Exam 2 Flashcards

1
Q

How is MTB transmitted?

A

Person-to-person via aerosol droplet nuclei

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2
Q

Who is the reservoir for MTB?

A

Humans only

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3
Q

Prosector’s Warts are indicative of inoculation with what disease?

A

MTB

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4
Q

MTB largely affects what age ranges?

A

Infants and older adults (bimodal age distribution)

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5
Q

MTB manifestations in infants/IMC? (2)

A
  1. Hematogenous dissemination

2. Meningitis

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6
Q

MTB manifestations in older pts? (2)

A
  1. Failure of immune sx

2. +/- reactivation of latent infection

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7
Q

Infection risk factor for children?

A

Close contact w/ infected caregiver

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8
Q

What are the causative agents of TB? (3)

A
  1. Mycobacterium tuberculosis&raquo_space;
  2. Mycobacterium bovis (Consumption of unpasteurized milk/ contact w/ infected animals)
  3. Mycobacterium africanum (West African Counties, no animal reservoirs, spread by food)
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9
Q

Strain of Mycobacterium used to make TB, BCG vaccine?

A

Mycobacterium bovis, given in highly endemic areas

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10
Q

MTB characteristics (shape, cell wall, oxygen status, motility, heat sensitivity, growth) ?

A
  1. Bacillus
  2. Mycolic acid
  3. Obligate aerobe
  4. Non-motile
  5. Heat sensitive, killed by pasteurization
  6. Alveolar macrophage
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11
Q

MTB staining

A
  • Acid Fast
  • Ziehl-Neelsen or Kinyoun stains
  • Cells resistant to staining and decolorization once stained
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12
Q

MTB virulence factors

A

No classic virulence factors or toxin, structure feature create issues for the pt

  1. Mycolic acid
  2. Cord factor - myoside,
  3. Lipoarabinomanna (LAM) - inhibits cell mediated immunity, scavenges ROI
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13
Q

CXR findings for TB?

A

Fibrotic and calcified tubercle

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14
Q

Risk of infection spread w/ latent TB?

A

No risk

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15
Q

Are pts w/ latent TB treated?

A

Yes

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16
Q

Are pts w/ reactivation or secondary TB infectious?

A

Yes

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17
Q

Cause of Miliary Tb? (2)

A
  1. Lypmhohematogenous spread of primary infection

2. Via latent focus w/ subsequent spread

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18
Q

Tests for DX of Tb? (5)

A
  1. XR consistent w/ TB
  2. Skin test reactivity
  3. Sputum stain/broth cx to detect acid fast bacteria
  4. Rapid blood test (release of IFN-Y)
  5. GeneXpert Rapid test for MTB and Rifampin resistance
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19
Q

Goal of tx for MTB?

A
  1. Recognize, isolate, and treat infected persons (Latent and active)
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20
Q

MAC characteristics (shape, cell wall, oxygen status, motility, growth)?

A
  1. Bacilli
  2. Acid fast, Weakly G+
  3. Aerobic
  4. Ubiquitous (water, soil, plants)
  5. Slow growing
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21
Q

MAC w/ person-to-person transmission?

A

NO

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22
Q

Pt isolation required w/ MAC infection?

A

No

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23
Q

MAC relationship w/ HIV pts?

A

Opportunistic pathogen. Leading cause of NTM infections in HIV+ pt

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24
Q

Lady Windermere’s syndrome is associated w/ what TB pathogen?

A

MAC

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25
Q

What gender/age range is Lady Windermere’s syndrome seen in?

A

Elderly, non-smoking female

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26
Q

Type of MAC disease in IMC (AIDs) pts?

A

Disseminated disease (no organ spared)

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27
Q

Findings/tests for NTM for dx? (3)

A
  1. Microscopy reveals acid fast bacteria and culture
  2. Must ecxlude other etiologies (Fungi, TB), sterile site isolation
  3. CXR w/ + pulmonary lesions
  4. Final ID via molecular techniques (PCR to determine 16S rRNA sequence)
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28
Q

MAC tx HIV- pts?

A

ABX until sputum cultures are negative for 1 yr

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29
Q

MAC tx in HIV + pt w/o infection?

A

Chemoprophylaxis w/ CD4 < 50 cell/uL, discontinue 3 months after CD4 > 100 cell/uL

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30
Q

MAC tx in HIV+ pt w/ MAC infection

A
  • Lifelong (if w/o immune reconstitution)

- Begin tx for 2 weeks then anti-HIV HAART

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31
Q

Mycobacterium abscessus is especially difficult to treat in what disease population?

A

CF

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32
Q

MTB pathogenesis?

A

Granulomas (2-6 weeks post infection) → caseous lesions (fibrotic tubercle) → calcifies & seen on x-ray → disease stops

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33
Q

MTB infection outcomes? (5)

A
  • Immediate resolution (no active TB) - innate immune system (alveolar macrophage) able to clear bacteria
  • Primary disease
  • Progressive primary (active) disease
  • Latent infection (inactive bacteria, - signs/sx, not infectious, treatment necessary)
  • Endogenous reactivation/secondary TB (+ signs/sx, infectious, insidious, lesions: caseous lesions → TB bacilli to bronchi → hematogenous spread
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34
Q

What is HAART?

A

Highly acute anti-retroviral therapy

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35
Q

Coryza, cough and conjunctivitis is concerning for what disease?

A

Measles

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36
Q

Koplick’s spots are diagnostic for what disease?

A

Measles

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37
Q

Mealse rash starts and spreads where?

A

Head, spread to body

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38
Q

When is a measles pt the sickest?

A

During rash/ highest fever (3-4 days after prodrome)

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39
Q

Acute symptomatic encephalitis is a complication associated with what disease?

A

Measles

also some associated w SSPE = subacute sclerosing panencephalitis

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40
Q

What complication is responsible for most deaths in measles pts?

A

Pneumonia

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41
Q

Is there a healthy carrier state associated with measles?

A

No, none known

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42
Q

Transmission of measles is via?

A

Respiratory droplets (highly contagious)

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43
Q

Is measles a disease of adulthood or childhood?

A

Primarily a disease of childhood (might be changing)

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44
Q

FA test for pt w/ measles will show?

A

Multinucleated giant cells

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45
Q

Largest preventative measure for measles?

A

MMR vaccine

also immune globulin BayGam for exposed non-immune subjects

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46
Q

MMR II is what type of vaccine?

A

Live, attenuated vaccine

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47
Q

Who should never receive MMR vaccine?

A

Pregnant, IMC

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48
Q

What % of population must be vaccinated to halt measles persistence?

A

95%

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49
Q

Rubella is also referred to as? (2)

A
  1. German Measles

2. “little red”

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50
Q

What age group often escaped rubella infection?

A

Children

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51
Q

Congenital rubella syndrome (CRS) is a complication due to what?

A

Maternal rubella infection during first trimester (worst prognosis earlier then infection, 1st month > 4th month)

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52
Q

Cataracts, hearing loss, and cardiac defects are sx of what?

A

Congenital rubella syndrome (CRS)

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53
Q

2 unique properties of HSV?

A
  1. Capacity to invade and replicate in CNS

2. Ability to establish latent infection

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54
Q

Shallow vesicles on erythematous +/- crusting and ballooning is concerning for?

A

HSV

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55
Q

Can the primary HSV infection be asymptomatic?

A

Yes

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56
Q

How does HSV become a latent virus?

A

Retrograde transport of virus through sensory neurons –> infection of dorsal root ganglia

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57
Q

What is the timeframe for completely clearing an HSV infection from the body?

A

None. HSV is for life!

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58
Q

Stress, menses, sunlights and nutrition are all triggers for what viral infection?

A

HSV

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59
Q

If a pt has a larger and more extensive initial outbreak with HSV, will their probability of recrudescence be higher or lower?

A

Higher

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60
Q

Will recrudescence of HSV occur in the presents of active humoral and cellular immunity?

A

Yes

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61
Q

Who is the reservoir for HSV?

A

Humans only

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62
Q

Can you transmitted HSV infection even if asymptomatic?

A

Yes

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63
Q

Are HSV-1 infection common in early life or later life?

A

Early life via casual contact

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64
Q

How are HSV-2 infections transmitted?

A

Sexual contact

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65
Q

Presence of enlarged or fused cells on Tzanck smear is concerning for what disease?

A

HSV

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66
Q

ACV (Acyclovir) is effective in treating HSV because viral enzyme thymidine kinase phosphorylates the drug for activation and then what?

A

Halts viral DNA replications b/c it lacks 3’-OH group

Will only get into infected cells when active

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67
Q

Varicella-zoster virus is responsible for what 2 disease states?

A
  1. Chickenpox

2. Shingles

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68
Q

Asymmetrical vesicular pruritic rash is concerning for what disease?

A

Chickenpox

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69
Q

Viral infection through conjunctiva or respiratory tract mucosa is concerning for what disease?

A

Chickenpox

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70
Q

Who is the only reservoir for chickenpox?

A

Humans

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71
Q

VZV infections peak during what seasons?

A

Winter-SPring

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72
Q

What age group has the highest incidence of VZV?

A

5-9 y/o

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73
Q

When is VZV pt most contagious?

A

1-2 before appearance of lesions and 4-5 days after

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74
Q

Are prodromal VZV present in older children and adults or younger children?

A

Younger children

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75
Q

VZV rash is primarily located where?

A

On the trunk

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76
Q

Is aspirin recommended in tx of chickenpox?

A

No, concerning for Reyes syndrome

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77
Q

TX for Chicken pox?

A

Sx relief - self limited
Acyclovir
Immune serum VariZig (high risk)

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78
Q

Varivax is the vaccine for what disease?

A

VZV

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79
Q

IS the VZV vaccine safe in pregnancy?

A

No

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80
Q

Will shingles cross midline?

A

No, unilateral dermatomal distribution

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81
Q

Shingles is recrudescence of what viral infection?

A

VZV

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82
Q

Searing, burning, stabbing lesions that don’t cross midline are concerning for?

A

Shingles

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83
Q

Most common complication fo shingles?

A

Postherpetic neuralgia

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84
Q

Can a pt present with shingles but never have had or been vaccinated against chicken pox?

A

No

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85
Q

Zostavax and Shingrix are vaccines against what?

A

Shingles

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86
Q

Is Zostavax or Shingrix a live vaccine?

A

Zostavax

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87
Q

Is Zostavax or Shingrix given in 2 doses?

A

Shingrix

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88
Q

Exanthem subitum, roseola infantum/6th disease are caused by what?

A

Human Herpes Virus-6 (HHV-6)

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89
Q

HHV-6 is dx by what? (2)

A
  1. Detection of AB by EIA

2. PCR

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90
Q

High fever w.o any obvious sources is concerning for what?

A

HHV-6

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91
Q

TX of HHV-6 does not require? (3)

A
  1. Isolation
  2. Anti-viral therapy
  3. Primary preventative measures
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92
Q

Fifth’s disease/ Erythema infectiosum is causes by?

A

Parvovirus B19

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93
Q

Prodrome of this disease is follow by maculopapular rash in “slapped cheeked” appearance?

A

Parvovirus B19

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94
Q

Arthralgia or arthritis follow maculopapular rash may be concerning for?

A

Parvovirus B19

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95
Q

Parvovirus B19 is most common in what seasons?

A

Later winter and spring

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96
Q

Virus that produces warts?

A

HPV

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97
Q

HPV 6 & II produce anogenital warts or cervical dysplasia and cancer?

A

Anogenital warts

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98
Q

HPV 16 & 18 produce anogenital warts or cervical dysplasia and cancer?

A

Cervical dysplasia and cancer?

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99
Q

Age range for Gardasil 9?

A

M/F 9-45

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100
Q

Dermatophytes require what for growth?

A

ketatin (hair, skin, nails)

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101
Q

Do dermatophytes infect mucosal surfaces?

A

No

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102
Q

What enzymes allows dermatophytes to inhabit keratinized regions of the body>

A

Keratinase

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103
Q

Dermatophyte test medium (DTM) allows for early detection of infection or can only be used to different source of dermatophyte?

A

Early detection

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104
Q

Arthroconidium is what?

A

The infective stage of disease for dermatophytes

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105
Q

Trichophytin is what? (2)

A
  1. Galactomannan peptide

2. Crude antigen of dermatophytes (CHO component = immediate response, Peptide component = delayed response)

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106
Q

How does 10% potassium hydroxide allow for visualization of fungi?

A

Digests human tissues, leaving fungal components intact

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107
Q

Dermatophytes utilize nitrogen compounds preferentially over carbs. DTM will turn what color?

A

Red (alkaline)

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108
Q

Dermatophyte test medium (DTM) is selective and differential for what?

A

Selective: Cyclohexamide and ABX
Differential: fermentation of sugars

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109
Q

Animal pathogens that may be transmitted to people are what?

A

Zoophilic

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110
Q

Antropholilic Dermatophytes are spread via what transmission?

A

Human to human

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111
Q

Soil to people transmission is what?

A

Geophilic

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112
Q

Geophilic dermatophytes will invade non-viable or viable keratinized tissue?

A

Non-viable

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113
Q

Fungi prefer dry or moist areas of the body?

A

Moist

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114
Q

Globally where are fungal infections more prevalent?

A

Tropics

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115
Q

Microconidia, macroconidia and sexual spores are infectious or non-infectious?

A

Infectious

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116
Q

Fragmented hypheal elements in hair, nails, outer skin are what?

A

Arthrospores

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117
Q

Lesions with inflamed edges and a central clearings are concerning for what infectious pathogen?

A

Fungi

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118
Q

Transmission pattern for arthrospores?

A

Person to persons

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119
Q

Are arthrospores infectious?

A

Yes

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120
Q

Microconidia is uni or multi cellular?

A

Uni

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121
Q

Macroconidia is uni or multicellular?

A

Multi

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122
Q

Classification for an allergic dermal reaction to fungal antigen occurring in areas devoid of organisms

A

Dermatophytid

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123
Q

Most common dermatophytid?

A

Athlete’s foot

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124
Q

How are dermatophytid reactions spread?

A

Itching

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125
Q

Will dermatophytid be present at only 1˚ or 1˚ and 2˚ sites?

A

Only primary

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126
Q

“Id reaction” is associated with what fungal infection?

A

Dermatophytid

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127
Q

What is an “id reaction” treated as?

A

An allergy

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128
Q

What is the most common trichophyton species?

A

T. mentagrophytes

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129
Q

Are trichophyton often fluorescent or not fluorescent?

A

Not fluorescent

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130
Q

What do all trichophyton species make?

A

Pencil-shaped macroconidia w/ thin walls

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131
Q

What 3 things do trichophyton produce?

A

Hyphae (spindle shaped), microconidia, macroconidia

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132
Q

What is the most common causative agent of tinea captitis?

A

M. canis

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133
Q

What disease is described as mostly a childhood disease that involves the hair and scalp?

A

Tinea capitis

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134
Q

What are the 2 types of ringworm infections?

A

Endothrix (infects throughout follicle)

Ectothrix

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135
Q

What infection is associated with certain species producing a black dot ringworm, intense inflammation, scarring/ permanent alopecia, and can be zoonotic?

A

Tinea capitis

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136
Q

With tinea capitis, infected hair can break off and lead to what?

A

Alopecia

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137
Q

If a patient presents with itching, peeling, and crackling of the skin in the toe webs/ soles of feet, what should you be concerned about?

A

Tinea pedis (most prevalent of dermatophytoses)

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138
Q

What are predisposing factors for tinea corporis and tinea cruris?

A

Diabetes, obesity, excessive perspiration

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139
Q

How are tinea corporis and tinea cruris transmitted?

A

Direct and indirect contact objects (towels, clothing, bed linens)

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140
Q

What is tinea unguium?

A

Onychomycosis (ringworm of the nail)

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141
Q

What infection is associated w/ the following:

  • Finger/ toenails become discolored/ thick
  • May be mistaken for psoriasis
  • Usually has fungal involvement (Candida)
A

Tinea unguium

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142
Q

What are the most commonly encountered opportunistic mycoses?

A

Candidiases

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143
Q

What infection is associated with colonization of normal flora of the skin and mucous membranes?

A

Candidiases

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144
Q

What infection is associated with the following:

  • Absence of competing normal flora
  • Introduction to abnormal site
  • “Pathologic” change in microenvironment
  • Inborn or acquired immune defect
  • Use of broad-spectrum abx
A

Candidiases

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145
Q

Although candida albicans does not have many virulence factors, all species are capable of attachment, and what is the most adhesive?

A

Germ tube more adhesive than yeast cell

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146
Q

How is a Candida infection diagnosed?

A

Direct microscopic exam

  • Large G- cells
  • Yeast cells
  • Pseudohyphae
  • True hyphae
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147
Q

Besides direct microscopic exam, how is a Candida infection diagnosed?

A

Cultures (germ tubes)
Histology
Serology

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148
Q

What is tinea versicolor aka?

A

Malassezia furfur

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149
Q

What fungi is described as microscopically having short, unbranched hyphae and somewhat spherical cells and also has yeast like colonies?

A

Malassezia furfur

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150
Q

If you see a “spaghetti and meatballs” arrangement on a microscopic exam, what fungal infection should you be suspicious of?

A

Malassezia furfur

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151
Q

What type of GF is required for growth of Malassezia furfur?

A

Lipophilic (fat, sebaceous glands)

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152
Q

In what populations is Malassezia furfur most commonly found?

A

Tropics, young adults

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153
Q

What fungal infection is associated with macular patches of depigmented or hyper pigmented skin that may enlarge and can lead to dandruff?

A

Malassezia furfur

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154
Q

How can Malassezia furfur be identified?

A

Microscopic exam in skin scrapings, KOH prep

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155
Q

What fungal infection is tinea nigra aka?

A

Hortaea werneckii

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156
Q

What fungal species is dimorphic and can grow in saturated salt solutions?

A

Hortaea werneckii

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157
Q

What fungal species is identified as a tropical disease, results in brownish lesions (melanin), and is identified with KOH and microscopy?

A

Hortaea werneckii

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158
Q

When is a bacterial skin infection considered complicated?

A
Pre-existing wound care
Deeper tissues
Requires surgery
Unresponsive to therapy/ recurrent
Associated w/ underlying disease
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159
Q

Recurrent infections raise concern over colonization with what?

A

Resistant bacteria or underlying issues

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160
Q

Although normally inoculum of bacteria (staph) introduced through breaks in skin is not large, what happens if a foreign body (splinter, stitches) is present?

A

Infectious dose drops dramatically

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161
Q

What disease is associated with the sebaceous follicles and is a noninfectious form of folliculitis?

A

Acne vulgaris

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162
Q

What is often the initial trigger for acne vulgaris?

A

Androgen hormones

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163
Q

What bacteria responsible for acne vulgaris is G+, anaerobic rod, and on normal skin flora (sebaceous glands)

A

Propionibacterium acnes

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164
Q

What does inflammatory acne develop?

A

When follicular contents rupture into dermis

papule > pustule > nodule

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165
Q

What is the usual cause of Folliculitis?

A

Staph. aureus

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166
Q

If a pt presents w/ mild pain, itching/ irritation with pustules or nodules surround hair follicles?

A

Folliculitis

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167
Q

If folliculitis is not responding to tx, what should be performed to r/o other possible causes?

A

Gram stain

r/o G- etiology or MRSA

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168
Q

What are the 2 primary pathogens responsible for superficial folliculitis?

A

Staph. aureus and Pseudomonas aeruginosa

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169
Q

Which pathogen is responsible for the majority of abscess-type infections, is G+, and coagulase-+ cocci in clusters?
(superficial folliculitis)

A

Staph. aureus

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170
Q
Which pathogen is described by the following:
- G- rod
- Opportunistic pathogen
- Ubiquitous
- Pyocyanin/ pyoverdin
(superficial folliculitis)
A

Pseudomonas aeruginosa

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171
Q

P. aeruginosa is often the cause of what type of folliculitis?

A

“Hot tub” folliculitis

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172
Q

If a pt presents 8-48 hrs post exposure to contaminated water and is complaining of an itchy maculopapular rash with some pustules, what is the likely responsible pathogen?

A

Pseudomonas aeruginosa

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173
Q

A furuncle (boil) is an abscess caused involving a hair follicle and surrounding tissue caused by what pathogen?

A

S. aureus

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174
Q

What are clusters of furuncles with subcutaneous connections that extend into the dermis and subcutaneous tissue?

A

Carbuncles

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175
Q

What other sxs might accompany carbuncles?

A

Fever and prostrations

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176
Q

What populations are more commonly affected by furuncles and carbuncles?

A

Obese, immunocompromised, diabetic, elderly

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177
Q

If furuncles or carbuncles are > 5mm, do not resolve w/ drainage, are spreading, or occur in IMC/ subjects at risk of endocarditis, how are they treated?

A

Abx (effective against MRSA)

More aggressive combo therapy with rifampin if + fever/ multiple

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178
Q

What condition is a superficial skin infection with crusting or bullae and what is the most common pathogen cause?

A

Impetigo

Cause= steph, strep (or both)

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179
Q

What is the deeper, ulcerative form of impetigo?

A

Ecthyma

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180
Q

Moist environment, poor hygiene or chronic nasopharyngeal carriage of agents are RF’s for what disease?

A

Impetigo/ ecthyma

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181
Q

If a pt presents with clusters of vesicles that rupture and crust over around the nose and mouth, what should you be concerned for?

A

Non-bullous impetigo

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182
Q

What is the #1 cause of non-bullous impetigo?

A

S. aureus (with MRSA in 20%)

Strep. pyogenes co-infects frequently

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183
Q

In bullous impetigo, exfoliative toxin that disrupts epidermal cell connections results in vesicles enlarging to form what?

A

Bacteria-colonized fluid-filled bullae

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184
Q

What is the most common pathogen involved with bullous impetigo and what role does the toxin play?

A

S. aureus (specific strains)

Toxin does not disseminate beyond local sites of infection

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185
Q

A severe form of impetigo featuring deep invasion of the dermis caused by the same agent producing non-bullous impetigo is known as what?

A

Ecthyma

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186
Q

Lesions with hard crust that is deeper and thicker than impetigo underlying ulcerated tissue is known as what?

A

Ecthyma

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187
Q

Staphylococcal scalded skin syndrome is aka?

A

Ritter’s disease

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188
Q

Acute and extensive epidermolysis due to action of staph toxin (exfoliation) that splits the skin just beneath the granule cell layer is what?

A

Staphylococcal scalded skin syndrome

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189
Q

Why are the bullae in Staphylococcal scalded skin syndrome sterile (no bacteria or leukocytes)?

A

Due to toxin

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190
Q

Positive Nikolsky’s sign, skin peels easily, and desquamated areas look scalded fits the description for what condition?

A

Staphylococcal scalded skin syndrome

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191
Q

Is the mortality rate for scaled skin syndrome high or low?

A

Low

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192
Q

Erythema and edema to R LE (unitlateral) the appears deep w/in the dermis and has less distinct borders is concerning for erysipelas or cellulitis?

A

Cellulitis

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193
Q

Superficial cellulitis (erythema with raised lesions) w/ focal dermal involvement and distinct borders is concerning for what?

A

Erysipelas (st. Anthony’s Fire)

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194
Q

Most common pathogen for erysipelas?

A

Group A, B-hemolytic Streptococci, Strep pyogenes

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195
Q

How do erysipelas spread once dermis is infected?

A

Superficial lymphatic vessels

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196
Q

Will you always be able to pinpoint the source of cellulitis infection?

A

No, wound may not be evident

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197
Q

HEET (heat, erythema, edema, tenderness) is the hallmark for what bacterial skin infection?

A

Cellulitis

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198
Q

When treating cellulitis should you assume the infection is caused by a single pathogen?

A

No, may be mixed etiology

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199
Q

Why should NSAIDs be avoided in the treatment of cellulitis?

A

Can mask pain of developing myonecrosis (something more serious than cellulitis)

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200
Q

What is a warning sign that cellulitis infection might be necrotizing fascitis?

A

Out of proportion pain

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201
Q

Cellulitis pathogen associated w/ cat bite?

A

Pasteurella multocida

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202
Q

Redness, swelling warmth, pain + what signs/sx would make you concerned for a MRSA infection? (4)

A
  1. Fluctuance (evidence of fluid)
  2. Yellow/white center
  3. Central point (head)
  4. Draining pus or ability to aspirate pus w/ syringe
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203
Q

What gene can you screen for that might tell if you are Methicillin resistant?

A

MecA

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204
Q

Infections of the epidermis? (3)

A
  1. Erysipelas
  2. Impetigo
  3. Follicutlits
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205
Q

Infections of the dermis? (3)

A
  1. Ecthyma
  2. Furunculosis
  3. Cabunculosis
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206
Q

Infection of the superficial fascia? (1)

A

Cellulitis

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207
Q

Infection of the subQ tissue and fascia? (1)

A

Necrotizing fasciitis

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208
Q

Infection of the muscles? (1)

A

Myonecrosis (clostridial and nonclostridial)

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209
Q

Why is it difficult to dx NF w/o surgical intervention?

A

Initially overlying tissues appear unaffected

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210
Q

Why is muscle tissue spared from NF infection?

A

Generous blood supply

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211
Q

Type 1 NF pathogens are most common. What disease state disease state puts you at increased risk?

A

DM

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212
Q

If you have a hx of surgery, previous abscess or GI perforation are you at risk for Type 1 or Type 2 NF infection?

A

Type 1

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213
Q

Flesh eating bacteria or streptococcal gangrene more common in abdominal/groin area or the extremities?

A

Extremities

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214
Q

Pain out of proportion and skin color changes w/ bullae within 3-5 day of onset is concerning for?

A

Necrotizing fasciitis

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215
Q

What differentiates NF from cellulitis?

A

Failure to respond to ABX (cellulitis will respond w/in 24-48hrs to abx)

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216
Q

What is the tx for NF?

A

Surgical debridement/apmutation w/ IV ABX

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217
Q

Presence of no true pus, but brownish exudate and pain out of proportion/ rapid progression is concerning for?

A

NF

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218
Q

Gas gangrene is most caused by what pathogen?

A

Clostridium perfringens type A (90%)

- spore forming, G+, anaerobic bacillus

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219
Q

Gas gangrene primarily affects what tissue?

A

Muscle

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220
Q

Gas gangrene is also known as?

A

Clostridial myonecrosis

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221
Q

Skin that is tense/edematous, intensely tender, and crepitant (due to H2 gas) with bronze appearance is concerning for?

A

Gas gangrene

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222
Q

Rapid onset of pain ≤24 hrs following anaerobic cell/spore infection is concerning for?

A

Gas gangrene

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223
Q

Gram stain of tissue biopsy for gas gangrene will show what?

A

Muscle necrosis , gram variable rods, and tissue destruction

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224
Q

Hyperbaric oxygen therapy, surgery, and IV abx are tx for what dermal infection?

A

Clostridial myonecrosis

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225
Q

Causative agents for toxic shock syndrome? (2)

A

Staph aureus and strep pyogenes

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226
Q

Fever and sunburn like rash to entire body is concerning for what?

A

TSS

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227
Q

Early presentation for Strep TSS?

A

Soft tissue inflammation at site of skin infection

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228
Q

True or False: Pt’s w/ strep TSS are usually bacteremic and have NF?

A

True

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229
Q

Enterotoxin type B superantigen is associated with strep or staph TSS?

A

Staph

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230
Q

True or false: Pt’s with staph TSS are otherwise healthy w/ no pre-existing skin infections?

A

True

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231
Q

Which pathogen of TSS is associated with tampon use?

A

Staph

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232
Q

What pathogen is a burrowing mite that is the most serious of the mites, a close relative of ticks, and leads to scabies, crusted scabies, mange, and seven year itch?

A

Sarcoptes scabiei

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233
Q

What is the morphology of Sarcoptes scabiei?

A

Small mite w short legs

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234
Q

Is a male or female Sarcoptes scabiei fertilized on the skin surface, burrows into the epidermis, and completes its life cycle in 5 weeks then dies in the burrow?

A

Female

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235
Q

Does a male or female Sarcoptes scabiei have a shorter life span and remains on the skin surface or produces a shallow burrow?

A

Male

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236
Q

Where are the eggs of Sarcoptes scabiei laid and how soon after incubation do larva emerge?

A

Under the skin

Larva emerge after 4 days

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237
Q

How long after Sarcoptes scabiei hatch do adult mites develop?

A

2 weeks

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238
Q

How long after someone is infested with Sarcoptes scabiei does it take for sxs (itching) to develop?

A

First infestation = weeks

Re-infection = 24 hours

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239
Q

What causes the majority of clinical issues (intensely pruritic eruption that is worse at night) with Sarcoptes scabiei?

A

Burrowing

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240
Q

What pathogen has an incubation period of 1 month and results in crusted scaling lesions that are intensely pruritic, with lesions having hundreds to thousands of mites?

A

Sarcoptes scabiei- crusted (Norwegian) scabies

241
Q

What population is readily infected w/ crusted scabies?

A

HIV

242
Q

What condition is similar to Norwegian scabies, but the lesions may be blood filled?

A

Pediatric scabies

243
Q

How is scabies most commonly spread?

A

Direct person contact (STI)

Crowded living conditions

244
Q

How are scabies identified?

A

Apply mineral oil, scrape lesion and visualize microscopically (look for whole mite or mite parts, eggs, or fecal pellets in burrows)

245
Q

What is the pathogen responsible for pubic lice/ “crabs”?

A

Phthirus pubis

246
Q

How does Phthirus pubis infected the pubic area?

A

Nits (eggs) cemented to hair, adults bite and feed in pubic area

247
Q

How is Phthirus pubis transmitted and identified?

A

Transmitted by sexual contact or contaminated bedding

ID by visualizing louse or nit

248
Q

What is the pathogen responsible for pediculosis?

A

Pediculus humans

249
Q

What pathogen is a vector for epidemic typhus?

A

Pediculus humans

250
Q

What pathogen is a nit cemented to a fiber in clothing or human hair and has an egg-to-egg cycle that takes about 3 weeks?

A

Pediculus humans

251
Q

If a pt presents with bite irritation (parasite is bloodsucking), “vagabonds disease” (years of infestation) and darkened, thickened skin, what should you be concerned about?

A

Pediculus humans/ pediculosis

252
Q

How is P. humanus spread?

A

Easily- crowded conditions, conditions where clothing cannot be changed often

253
Q

What pathogen is 1-4mm in length, laterally compressed, and has short spikes on its legs that allow attachment to the host?

A

Pulex irritans (human flea)

254
Q

What does Pulex irritans need to survive?

A

Blood (it is a parasite)

255
Q

What do Pulex irritans inject during a blood meal?

A

Saliva that initiates an allergic response

256
Q

What is the main manifestation of an infection w Pulex irritans?

A

Rash

257
Q

What is a tick-borne disease via a brown dog tick (AZ)?

A

Rocky Mountain Spotted Fever

258
Q

What pathogen is responsible for Rocky Mountain Spotted Fever?

A

Rickettsia rickettsii

259
Q

What pathogen is described as G-, obligate intracellular, non-motile, and pleomorphic and can cause a potentially fatal disease if not tx in the first few days of sxs?

A

Rickettsia rickettsii

260
Q

During what time of year is Rocky Mountain Spotted Fever seen more frequently?

A

Summer months (peak in June and July)

261
Q

If a pt presents w hx of a painless bite and didn’t notice sxs until 2-14 days post bite, what disease should you be concerned about?

A

Rocky Mountain Spotted Fever

262
Q

What parts of the body does Rickettsia rickettsii invade?

A

Endothelial cells that line blood vessels

263
Q

What early sxs and sudden onset sxs are seen with Rocky Mountain Spotted Fever?

A

Early sxs are non-specific

Sudden onset sxs = fever, HA

264
Q

What 2 types of rash are seen with Rocky Mountain Spotted Fever?

A
  1. small, flat, pink non-itchy spots (macules)

2. red to purple spotted petechial rash +/- pinpoint hemorrhages

265
Q

Which type of Rocky Mountain Spotted Fever rash will likely be seen on wrists, forearms, ankles and spreads to trunk, palms and soles 2-5 days post infection?

A

small, flat, pink non-itchy spots (macules)

266
Q

Which type of Rocky Mountain Spotted Fever rash will likely be seen after 6 days post infection, and is a sign of late infection/ severe disease?

A

red to purple spotted petechial rash

267
Q

If you suspect a pt is infected with Rocky Mountain Spotted Fever, do you wait to treat until receiving laboratory confirmation?

A

No- most successful if tx initiated w/i first 5 days

268
Q

Why is Rocky Mountain Spotted Fever a difficult disease to deal with?

A

Similarity to other diseases

Difficult to detect until disease is in late stages

269
Q

Why are diagnostic tests not a good option for Rocky Mountain Spotted Fever?

A

Detectable antibody titers are not visible for 7-10 days post infection

270
Q

What is the gold standard for dx of Rocky Mountain Spotted Fever?

A

Indirect immunofluorescence w/ a R. rickettsii antigen (2 samples 2-4 weeks apart)

271
Q

What pathogen is responsible for African sleeping sickness?

A

Trypanosoma brucei

272
Q

What pathogen is responsible for Chagas disease?

A

Trypanosoma cruzi

273
Q

What pathogen is responsible for Leishmaniasis?

A

Leishmania spp.

274
Q

What disease is prevalent in Mexico, Central America, and South America, is considered a neglected parasitic infection (NPI) by the CDC in the US and is associated w survivors that typically exhibit altered organ function?

A

Chagas disease

275
Q

What is the vector for Chagas disease?

A

Triatomine bugs (“kissing bugs”)

276
Q

What parasitic protozoan is transmitted through feces of the triatomine bug, blood transfusions, organ transplants, and congenital?

A

Trypanosoma cruzi

277
Q

What happens once the trypomastigote (T. cruzi) enters near the inoculation site?

A

It differentiates into amastigotes

278
Q

What happens to the amastigotes (T. cruzi) once differentiated into?

A

Replicate by binary fission in cells, differentiate, and release into circulation to rupture host cells

279
Q

What are the key characteristics of the acute stage of Chagas disease?

A

Asx to mild manifestation
Non-specific signs/ sxs, +/- Chagoma
Romanas sign- swelling of eyelid near entry site

280
Q

What are the key characteristics of the chronic stage of Chagas disease?

A

Pseudocysts of amastigotes in cells (muscles and nerves affected, degeneration and necrosis)
Chronic inflammation
Cardiac > intestinal complications

281
Q

How long can the infection with Chagas disease be asx?

A

Years, or even for life

282
Q

How is Chagas disease diagnosed?

A

Parasite under microscopy- blood smear (acute) or biopsy (chronic)
Serological tests

283
Q

What is involved with prevention and control of Chagas disease?

A
Insecticides/ housing improvements
Bednets
Screening of blood donors
Testing of organ, tissue, cell donors
Screening of newborns/ children of infected mothers for early dx/ tx
284
Q

Viral infection that causes infectious mononucleosis (IM)?

A

EBV

285
Q

EBV is linked to what form of cancer?

A

Burkitt’s lymphoma

286
Q

IM is a B or T cell infection?

A

B cell. Induces polyclonal expansion of lymphocytes

287
Q

Sore throat, symmetrical lymphadenopathy, and fever +/- hepatomegaly is concerning for what?

A

IM

288
Q

Downey cells (atypical lymphcytes) appear in the circulation for pt’s infected with what disease?

A

IM

289
Q

In IM does B cells or T cells generate most of the pt’s sx?

A

T cells

290
Q

Transmission pattern for EBV?

A

Person to person

291
Q

Peak incidence of EBV causing IM?

A

17-25 yrs

292
Q

Early infection w/ EBV in a pt from regions of Africa is concerning for what?

A

Burkitt’s Lymphoma

293
Q

Presence of what type of antibodies are help dx EBV IM?

A

Heterophile AB

294
Q

Why might the monospot test give a false negative?

A

Age-specific reactivity. Less useful in kids so use IgM anti virus capsid antigen serology

295
Q

When treating IM pt with penicillin you must warn them about?

A

Penicillin reaction rash

296
Q

Which virus, CMV or EBV, DOES NOT produce heterophile antibodies?

A

CMV

297
Q

What populations are most at risk for CMV?

A

IMC, transplant pts, infections occurring during pregnancy

298
Q

Does MMR provided lifelong immunity to mumps for all recipients?

A

Not for egg or neomycin sensitive pts. Pts that have been vaccinated are still getting the disease.

299
Q

How is mumps controlled?

A

Vaccination

300
Q

Borrelia burgdorferi is the pathogen for what disease?

A

Lyme disease

301
Q

Pt presents with erythema migrans/red bulls eye rash. What stage of lyme disease are you suspecting?

A

Stage 1: Acute localized disease

302
Q

Flu sx, brief asymmetric arthritis attaches and/or secondary annular skin lesions may be concerning for what stage of lyme disease?

A

State 2: Subacute disseminated disease

303
Q

Chronic lyme disease is easier or harder to treat?

A

Hard the further the disease process

304
Q

Chronic lyme disease (stage 3) is associated with primarily what sx?

A

Musculoskeletal.

Arthritis attacks become more persistent and last long

305
Q

What general location of the US has the highest reported cases of lyme disease?

A

NE

306
Q

Vector for lyme disease?

A

Tick vector (deer or black-legged)

307
Q

Ticks exhibit what type of behavior?

A

Questing behavior

308
Q

Lyme disease reservoir hosts?

A

Small mammals and birds

309
Q

What form of the black legged tick causes large portion of infections in humans?

A

Nymphal

310
Q

Serology test for lyme disease?

A

EIA w/ western blot follow up if positive (positive by 4th week of infection)

311
Q

What disease states might cause false positive on lyme disease serology test?

A

Syphilis, mono, SLE, RA, oral infection w/ spirochetes

312
Q

How can you prevent lyme disease?

A

Control and avoidance of vector contact (Deet, tick checks following outdoor activity)

313
Q

Post TX Lyme Disease Syndrome is chronic or will improve with time?

A

Most should improve with time

314
Q

Source of Hep A and Hep E?

A

Feces

315
Q

Route of transmission for Hep A and E?

A

Fecal-oral

316
Q

Are Hep A and E a chronic infections?

A

No

A= infectious

317
Q

Source of Hep B, C, and D?

A

Blood/blood-derived body fluids
B= serum
C= transfusion-associated

318
Q

Route of transmission for Hep B, C, and D?

A

Percutaneous, permucosal

319
Q

Is Hep B a chronic or acute infections?

A

Chronic

320
Q

True or false: Hep C and D are chronic infections?

A

true

321
Q

Hep A will have IgM antibody on ELISA, True or False?

A

True

322
Q

HAV prevention measures? (5)

A
  1. Hand washing
  2. Avoidance of contaminated food/water
  3. Post exposure prophylaxis
  4. Vaccine
  5. Education
323
Q

Which Hepatitis virus is infectious cause of primary hepatocellular carcinoma?

A

Chronic HBV

324
Q

Presence of double walled Dane particle is indicative of infectious or non-infectious form of Hep B?

A

Infectious

325
Q

Largest reservoir for HBV?

A

Chronic hepatitis pts

326
Q

Are HBeAg positive pts at risk of transmitting HBV infection?

A

Yes

327
Q

What are newborns vaccinated against HBV?

A

90% of infections become chronic

328
Q

IgG and anti-HBc indicated past or present HBV infection?

A

Past

329
Q

Rapid Hepatitis virus test detect what type of HBV antigen?

A

Surface

330
Q

Is HBV a self limited disease for most adults?

A

Yes, no specific curative tx exisits

331
Q

Do tx for chronic HBV result in a cure?

A

No only inhibit viral replications, prevent liver damage progression

332
Q

True or false, Subunit vaccine is available for HBV?

A

True

333
Q

True or false: immunoglobulin is available for HBV prophylaxis?

A

True

334
Q

Which form of hepatitis requires presence of chronic HBV and superinfection?

A

HDV

335
Q

HDV will increase or decrease the severity of HBV?

A

Increase

336
Q

Pts with chronic HBV are a reservoir for what disease?

A

HDV

337
Q

Positive delta antigen on ELISA is indicative of what hepatitis infection?

A

HDV (but must also have active HBV)

338
Q

True or false: HBV vaccine will protect against HBV and HDV?

A

True

339
Q

Form of hepatitis associated with needle sticks and M/M unprotected sex?

A

Hep B

340
Q

Form of hepatitis that most often occurs post transfusion?

A

Hep C

341
Q

Establishment of chronic infection is the hallmark for what form of hepatitis?

A

HCV

342
Q

True or false HCV often does not progress to cirrhosis and liver failure

A

False. It often does!

343
Q

Serologic tests will show increased or decreased anti-HCV over time?

A

Increased

344
Q

Acute HCV will most often develop into what disease?

A

Chronic

345
Q

Factors that promotes HCV infection progression? (5)

A
  1. Alcohol use
  2. Infection at age ? 40
  3. Male sex
  4. Hep B co-infection
  5. HIV co-infection
346
Q

What is dx of HCV difficult?

A

chronic state and acute phase viremic patients often escape detection

347
Q

TX for HCV ?

A

Direct acting antiviral agents (DAAs) , possibly curable

348
Q

Are combination regiments the same for all 6 HCV genotypes?

A

No, vary with virus genotype

349
Q

If HBV and HVC co infection which form usually dominates and is thus treated first?

A

HCV

350
Q

DAA tx that eliminates HCV will:

  1. Eliminate HBV?
  2. Activate HBV?
A

Activate

351
Q

True or false: because HCV tends to suppress HBV activity, we are not sure how often the two viruses are found together?

A

True

352
Q

HCV prevention? (2)

A
  1. Blood screening

2. Effect to ID compensated, unrecognized infections

353
Q

What are the two leading causes for liver transplant?

A

Cirrhosis and hepatocellular carcinoma

354
Q

Will life transplant be curative for HBV and HCV confection?

A

Yes

355
Q

Is a liver transplant pt at risk for recurrent infection?

A

Yes, if no edu/lifestyle change AND b/c IMC

356
Q

Pt presents w non-specific sore throat and swollen lymph glands mimicking a mono-like condition… what are you concerned for?

A

Initial HIV infection

357
Q

When is HIV in a period of high transmission risk?

A

Early stages when pt unaware they are HIV- infected (high levels of virus in circulation)

358
Q

All pts with HIV are considered what?

A

Life-long carriers and continually infectious

359
Q

When is AIDS (stage 3 HIV) diagnosed?

What are CD4 T cell levels at?

A

When severe damage to immune system is evident

CD4 T cells < 200 uL

360
Q

AIDS defining conditions emerge as what declines?

A

Immune system function

361
Q

What disease is associated w/ Kaposi’s sarcoma, pneumocystis pneumonia, MAC infection, severe CMV disease, cryptosporidiosis, and candidiasis?

A

AIDS

362
Q

What defines the “fast” HIV disease course class?

A

3 years or less to AIDS

363
Q

What defines the “intermediate” HIV disease course class?

A

AIDS emergence ~ 1 decade post infection

364
Q

What defines the “long term non-progressors” HIV disease course class?

A

> 10 yrs (under 5% of cases)

365
Q

What pathogenic agents has the following characteristics:

  • Human retrovirus
  • RNA genome
  • Enveloped
  • Reverse transcriptase
A

HIV/ AIDS

366
Q

AIDS is now considered to be a probable what that has entered human populations?

A

Zoonosis (animal disease)- contact via primates/ bushmeat

367
Q

What has sequencing of the HIV/ AIDS viral genome revealed?

A

A focus in African and entry of HIV into human populations several times

368
Q

How is HIV/ AIDS most commonly spread?

A

STIs

369
Q

What are 3 myths about HIV?

A

Polio vaccine = source of HIV-1
Pt zero
Deliberate spread

370
Q

How can HIV-1 become a latent disease?

A

Entry into T/B memory cells (reverse transcription)

371
Q

How does HIV exhibit cytopathic effects?

A

TH cell loss = immunosuppression
Formation of “swarms”
mechanism of viral killing uncertain

372
Q

Is you notice Gohn lesions and ipsilateral calcified hilar lymph nodes on CXR, what is this concerning for?

A

Ranke complex, concerning for healed primary TB

373
Q

What are the 3 most common HIV routes of transmission?

A
  1. sexual contact
  2. parenteral (IV drug use, needle sticks)
  3. perinatal
374
Q

Is HIV-1 or HIV-2 more common worldwide?

Is HIV-1 or HIV-2 less easily transmitted?

A

HIV-1 = worldwide, HIV-2 = W Africa

HIV-2 less easily transmitted, exhibits slower progression to AIDS, resistant to NNRTIs

375
Q

What is the progression pattern of HIV?

A
  1. Infection
  2. Free replication
  3. Pt ab response
  4. Latent virus changes and no longer immune
376
Q

What is the goal of HIV tx?

A

Keep virus @ low levels and keep from killing CD4 lymphocytes

377
Q

What 2 steps are used for dx of HIV? (HIV ab)

A
  1. EIA screen (general)

2. Western blot

378
Q

What designates an HIV + test on Western blot for CDC?

A

2 cross-reacting bands

379
Q

What is the role of direct tests for HIV?

A

Determine how much virus is present

Protect blood supply (donated blood screened)

380
Q

Which direct test is able to detect and quantify the HIV virus?

A

Nucleic acid test (NAT)

381
Q

Why should you do direct tests and not just AB tests for HIV?

A

Early disease may not have ab yet

382
Q

What is the general tx for HIV but what is important to know about it?

A

Tx = combo of antiviral agents, but NOT curative

383
Q

What 3 types of antiviral agents are included in combo treatment for HIV?

A

Reverse transcriptase inhibitors
Protease inhibitors
Fusion-penetration inhibitors

384
Q

What is the role of viral load tests for HIV pts?

A

Tests amount of HIV in blood
Watch trend of counts
Run frequently if early in disease

385
Q

Why does HIV impact cognitive function?

A

Neuron damage

386
Q

What is the best control method for HIV?

A

Prevention/ education

387
Q

Anti-retroviral therapies drive virus levels to undetectable levels… why is this important?

A

Undetectable = un-transmissible

388
Q

What are new strategies for ending HIV transmission?

A

PrEP if at risk

Early ID/ therapeutic tx

389
Q

How is malaria transmitted?

A

Plasmodia from salivary glands of Anopheles female mosquito

390
Q

What are the Malaria important species, and which are the 2 most common?

A
Plasmodium vivax (most common)
P. falciparum (most common)
P. malariae
P. ovale
P. knowlesi
391
Q

What are the 2 phases of malaria life cycle, contributing to its ability to evade host defenses?

A

Human phase and mosquito phase

392
Q

How is the malaria life cycle initiated in humans?

A

Injected of Plasmodium sporozites (motile forms) in saliva

393
Q

How do sporozoites divide once they migrate to the liver?

A

Asexual division = schizogony

394
Q

What is the name of the life cycle form released from the schizogony phase of the malaria life cycle?

A

Merozoites

395
Q

What stage of the malaria life cycle is the vaccine target?

A

Sprorozoites

396
Q

What do merozoites infect?

A

Other liver cells or RBCs (erythrocytic cycle)

397
Q

Once in the RBC, merozoites enlarges and undergoes a differentiation into what?

A

Ring trophozoite (uninucleate)

398
Q

As trophozoites age, what can they develop into?

A

Amoeboid trophozoites

399
Q

In the malaria life cycle, a single nucleus can also divide to produce what?

A

Schizont

400
Q

Erythrocytic schizonts are multinucleated cells that produce what?

A

Erythrocytic merozoites

401
Q

After an infected RBC ruptures and merozoites escape to invade new cells, what happens?

A

Schizogony begins again or gametogony (sexual cycle) is initiated

402
Q

What leads to sexual reproduction within the mosquito?

malaria life cycle

A

Erythrocytic merozoites develop into gametocytes, which are then taken up by mosquito

403
Q

Sporozoites produced in the mosquito and traveling to the salivary glands of the mosquito contribute to treatment difficulty?

A

Exchange of DNA allowing the mosquito to change and gain drug resistance

404
Q

What does the malaria organism consume?

A

Hemoglobin

405
Q

Release of pyrogenic waste from rupture of RBCs travel to hypothalamus and cause what?

A

Increased thermal set point = fever and chills (sxs)

406
Q

If a pt presents with episodes of 1-2 hours of severe shivering and high fever following it, what is the cause? (Malaria)

A

TNF release (inflammation) after pyrogen travels to hypothalamus

407
Q

What is one of the first signs of malaria?

A

Anemia due to RBC destruction

408
Q

Why is malaria difficult to treat?

A

Mimics other diseases

409
Q

What 2 things can provide a pt with malaria resistance? What forms are they specifically resistant to?

A

Sickle cell anemia (all forms)

Lack of Duffy antigen (P. vivax)

410
Q

What is the malaria vaccine and what is the issue with it?

A

RTS, S (Mosquirix)

Low efficacy

411
Q

What are the reservoirs for malaria?

A

Humans and simians

412
Q

What role will climate change play in the spread of malaria?

A

Increasing land mass and population being exposed to disease

Organism can survive in areas it didn’t used to be able to

413
Q

Plasmodium vivax is aka what?

A

Vivax malaria, benign tertian malaria

414
Q

Why is Plasmodium vivax is seldom fatal?

A

Infects young erythrocytes (receptor no longer available once erythrocyte ages)

415
Q

Pt prevents with relapse of malaria infection 3-5 years after initial disease. What organism are you concerned about and what is the reason for the relapse?

A

Plasmodium vivax

Activation of liver hypnozoites

416
Q

If Plasmodium vivax is microscopically evaluated, what should you see?

A

Enlarged infected RBCs with Schuffner’s dots

417
Q

How is infection with Plasmodium vivax controlled?

A

Protection from mosquitos (nettings, insecticides, repellants)

418
Q

What malaria organism has the capability to infect any age RBC?

A

Plasmodium falciparum (malignant tertian malaria)

419
Q

Rapid multiplication and high parasite numbers lead to what sxs?

A

High fever/ Blackwater fever

420
Q

Pt presents w/ high levels of free Hgb in urine. What are you concerned about and what might this lead to?

A

Blackwater fever

Concerned for autoimmune rxn w destruction of kidney tissue

421
Q

RBCs infected with Falciparum malaria stick to capillary linings leading to what?

A

Capillary obstruction

422
Q

Pt presents with cold skin temp but high internal malaria. What should you be concerned about?

A

Algid malaria (releated to Plasmodium falciparum)

423
Q

How can Plasmodium falciparum be distinguished from Plasmodium vivax?

A

Plasmodium falciparum is non relapsing due to lack of hypnozoite stage and absence of Schuffners dots on microscopic eval

424
Q

Pt presents w/ hx of mosquito bite and signs of necrosis, hemorrhages, extreme fever, mania, convulsions, and is at risk of death. What is the infecting species and what type of malaria are you concerned about?

A

Plasmodium falciparum

Cerebral malaria

425
Q

Gastric falciparum malaria from the Plasmodium falciparum species leads to what sxs?

A

Frequent vomiting

426
Q

On microscopic eval of blood of a malaria infected pt you see erythrocytes with double or multiple ring stages, crescent shaped gametocytes, and Maurer’s clefts. What organism are you concerned about?

A

P. falciparum

427
Q

On microscopic eval of blood of a malaria infected pt you see young trophozoites and gametocytes but not schizonts in the periphery. What infecting organism are you concerned about?

A

P. falciparum

428
Q

How is P. falciparum controlled?

A

Protection from mosquitos (nettings, insecticides, repellants)

429
Q

What malaria organism has the following characteristics:
Infects older RBCs
Paroxysms every 4th day
Zoonotic from primate reservoirs

A

P. malariae

430
Q

On microscopic eval of blood of a malaria infected pt you see trophozoites (basket and band shaped) and schizonts (rosette shaped). What infecting organism are you concerned about?

A

P. malariae

431
Q

What malaria organism has the following characteristics:
Similar to vivax malaria
Relapses common
Common to W coast of Africa

A

P. ovale

432
Q

What malaria organism has the following characteristics:
Zoonotic
May be life-threatening if heavy parasite burden
Common to SE Asia

A

P. knowlesi

433
Q

Why is medication targeting Duffy antigen becoming less effective?

A

Increasingly independent binding to Duffy antigen

434
Q

What is the main cause of drug resistance for malaria organisms?

A

Efflux pumps

435
Q

What is the causative agent of Babesiosis (Nantucket island fever)

A

Babesia microti

436
Q

What does Babesia microti infect?

A

RBCs

437
Q

When do you have increased transmission of Babesia microti?

A

Warmer months/ summer

438
Q

Lack of ability to test for Babesia microti in the blood leads to issues why?

A

Transmission through blood donation

439
Q

What is the vector for Babesia microti?

A

Deer tick

440
Q

Pt presents w small pinpoint lesions and are diagnosed w anemia. What organism should you be suspicious of?

A

Babesia microti

441
Q

Babesia microti often presents with a co-infection of what disease?

A

Lyme disease

442
Q

If under microscopic examination you note a “cross like” morphology in RBCs, what infecting organisms should you be concerned for?

A

Babesia microti

443
Q

How is infection with Babesia microti controlled?

A

Insect repellants when outdoors

444
Q

How did water treatment plants affect infection with polio?

A

Shifted from infants getting infected (fewer complications) to children getting infected

445
Q

What disease affects the brain stem and cerebellum?

A

Rabies

446
Q

What disease affects the cerebral cortex and cerebellum?

A

Creutzfeldt-Jakob encephalitis

447
Q

What is the only disease that you vaccinate after exposure for?

A

Rabies

448
Q

What disease affects the anterior horn cells and bulbar motor nuclei?

A

Poliomyelitis

449
Q

What disease is associated with asymmetric flaccid paralysis?

A

Poliomyelitis

450
Q

What causes asymmetric flaccid paralysis seen with poliomyelitis?

A

Destruction of motor neurons in spinal cord

451
Q

What is the virus responsible for poliovirus?

A

Picorna virus

452
Q

What are the 5 main clinical syndromes of the polio virus infection?

A
  1. Inapparent infection (most common)
  2. Abortive illness
  3. Nonparalytic poliomyelitis
  4. Paralytic poliomyelitis
  5. Post polio syndrome
453
Q

What is the rarest/ more severe manifestation of the polio virus infection?

A

Paralytic poliomyelitis

454
Q

What device is used for pts with paralytic poliomyelitis to continue breathing?

A

Iron lung

455
Q

What polio syndrome is associated with muscle weakness, pain and fatigue in paralyzed polio pts?

A

Post polio syndrome (30 yrs post)

Only in paralyzed pts

456
Q

In a pt with post polio syndrome, has the latent polio virus returned?

A

No, remaining motor units of CNS react to overuse and fail

457
Q

How can polio be prevented?

A

Inactivated polio vaccine (IPV) (Salk)

Live polio vaccine, trivalent oral polio vaccine (OPV)

458
Q

Does the inactivated polio vaccine prevent infection?

A

No, prevents disease/ paralysis (not infection)

459
Q

Why is the live polio vaccine (OPV) no longer used in the US?

A

Possibility for back mutation to wild type

460
Q

Why is it important to continue to vaccinate against polio?

A

The polio virus is still present in some countries

461
Q

What is the cause of the newest/ uncontrolled strain of polio?

A

Circulating vaccine-derived polioviruses (cVDPVs)

462
Q

What arbovirus is the most concerning in the US and how is it transmitted?

A

West Nile virus

Vector= mosquito, tick

463
Q

What is the reservoir for West Nile virus?

A

Animals

464
Q

Are humans active hosts for arbovirus (West Nile virus)?

A

No (dead end hosts)

465
Q

What is the most concerning agent of disease for arbovirus?

A

Flavivirdae group (yellow fever group)

466
Q

What is important in the treatment/ prevention of arbovirus?

A

Break chain of transmission

467
Q

Pt presents w fever, HA, vertigo, photophobia, nausea, vomiting, confusion/ personality changes, focal/ general seizures. What are you concerned for?

A

Arbovirus

468
Q

What serious complication is caused by WNV?

A

Encephalitis

469
Q

What population is typically affected by WNV?

A

Older pts

470
Q

What time of year is WNV most prevalent?

A

Summer/ fall (higher mosquito activity)

471
Q

Does WNV have the potential to cause viral encephalitis?

A

Yes

472
Q

What test is used for the dx of WNV?

A

MAC-ELISA (look for IgM antibody)

473
Q

In pts with yellow fever, dengue, Japanese encephalitis St Louis encephalitis viruses, what should you beware of when performing tests such as MAC-ELISA?

A

Antigenic cross reactions

474
Q

Vaccination against yellow fever and/ or Japanese encephalitis may induce what?

A

Long-lasting positive IgM titers (for 9 mos past vaccine)

travel hx important

475
Q

What test is best for dx of Zika?

A

RT-PCR

476
Q

For all arboviruses besides Zika, what is the best dx test?

A

IgM ELISA

477
Q

How is infection w arbovirus prevented?

A

Interrupt chain of transmission

478
Q

What is the major concern w Zika virus?

A

Teratogenic potential and GBS

479
Q

What are most US cases of Zika virus associated with?

A

Travel

480
Q

How can Zika virus be prevented?

A

Mosquito avoidance and pt edu (including potential to transmit as STI)

481
Q

What is the target of rabies disease?

A

Salivary glands

482
Q

Only touch with rabid animal can cause what?

A

Cryptic rabies

483
Q

What affected organism exhibits a “furious” excitatory phase?

A

Dogs only

Humans experience anxiety and apprehension hydrophobia

484
Q

Pt presents w mild fever, pharyngitis, HA, and abnormal sensations such as pain and burning. What should you be concerned for?

A

Rabies

485
Q

What phase of rabies is characterized by coma, hypotension, and possible death?

A

Paralytic phase

486
Q

How is rabies dx’d?

A

Exposure to bite + sxs

487
Q

In what case do you always treat/ should you be especially cautious for with regards to rabies?

A

Contact w a bat

488
Q

Microscopy shows a “bullet shaped” organisms. What should you be concerned about?

A

Rabies

489
Q

What “tx” for rabies has failed as often as it has succeeded?

A

“Milwaukee” protocol

490
Q

How is rabies prevented in animals?

A

Prophylactic vaccination in companion/ herd animals

491
Q

How is rabies treated in humans?

A

Vaccine (HDCV) + hyperimmune serum after contact w reservoir animal

492
Q

What are the 2 broad categories of CNS infections?

A

Meningitis and encephalitis

493
Q

What CNS infection is defined as inflammation resulting from an infection within the subarachnoid space?

A

Meningitis

494
Q

What CNS infection is defined as inflammation in the parenchyma?

A

Encephalitis

495
Q

What organism-dependent skin complication can occur from CNS infections?

A

Abscess formation

496
Q

What time frame defines acute v chronic meningitis?

A
Acute = hours to several days
Chronic = ≥ 4 weeks (w over exaggerated immune response)
497
Q

What is the danger with respiratory pathogens?

A

Can enter blood and cause CNS infection

498
Q

Why has the cause of bacterial meningitis infections shifted from H. influenzae to S. pneumoniae?

A

Vaccine against H. influenzae

S. pneumoniae is cause of resp infections which lead to CNS infections

499
Q

Why has the incidence of meningitis declined significantly over time?

A

Vaccines

Screening of pregnant women for GBS (group B strep)

500
Q

What can manifest as an “aseptic” case of meningitis (and classified as virus) due to difficulty in making a positive ID of pathogen?

A

Bacterital meningitis

501
Q

Which type of meningitis is usually caused by organisms able to colonize the resp tract?

A

Community acquired

502
Q

Which type of meningitis results after iatrogenic procedures or in patients with altered immune status and often GI/ skin pathogens?

A

Hospital acquired

503
Q

What is step 1 in pathogenesis of bacterial meningitis?

  1. Entry into blood stream
  2. Penetration of BBB
  3. Release of inflammatory cytokines
  4. WBC diapedesis into CSF
  5. Increased permeability of BBB
  6. Exudation of serum
  7. Edema, increased intracranial pressure, altered BF
A

Mucosal colonization

504
Q

What is step 2 in pathogenesis of bacterial meningitis?

  1. Mucosal colonization
  2. Penetration of BBB
  3. Release of inflammatory cytokines
  4. WBC diapedesis into CSF
  5. Increased permeability of BBB
  6. Exudation of serum
  7. Edema, increased intracranial pressure, altered BF
A

Entry into blood stream

505
Q

What is step 3 in pathogenesis of bacterial meningitis?

  1. Mucosal colonization
  2. Entry into blood stream
  3. Release of inflammatory cytokines
  4. WBC diapedesis into CSF
  5. Increased permeability of BBB
  6. Exudation of serum
  7. Edema, increased intracranial pressure, altered BF
A

Penetration of BBB

506
Q

What is step 4 in pathogenesis of bacterial meningitis?

  1. Mucosal colonization
  2. Entry into blood stream
  3. Penetration of BBB
  4. WBC diapedesis into CSF
  5. Increased permeability of BBB
  6. Exudation of serum
  7. Edema, increased intracranial pressure, altered BF
A

Release of inflammatory cytokines

507
Q

What is step 5 in pathogenesis of bacterial meningitis?

  1. Mucosal colonization
  2. Entry into blood stream
  3. Penetration of BBB
  4. Release of inflammatory cytokines
  5. Increased permeability of BBB
  6. Exudation of serum
  7. Edema, increased intracranial pressure, altered BF
A

WBC diapedesis into CSF

508
Q

What is step 6 in pathogenesis of bacterial meningitis?

  1. Mucosal colonization
  2. Entry into blood stream
  3. Penetration of BBB
  4. Release of inflammatory cytokines
  5. WBC diapedesis into CSF
  6. Exudation of serum
  7. Edema, increased intracranial pressure, altered BF
A

Increased permeability of BBB

509
Q

What is step 7 in pathogenesis of bacterial meningitis?

  1. Mucosal colonization
  2. Entry into blood stream
  3. Penetration of BBB
  4. Release of inflammatory cytokines
  5. WBC diapedesis into CSF
  6. Increased permeability of BBB
  7. Edema, increased intracranial pressure, altered BF
A

Exudation of serum

510
Q
What is step 8 in pathogenesis of bacterial meningitis?
1. Mucosal colonization
2. Entry into blood stream
3. Penetration of BBB
4. Release of inflammatory cytokines
5. WBC diapedesis into CSF
6. Increased permeability of BBB
7. Exudation of serum
8.
A

Edema, increased intracranial pressure, altered BF

511
Q

What is the most common pathway for a pathogen gaining access to the CNS?

A

Invasion of the bloodstream and seeding of the CNS

512
Q

Besides invasion of the bloodstream and seeding of the CNS, what are the other 2 pathways for a pathogen gaining access to the CNS?

A

Retrograde neuronal pathway

Direct contiguous spread

513
Q

What allows fluid, WBCs and other immune components to enter the blood during a CNS infection?

A

“Leaky” blood vessels

514
Q

What is the classic triad of sxs for CNS infections?

A

Fever, HA, neck stiffness

515
Q

What would you expect to see with CSF glucose levels in a pt with a CNS infection?

A

Decreased; organism uses as energy source

516
Q

Neonatal meningitis can be caused by what factors?

A

Neonatal or maternal factors

517
Q

What are the most important signs/ sxs seen with neonatal bacterial meningitis?

A

Bulging fontanelle, high pitched cry, hypotonia, paradoxic irritability

518
Q

What is paradoxic irritability seen with neonatal bacterial meningitis?

A

Quiet when stationary and crying when held

519
Q

How can neonatal bacterial meningitis be classified that differentiates it from meningitis seen in adults?

A

Hyperthermia +/- GI disturbance

520
Q

What are the predominant agents of neonatal bacterial meningitis, and are they G+ or G-?

A
Streptococcus agalactiae (G+) (GBS)
E. coli (G-)
Listeria monocytogenes (G+)
521
Q

Screening pregnant mothers for GBS and routine abx prophylaxis for culture + women contributes to what?

A

Prevention of neonatal bacterial meningitis

522
Q

Does a child who survives neonatal bacterial meningitis have long term effects?

A

Yes, usually permanent defects

523
Q

What is the most common cause of neonatal bacterial meningitis?

A

Streptococcus agalactiae (GBS)

524
Q

Which causative agent of neonatal bacterial meningitis will display gray-white colonies with a narrow zone of beta-hemolysis on microscopy?

A

S. agalactiae (GBS)

525
Q

When do most cases of neonatal bacterial meningitis caused by S. agalactiae occur?

A

Transmitted during delivery (remainder acquired postpartum)

526
Q

Capsular polysaccharide, hyaluronidase, collagenase, and hemolysin are virulence factors for what pathogen?
(dangerous bc neonates are IMC)

A

S. agalactiae (GBS)

527
Q

When can S. agalactiae (GBS) be seen in adults?

A

IMC

528
Q

With early onset neonatal bacterial meningitis, are maternal obstretric complications common or uncommon?

A

Common

529
Q

When do sxs develop with with early onset neonatal bacterial meningitis?

A

During first 5 days of life

530
Q

What type of neonatal bacterial meningitis is characterized by bacteremia, pneumonia, and meningitis?

A

Early onset

531
Q

What type of neonatal bacterial meningitis leads to systemic effects (bone/ joint infections, bacteremia w meningitis) and is often fatal?

A

Late onset

532
Q

How is infected by S. agalactiae diagnosed?

A

Lab tests detect CAMP factor (only works 25% of the time)

533
Q

How is S. agalactiae definitely diagnosed?

A

Isolation from blood, CSF

534
Q

Source of E. coli (causing bacterial meningitis) is rectal colonization of mother’s vagina and NOT what?

A

An endogenous infection

535
Q

What is the morphology of E. coli?

A

G- encapsulated bacillus

536
Q

What is the most common cause of bacterial meningitis, is most common agent in elderly, and is most common with recurrent meningeal infections?

A

S. pneumoniae

537
Q

What is the morphology of H. influenzae (causing bacterial meningitis)?

A

Non-motile, G- coccobacillus

538
Q

What causative agent of bacterial meningitis displays a usual pattern of several days of mild antecedent infection followed by deterioration, signs and sxs of meningitis?

A

H. influenzae

539
Q

What is the morphology of L. monocytogenes (causing bacterial meningitis)?

A

G+ motile coccobacillus, non-fastidious, facultative IC pathogen

540
Q

What pathogen causing bacterial meningitis is common in foodstuffs?

A

L. monocytogenes

541
Q

What temps allows survival of L. monocytogenes?

A

Low temps (freezer, refrigerator)

542
Q

What pathogen is considered the “exception” because it is not commonly a resp infection and is more common in summer?

A

L. monocytogenes

543
Q

What are the 2 primary virulence factors of L. monocytogenes?

A

Lipopolysaccharide-like surface component

Listeriolysin O

544
Q

What virulence factor of L. monocytogenes has the following characteristics:
Antiphagocytic
Presumably responsible for induction of complement- depdendent hemolytic antibodies

A

Lipopolysaccharide-like surface component

545
Q

What virulence factor of L. monocytogenes has the following characteristics:
Disrupts phagolysosome membrane
Inhibits antigen processing
Induces apoptosis

A

Listeriolysin O

546
Q

Why is pathogenesis listeriosis dangerous in an IMC host?

A

IMC cannot eliminate = IC and EC multiplication and systemic disease

547
Q

What are the 2 main clinical manifestations of listeriosis?

A

Sepsis and meningitis

548
Q

If you note “tumbling” motility in hanging drop preparation of a pathogen, what should you be concerned for?

A

Listeriosis

549
Q

How is listeriosis diagnosed?

A

DNA probe technology

550
Q

What is the causative agent of meningococcal meningitis?

A

Neisseria meningitidis

551
Q

What pathogen has a morphology that is fastidious, G-, kidney bean-shaped diplococcus and encapsulated?

A

Neisseria meningitidis

552
Q

What is the most important serogroup of Neisseria meningitidis?

A

B

553
Q

Who is the only reservoir for Neisseria meningitidis and what does infection require?

A

Humans

Close contact

554
Q

Pt presents with a skin rash consisting of petechiae and pink macules that is widespread and erupted within hours. What are you concerned for?

A

Meningococcemia

555
Q

If you note a + tumbler test in which the pts rash does NOT change color (aka is non-blanching), what should you be concerned about?

A

Meningococcal meningitis

556
Q

Thayer-Martin agar is selective for what pathogen due to presence of antibiotics?

A

Meningococcal meningitis

557
Q

Why don’t you give a group B vaccine with the A,C,Y,W135 vaccine on the same day in the same arm for prevention of Meningococcal meningitis?

A

Causes autoimmune rxn

558
Q

What is the pathogenesis for reactivation/ secondary TB after progression from caseous lesions with necrosis?

A

Erode and discharge TB bacilli into bronchi (infectious) > erode blood vessel > hematogenous spread

559
Q

What are the following used for?
Purified MTB protein derivative (PPD) in skin test
Boosters id’d by 2nd administration
BCG and NTM false pos

A

Serial screening programs to id latent TB

560
Q

How does infection w MAC occur?

A

Infection through contaminated water or food

561
Q

When can measles be especially severe?

A

Malnourished and/or vitamin A deficient persons

562
Q

How does measles cause encephalitis?

A

Viremia, dissemination to other tissues by monocytes

563
Q

What disease multiples in respiratory epithelium and lymph nodes?

A

Measles

564
Q

What are the 4 stages of measles?

A
  1. Incubation period (10-14 days)
  2. Prodromal stage
  3. Rash
  4. Resolution
565
Q

At what point do you have resolution of measles?

A

Rise in antibody titers, viremia stops, rash fades in same order it appears

566
Q

Who are the only known hosts of measles?

A

Humans and monkeys

567
Q

When is the measles vaccine given?

A
Initiation before school entry 
1st dose = 15 mos
2nd dose = 4-6 yrs
Monovalent measles vaccine if under 15 mos and high exposure likelihood 
Booster sometimes required
568
Q

How is rubella treated?

A

Symptomatic relief
MMR
Intravenous immunoglobulin (IVIG) “last ditch effort” if exposure of non-immune mother in 1st trimester

569
Q

How is continued spread of HSV halted?

A

Cell and humoral immune processes (disseminates if absent)

570
Q

Besides spreading via contact with vesicular fluid, saliva, and secretions, how else can HSV be spread?

A

Asx shedding possible

571
Q

Where does the chickenpox virus replicate?

A

Regional lymph nodes (4-6 days)

Liver and spleen (secondary viremia at 10-14 days)

572
Q

Who gets the zostavax vaccine?

A

Pts over 50 yo

High potency vaccine

573
Q

What is the treatment for parvovirus?

A
Sx relief (non-steroidal anti-inflammatory agents)
Immunoglobulin available for anemia patients
574
Q

What topical tx is used for folliculitis?

A

Clindamycin ointment or benzoyl peroxide

575
Q

What type of spores are microconidia and macroconidia?

A

Asexual

576
Q

What dermatophytid species is the most common cause of tinea capitis, fluoresces when examined with a wood lamp and produce hyphae, micro/ macroconidia (large, spindle shaped, multicellular, thick walled)?

A

Microsporum species

577
Q

What are the 3 most common pathogens responsible for Tinea pedis, Tinea corporis, Tinea cruris, and Tinea unguium?

A

E. floccosum, T. mentgrophytes, T. rubrum

Also M. canis for corporis, cruris, capitis

578
Q

How can recurrent furuncles be prevented?

A

Liquid soap containing chlorhexidine/ isopropyl alcohol and maintenance abx

579
Q

How can impetigo and ecthyma be managed?

A

Hygiene, wash with soap and water, topical abx ointment

580
Q

How is scalded skin syndrome treated?

A

Prompt dx and therapy w penicillinase- resistant anti-staph abx

581
Q

If scalded skin syndrome is extensive, how should it be treated?

A

Treat as for burns

582
Q

How is erysipelas treated?

A

Oral or IV abx targeted against most likely agent

583
Q

Is type 1 NF mono or poly microbic?

A

Type 1 = poly

Type 2 = mono

584
Q

Is type 1 or 2 “flesh eating bacteria”/ strep gangrene?

A

T2

585
Q

Pt presents with a thick pink/ purple fluid filled bullae on leg that is not tender. What are you concerned for?

A

NF

586
Q

What promotes split and invasion of nearby tissue in pts with NF?

A

Production of exotoxins and insoluble H2 gas

587
Q

On surgery, infected muscle is dark red to black, non-contractile and does not bleed when cut. What should you be concerned for?

A

Clostridial myonecrosis

588
Q

What is the treatment for Lyme disease?

A

Sx: amoxicillin or doxycycline for 10-21 days

589
Q

What are the 4 possible courses of viral hepatitis?

A
  1. Subclinical and anicteric
  2. Typical acute icteric hepatitis
  3. Fulminant hepatitis
  4. Chronic hepatitis
590
Q

Which course of viral hepatitis is associated with a high fatality rate?

A

Fulminant hepatitis

591
Q

How is the subclinical and anicteric course of viral hepatitis recognized?

A

Seroconversion

592
Q

What does the incubation period of typical acute icteric hepatitis course represent?

A

Dose dependent range

593
Q

While the prodrome or pre-icteric phase of hepatitis is marked by fatigue, malaise, and anorexia, what is the icterus phase marked by?

A

Dark urine, jaundice, hepatomegaly, elevation of serum enzymes

594
Q

What phase of the typical acute icteric hepatitis course includes disappearance of jaundice and other sxs?

A

Convalescent phase

595
Q

What is the treatment for HAV?

A

Bed rest, reduction of activities, hydrated, good nutrition, avoid hepatotoxins

596
Q

When should a pt with HAV be hospitalized?

A

If IV fluids needed or there is evidence of deteriorating liver function

597
Q

What are the following HBV antigens associated with?
HBsAg
HBcAg
HBeAg

A

HBsAg- surface antigen
HBcAg- core antigen
HBeAg- surface antigen + pt infectious

598
Q

HBV replicates almost exclusively where?

A

In the liver

599
Q

Who is Colleen’s best friend?

A

Abbey <3