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Clin Med I - Dermatology > Insects, Bacteria, & Viral > Flashcards

Insects, Bacteria, & Viral Flashcards

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1
Q

What type of parasite are lice?

A
  • ectoparasite
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2
Q

What species of lice causes head lice?

A
  • Pediculosis capitis
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3
Q

What species of lice causes body lice?

A
  • Pediculosis corporis
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4
Q

What type of lice causes pubic lice?

A
  • Pediculosis or Pthirus pubis
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5
Q

How is lice spread?

A
  • person to person by close contact

- fomites

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6
Q

How is lice NOT spread?

A
  • jumping
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7
Q

What is lice a vector for?

A
  • typhus
  • trench fever
  • relapsing fever
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8
Q

Describe the lice ‘workup’

A
  • distance of nits away from hair follicle
  • cellulose tape
  • UV light
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9
Q

What are the symptoms of lice?

A
  • visible nits

- pruritis

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10
Q

What are the treatments for lice?

A
  • topical pediculicidal agents

- oral antihelmintics

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11
Q

What are the lice treatments effective against?

A
  • killing nymphs and mature lice

- not so much against eggs

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12
Q

What is the great clinical imitator?

A
  • scabies
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13
Q

What are the symptoms of scabies?

A
  • pruritis
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14
Q

What is the pathophysiology of scabies?

A
  • female mite burrows into skin
  • lays eggs
  • move through layers and secrete proteases
  • feed on tissue but not blood
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15
Q

scybala

A
  • scabies feces
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16
Q

Why do humans react to scabies infestations?

A
  • type IV hypersensitivity reaction to scybala
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17
Q

What are the treatments for scabies?

A
  • scabicidal
  • antipruritic
  • antimicrobial if secondary infection
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18
Q

What is a characteristic of the brown recluse spider?

A
  • dorsal violin shape
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19
Q

What is dermonecrotic arachnidisim?

A
  • local skin/tissue injury resulting from envenomation
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20
Q

What is loxoscelism?

A
  • systemic clinical syndrome caused bye envenomation from brown recluse spiders
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21
Q

How does a brown recluse spider bite present?

A
  • edematous/ischemic bite site

- erythematous halo

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22
Q

Why does the margin enlarge peripherally in a brown recluse spider bite?

A
  • 2nd to gravitational spread of the venom into the tissues
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23
Q

What happens 24-72h after a brown recluse spider bite?

A
  • single clear or hemorrhagic vesicle at site

- later forms a dark eschar

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24
Q

What is the treatment for a brown recluse spider bite?

A
  • wound management
  • cool compress to hinder sphingomyelinase D activity
  • dapsone
  • hyperbaric oxygen
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25
Q

What causes latrodectism?

A
  • latrotoxin, a neurotoxin
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26
Q

What is characteristic of the black widow spider?

A
  • hourglass on its dorsum
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27
Q

What are the 3 phases of a black widow bite presentation?

A
  • exacerbation
  • dissipation
  • residual
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28
Q

What is ominous in the residual phase?

A
  • changes in heartbeat, breathing, or blood pressure
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29
Q

What is the treatment for a black widow spider bite?

A
  • pain medication
  • muscle relaxants
  • antivenom
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30
Q

What is cellulitis?

A
  • infection without formation of abscess and without purulent drainage or ulceration
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31
Q

When there is intact skin with cellulitis, what causes the majority of cases?

A
  • Strep pyogenes
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32
Q

When the skin is not intact with cellulitis, what causes the majority of cases?

A
  • Staph aureus
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33
Q

What is a ddx for cellulitis?

A
  • erysipelas
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34
Q

How does cellulitis with a systemic infection present?

A
  • violacious
  • bullae
  • lymphangitis
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35
Q

What causes facial cellulitis in children?

A
  • H. influenza B
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36
Q

What comorbidities put a patient with cellulitis at risk?

A
  • DM
  • chronic edema
  • splenectomy
  • liver disease
  • immunosuppression
  • prosthetic implant
  • arterial or venous disease
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37
Q

How is cellulitis with intact skin treated?

A
  • beta-lactam abx (PCN)
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38
Q

How is cellulitis without intact skin treated?

A
  • cefazlin
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39
Q

erysipelas

A
  • bacterial infection of upper dermis extending into superficial cutaneous lymphatics
  • not deep
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40
Q

What is the causative agent of erysipelas?

A
  • Strep pyogenes (St. Anthony’s Fire)
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41
Q

How does erysipelas present?

A
  • initially small erythematous patch progressing into a fiery-red indurated, tense, & shiny plaque with well demarcated borders
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42
Q

What is a ddx for erysipelas?

A
  • SJS/TENS
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43
Q

What is the treatment for erysipelas?

A
  • elevation
  • saline wet dressings
  • PCN
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44
Q

What are common complications of erysipelas?

A
  • abscess
  • gangrene
  • thrombophlebitis
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45
Q

What are the two types of impetigo?

A
  • nonbullous

- bullous

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46
Q

What causes impetigo?

A
  • S. aureus
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47
Q

How does impetigo present?

A
  • folliculitis

- superficial, yellow, crust

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48
Q

What are the treatments for nonbullous impetigo?

A
  • topical mupirocin

- antihistamines

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49
Q

What are the treatments for bullous impetigo?

A
  • systemic antibiotics

- antihistamines

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50
Q

What are the classic exanthems?

A
  • 1st-6th disease
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51
Q

What are the other names for 1st disease?

A
  • measles
  • rubeola
  • morbilli
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52
Q

What are the other names for 2nd disease?

A
  • scarlet fever
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53
Q

What are the other names for 3rd disease?

A
  • rubella (German measles)
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54
Q

What are the other names for 4th disease?

A
  • Duke’s disease

- staph scalded skin

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55
Q

What are the other names for 5th disease?

A
  • erythema infectiosum
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56
Q

What are the other names for 5th disease?

A
  • erythema infectiosum
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57
Q

What are the other names for 6th disease?

A
  • roseola infantum

- exanthem subitum

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58
Q

How does measles present?

A
  • incubation period
  • prodrome
  • rash
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59
Q

What is the incubation period for measles?

A
  • 10-12d
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60
Q

What is characteristic of the prodrome phase prior to measles?

A
  • febrile
  • cough
  • coryza
  • conjunctivitis
  • Koplik spots
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61
Q

coryza

A
  • heavy rhinorhea
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62
Q

Koplik spots

A
  • tiny white dots on mucous membranes inthantum
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63
Q

What is the time frame for the rash of measles?

A
  • 2-4d after prodrome, 14d after exposure
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64
Q

Describe the measles rash

A
  • discrete maculopapular that becomes confluent

- begins on face and head goes to trunk and extremities

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65
Q

How long does the measles rash last?

A
  • 5-6d
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66
Q

How does the measles rash disappear?

A
  • fades in order of appearance
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67
Q

How does scarlet fever develop?

A
  • within 24-48 hours of onset of symptoms in untreated group A strep infected children
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68
Q

What is characteristic of scarlet fever presentation?

A
  • scarletina rash
  • peeling of the skin
  • ‘hot potato’
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69
Q

What does hot potato mean in relation to scarlet fever?

A
  • beefy-red uvula preventing clear speech
70
Q

How is scarlet fever diagnosed?

A
  • throat culture

- rapid antigen test

71
Q

What is the acute presentation of untreated strep pharyngitis?

A
  • scarlet fever
72
Q

What is the presentation 3-6mo after untreated strep pharyngitis?

A
  • rheumatic fever
73
Q

What is the next step after a negative rapid strep test?

A
  • throat culture
74
Q

What is a ddx for failed or relapsed within 1 week strep pharyngitis?

A
  • mononucleosis
75
Q

What is rubella generally?

A
  • benign communicable exanthematous disease
76
Q

What is the causative agent of rubella?

A
  • rubella virus
77
Q

What is the epidemiology of rubella in young children?

A
  • mild constitutional symptoms
  • rash
  • suboccipital adenopathy
78
Q

What is the epidemiology of rubella in older children, adolescents, and adults?

A
  • complicated by arthralgia, arthritis, and thrombocytopenia purpura
79
Q

What is a rare complication with rubella?

A
  • encephalitis
80
Q

What is a concern for pregnant women with rubella?

A
  • teratogenic effects when contracted early in the pregnancy
81
Q

What is the diagnosis for a fetus born to a mother who contracted rubella while pregnant?

A
  • congenital rubella syndrome
82
Q

How does rubella present?

A
  • 2-3 after incubation
  • pharyngitis
  • Forchheimer sign
  • tender lymphadonopathy
83
Q

How does postnatal rubella present?

A
  • discrete rose-pink maculopapular rash
  • pruritic
  • febrile
  • enlarged lymph nodes
  • forchheimer sign
84
Q

What are serious complications from congenital rubella syndrome?

A
  • deaf
  • blind
  • cardiac issues
85
Q

What does a congenital rubella syndrome kid look like?

A
  • blueberry baby
86
Q

What is erythema infectiosum?

A
  • benign, childhood condition
87
Q

What causes erythema infectiosum?

A
  • human parvovirus (HPV) B19
88
Q

How is erythema infectiosum transmitted?

A
  • respiratory secretions
  • fomites
  • parenterally from mother to fetus
89
Q

Describe phase 1 of erythema infectiosum

A
  • bright red, raised, slapped-cheek rash

- spares the nasolabial folds

90
Q

What is associated with erythema infectiosum?

A
  • arthropathy

- anemia

91
Q

Describe phase 1 of erythema infectiosum

A
  • bright red, raised, slapped-cheek rash

- spares the nasolabial folds

92
Q

Describe phase 2 of erythema infectiosum

A
  • maculopapular rash fades into classic lace-like reticular pattern
93
Q

Describe phase 3 of erythema infectiosum

A
  • recurrence of lacy rash worse with heat or exercise
94
Q

What is fetal hydops?

A
  • fetal transmission of erythema infectiosum
95
Q

How does erythema infectiosum present?

A
  • pruritic
  • exanthem only
  • rash in children
96
Q

What is exanthem subitum?

A
  • roseola
97
Q

What causes roseola?

A
  • human herpesvirus 6 (HHV-6)
98
Q

What is the classic presentation of roseola?

A
  • 9-12mo
  • acute
  • high febrile
  • seizure
  • Nagayama spots
  • 72 hr later, defervescence
99
Q

What patient population gets recurrence of roseola?

A
  • immunocompromised
100
Q

What are Nagayama spots?

A
  • small, white dots on soft palate
101
Q

What is the causative agent of varicella?

A
  • varicella-zoster virus
102
Q

How is varicella transmitted?

A
  • respiratory droplets
103
Q

Where are high viral titers found in a patient with varicella?

A
  • vesicles
104
Q

What does varicella infect?

A
  • conjunctiva

- mucosae of upper respiratory tract

105
Q

What is the 2nd viremia characterized by with varicella?

A
  • diffuse viral invasion of capillary endothelial cells and the epidermis
106
Q

What happens to varicella after the initial infection?

A
  • VZV spreads to local sensory nerves

- remains latent in the dorsal ganglion cells of sensory n.

107
Q

What is reactivation of VZV?

A
  • shingles
108
Q

How does varicella present?

A
  • intensely pruritic with vesicles

- head to neck to trunk to extremities

109
Q

When can children return to school?

A
  • when the most distal lesion has scabbed
110
Q

What are ‘dew drops on a rose petal’?

A
  • description of varicella vesicles

- reddish irregular papule with clear vesicle on top

111
Q

What are the complications of varicella?

A
  • secondary bacterial infection
  • disseminated primary varicella infection
  • CNS
  • hemorrhagic
112
Q

When there is a secondary bacterial infection of varicella, what is often suspected?

A
  • strep pyogenes
113
Q

What is the patient population with the complication from varicella of disseminated primary varicella infection?

A
  • immunocompromised

- adult

114
Q

What are the CNS complications from varicella?

A
  • Reye’s
  • Guillain-Barre
  • acute cerebellar ataxia
  • encephalitis
115
Q

What is in utero VZV infection?

A
  • primary maternal varicella during pregnancy

- produces latency of VZV in DRG of fetus

116
Q

What is reactivation of VZV associated with?

A
  • aging
  • immunosuppression
  • intrauterine exposure
  • varicella younger than 18mo
117
Q

What is an after effect of healed, reactivated VZV?

A
  • postherpetic neuralgia (phantom pains)
118
Q

How is varicella diagnosed?

A
  • Tzanck smear
  • vesicular fluid culture
  • serological testing for IgG
  • chest XR
  • histological exam
119
Q

What is the treatment for varicella?

A
  • clip nails
  • antihistamines
  • abx for 2ndary infection
120
Q

How is varicella prevented?

A
  • vaccine
121
Q

What does HPV (human papilloma virus) cause?

A
  • epithelial tumors of skin and mucous membranes
122
Q

Who are at risk of getting HPV?

A
  • people with multiple sexual partners

- people with HPV

123
Q

What are the three clinical categories of HPV?

A
  • anogenital or mucosal
  • nongenital cutaneous
  • epidermodysplasia verruciformis (EV)
124
Q

What is not a prevention for HPV spread?

A
  • condoms
125
Q

What does nongenital cutaneous HPV cause?

A
  • verruca vulgaris
126
Q

Where do verruca vulgaris present?

A
  • keratinized skin
127
Q

How are verruca vulgaris transmitted?

A
  • autoinoculation yields kissing warts
128
Q

What is verruca vulgaris?

A
  • common cutaneous warts
129
Q

What are verruca plana?

A
  • flat warts
130
Q

How is epidermodysplasia verruciformis genetically transfered?

A
  • autosomal recessive familial trait
131
Q

What are the low risk HPV types?

A
  • 6 & 11
132
Q

What is condylomata acuminata?

A
  • genital warts

- benign proliferations of the anogenital skin and mucosa

133
Q

What are the high risk HPV types?

A
  • 16 & 18
134
Q

What do HPV 16 & 18 lead to?

A
  • high-grade intraepithleial lesions that may progress to carcinomas
135
Q

What is the immune response to HPV?

A
  • weak cell mediated

- humoral does not occur until viral particles released from superficial cells

136
Q

How do HPV lesions resolve?

A
  • spontaneously
137
Q

What are the HPV malignancy factors?

A
  • oral contraceptives
  • chewing Indian betel quid
  • UV and XR irradiation
138
Q

What is laryngeal papillomatosis?

A
  • warts on the larynx
139
Q

Which HPV virus is implicated in laryngeal papillomatosis?

A
  • 6, 11, & 16
140
Q

What symptoms are involved with laryngeal papillomatosis?

A
  • hoarseness
  • voice change
  • croupy
  • cough
  • stridor
141
Q

How is laryngeal papillomatosis diagnosed?

A
  • direct laryngoscopy
142
Q

How is laryngeal papillomatosis transmitted?

A
  • vaginal delivery
143
Q

How is HPV diagnosed?

A
  • clinically
  • visually with acetic acid
  • PAP smear
144
Q

What is the treatment for HPV?

A
  • no single cure

- ablate the lesions

145
Q

How does molluscum contagiosum present?

A
  • multiple, rounded, dome-shaped, pink waxy papules
  • 2-5mm
  • umbilicated
  • with a caseous plug
146
Q

Where does molluscum contagiosum present?

A
  • along a line of minor skin trauma
147
Q

What are the three different patient populations who get molluscum contagiosum?

A
  • children
  • immunocompetent adults
  • immunocopromiesd children and adults
148
Q

How do children get mollusucm contagiosum?

A
  • direct skin-to-skin contact

- fomites

149
Q

How doe immunocompetent adults get molluscum contagiosum?

A
  • STD

- lesions limited to perineum, genitalia, lower abdomen, or buttocks

150
Q

Describe the molluscum contagiosum lesions in immunocompromised patients

A
  • widespread
  • persistant
  • atypical
151
Q

Where is the distribution for molluscum contagiosum in children v. adults?

A
  • children: face, trunk, and extremities; not pathognomic of abuse in groin, perineal, or genital
  • adults: groin and genitalia
152
Q

Where is molluscum contagiosum not found and why?

A
  • palms, soles, oral mucosa, conjunctiva

- thick skin

153
Q

How does molluscum contagiosum resolve?

A
  • spontaneously
154
Q

What are the treatment options for molluscum contagiosum?

A
  • benign neglect
  • direct trauma to lesions
  • antiviral therapy
  • immune response stimulation
155
Q

What HSV is associated with orofacial disease?

A
  • HSV 1
156
Q

What HSV is associated with genital disease?

A
  • HSV 2
157
Q

What is a good preventative measure for transmission of HSV?

A
  • condoms
158
Q

What makes HSV biologically unique?

A
  • neurovirulence
  • latency
  • reactivation
159
Q

How is HSV transmitted?

A
  • close personal contact
160
Q

What is acute herpetic gingivostomatisis?

A
  • primary HSV 1 infection in children
161
Q

What are the clinical features of acute herpetic gingivostomatisis?

A
  • abrupt onset
  • high T
  • anorexia
  • gingivitis
  • vesicular lesions
  • perioral skin involvement
162
Q

How are infections differentiated between HSV 1 and HSV 2?

A
  • culture
163
Q

What is the most common manifestation of recurrent HSV1?

A
  • acute herpetic labialis (lip sore)
164
Q

What are the characteristics of the primary v. recurrent HSV 2 genital infection?

A
  • primary: more severe and prolonged

- recurrent: less severe and shorter

165
Q

How do HSV 1 and 2 ‘protect’ against each other?

A
  • HSV1 protects against HSV2 severity

- orolabial HSV1 protects against genital HSV1 but not 2

166
Q

How does genital herpes present in women?

A
  • vesicles in moist areas that rupture leaving tender ulcers
  • cervix involvement in 70-90%
  • dysuria
167
Q

How does genital herpes present in men?

A
  • vesicles in dry areas that progress to pustules then encrust
  • urethritis
  • dysuria
  • proctitis
168
Q

How is HSV diagnosed?

A
  • culture
  • immunoflorescent staining
  • punch biopsy
169
Q

What are complications from HSV?

A
  • bacterial and fungal superinfections
  • candidal vaginitis
  • ocular infections
  • skin
  • CNS complications
  • pregnancy needs c-section
170
Q

What is the treatment for HSV?

A
  • based on specific antiviral treatment

- symptomatic

Clin Med I - Dermatology (10 decks)

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