprotein of SARS-CoV-2

117
Q

COVID-19

Moderna Vaccine

A

mRNA
MOA: encodes the prefusion spike glycoprotein of SARS-CoV-2

118
Q

COVID-19

Janssen (J&J) Vaccine

A

Replication-incompetent adenovirus vector
MOA: vector expresses the SARS-CoV-2 spike glycoprotein

119
Q

What is Antigenic drift?

A

small mutations in the genes that lead to changes in surface proteins of the virus

120
Q

What is Antigenic shift?

A

Abrupt, major change due to reassortment that lead to changes in surface proteins of the virus

121
Q

Influenza

A

“the flu”
Sx: malaise, headache, fever, chills, loss of appetite, weakness, fatigue
Tx: supportive care, Oseltamivir, Influenza cap-dependent endonuclease inhibitor

122
Q

Influenza vaccine is recommended to?

A

Everyone at least 6 y/o once a year

123
Q

What are the HIV risk factors?

A
  • unprotected sex
  • sharing contaminated injecting equipment
  • accidental needle stick
124
Q

How is HIV transmitted?

A

sexual contact, blood, breast milk, semen, vaginal secretions, and perinatal

125
Q

HIV MOA

A

preferentially infects and kills helper T-lymphocytes (CD4+ cells) which results in a loss of cellular immunity and vulnerability to opportunistic infections

126
Q

What is the HIV life cycle?

A
  1. Binding
  2. Fusion
  3. Reverse transcription
  4. Integration
  5. Replication
  6. Assembly
  7. Budding
127
Q

HIV drug

What is an NRTI?

A

Nucleoside Reverse Transcriptase Inhibitor
- works on reverse transcription step

128
Q

HIV drug

What is an NNRTI?

A

Non-nucleoside Reverse Transcriptase Inhibitors

129
Q

HIV drug

What is an INSTI

A

Integrase inhibitors

130
Q

HIV drug

What is a PI?

A

Protease inhibitor

131
Q

How to diagnose HIV?

A

HIV serology: detection of Ab against virus
HIV viral load: amount of HIV in blood
CD4 cell count: indicator of HIV progression

132
Q

HIV treatment

A

2 NRTI’s + INSTI or NNRTI or PI with PK enhancer

133
Q

What is zoonoses?

A

diseases/infections naturally transmitted to humans from vertebrate animals either directly or indirectly through an insect vector

134
Q

What does “vector-borne” mean?

A

When a blood-feeding arthropod is involved
ex: mosquito/tick

135
Q

Dog Bite/Scratches organisms

A

Pasteurella canis or Pasteurella multocida
OR rarely Rabies lyssavirus

136
Q

Cat bite organism

A

Pasteurella multocida

137
Q

Cat scratch organism

A

Bartonella henselae

138
Q

Small rodent bites organism

A

Streptobacillus moniliformis

139
Q

Pasteurella canis and multocida Treatment

A

Amoxicillin/Clavulanate

140
Q

Rabies treatment

A

Pre-exposure prophylaxis: rabies vaccine
Post-exposure prophylaxis: rabies vaccine + rabies immunoglobulin

141
Q

Cat scratch disease treatment

A

Azithromycin +/- rifampin
or
Doxycycline +/- rifampin

reminder this is Bartonella henselae

142
Q

Rabbit/muskrat/praire dog/ticks/deer flies organism

A

Francisella tularensis

143
Q

Francisella tularensis treatment

A

Gentamicin or doxycycline

144
Q

TIcks

Lyme Disease is caused by

A

Borrelia burgdorferi

145
Q

ticks

Ehrlichiosis is caused by

A

Ehrlichia spp.

146
Q

tick

Rocky Mountain Spotted Fever is caused by

A

Rickettsia rickettsii

147
Q

How do you treat a tick-borne illness?

A

Doxycycline!

148
Q

How do you get Toxoplasmosis?

A

CD4 counts <50-100
Cat feces
Eating undercooked meat
Gardening

149
Q

Toxoplasmosis Prophylaxis and Treatment

A

Prophylaxis: TMP/SMX if CD4<100 and toxoplasma IgG is positive
Tx: Pyrimethamine + sulfadiazine + leucovorin

150
Q

What is a Trophozoite?

A

Motile, active feeding stage of protozoa

151
Q

Parasite

What is a Cyst?

A

Nonmotile, nonmetabolizing, nonreproducing form. This form is dormant and resting. This is how it can survive outside of the host.

152
Q

Trichomonas vaginalis

A

one of the most common STD’s that infects squamous epithelium in the urogenital tract
- exists only in trophozoite form
- transmission is via sexual contact

153
Q

Trichomoniasis treatment

A

Metronidazole whether asymptomatic or symptomatic

154
Q

Malaria

A

Caused by Plasmodium and spreads to humans via Anopheles mosquitoes

155
Q

4 different Malaria species

A

P. falciparum, P. vivax, P. ovale, P. malariae

156
Q

Mild Malaria Treatment

A

Artemisinin-based combination therapy

157
Q

Severe Malaria treatment

A

Start with Parentaral artesunate for 24 hours then complete treatment with artemisinin-based combination therapy

158
Q

Enterobiasis

A

Pinworms
diagnosed by finding eggs on perianal tape swabs. eggs are rarely fond in stool.

159
Q

Enterobiasis treatment

A

Albendazole
OTC: pyrantel pamoate

Clinical Micro (1 decks)

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