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CHEST SEEK Library > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

HIV/AIDS opportunistic infections based on CD4 count

  • 250-500 (x 10^6/L)
A
  • ORAL Candidiasis
  • TB
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2
Q

HIV/AIDS opportunistic infections based on CD4 count

  • 150-200 (x 10^6/L)
A
  • Kaposi’s sarcoma
  • lymphoma
  • Cryptosporidiosis
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3
Q

HIV/AIDS opportunistic infections based on CD4 count

  • 75-125 (x 10^6/L)
A
  • PJP
  • Toxoplasmosis
  • Cryptococcal meningitis
  • recurrent HSV ulceration
  • ESOPHAGEAL Candidiasis
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4
Q

HIV/AIDS opportunistic infections based on CD4 count

  • < 50 (x 10^6/L)
A
  • CMV
  • MAC (Mycobacterium avium complex)
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5
Q

esophagitis w/ symptoms refractory to treatment to Candida, think of

A

CMV esophagitis

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6
Q

HIV/AIDS patient w/ these symptoms;

  • urinary retention
  • b/l leg weakness
  • sacral paresthesia

think of

A

polyradiculomyelopathy 2/2 CMV

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7
Q

legs spasticity indicative of upper motor neuron disease in a patient w/ HIV and a CD4 count < 50 (x 10^6/L), think of

A

ventriculoencephalitis 2/2 CMV

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8
Q

ulcers scattered throughout bowel, especially in cecum, w/ symptoms of abdominal pain and debilitating diarrhea in a patient w/ HIV and a CD4 count < 50 (x 10^6/L), think of

A

CMV involvement of the GI tract

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9
Q

in a patient w/ HIV and a CD4 count < 50 (x 10^6/L) w/ the following;

  • NAGMA
  • hyponatremia
  • hyperkalemia

think of

A

adrenal insufficiency 2/2 CMV

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10
Q

should patients at high risk for CMV infection, including MSM and IVDU, be tested for CMV, and why or why not?

A
  • no
  • because, they are assumed to be positive
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11
Q

HIV-infected patient w/ cerebral involvement w/ ring-enhancing lesions that demonstrate mass effect

A

Toxoplasma infection

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12
Q

which pathogen enters the respiratory tract and can disseminate to the nervous system leading to meningitis?

A

Cryptococcus neoformans

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13
Q

what organ is a reservoir for Cryptococcus?

A

prostate

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14
Q

which granulomatous pathogens can infect the adrenal glands and cause adrenal insufficiency?

A
  • Mycobacterium tuberculosis
  • Histoplasma capsulatum
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15
Q

what happens during passive lung inflation on a MV w/ a closed chest?

A

rising intrathoracic pressure reduces venous return to the RV, and after a delay of a few cardiac cycles, LV SV falls

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16
Q

in which patients w/ large variations in pulse pressure reflect limited venous return function and therefore could be used as a rationale for fluid administration in a patient w/ shock?

A

patients in NSR AND w/ passive breathing on MV

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17
Q

pulse pressure variation calculation

A

[(PPmax - PPmin) / (PPmax + PPmin) / 2] x 100

where PP = SBP - DBP

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18
Q

what percentage of PPV has a sensitivity and specificity of 88% and 89%, respectively, of predicting fluid responsiveness in patients passive on MV?

A

> 13%

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19
Q

in most trials, what percentage increase in CO is considered fluid responsive and how much fluid is required to achieve this?

A
  • 15%
  • 500 mL fluid bolus
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20
Q

when is PPV not a reliable predictor of fluid responsiveness?

A

spontaneous breather, whether on or off MV

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21
Q

what percentage of patients w/ septic shock will still be fluid responsive at the time of ICU admission even if “adequately” resuscitated?

A

about 25%

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22
Q

even if a patient turns out to be fluid responsive, does that mean giving more fluid will improve clinical outcome?

A

no

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23
Q

is there data to demonstrate that patients who are not fluid responsive cannot occasionally benefit from additional fluids?

A

no

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24
Q

convert 37°C to °F

A

98.6

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25
Q

convert 37.5°C to °F

A

99.5

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26
Q

convert 38°C to °F

A

100.4

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27
Q

convert 38.5°C to °F

A

101.3

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28
Q

growth of Staphylococcus lugdunensis in 2 separate BCs should prompt consideration of w/u for what?

A

IE

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29
Q

catheter-related bloodstream infection d/t Staphylococcus lugdunensis should be managed similar to recommendations for what pathogen?

A

Staphylococcus aureus bacteremia

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30
Q

how should catheter-related bloodstream infection d/t Staphylococcus aureus?

A
  • prolonged course of abx
  • catheter removal
  • TEE
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31
Q

which coagulase-negative staphylococci characteristically causes lower UTI?

A

S saprophyticus

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32
Q

which coagulase-negative staphylococci have been a/w clinical disease and characteristically cause systemic infection?

A
  • S epidermidis
  • S haemolyticus
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33
Q

if there is an uncomplicated catheter-related bloodstream infection 2/2 S epidermidis or S haemolyticus what are the IDSA management guidelines?

A

abx for 5-7 days if the catheter is removed

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34
Q

HAP abx course duration

A

7 days

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35
Q

VAP abx course duration

A

7 days

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36
Q

GN bacteremia abx course duration if;
- afebrile x ≥ 48 hours
- hemodynamically stable x ≥ 48 hours
- adequate source control

A

7 days

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37
Q

abx course management in patients w/ Enterobacteriaceae bacteremia w/ adequate source control and appropriate clinical response by day 5 of parenteral abx

A

can switch to PO for rest of 7 day abx course

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38
Q

what should be done as an important antibiotic stewardship in the management of uncomplicated gram-negative bacteremia?

A
  • reducing abx duration
  • switching from IV to PO
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39
Q

abx course management for S aureus even if uncomplicated bacteremia and catheter removal leads to a patient quickly becoming afebrile w/ a normal WBC count

A

14 days

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40
Q

why does S aureus bacteremia abx duration need to be a minimum of 14 days?

A

endovascular adhesiveness (S aureus is “sticky”)

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41
Q

the risk of endocarditis from enterococcal bacteremia is higher in which situation?

A

community-acquired

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42
Q

how is Enterococcus similar to S aureus

A

endothelial adhesiveness (“sticky”)

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43
Q

candidemia treatment course duration W/O obvious metastatic complications

A

14 days after documented clearance of Candida species from bloodstream and resolution of symptoms attributable to candidemia

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44
Q

what condition must be excluded and therefore exam is mandatory in a patient w/ candidemia?

A
  • endophthalmitis
  • ophthalmologic evaluation
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45
Q
  • hypersalivation
  • dysphagia
  • marked instability of temperature regulation
  • myoclonus
A

rabies

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46
Q

this viral pathogen transmits from peripheral nerves to the spinal cord and ascends into the brain; can be conceptualized as being myeloencephalopathy

A

rabies virus

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47
Q

main source for rabies transmission worldwide

A

dog bites

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48
Q

postexposure prophylaxis for rabies is indicated for which HCPs?

A

healthcare professionals exposed to mucous membranes, or open skin contact w/ saliva, tears, or nervous tissue

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49
Q

the CDC emphasizes considering which diagnosis in any patient w/ acute unexplained encephalitis before organ transplantation?

A

rabies

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50
Q

neurotropic virus that may present as a stroke-like syndrome

A

West Nile virus

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51
Q

can West Nile virus present as altered level of consciousness?

A

yes, because, it can cause meningitis

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52
Q

what are the signs/symptoms of meningitis?

A
  • headache
  • fever
  • nuchal rigidity (meningismus)
  • lethargy/obtunded
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53
Q

how can you distinguish nuchal rigidity (meningismus) from cervical spine osteoarthritis or influenza w/ severe myalgia?

A
  • w/ OA or myalgia from influenza, neck movement in ALL directions is affected
  • meningismus d/t meningeal irritation affects mostly neck FLEXION
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54
Q

what are the signs/symptoms of encephalitis?

A
  • headache
  • fever
  • AMS
  • seizures, possibly status epilepticus
  • focal neurologic deficits
  • GI or respiratory prodrome
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55
Q

olfactory seizures (manifested as aura of foul smells; rotten eggs, burnt meat), indicate what?

A
  • temporal lobe involvement
  • suggest HSV encephalitis
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56
Q

rabies can be difficult to distinguish from what disease?

A

Guillain-Barré syndrome

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57
Q

Guillain-Barré syndrome typical characteristics

A
  • demyelination of nerves
  • sharp pain
  • autonomic neuropathy (only 20%)
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58
Q

spastic complication occurring after infection w/ Clostridium tetani

A

tetanus

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59
Q

marked degrees of autonomic dysfunction, including hypersalivation, can occur as a complication from what infection?

A

tetanus

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60
Q

what liver injury pattern is this?

  • indirect bili = high
  • direct bili = normal
  • urine urobilinogen = high
  • AST/ALT = normal
  • ALP = can be markedly LOW
A

hemolytic

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61
Q

what liver injury pattern is this?

  • indirect bili = high
  • direct bili = high
  • urine urobilinogen = high
  • AST/ALT = high
  • ALP = normal
A

hepatocellular

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62
Q

what liver injury pattern is this?

  • indirect bili = normal
  • direct bili = high
  • urine urobilinogen = LOW
  • AST/ALT = normal to high
  • ALP = disproportionately HIGH
A

cholestatic

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63
Q
  • biliary stasis (cholestasis)
  • infection
  • cholelithiasis w/o GB thickening but dilated CBD
A

acute cholangitis

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64
Q

if cholangitis is suspected, what initial imaging should be done?

A

US

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65
Q

if cholangitis is suspected, but US does not show biliary dilation, and there’s still high clinical suspicion, what imaging should be done next?

A

MRCP (magnetic resonance cholangiopancreatography)

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66
Q

if there is evidence for cholestasis on labs, what’s the next step for definitive diagnosis and biliary decompression?

A

ERCP (endoscopic retrograde cholangiopancreatography)

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67
Q

management of severe cholangitis (manifested by organ dysfunction)

A

ERCP w/i 24 hours

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68
Q

management of moderate cholangitis (manifested by at least 2 of the following; abnormal WBC count, fever, age > 74 years, hyperbilirubinemia, hypoalbuminemia) that hasn’t responded to abx for 24 hours

A

immediate drainage

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69
Q

management of mild to moderate cholangitis responding to abx

A

drainage w/i 24-48 hours

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70
Q

what are the most common organisms isolated from cultures of bile and stones 2/2 cholangitis?

A
  • Escherichia coli
  • Klebsiella
  • Enterobacter
  • Enterococcus
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71
Q

does acute cholecystitis cause hyperbilirubinemia?

A

no, it shouldn’t, because biliary tract drainage is preserved

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72
Q

what type of isolation precaution for the following pathogens?

  • CPO
  • MRSA
  • VRE
  • lice
  • scabies
A

contact

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73
Q

what type of isolation precaution for the following pathogens?

  • C difficile
A

contact plus

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74
Q

what type of isolation precaution for the following pathogens?

  • N meningitidis
  • mumps
  • pertussis
A

droplet

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75
Q

what type of isolation precaution for the following pathogens?

  • influenza
  • invasive group A Streptococcus
A

contact AND droplet

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76
Q

what type of isolation precaution for the following pathogens?

  • TB
  • measles
A

airborne

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77
Q

what type of isolation precaution for the following pathogens?

  • varicella; chickenpox, and disseminated herpes zoster
A

contact AND airborne

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78
Q

what are the 2 important considerations in recent guidelines for early valve replacement in a patient w/ left-sided native valve IE?

A
  1. vegetation size; > 10 mm in diameter, especially when they’re mobile
  2. valve location; anterior leaflet
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79
Q

early valve replacement for left-sided native valve IE might be considered in patients w/ which complication if appropriate abx have been given x 48 hours?

A
  • recurrent emboli
  • HF not improving w/ medical therapy
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80
Q

what is persistent bacteremia?

A

positive BCs x 5-7 days despite abx

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81
Q

is it normal for S aureus bacteremia to persist > 72 hours?

A

yes

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82
Q

what is complicated S aureus and how should management be adjusted?

A
  • persistent bacteremia > 72 hours
  • abx duration should be > 14 days
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83
Q

what are the different ways FMT can be administered?

A
  • swallowing pills
  • upper endoscopy
  • through a NG tube
  • colonoscopy
  • retention enema directly in the colon
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84
Q

what therapy can be considered to avoid emergent colectomy in severe CDI?

A

FMT

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85
Q

empiric bacterial meningitis therapy

A
  • ceftriaxone
  • ampicillin
  • vancomycin
  • dexamethasone
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86
Q

dexamethasone dose and duration for Streptococcus pneumoniae meningitis

A
  • 0.15 mg/kg q6h
  • 4 days
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87
Q

should dexamethasone empirically started for Streptococcus pneumoniae meningitis be stopped before 4 days duration if CSF or BCs are negative?

A

yes

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88
Q

is there a role for routine monitoring of ICP in patients w/ bacterial meningitis?

A

no

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89
Q

if intracranial hypertension in bacterial meningitis is suspected, what is the goal ICP?

A

< 20 mm Hg

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90
Q

aside from abx therapy, what other treatments may also lower ICP in patients w/ bacterial meningitis and IC hypertension?

A
  • HOB > 30° but NOT > 60° as this is a/w decreased cerebral perfusion
  • hyperventilation w/ a goal PaCO2 < 30 mm Hg
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91
Q

ddx for;

  • recurrent fevers
  • night sweats
  • pulmonary abnormalities
  • noncaseating granulomas on lung biopsy
  • recent travel
A
  • TB
  • sarcoidosis
  • lymphoma
  • fungal d/o’s
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92
Q
  • recurrent fevers, night sweats, pulmonary abnormalities, noncaseating granulomas on lung biopsy, recent travel

PLUS

  • severe leukopenia
  • anemia
A

intracellular pathogen

  • Brucella
  • Salmonella
  • Ehrlichia
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93
Q
  • negative acid-fast bacilli smears/cultures
  • negative fungal stains/cultures
  • recent exposure to unpasteurized dairy
A

brucellosis

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94
Q

treatment for brucellosis

A

doxycycline and an aminoglycoside (streptomycin or gentamicin)

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95
Q

what percentage of patients w/ brucellosis can p/w pulmonary nodules?

A

1-4% (uncommon)

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96
Q

how is Brucella transmitted?

A

ingestion of contaminated meat or unpasteurized dairy products

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97
Q
  • undulating fever
  • cough w/ mucopurulent sputum
  • myalgias
  • arthralgias
  • leukopenia
  • AST/ALT elevation
  • abnormal chest imaging

diagnosis?

A

brucellosis

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98
Q

is there a high rate of false negative BCs when diagnosing brucellosis?

A

yes; need to have high clinical suspicion

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99
Q

what has the highest sensitivity and is the gold standard for diagnosing brucellosis?

A

bone marrow cultures

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100
Q

what is the typical finding on BM, liver, or lung tissue cultures for brucellosis?

A

noncaseating granulomas

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101
Q

what are the 3 mechanisms of resistance Pseudomonas aeruginosa possesses?

A
  1. AmpC β-lactamases
  2. efflux pumps
  3. outer membrane porin alterations
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102
Q

which cephalosporin is structurally similar to ceftazidime but is modified and has increased antipseudomonal activity and some activity against some ESBL strains?

A

ceftolozane

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103
Q

which β-lactamase inhibitors don’t possess a β-lactam?

A
  • avibactam
  • vaborbactam
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104
Q

what are the underlying conditions a/w severe pneumococcal infection and are also indications for pneumococcal vaccine?

A
  • functional or anatomical asplenia
  • HIV infection
  • lymphoma (both Hodgkin’s and NHL)
  • MM
  • alcoholism
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105
Q

Austrian triad

A
  • pneumococcal PNA
  • meningitis
  • endocarditis
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106
Q

acute illness is suggested by what clinical scenario?

A

histamine-mediated phenomenon

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107
Q

the following are classical features of what pathology in a patient w/ a h/o malignancy and/or is on chemotherapy?

  • fever
  • abdominal pain w/ cramping
  • diarrhea
  • GI bleeding
A

neutropenic enterocolitis

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108
Q

diagnostic procedure of choice for neutropenic enterocolitis

A

CT a/p w/ iv contrast

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109
Q

the following are risk factors for what?

  • prolonged broad spectrum abx
  • extended ICU stay (> 8 days)
  • respiratory failure w/ MV
  • parenteral nutrition
  • AKI
  • abdominal surgery
  • neutropenia
  • severe sepsis
A

fungemia

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110
Q

Candida species COLONIZATION from which sites increases deep-seeded Candida infection by 3-fold?

A

nonsterile sites such as, lung or urine

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111
Q

what is the gold standard for diagnosis of Candida species?

A

isolation from an otherwise sterile site, such as, blood or peritoneal cavity

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112
Q

false positives w/ galactomannan and beta-D glucan can occur, especially under what circumstances?

A

administration of piperacillin/tazobactam and other fungal-derived abx

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113
Q

guidelines recommend which antifungal for candidemia?

A

an echinocandin

  • caspofungin
  • micafungin
  • anidulafungin
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114
Q

which empiric therapy should be considered in LOW-risk, clinically stable patients w/ candidemia?

A

fluconazole

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115
Q

which step-down therapy from an echinocandin is recommended?

A

fluconazole

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116
Q

what is the treatment of choice for endophthalmitis d/t their ocular penetration?

A

azoles

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117
Q

management of candidemia aside from antifungals

A
  • removal of central venous catheters
  • retinal exam at least once
  • BCs q48h
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118
Q

antifungal duration for candidemia

A

14 days from last negative BC

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119
Q

facultative anaerobic GNR that can cause sepsis w/ meningitis, particularly in postsplenectomy patients, after DOG exposures

A

Capnocytophaga canimorsus

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120
Q

skin lesions a/w Capnocytophaga canimorsus which are characteristically nonblanching

A

purpura fulminans

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121
Q

treatment for Capnocytophaga canimorsus

A
  • usually susceptible to penicillin, but some prefer
  • third-generation cephalosporin, or
  • β-lactamase inhibitor combination
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122
Q

classic skin lesion in patients w/ Pseudomonas aeruginosa

A

ecthyma gangrenosum

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123
Q

halophilic (“salt-loving”), GNR that is found worldwide in warm coastal salt waters

A

Vibrio vulnificus

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124
Q

Vibrio vulnificus can cause primary sepsis in certain high-risk populations, which include?

A
  • chronic liver disease
  • immunodeficiency
  • iron storage d/o’s
  • ESRD
  • DM
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125
Q

most reports of primary sepsis in the USA from Vibrio vulnificus are a/w what?

A

ingestion of raw or undercooked oysters harvested from the Gulf Coast

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126
Q

Rocky Mountain spotted fever (RMSF) is caused by

A

Rickettsia rickettsii

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127
Q

the clinical spectrum of RMSF includes

A

skin lesions and CNS involvement

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128
Q

why do the skin lesions caused by Rickettsia rickettsii typically involve the wrists, palms of the hands, ankles, and soles of the feet?

A

because of enhanced proliferation in cooler body parts

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129
Q

what type of skin rash is classically seen w/ Rickettsia rickettsii?

A

petechial rash

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130
Q

what does MIC stand for?

A

minimum inhibitory concentration

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131
Q

are bactericidal abx more efficacious than bacteriostatic abx?

A

no, studies have shown they are equally efficacious; even in neutropenia, endocarditis, and meningitis

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132
Q

what pharmacologic property when administering abx against resistant gram-negative pathogens in the ICU has been most consistently a/w improved outcomes in patients w/ pulmonary infections, including HAP and VAP?

A

time above MIC

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133
Q
  • fever
  • generalized erythroderma
  • profound shock
  • MOF
  • result of capillary leak and tissue damage induced by bacterial toxins
A

TSS (toxic shock syndrome)

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134
Q

what is positive ice pack test?

A

ptosis improves following application of ice to orbits for 2 minutes

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135
Q

what are the neurotoxin-producing, spore-forming anaerobic bacteria that may contaminate food or illicit IV drugs?

A
  • Clostridium botulinum
  • Clostridium butyricum
  • Clostridium baratii
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136
Q

how many forms of botulinum toxin are there and how many can cause human botulism?

A
  • 7 forms (A-G)
  • 4 forms (types A, B, E, and occasionally F)
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137
Q

when can botulism symptoms appear after inoculation?

A

≥ 10 days

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138
Q

botulism classically causes descending FLACCID paralysis characterized by

A
  • ptosis
  • diplopia
  • dysphagia
  • dilated nonreactive pupils
  • respiratory distress
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139
Q

how does food botulism classically occur?

A

ingesting contaminated food, classically during HOME CANNING

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140
Q

how does wound botulism occur?

A
  • following trauma or surgery
  • IV drug use
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141
Q

what empiric treatment should be started for botulism if high on the ddx?

A

botulinum antitoxin

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142
Q

what additional therapy aside from botulinum antitoxin should be done for botulism?

A
  • wound debridement if present
  • empiric abx
  • organ failure support
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143
Q

how long does regeneration of new neuromuscular junctions and restoration of muscle strength take?

A

weeks to months

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144
Q

should a positive ice pack test be used to confirm myasthenia gravis?

A

no

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145
Q

definition of VAP (ventilator-associated PNA)

A

PNA in patient receiving MV that occurs 48 hours AFTER intubation

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146
Q

definition of HAP (hospital-acquired PNA)

A

PNA NOT a/w MV that occurs at least 48 hours after admission in a patient who has NOT been intubated at the time of admission to the hospital

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147
Q

the use of combination therapy to cover Pseudomonas aeruginosa has been demonstrated to do what?

A

cover multiple resistance mechanisms

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148
Q

what are risk factors a/w Candida auris, which is a multiresistant pathogen that can cause in-hospital epidemics?

A
  • DM
  • recent surgery
  • CVC
  • receiving systemic antifungal therapy
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149
Q

which dimorphic fungus characteristically causes infection in HIV-infected and other immunosuppressed patients, particularly those who live or have traveled to Southeast Asia?

A

Talaromyces marneffei (formerly Penicillium marneffei)

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150
Q
  • dimorphic fungus
  • fever
  • weight loss
  • nonproductive cough
  • skin lesions
  • hepatosplenomegaly
  • lymphadenopathy
  • endemic to Southeast Asia
A

Talaromyces marneffei (formerly Penicillium marneffei)

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151
Q
  • mold
  • usually cause bloodstream infection in severely immunocompromised patients; especially w/ neutropenia or severe T-cell immunodeficiency
  • multidrug-resistant
A

Fusarium species

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152
Q
  • ubiquitous, filamentous fungi present in soil, sewage, and polluted waters
  • can be colonizers of previously damaged bronchopulmonary system
  • can be acquired from a near-drowning even
A

Scedosporium apiospermum (sexual state; Pseudallescheria boydii), and Scedosporium prolificans

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153
Q

Scedosporium apiospermum (sexual state; Pseudallescheria boydii), and Scedosporium prolificans can cause what?

A
  • PNA
  • brain abscess
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154
Q

what is the most common species of malaria that makes up > 90% of all cases?

A

Plasmodium falciparum

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155
Q
  • AMS
  • anemia
  • thrombocytopenia
  • AKI
  • ARDS w/ DAH
  • metabolic acidosis
  • shock
  • endemic in tropical areas, especially sub-Saharan Africa
A

severe malaria

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156
Q

management of severe malaria

A
  • interim oral treatment w/ artemether-lumefantrine (Coartem)
  • call CDC Malaria Hotline to see if patient qualifies for artesunate iv
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157
Q

which medication has been shown to reduce risk of death in the treatment of severe malaria compared to quinidine?

A

artesunate iv

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158
Q

what medication can be used to treat uncomplicated malaria but would NOT be appropriate to treat severe malaria?

A

doxycycline iv

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159
Q

what age should empiric treatment for Listeria monocytogenes be given in bacterial meningitis?

A

adults > 50 yoa

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160
Q

what medication should be given to empirically treat for Listeria monocytogenes?

A

ampicillin

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161
Q

what medications should be given to cover for Streptococcus pneumoniae?

A

ceftriaxone or cefotaxime AND vancomycin (until c&s come back in case it’s resistant to 3rd-gen cephalosporins)

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162
Q

what medication should be given to reduce neurologic sequelae of bacterial meningitis 2/2 pneumococcus?

A

dexamethasone

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163
Q
  • AMS
  • seizure
  • CSF w/ lymphocytic pleocytosis w/o hemorrhage
  • MRI w/ symmetric hyperintensities in the basal ganglia and thalami
  • mosquito bites while camping
  • summertime
A

viral encephalitis, most likely from West Nile virus

164
Q
  • AMS
  • seizure
  • CSF w/ lymphocytic pleocytosis w/ hemorrhage
  • hemorrhagic lesion in the temporal lobe on MRI
A

viral encephalitis, most likely from herpes virus

165
Q

CNS involvement in the setting of immunosuppression (HIV) which leads to primary CNS lymphoma, not encephalitis

A

Epstein-Barr virus

166
Q
  • can cause severe encephalitis, but is exceedingly rare
  • largely occurs in children
  • typically occurs in winter months
A

influenza

167
Q

how do meningitis and encephalitis differ?

A

w/ meningitis cognition should be preserved

168
Q

what are the neurologic manifestations of encephalitis?

A
  • AMS
  • seizures
  • focal neurologic abnormalities (hemiparesis, CN palsies, exaggerated or pathologic DTRs)
169
Q

therapy for WNV, WEE, EEE, and other arboviruses

A

supportive

170
Q

treatment for HSV-1 encephalitis

A

acyclovir 10 mg/kg/dose q8h

171
Q

are neurologic deficits common after recovery from viral encephalitis?

A

yes, regardless of etiology

172
Q

what neurologic deficits can occur after recovery from viral encephalitis?

A
  • behavioral abnormalities
  • amnesia
  • severe cognitive impairment
  • dysnomia (difficulty recalling words, names, numbers)
  • impaired new learning
173
Q

main therapy for lung abscess

A

empiric abx therapy for an extended period of time

174
Q

what characteristics should empiric abx for treatment of lung abscess have?

A
  • should penetrate lung tissue
  • should provide good anaerobic coverage
175
Q

what empiric abx should be used for lung abscess?

A
  • β-lactam/lactamase inhibitor combination, OR
  • carbapenems, OR
  • clindamycin
176
Q

duration of abx for lung abscess

A
  • 6 weeks to 6 months
  • iv for the first 1 to 2 weeks then po for the rest if good clinical response
177
Q

when should surgical resection of lung abscess be considered?

A
  • no response to abx
  • size > 6 cm
178
Q

why is surgical resection of lung abscess not first-line therapy?

A

a/w higher mortality

179
Q

what procedures should NOT be attempted for management of lung abscess and WHY?

A
  • thoracentesis, chest tube, and transthoracic biopsy
  • can contaminate the pleural space and lead to empyema
180
Q

what are lung abscesses often 2/2?

A

recurrent aspiration

181
Q

which abx cannot be used to treat lung abscesses because they don’t have sufficient anaerobic coverage?

A
  • cephalosporins
  • macrolides
  • fluoroquinolones
182
Q

tissue plasminogen activator and deoxyribonuclease are effective in improving pleural fluid drainage and reducing the need for surgery in treating which conditions?

A
  • complicated pleural effusion
  • empyema
183
Q

what pathogen is defended against by cell-mediated immunity and can cause sepsis in up to 10% so should be suspected in HIV-infected patients?

A

Histoplasma capsulatum

184
Q

what is the classic pattern of involvement of Histoplasma capsulatum?

A

infection of the lungs followed by dissemination to reticuloendothelial structures (liver, spleen, BM, LNs) and to mucocutaneous sites

185
Q

what are the expected physical exam findings and laboratory findings of Histoplasma capsulatum based on its classic pattern of involvement?

A
  • transaminitis
  • pancytopenia
  • lymphadenopathy
  • GI bleed
186
Q

like TB, histoplasmosis can infect which organ leading to what?

A
  • adrenal glands
  • primary adrenal insufficiency
187
Q

diagnosis of histoplasmosis

A
  • BCs
  • cultures from BM
  • respiratory cultures, OR
  • cultures from other involved sites
188
Q

severe disseminated histoplasmosis can show what on PBS?

A

Histoplasma organisms ENGULFED by WBCs (yeah! get’em!)

189
Q

what method is sensitive for rapid diagnosis of disseminated histoplasmosis but not for chronic forms of pulmonary histoplasmosis?

A

Histoplasma antigen in blood or urine

190
Q

treatment of moderately severe to severe disseminated histoplasmosis?

A

liposomal amphotericin B for at least 2 weeks w/ possible step-down to po itraconazole

191
Q

Histoplasma can result in a secondary form of hemophagocytic syndrome aka

A

hemophagocytic lymphohistiocytosis (HLH)

192
Q

hemophagocytic syndrome aka hemophagocytic lymphohistiocytosis (HLH) is characterized as a hematologic d/o manifested by what clinical findings?

A
  • extreme inflammation
  • unregulated immune activation
193
Q

what organs are classically affected 2/2 HLH?

A
  • GI tract
  • endocrine glands
  • skin
  • liver
194
Q

HLH can be divided into primary (genetic or familial forms), and secondary forms; what are the causes of secondary HLH?

A
  • infection
  • AI disease
  • malignancy
  • immunodeficiency 2/2 organ transplantation
195
Q

what specific form of secondary HLH occurs in a/w AI diseases, most classically systemic juvenile idiopathic arthritis?

A

macrophage activation syndrome (MAS)

196
Q

what are the characteristic features of HLH?

A
  • prolonged fever
  • hepatosplenomegaly
  • cytopenia
  • very high ferritin
  • high triglycerides
  • transaminitis
  • high bilirubin
  • LOW fibrinogen
197
Q

what disease marker is typically very high, but if negative does not exclude HLH?

A

IL-2 receptor; particularly the apha (CD25) subunit

198
Q

primary HLH is a diagnosis of exclusion so what needs to be ruled out first?

A

secondary causes of hyperferritinemia

199
Q

the following Yamaguchi criteria are used to diagnose what disease?

  • major criteria
    1. fever ≥ 39°C ≥ x 1 week
    2. arthralgia/arthritis x ≥ 2 weeks
    3. nonpruritic salmon-colored rash on trunk/extremities, and
    4. granulocytic leukocytosis (≥ 10,000)
  • minor criteria
    1. sore throat
    2. lymphadenopathy
    3. hepatomegaly or splenomegaly
    4. transaminitis, and
    5. negative tests for RF and ANA
A

adult-onset Still’s disease

200
Q

if prolonged use of nasal tamponade devices leading to profound hypotension and skin rash, think of

A

toxic shock syndrome (TSS)

201
Q

aside from source control but removing the offending agent, treatment for TSS must include what?

A

MRSA coverage w/ vancomycin

202
Q

diagnosis of CDI

A
  • clinically significant diarrhea (≥ 3 loose stools w/i 24 hours)
  • relevant risk factors; recent abx use, hospitalization, advanced age
  • positive stool C diff toxin by EIA or PCR
203
Q

does testing for C diff distinguish between CDI and asymptomatic carriage?

A

no

204
Q

should you test patients who are asymptomatic for C diff or are actively receiving treatment for CDI?

A

no

205
Q

can stool assays remain positive for C diff during or after clinical recovery from CDI?

A

yes

206
Q

treatment for initial cases of CDI

A
  • vancomycin 125 mg po q6h, OR
  • fidaxomicin
207
Q

treatment for CDI in critically ill patients for whom oral therapy can’t be given

A

metronidazole 500 mg iv q8h w/ colonic administration of vancomycin

208
Q

definitive treatment of CDI in severely critically ill patients who are > 60 yoa w/ acute abdominal distention and ileus

A

colectomy

209
Q

treatment of recurrent CDI (> 1 episode) (no rigorous studies of management)

A
  • vancomycin 250 to 500 mg po q6h, OR
  • fidaxomicin, OR
  • rifaximin, OR
  • addition of an antitoxin MAB
210
Q

treatment of refractory CDI for those whom surgery is extremely high risk

A
  • FMT, OR
  • toxin A/B MAB
211
Q

should patients who are C diff toxin-positive but asymptomatic be treated?

A

no!

212
Q

what should be done regarding concomitant abx when treating CDI?

A
  • stop any abx that can be stopped
  • narrow the spectrum and/or shorten abx duration if possible
213
Q

nocardiosis typically presents as

A
  • pulmonary infiltrates
  • CNS infiltrates
  • can be protean (able to change frequently or easily)
214
Q

the order Actinomycetales has which 3 genuses (or genera) which cause human infection

A
  • Nocardia
  • Mycobacteria
  • Actinomyces
215
Q

Actinomyces infections typically affect

A

head, neck, and abdomen w/ a tendency to form abscesses and fistulous tracts

216
Q

what diagnostic information is highly suggestive of Nocardia infection?

A

weakly acid-fast staining on BC

217
Q

treatment for nocardiosis

A

trimethoprim-sulfamethoxazole

218
Q

what are the most common adverse effects of trimethoprim-sulfamethoxazole?

A
  • GI upset
  • allergic skin reactions
219
Q

treatment for Actinomyces

A

high-dose PCN

220
Q

adverse effect of PCN

A

anaphylaxis

221
Q

Nocardia infection can occasionally be mistaken for what infection?

A

TB and nontuberculous mycobacterial infection

222
Q

type of infection a/w solid organ or hematologic transplant

  • first month
A

hospital acquired infection

223
Q

type of infection a/w solid organ or hematologic transplant

  • 1 to 6 months
A

opportunistic infection

224
Q

type of infection a/w solid organ or hematologic transplant

  • 6 months to 1 year or more
A

community acquired infection

225
Q

infections a/w types of immunosuppression

  • antilymphocyte globulins
A

activation of latent viruses

226
Q

infections a/w types of immunosuppression

  • glucocorticoids
A
  • bacteria
  • PJP
  • hepatitis B
  • hepatitis C
227
Q

infections a/w types of immunosuppression

  • azathioprine
A

neutropenic infections

228
Q

infections a/w types of immunosuppression

  • MMF
A
  • late-onset CMV
  • bacterial
229
Q

infections a/w types of immunosuppression

  • cyclosporine
  • tacrolimus
A
  • viral
  • intracellular pathogens
230
Q

infections a/w types of immunosuppression

  • plasmapheresis
A

encapsulated organisms

231
Q

infections a/w types of immunosuppression

  • MAB
A
  • bacterial
  • viral
232
Q

what are the most common sites of infection in renal transplant patients?

A
  • same as nontransplant patients
  • lung
  • urinary tract
  • abdomen
233
Q

in patients who have transplanted > 1 year ago the most common organisms causing infection are similar to nontransplanted patients, which are?

A
  • mainly gram-negative bacteria
  • Escherichia coli
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa

followed by gram-positive bacteria
- Staphylococcus aureus
- Streptococcus pneumoniae
- Enterococcus species

  • fungi, such as Pneumocystis jirovecii, can also be important
234
Q

in a retrospective observational study of renal transplant patients w/ severe sepsis or septic shock in the ICU, hospital mortality was independently a/w what factors?

A
  • male sex
  • hematologic dysfunction
  • MV
  • graft dysfunction
235
Q

which abx is stable in the presence of all 3 classic mechanisms of gram-negative resistance to carbapenems;

  • inactivation by β-lactamases
  • impermeability
  • efflux
A

cefiderocol

236
Q

nosocomial PNA is broken down into 2 clinical entities, which are?

A
  • hospital-acquired bacterial PNA (HABP)
  • ventilator-associated bacterial PNA (VABP)
237
Q

ventilator-associated bacterial PNA is broken down into what 2 stages?

A
  • early
  • late
238
Q

hospital-acquired bacterial PNA is broken down how?

A
  • non-ventilated;
    = wards
    = ICU
  • ventilated
    = vHABP
239
Q

which GNRs have a high-level resistance to β-lactams, cephalosporins, and carbapenems?

A
  • Pseudomonas spp
  • Stenotrophomonas maltophilia
  • ESBL Klebsiella pneumoniae (including carbapenem-producing strains)
240
Q

GNR that is lactose fermenting, and carbopenamase-producing

A

Klebsiella pneumoniae

241
Q

what are the lactose-fermenting GNRs that can develop resistance to abx through extended spectrum beta-lactamases (ESBLs)?

A
  • Klebsiella pneumoniae
  • Enterobacter cloacae
  • Escherichia coli
242
Q

ESBLs are enzymes that allow bacteria to be resistant to which abx?

A
  • beta-lactam abx
    = penicillins
    = cephalosporins
    = aztreonam (monobactam)
243
Q

what bacterial strain, present in North America and the Middle East, has carbopenemase conferring resistance to all beta-lactam abx?

A

KPC strain (Klebsiella pneumoniae carbopenemase)

244
Q

what bacterial strain contain zinc for activity and is therefore dubbed a metall-beta-lactamase, and is commonly found in southeast Asia?

A

NDM-1 strain (New Delhi metallo-beta lactamase)

245
Q

what therapy is now being used to combat resistant strains such as KPC and NDM-1?

A

combination of antipseudomonal abx w/ a carbopenemase inhibitor, usually avibactam or vaborbactam

246
Q

what are the 2 most frequently used abx w/ activity against KPC?

A
  • ceftazadine-avibactam
  • meropenem-vaborbactam
247
Q

what other abx can be used for KPC, but limited d/t their side effect profile (AKI)?

A
  • colistin
  • tigecycline
248
Q

treatment choice for Stenotrophomonas maltophilia

A

trimethoprim-sulfamethoxazole

249
Q

when administering beta-lactam abx to critically ill patients w/ bacteremia, what best correlates w/ successful microbiologic eradication?

A

prolonged infusion (time-dependent effect)

250
Q

bacteremia from what organism is a common problem in OLT patients?

A

Pseudomonas aeruginosa

251
Q

what should be on the ddx for recurrent Pseudomonas aeruginosa bacteremia despite adequate abx in an OLT patient that’s admitted for small bowel perforation 2/2 duodenal ulcer?

A

occult intraabdominal abscess

252
Q

bacteremic seeding of the kidneys w/ development of small renal abscesses occurs as a complication of which 2 organisms?

A
  • Staphylococcus aureus bacteremia
  • Candida species fungemia
253
Q

how does Mycobacterium tuberculosis contribute to HIV-1 replication?

A

activation of the transcription factor, nuclear factor-kappa B

254
Q

can active disease caused by Mycobacterium tuberculosis directly increase the level of HIV-1 infection?

A

yes

255
Q

should ART be withheld until completion of TB treatment given drug-drug interactions?

A

no! since active Mycobacterium tuberculosis directly increase the level of HIV-1 infection

256
Q

which pathogen is angioinvasive and in neutropenic patients occlude blood vessels thereby mimicking the physiology of a PE?

A

Aspergillus infection

257
Q

Streptococcus pneumoniae, in asplenic patients, particularly those who required splenectomy 2/2 a hemoglobinopathy, what 2 clinical problems may occur and result in elevated right-sided pressures?

A
  • increased rate of thrombosis, including PE
  • recurrent inflammation and thrombosis leading to pHTN
258
Q

what are the 3 main ways a pathogen can cause disease?

A
  • direct destruction or inflammatory effect
  • toxin production
  • immunologic effect
259
Q

what metric is used to guide preemptive treatment in hematopoietic-cell transplant patients that are CMV positive to prevent a direct effect of the virus?

A

CMV viral load

260
Q

in HCT patients, indirect effects of CMV include increased incidence of graft rejection and graft-vs-host disease; even if patients have low seropositivity or undetectable viral loads, patients should be considered for what?

A

CMV ppx w/ letermovir

261
Q

what are the most characteristic pathogens to cause meningitis after trauma, neurosurgical procedures, or intracranial device placement?

A
  • MRSA
  • Pseudomonas aeruginosa
262
Q

patients that are s/p trauma, neurosurgical procedures, or intracranial device placement that p/w minimal if any elevation in CSF WBCs, and normal or minimally depressed CSF glucose, think of

A

healthcare-associated ventriculitis or meningitis

263
Q

ventriculitis or meningitis 2/2 what organism can take at least 10 days to grow?

A

Propionibacterium acnes

264
Q

what are the 4 mechanisms that CSF shunts may become infected?

A
  • colonization of the shunt at the time of surgery
  • retrograde infection from the distal end of the shunt
  • pathogen entry through the skin while entering the shunt
  • hematogenous seeding
265
Q

acute, febrile, and focal encephalitis

A

HSV encephalitis

266
Q

type of meningitis that is an underreported clinical phenomenon, thought to be a T-cell-mediated delayed hypersensitivity reaction

A

drug-induced meningitis (aka, drug-induced aseptic meningitis; DIAM)

267
Q

what drug classes have been reported to cause drug-induced meningitis?

A
  • NSAIDs (MCC)
  • abx, most notably, sufla and fluoroquinolones
  • immunosuppressive-immunomodulatory drugs
  • AEDs
  • SLE drugs
268
Q

severe demyelinating disease of the CNS caused by activation of previous John Cunningham polyomavirus (JCV) infection earlier in life

A

progressive multifocal leukoencephalopathy (PML)

269
Q

in PML, JCV leads to demyelination that affects primarily white matter and leads to subacute deficits that include what?

A
  • AMS
  • ataxia
  • visual disturbances (hemianopia and diplopia)
270
Q

about 40% of patients w/ PML can develop

A

seizures

271
Q
  • affects ALL white matter tracts, including those closest to the cortex
  • tracts closest to the cortex are often spared in other demyelinating d/o’s
A

progressive multifocal leukoencephalopathy (PML)

272
Q

diagnosis of progressive multifocal leukoencephalopathy (PML) is suggested by what?

A
  • h/o immunosuppression
  • progressive neurologic symptoms
  • MRI lesions localized to subcortical white matter w/ T2-weighted (T2W) images demonstrating fluid-attenuated inversion recovery
273
Q

diagnosis of progressive multifocal leukoencephalopathy (PML) is confirmed by

A

LP w/ CSF positive by PCR for JCV

274
Q

what immunocompromised conditions are a/w JCV infection?

A
  • malignancy (lymphoproliferative/myeloproliferative d/o’s)
  • HIV
  • immunosuppressive therapy for organ transplant or AI d/o’s (sarcoidosis, SLE)
275
Q

treatment for PML

A

supportive, and reconstitution of the immune system asap

276
Q

most common immune-mediated, inflammatory, demyelinating disease of the CNS

A

multiple sclerosis (MS)

277
Q

multiple sclerosis onset

A

acute manifestation (days to weeks) w/ periods of remission

278
Q

progressive multifocal leukoencephalopathy (PML) onset

A

progressive over weeks to months WITHOUT periods of remission

279
Q

MS is often a/w what condition that is not characteristic of PML?

A

focal eye findings;
- optic neuritis
- internuclear ophthalmoplegia

280
Q

what MRI findings are seen w/ acute MS exacerbation?

A

lesions (plaques) w/ peripheral enhancement on axial contrast-enhanced T1-weighted images

281
Q

patients w/ poorly controlled HIV are at risk for HIV encephalopathy which manifests as the classic triad of which symptoms?

A
  • subcortical dementia (memory and psychomotor speed impairment)
  • depressive symptoms
  • movement d/o’s
282
Q
  • can manifest w/ oculomotor symptoms
  • symptoms are typically acute
A

acute cerebellar strokes

283
Q

what are the MRI findings in acute stroke?

A
  • hyperintense areas on diffusion-weighted images because of cytotoxic edema w/ restricted diffusion
  • then hyperintense on fluid-attenuated inversion recovery and T2W images
284
Q

how can you tell if an MRI is T1?

A

if gray matter is DARKER than white matter (like it’s supposed to be)

285
Q

how can you tell if an MRI is T2?

A

if gray matter is LIGHTER than white matter

286
Q
  • vesicles or bullae w/ underlying purpura
  • septic shock
  • lactic acidosis
A

necrotizing infection

287
Q

treatment for necrotizing skin/soft-tissue infection

A
  • vancomycin
  • piperacillin/tazobactam
  • clindamycin (theoretical reduction of toxin production)
  • +/- IVIG (small RCTs suggest benefit)
  • urgent surgical consultation
288
Q

what is the utility of imaging studies in the diagnosis of necrotizing infection?

A

insensitive

289
Q

what abx is critical in the treatment of leptospirosis and rickettsial diseases?

A

doxycycline

290
Q

can leptospirosis or rickettsial diseases cause necrotizing skin or soft-tissue infection?

A

no

291
Q

routine testing for the presence of ESBLs is NOT performed by most clinical microbiology labs, so instead, nonsusceptibility to what abx is used as a PROXY for ESBL production?

A

ceftriaxone (MIC > 2 μg/ml)

292
Q

if susceptible, the use of which abx will effectively treat ESBL Klebsiella while also minimizing the risk of developing resistance to meropenem for possible future infections w/ Pseudomonas or Acinetobacter?

A

ertapenem

293
Q

what classic tenet in ID should always be remembered regarding abx activity against Pseudomonas aeruginosa?

A

when treating another pathogen there’s a risk for selecting resistant strains of Pseudomonas aeruginosa so abx that don’t have activity against Pseudomonas aeruginosa should be chosen

294
Q

which abx should be avoided for the treatment of infections caused by ESBL-producing Enterobacterales even if susceptible?

A

cefepime

295
Q

what are 2 examples of ESBL-producing Enterobacterales bacteria?

A
  • Escherichia coli
  • Klebsiella pneuomoniae
296
Q

which abx is a/w a significantly higher mortality rate than those treated w/ meropenem for the treatment of ESBL-producing bacterial bloodstream infections?

A

piperacillin/tazobactam

297
Q

what test bolus can be given to determine if a patient is fluid responsive and by what percentage does the stroke volume need to increase?

A
  • 4 ml/kg bolus
  • ≥ 10%
298
Q

how much whole blood enters the central circulation w/ a passive leg raise maneurver?

A

250-350 ml

299
Q

lactose-fermenting GNR that is unusually “sticky”

A

hypervirulent (hypermucoviscous) Klebsiella pneumoniae (hvKp)

300
Q
  • subgroup of viridans streptococci that is normal human flora (found in the mouth, throat, stool, and vagina) but can lead to pyogenic abscess formation
  • can lead to liver abscesses, but typically responds to drainage and abx
A

Streptococcus milleri group

  • Streptococcus anginosus
  • Streptococcus intermedius
  • Streptococcus constellatus
301
Q
  • protozoan that usually does not produce symptoms but can lead to dysentery
  • can lead to invasive infections in the lungs, heart, brain, and liver
  • liver abscess is the most common extraintestinal site
  • most commonly seen in India, Africa, Mexico, and Central and South America
A

Entamoeba histolytica

302
Q

GNR that causes liver abscesses, but is NOT a/w metastasis and responds to drainage and abx

A

Escherichia coli

303
Q

CN 1

A

olfactory nerve

304
Q

CN 2

A

optic nerve

305
Q

CN 3

A

oculomotor nerve

306
Q

CN 4

A

trochlear nerve

307
Q

CN 5

A

trigeminal nerve

308
Q

CN 6

A

abducens nerve

309
Q

CN 7

A

facial nerve

310
Q

CN 8

A

vestibulocochlear nerve

311
Q

CN 9

A

glossopharyngeal nerve

312
Q

CN 10

A

vagus nerve

313
Q

CN 11

A

spinal accessory

314
Q

CN 12

A

hypoglossal nerve

315
Q
  • vomiting followed by
  • oculobulbar findings
  • flaccid DESCENDING paralysis
A

botulism

316
Q

what are the CN 3 (ocular nerve) and CN 6 (abducens nerve) signs/symptoms that occur from botulism?

A
  • accommodative paresis
  • ptosis
  • ophthalmoparesis
  • mydriasis
317
Q

what other CNs besides 3 and 6 can be involved 2/2 botulism?

A

CNs 9, 10, 11, and 12

318
Q

how does involvement of CNs 9, 10, 11, and 12 present in botulism?

A
  • dysarthria (poor articulation)
  • dysphagia
  • dysphonia (hoarse voice)
319
Q

are the neuro-ophthalmic signs in botulism unilateral or bilateral?

A

usually bilateral

320
Q

in botulism how does descending paralysis progress after the development oculobulbar findings?

A

quickly

321
Q

if botulism is suspected who does the CDC recommend to contact?

A

local or state health department’s emergency on-call staff to arrange emergency expert clinical consultation because laboratory confirmation can only be performed by certain municipal and state public health laboratories

322
Q

CO poisoning usually presents w/ what symptoms?

A
  • headache
  • encephalopathy
323
Q
  • ASCENDING paralysis
  • 2/2 nerve demyelination
  • AREFLEXIA
  • 2/2 immunologic sequela of a diarrheal illness, most commonly Campylobacter jejuni
A

Guillain-Barré syndrome

324
Q

Guillain-Barré syndrome tends to follow GI illness by what timeframe?

A

weeks

325
Q
  • neuromuscular junction d/o
  • may occur as a paraneoplastic phenomenon or a primary AI d/o
A

Lambert-Eaton myasthenic syndrome

326
Q

> 50% of cases of Lambert-Eaton myasthenic syndrome are a/w what?

A

small cell lung cancer

327
Q
  • proximal muscle weakness
  • DTRs are usually absent
  • there is often autonomic dysfunction
A

Lambert-Eaton myasthenic syndrome

328
Q
  • reticulonodular pattern
  • recent travel to Southwestern USA
  • severe PNA
A

coccidioidomycosis

329
Q

in patients w/ severe disease and immune compromise, what is the recommended approach to dialysis Coccidioides?

A

to use multiple modalities, including;
- serologic testing for Abs
- direct visualization
- culture of sputum or BAL

330
Q

in addition to serologic testing for Abs, direct visualization, and culture of sputum or BAL, what is another potential way to test for Coccidioides in patients who are immunocompromised?

A

serum and urine Ag testing; but again, this shouldn’t be the only diagnostic test done

331
Q

what test is typically used to diagnose invasive candidiasis in critically ill patients, but is a nonspecific cell wall component of most fungal pathogens?

A

serum (1-3)-β-D-glucan measurement

332
Q

when is LP recommended in a patient w/ suspected meningitis 2/2 Coccidioides?

A
  • headache
  • AMS
  • focal neurologic deficits
333
Q
  • mold infection
  • in immunocompetent hosts, manifests as superficial infections such as keratitis or onychomycosis
A

Fusarium species

334
Q
  • mold infection
  • in severely immunocompromised hosts, manifests as sinusitis, endophthalmitis, PNA, skin infection, and fungemia
A

Fusarium species

335
Q
  • disseminated skin lesions are characteristically reddish gray macules, some w/ central ulceration but others w/ black eschar formation
  • pathogen has angioinvasive properties
A

Fusarium species

336
Q

treatment for Fusarium species

A

amphotericin B

337
Q

what mold infection can breakthrough in a patient on azole ppx?

  • much less likely for Candida or Aspergillus to breakthrough
A

Fusarium species

338
Q

what group of antifungals lack clinically significant activity against the Fusarium species?

A

echinocandins (micafungin, caspofungin, and anidulafungin)

339
Q

what mold infection clinically mimics Aspergillus?

A

Fusarium species

340
Q
  • pathogen has angioinvasive properties
  • clinical manifestations often include evidence of infarction at the classic site of infection;
  • lungs
  • sinuses
  • skin
  • CNS
A

Aspergillus

341
Q

mold infection that can grow in blood cultures (up to 40% of patients) and is highly characteristic of its clinical presentation

A

Fusarium species

342
Q

pathogenic mold infection that does NOT commonly grow in blood cultures

A

Aspergillus

343
Q

skin lesions 2/2 to mold infection that present in patients w/ neutropenia, usually occur as a single lesion, often at a site of inoculation (such as a previous IV catheter)

A

Aspergillus

344
Q

mold that act as either primary or opportunistic pathogens to cause infections in both immunocompetent AND immunocompromised hosts

A

Scedosporium species

345
Q

what are the spectrum of infection that Scedosporium species causes?

A
  • asymptomatic colonization of respiratory tract
  • superficial infections
  • allergic reactions
  • severe invasive localized or disseminated fungal infections
346
Q

what is an important predisposition to infection by Scedosporium?

A

prior antifungal ppx NOT active against it

347
Q

how can immunocompetent hosts develop clinical disease 2/2 Scedosporium?

A

near-drowning events in water polluted w/ fungal organisms

348
Q

infection 2/2 Scedosporium typically involves which organ systems?

A
  • sinuses
  • lungs
  • CNS
349
Q

does Scedosporium grown in blood cultures?

A

rarely

350
Q

does Scedosporium typically cause skin lesions?

A

no

351
Q

which molds are in the Mucorales family?

A
  • Rhizopus species
  • Mucor species
352
Q

mold infection that is second most common in patients w/ hematological malignancy or after transplant w/ mortality rates > 90% when infection is disseminated

A

mucormycosis

353
Q

because of this mold’s propensity to use iron as an element for growth, repeat blood transfusions in patients w/ MDS who have undergone BMT are at risk of high fatality rates from this mold

A

Murcorales family (Rhizopus species and Mucor species)

354
Q
  • siderophilic (iron-loving)
  • angioinvasive, inducing blood vessel thrombosis and tissue necrosis
  • BCs are rarely positive w/ this pathogen
  • disseminated skin lesions are NOT part of the clinical picture
A

Murcorales family (Rhizopus species and Mucor species)

355
Q

compared to CVCs (central venous catheters), PICCs (peripherally inserted central catheters) have what risk of CLABSI and DVT?

A
  • fourfold greater risk of BSI (bloodstream infection)
  • 2.5x higher risk of DVT
356
Q

HCPs who are NOT vaccinated or do NOT have other evidence of immunity to varicella are considered susceptible to varicella-zoster virus infection and are potentially infectious during what time period?

A

days 8 to 21 after exposure

357
Q

if an HCP who is NOT vaccinated or does NOT have other evidence of immunity to varicella is exposed to a patient w/ acute varicella infection what is the most appropriate next step?

A

temporarily reassign to a location remote from patient-care areas from day 8 to 21 after the last exposure

358
Q

if an HCP is exposed to a patient w/ acute varicella infection what is the treatment?

A

varicella vaccination

359
Q

if an HCP is exposed to a patient w/ acute varicella infection, what is the treatment if there is a contraindication to give the varicella vaccine?

A

varicella-zoster immune globulin

360
Q

varicella vaccination is contraindicated in which persons?

A
  • pregnant HCP
  • leukemia/lymphoma patients
  • patients on immunosuppressive medications
  • cellular immune deficiencies
361
Q

when should varicella vaccine be given if someone is exposed to a patient w/ acute varicella infection?

A

w/i 3 to 5 days, but even after 5 days in case of repeat exposure

362
Q
  • incubation period usually 1 to 2 weeks, but can be as long as 4 weeks
  • nonspecific prodrome followed by rapid development of ARDS and hemodynamic compromise
  • ARDS is often hemorrhagic
A

hantavirus cardiopulmonary syndrome

363
Q

human acquisition of hantavirus is through contact w/ what?

A

rodents

364
Q

what phase of disease 2/2 hantavirus is characterized by significant capillary leak, resulting in noncardiogenic pulmonary edema and hypotension?

A

cardiopulmonary phase

365
Q

progression to shock, respiratory failure, coagulopathy, and even death is often quite rapid in which viral illness?

A

hantavirus cardiopulmonary syndrome

366
Q

hantavirus pulmonary syndrome is characterized by what?

A
  • hemoconcentration
  • thrombocytopenia
367
Q
  • transaminitis
  • elevated LDH
  • lactic acidosis
  • leukocytosis, sometimes up to 90,000/µL, and circulating immunoblasts
A

hantavirus

368
Q

this diagnostic triad is in reference to which viral illness?

  • thrombocytopenia
  • left-shifted, predominantly granulocytic leukocytosis
  • > 10% immunoblasts
A

hantavirus

369
Q

this viral illness is diagnosed by serology w/ results taking a month or more after the patient is d/c’d from the hospital

A

hantavirus

370
Q

when a patient diagnosed w/ PNA fails to respond to empirical abx treatment, what things should be considered?

A
  • obstructing airway lesion
  • immunocompromise
  • unusual pathogen
  • incorrect diagnosis
371
Q

histopathological findings

  • thick-walled
  • round to oval fungal yeast forms
  • ~ 8 to 15 µm
A

disseminated blastomycosis

372
Q

histopathological findings

  • spherules, containing multiple endospores
  • ~ 10 to 100 µm
A

coccidioidomycosis

373
Q

histopathological findings

  • narrow-based budding
  • ~ 5 to 10 µm
A

cryptococcosis

374
Q

histopathological findings

  • yeasts
  • often w/ pseudohyphae
  • ~ 3 to 5 µm
A

candidemia

375
Q

histopathological findings

  • yeasts w/ narrow-based budding
  • ~ 2 to 4 µm
A

histoplasmosis

376
Q

treatment for life-threatening blastomycosis, including ARDS

A

liposomal amphotericin B until clinical improvement, then itraconazole for 6 to 12 months

377
Q

what additional treatment, besides liposomal amphotericin B, for severe pulmonary blastomycosis, such as ARDS, should be considered?

A

corticosteroids (prednisone 40-60 mg/day or equivalent x 1-2 weeks)

378
Q

treatment of invasive aspergillosis

A

IV voriconazole

379
Q

histopathological findings

  • thin, septate, acute-angle branching hyphae
A

Aspergillus species

380
Q

AC is not considered for what time periods if a patient has an ischemic stroke vs hemorrhagic?

A
  • ischemic = 48 hours
  • hemorrhagic = up to 7 days after
381
Q

what is the recommend for starting AC for embolic stroke in the setting of endocarditis?

A

considered risky and is typically NOT recommended

382
Q

in a patient w/ a bleeding risk 2/2 cerebral abscess from septic embolization and mycotic aneurysm in other parts of the cerebral vasculature what imaging study should be done before starting AC?

A

digital subtraction cerebral angiography

383
Q

a patient in septic shock, what physical exam finding is equivalent to lactate clearance as an end point guiding fluid and vasoactive drug treatment?

A

measuring peripheral circulation adequacy

384
Q

what abx should be added to an empiric regimen for spontaneous gas gangrene to inhibit toxin production?

A

clindamycin

385
Q

Clostridial myonecrosis can be caused by what 2 processes?

A
  • trauma
  • spontaneous seeding of muscle through hematogenous spread
386
Q

what type of malignancy is a well-recognized risk factor for spontaneous Clostridial myonecrosis w/ the malignancy being the source of hematogenous spread of Clostridium from the GI tract to the muscle?

A

colorectal malignancy

387
Q
  • wound exposed to salt water or shellfish (opening oysters)
  • eating raw shellfish (mainly seen in underlying liver disease)
  • case reports from eating raw shellfish in patients w/ DM or CKD
A

Vibrio vulnificus

388
Q

Enterobacterales was previously known as?

A

Enterobacteriaceae

389
Q

what are the three categories pharmacokinetic/pharmacodynamic considerations when choosing abx in the ICU?

A
  • time-dependent killing
  • concentration-dependent killing
  • concentration-dependent w/ time-dependent killing
390
Q
  • β-lactam abx
  • hydrophilic
  • time-dependent killing
A

piperacillin

391
Q
  • hydrophilic
  • both time- and concentration-dependent killing
A

vancomycin

392
Q
  • lipophilic
  • concentration dependent w/ time dependence
  • is able to pass through alveolar epithelial cells to reach the epithelial lining fluid w/ concentrations approximated to be 100% of corresponding plasma values
A

linezolid

393
Q
  • hydrophilic
  • concentration-dependent killing
  • plasma concentrations needed to achieve an antibacterial effect often overlap w/ clinical levels that result in nephrotoxicity
A

colistin

394
Q

oral antiviral for influenza

A

oseltamivir

395
Q
  • inhaled antiviral that is approved for ppx among close contacts of patients w/ influenza and for treatment of patients who are not at high risk
  • not recommended for patients w/ uncontrolled asthma or COPD
A

zanamivir

396
Q

IV antiviral that should be reserved for patients who cannot receive enteral oseltamivir

A

peramivir

397
Q
  • novel oral antiviral that inhibits viral cap-dependent endonuclease
  • has demonstrated activity against both influenza A and B viruses
A

baloxavir

398
Q
  • inhibit viral matrix protein 2 in influenza A viruses
  • have NO activity against influenza B viruses
  • because of side effects and high levels of resistance, are no longer recommended for use as anti-influenza drugs in the US
A

amantadine and rimantadine

399
Q
  • exposure to this fungus is normally of little consequence
  • some individuals can develop hypersensitivity leading to severe asthma, bronchiectasis, and fleeting lung infiltrates
A

allergic bronchopulmonary aspergillosis

400
Q

exposure to this fungus in patients w/ structural lung disease such as emphysema or cystic sarcoidosis may develop this

A

fungus balls (aspergillomas) in lung cavities

401
Q

invasive aspergillosis occurs in which patients?

A

immunocompromised;

  • neutropenic undergoing BMT
  • solid organ transplant recipients
  • patients undergoing CAR-T cell therapy
  • maybe advanced cirrhosis
402
Q

ideal method of diagnosing invasive aspergillosis

A

tissue biopsy

403
Q

if tissue biopsy is not possible, what other methods can be used to diagnose invasive aspergillosis?

A
  • galactomannan or β-D-glucan (fungal Ag)
  • BAL
  • PCR
404
Q

treatment of choice for invasive aspergillosis

A

posaconazole (less adverse effects) or voriconazole

405
Q

what causes type A lactic acidosis?

A

marked tissue hypoperfusion 2/2

  • hypovolemia
  • cardiac failure
  • sepsis
  • cardiopulmonary arrest
406
Q

what causes type B lactic acidosis?

A

toxin-induced impairment of cellular metabolism and regional areas of ischemia

  • metformin
  • malignancy
  • alcoholism
  • toxic alcohols (methanol and ethylene glycol)
  • HIV infection = from sepsis and/or ART
  • beta-adrenergic agonists = epinephrine
  • severe bronchospasm treated w/ high-dose, inhaled beta agonists
  • mitochondrial dysfunction 2/2 inherited d/o’s
  • mitochondrial dysfunction 2/2 thiamine deficiency
  • drug-induced mitochondrial dysfunction 2/2 propofol
  • drug-induced mitochondrial dysfunction 2/2 linezolid

CHEST SEEK Library (11 decks)

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