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Dermatology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

THis is a collection of pus (neutrophils) that has accumulated within a tissue because of an inflammatory process.

A

Abscess

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2
Q

This is an infection of the hair follicle, which may progress to cutaneous tissue, leading to furuncles (boils).

A

Folliculitis

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3
Q

These are large, painful, raised nodules that contain underlying collections of dead and necrotic cells in cutaneous tissues.

A

Furuncles (boils)

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4
Q

These are an extension of furuncles into subQ tissues.

A

Carbuncles

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5
Q

This is a spreading infection that is limited tot he epidermis and presents as a bullous, crusted, or pustular eruption of the skin.

A

Impetigo

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6
Q

What characteristic color are the lesions in impetigo?

A

Honey-crusted lesions

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7
Q

This is a spreading infection that involves the blocking of dermal lymphatics and presents as a well-defined, spreading erythematous inflammaton, and often accompanied by pain and fever.

A

Erysipelas

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8
Q

In which age does a malar (butterfly) bright red rash occur on the face as an erysipelas?

A

Children

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9
Q

This is a spreading infection where the focus of the infection is in the subQ fat.

A

Cellulitis

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10
Q

This is the inflammatory response to infection of the soft tissue below the dermis, rapid spread along the fascial planes, disrupting the blood suppy.

A

Necrotizing fasciitis

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11
Q

Ischemia of the muscle layer can cause this condition, where there is gas resulting from the fermentative metabolism of anaerobic organisms.

A

Gas Gangene

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12
Q

This is a flat red local inflammation in response to an infiltrating leukocyte (esp their toxins in the dermis).

A

Macule

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13
Q

This is a raised red inflammation with invasion of neighboring tissues.

A

Papule

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14
Q

This is a small blister, from a microbe that invades the epithelium (HSV, VZV).

A

Vesicle

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15
Q

This is the ruptured epithelium from a vesicle, where the microbe is discharged.

A

Ulder

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16
Q

This is when the microbe grows into the epitheliu, which proliferates, and the microbe sheds with epithelial cells (wart).

A

Papilloma

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17
Q

What is the most common cause of skin infections?

A

S. aureus

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18
Q

What are the lab chracteristics of S. aureus?

A

G+ cocci
Catalase +
Coag +
B-hemolytic

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19
Q

After S. aureus invasion to the skin, what forms within 2-4 days?

A

Boil

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20
Q

After the boil in the S. aureus forms, it triggers an inflammatory response and the invasion of Neutrophils to cause what to form?

A

Abscess

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21
Q

What happens to the abscess in S. aureus infections?

A

Expands and eventually drains.

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22
Q

What is the DOC for bacteria that produce B-lactamase?

A

Methcillin

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23
Q

What is the DOC for MSSA?

A

Nafcillin

susceptible

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24
Q

What is the DOC for MRSA?

A

Vancomycin

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25
Q

Nasal carries of MRSA can be treated with nasal creams, like what drug?

A

Mupirocin

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26
Q

What does MRSA secrete, which has a lower affinity for B-lactams than normal PBPs, allowing it to continue cell wall synthesis when other PBPs are inhibited.?

A

PBP2a

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27
Q

What gene codes for PBP2a?

A

MecA

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28
Q

Vancomycin resistance comes from a ligase producing pentapeptides terminating in what sequence?

A

D-Ala D-lactate

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29
Q

Which Van genes can be transmitted (chromosomal or plasmid) and inducible?

A

VanA and VanB can be transmitted and is inducible.

VanD cannot be transmitted (chromosomal) and expressed constitutively

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30
Q

True or False: S. aureus have decreased susceptibility to vancomycin from Van genes.

A

False

Decreases susceptibility is associated with cell wall composition (↑ thickness) and not a Van gene.

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31
Q

Which Van comes from VRE from a plasmid and has high-level glycopeptide resistance?

A

VanA gene

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32
Q

Which toxin causes SSSS?

A

Exfoliatin or SSS toxin

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33
Q

Which ages is SSSS common?

A

Neonates

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34
Q

What is the manifestations of SSSS?

A

Large blisters with clear fluid and skin loss, mimics burns.

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35
Q

What is the mechanism of action of the TSST1 to cause TSS?

A

Superantigen (overstimulation of T cells and macrophages)

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36
Q

What “device” causes young girls to be susceptible to TSS?

A

Tampons

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37
Q

What are the Sx to TSS?

A

Fever, hypoTN, diffuse macular erythematous rash followed by desquamation of the skin (esp soles/palms)

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38
Q

What is the main virulence factor for S. pyogenes?

A

M protein

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39
Q

How does M protein provide resistance from S. pyogenes infections?

A

Inhibition of opsonization

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40
Q

After 1-2 days, there is an inflammatory response made from S. pyogenes infections, and it spreads using what protein?

A

Hyaluronidase

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41
Q

What are the superantigens called in S. pyogenes?

A

SPE’s (A, B, and C)

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42
Q

This is the superficial infection of S. pyogenes.

A

Impetigo

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43
Q

What is the deeper infection of the dermis called in S. pyogenes, where there can be bacteriemia and death?

A

Erysipelas

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44
Q

What is the condition from S. pyogenes where there is immune complex deposition on the BM of the glomerulus 2-3 weeks after infection?

A

PSGN

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45
Q

What is teh condition from S. pyogenes infection that is a mixed infection of anaerobes and faculative anerobes, and there is widespread necrosis of the skin and possible death?

A

Necrotizing fasciitis

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46
Q

What are the 2 main suspects to Cellulitis?

A

S. pyogenes

S. aureus

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47
Q

Which bacteria is G+, cocci, catalase -, B hemolytic, bactitracin sensitive, PYR+, and ASO+?

A

S. pyogenes

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48
Q

What is the source for S. pyogenes cellulitis?

A

Normal flora –> trauma causes inoculation

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49
Q

Which bacteria is G+, cocci, catalase +, coag +, and mannitol fermenting?

A

S. aureus

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50
Q

Which VF from S. aureus binds the Fc portion of host IgG?

A

Protein A

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51
Q

What cause of cellulitis is a G+ rod, catalase-, non-spore forming, and nonmotile?

A

Erysipelothrix rhusiopathiae

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52
Q

What is the host for Erysipelothrix rhusiopathiae infections?

A

Pigs

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53
Q

What is the cause of cellulitis that is G- rod, comma shaped, lactose non-fermenter, oxidase +, and motile?

A

Vibrio vulnificus

Vibrio algionlyticus

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54
Q

Where can u get vibrio?

A

Marine invironments

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55
Q

Which bug can cause gas gangrene from the soil and feces?

A

C. perfringens

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56
Q

What does the Lecithinase (alpha toxin) cleave on the host cell membranes, leading to cell lysis and death?

A

Phospholipids

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57
Q

What are the 2 risk factors for gas gangrene?

A

Ischemic vascular disease

Peripheral arteriosclerosis

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58
Q

Which specialized agar differentiates C. perfrinegens from other bacteria?

A

+ Nagler rxn (egg yolk agar)

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59
Q

These are greasy plugs of keratin, sebum, and bacteria, capped by a layer of melanin.

A

Comedones (black heads)

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60
Q

What is the main cause of comedones, which an aerotolerant anaerobic G+ rod?

A

Proprionibacterium acnes

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61
Q

What hormones ↑ in the body to ↑ sebum and keratinization/desquamation in pilosebaceous ducts to cause acne/comedones?

A

Androgenic H’s

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62
Q

These are acid fast rods that stain with Ziehl-Neelsen or auramine stain.

A

M. leprae

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63
Q

Which 2 cells does M. leprae grow in?

A

Skin histiocytes

Schwann cells

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64
Q

True or False: like TB, M. leprae can be grown in vitro.

A

FALSE

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65
Q

Where can u find M. leprae in infected individuals?

A

Nasal secretions

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66
Q

How long is the incubation period for M. leprae?

A

Years

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67
Q

This is the form of leprosy where there is a vegrous CMI response, leading to phagocytic destruction of bacteria and exaggerated allergic response.

A

Tuberculoid leprosy

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68
Q

What is a common Sx of Tuberculoid leprosy?

A

Local anethesia from thickening of peripheal nerves

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69
Q

What is the CMI response to M. leprae to cause Lepromatous leprosy?

A

Weak CMI response

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70
Q

Which is worse, Lepromatous leprosy or Tuberculoid?

A

Lepromatous leprosy

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71
Q

What are the Sx to Lepromatous leprosy?

A

Loss of eyebrows
Thickening and enlargement of nostrils, ears, and cheeks
Lion-like face
Lose nasal septum

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72
Q

Which form of Leprosy (L or T) will have numerous organisms on staining?

A

Lepromatous leprosy

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73
Q

Which mycobacterium do u associate with fish tanks?

A

M. marinum

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74
Q

What usually happens to you to allow M. marinum into your skin?

A

Some sort of trauma

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75
Q

What is the initial lesion of M. marinum after 2-8 weeks?

A

Small papules –> enlarge and may ulcerate.

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76
Q

What are Mycobacterium genus that causes chronic, relatively painless cutaneous “buruli” ulcers?

A

M. ulcerans

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77
Q

Where can u find M. ulcerans?

A

Africa and Australia

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78
Q

Which form of fungi (yeast or mold) are unicellular, reproduce by budding, and can form pseudohyphae?

A

Yeast

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79
Q

So we can guess that molds are multicellular and have hyphae, but what are hyphae?

A

Elongated tubes of cells attached end to end

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80
Q

What are the form of hyphae that have membranes separating individual cells?

A

Septate hyphae

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81
Q

What are the 4 dimorphic fungi?

A

C. immitis
H. capsulatum
B. dermatidis
S. schenkii

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82
Q

Tinea pedis and vaginal candidiasis are of what type of mycoses infection?

A

Superficial

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83
Q

What is involved in subcutaneous mycoses?

A

Nails and deeper layers of the skin

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84
Q

What is it called when there are mycoses of the internal organs?

A

Systemic/Deep mycoses

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85
Q

Malassezia furfur- conditions

A

Pityriasis or Tinea versicolor

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86
Q

Malassezia furfur- lesion morphology

A

Hypo or Hyperpigmented macules that coalesce to form scaling plaques.

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87
Q

Malassezia furfur- Sx

A

Itchy lesions, resolve spontaneously

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88
Q

Malassezia furfur- findings on KOH prep

A

Spaghetti and meatballs

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89
Q

Malassezia furfur- Tx

A

Miconazole, selenium sulfide

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90
Q

This is is a common label for a group of 3 types of fungus that common causes skin disease in animals and humans.

A

Dermatophytes

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91
Q

What contacts the skin to cause dermatophytes?

A

Anthospores

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92
Q

What are the most common cause of dermatophyte infections, where the anthrospores are spread shed from human skin scales and hair?

A

Antropohphilic

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93
Q

What is the most common dermatophyte from animals?

A

Zoophilic

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94
Q

Where do the following Zoophilic dermatophytes come from?

Trichophyton verrucosum
T. mentagrophytes
Microsporum canis

A

Trichophyton verrucosum- cows
T. mentagrophytes- rodents
Microsporum canis- dogs and cats

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95
Q

What are the type of dermatophytes from soil, and includes species like Microsporum gypseum?

A

Geophilic

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96
Q

Which epidermal protein do the tinea spp like to infect?

A

Keratin (skin, hair, nails)

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97
Q

What is the typical lesion morphology in tinea infections?

A

Serpentine scaling patch with raised margin

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98
Q

Which tinea spp infects the hair and scalp, leading to hair loss?

A

Capitis

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99
Q

Which tinea spp infects the body?

A

Corporis

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100
Q

Which tinea spp infects the crotch?

A

Cruris

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101
Q

Which tinea spp infects the feet?

A

Manuum and Pedis

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102
Q

Which tinea spp infects the nails?

A

Unguium

these names are freakin weird

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103
Q

What are the 3 genera responsible for dermatophytoses?

A

Microsporum
Epidermophyton
Trichophyton

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104
Q

What type of “light” do you use to see the microsporum spp?

A

UV-emitting Wood’s light

105
Q

Using a UV-emitting Wood’s light, what color do the hairs flouresce if they are contaminated with microsporum spp?

A

Bright green

106
Q

If you have a bright red rash in a skin fold because youre 500 pounds and you need an innocent EMT working in the ICU to help cleanse your cheesy smelly skin folds, what fungi is prolly growing there?

107
Q

Which WBC are important for the prevention of superficial candida infections?

108
Q

Which WBC are important for the prevention for hematogenous spread of candida?

A

Neutrophils

109
Q

If you get pricked by a rose bush and develop a small papule that subsequently spreads to the lymphatics, what fungi might be the cause?

A

Sporothrix schenckii

110
Q

What agar is used to Dx Sporothrix schenckii?

A

Sabouraud dextrose agar

111
Q

Which 3 viruses do not spread systemically?

A

Papillomas
Molluscum contagiosum
Orf

112
Q

What is the type of lesion of HSV, VZV, CoxA, and CoxB?

113
Q

A vesicular lesion shows a icosahedral, non-enveloped, dsDNA virus. What is the cause?

A

Papillomavirus

114
Q

Which HPV types cause plantar warts?

115
Q

Which HPV types cause genital warts?

116
Q

Which HPV types cause warts on the knees and fingers?

117
Q

Papillomavirus- transmission

A

Direct contact

118
Q

Papillomavirus- layer of skin infected

A

Basal layer

119
Q

Papillomavirus- cancer associations

A

Cervical
Vulva
Penis
Rectum

120
Q

Molluscum contagiosum- genus

121
Q

Molluscum contagiosum- lesion morphology

A

Fleshy, umbilicated

122
Q

Molluscum contagiosum- transmission

123
Q

Orf- host

124
Q

Orf- lesion morphology

A

Papulovesicular, generally on hands, may ulcerate

125
Q

What type of host envelope do the herpesviridae acquire?

A

Nuclear membrane envelope

126
Q

What type of cells are seen on Tzanck smear for herpes?

A

Multinucleated Giant cells

127
Q

What “bodies” are seen in herpes?

A

Eosinophilic Cowdry intranuclear inclusion bodies

128
Q

HSV1- diseases

A

Gingivostomatitis, keratoconjunctivitis, herpes, ENCEPHALITIS

129
Q

HSV1- transmission

130
Q

HSV1- location for focal necrotic lesions

A

Temporal lobe

131
Q

HSV1- site of latency

A

Trigeminal gangkion

132
Q

HSV1- triggers

133
Q

HSV2- diseases

A

genital herpes, neonatal herpes

134
Q

HSV2- transmission

A

sexual contact

135
Q

HSV2- Sx

A

local vesicular lesions

136
Q

HSV2- group at complication risk

A

Pregnant ladies

137
Q

HSV2- site of latency

A

Sacral ganglia

138
Q

HSV2- trigger

139
Q

VZV- diseases

A

varicella (chickenpox) and zoster (shingles)

140
Q

VZV- transmission

A

Respiratory secretions

141
Q

VZV- morphology of vesicles in respiratory tract

A

Dew on a rose petal

142
Q

VZV- primary presentation

A

Rash with vescicles (varicella), resolves in 2 weeks

143
Q

VZV- secondary presentation

A

Shingles, painful vesicular rash over 1 dermatome

144
Q

VZV- 3 complications

A

Interstitial PNA
CNS involvement
Blindness

145
Q

VZV- site of latency

146
Q

VZV- triggers

A

Stress, IC state, ↑ age, local injury

147
Q

Which viral family does coxsackie virus A16 belong to?

A

Picornaviruses

148
Q

Coxsackie A16- viral characteristics

A

ss + linear RNA, nonenveloped, iscosahedral

149
Q

Coxsackie A16- 2 diseases

A

Herpangina (mouth blisters, fever)

Hand, Foot, Mouth disease

150
Q

Coxsackie A16- transmission

A

Fecal oral or direct contact or aersolization

151
Q

Parvovirus B19- genome morphology

152
Q

Parvovirus B19- 2 diseases

A 
Erythema Infectiosum (5th disease)
Aplastic anemia crisis
153
Q

Parvovirus B19- 5th disease Sx

A

Cheek rash (slapped cheeks) –> move down to trunk

154
Q

Parvovirus B19- transmission

A

Respiratory aerosols

155
Q

Parvovirus B19- vertical transmission conditions

A

Fetal anemia

Hydrops fetalis

156
Q

HHV6- disease

157
Q

HHV6- Sx

A

Fever followed by a lacy body rash within 2 days

possible szrs

158
Q

HHV6- transmission

159
Q

HHV7- disease

A

Roselia (though not as frequently)

160
Q

HHV8- disease

A

Kaposi sarcoma

161
Q

HHV8- pts at risk

162
Q

HHV8- lesion morphology

A

Nodular and dark (purplish)

163
Q

HHV8- transmission

164
Q

Poxvirus- morphology

A

Complex (not enveloped)

165
Q

Poxvirus- site of replication

A

Cytoplasm (not in nucleus, despite being a DNA virus)

166
Q

Since poxvirus replicates in the cytoplasm, what enzyme must it contain to replicate within the cytoplasm?

A

DNA-dependent RNA polymerase

167
Q

Poxvirus- transmission

A

Person-person with skin lesions and via respiratory tract

168
Q

Poxvirus- disease

169
Q

Poxvirus- lesion morphology

A

Vasiculopapular rash with later scarring, especially on the face

170
Q

Poxvirus- vaccine type

A

Live attenuated

171
Q

What was it about the following things that made it possible for smallpox to be eradicated?

Subclinical features
Carriers
Host
Vaccine

A

No subclinical features
No carriers
Humans were the only host
Effective vaccine was available.

172
Q

What was the most recent scare in the US related to smallpox due to?

173
Q

What was the carrier for monkeypox to infect 80 people in the US?

A

Prairie dogs

174
Q

Measles- virus morphology

A

dsDNA, linear

175
Q

Measles- transmission

A

Respiratory droplets

176
Q

What was the name of the Arabian physician that first recognized measles over 1000 years ago?

177
Q

Measles- first Sx

A

Runny nose, fever, cough, conjunctivits

178
Q

Measles- lesion morphology

A

Koplik spots- white spots on buccal mucosa

179
Q

Measles- spread of rash

A

Starts on the face and then spreads down the trunk to the limbs

180
Q

Rubella- class of virus

181
Q

Rubella- viral characterisitics

A

+ ssRNA, linear, icosahedral, envelope with E1, E2 surface glycoproteins

182
Q

Rubella- transmission

A

Transplacental or Airborne

183
Q

After entering the respiratory tract, where does rubella enter?

A

Lymph nodes and spleen

184
Q

After multiplying in the lymph nodes, where does the virus then invade?

A 
Respiratory tract
Skin
Placenta
Joints
Kidneys
185
Q

What are the Sx of rubella invasion of the respiratory tract?

A

Sore throat, coryza, cough

186
Q

What are the Sx of rubella invasion of the skin?

A

rash from forehead –> down

187
Q

What are the Sx of rubella invasion of the placenta?

A

Congential rubella (PDA, cataracts, deafness, microcephaly)

188
Q

What are the Sx of rubella invasion of the joints?

189
Q

R. rickettsi- disease

190
Q

R. rickettsi- vector

A

Wood tick (dermacentor andersoni)

191
Q

R. rickettsi- spread of rash

A

palms/soles –> trunk

192
Q

R. rickettsi- complications

A

edema + hemorrhage –> hypovolemia

193
Q

R. rickettsi- area of infection in the US

A

North Carolina and Oaklahoma

194
Q

Borrelia burgdoferi- disease

A

Lyme disease

195
Q

Borrelia burgdoferi- vector

A

Ixodes tick

196
Q

Borrelia burgdoferi- stages

A
  1. erythema migrans
  2. neuropathy
  3. arthritis
197
Q

Borrelia burgdoferi- rash morphology

A

Bulls eye that expands

198
Q

Bacillus anthracis- disease

199
Q

Bacillus anthracis- population at risk

A

herbivores

200
Q

Bacillus anthracis- bacterium morphology

A

G+ rod (boxcar shaped)

201
Q

Bacillus anthracis- capsule morphology

A

D-glutamic acid

protein capsule. the only bacteria to have a protein capsule. super important

202
Q

Bacillus anthracis- toxins

A

PA
EF- ↑ cAMP
LF- protease

203
Q

Bacillus anthracis- skin manifestations

A

Painless ulcer with black eschar and edema called a malignant pustule

204
Q

Bacillus anthracis- pulmonary findings

A

If inhaled –> hemorrhagic mediastinitis (widened) –> septic shock and death

205
Q

Bacillus anthracis- GI findings

A

Ingestion of contaminated meats –> N/V, bloody diarrhea, death

206
Q

Bacillus anthracis- Tx

207
Q

Yersinia pestis- disease

208
Q

Yersinia pestis- vector

209
Q

Yersinia pestis- host

210
Q

Yersinia pestis- VF

211
Q

Yersinia pestis- morphology

A

non-motile, non-lactose fermenting, SAFETY PIN, growth at 4 degrees

212
Q

Yersinia pestis- plague Sx

A

High fever, buboes

No human-human

213
Q

Yersinia pestis- penumonic plague transmission

A

Human-human

214
Q

Pasteurella multocida- host

A

Cats and Dogs

215
Q

Pasteurella multocida- transmission

A

Cat/Dog bite

216
Q

Pasteurella multocida- Sx

A

Cellulitis

217
Q

Pasteurella multocida- lab characterisitics

A

G- rod, bipolar (safety pin) staining, capsule, musty odor

218
Q

Pasteurella multocida- agar

A

Chocolate or blood at 37 degrees

219
Q

Ancylostoma braziliense- appearance

220
Q

Ancylostoma braziliense- host

A

Dog and cat intestines

221
Q

Ancylostoma braziliense- people at risk

A

Kids who play with dog and cat poop

222
Q

Ancylostoma braziliense- distribution

A

Beaches throughout the US

223
Q

Ancylostoma braziliense- Sx

A

Severe erythematous and vesicular reactions

224
Q

Ancylostoma braziliense- syndrome at risk

A

Loffler syndrome- transient pulmonary infiltrate with peripheral eosinophilia

225
Q

Ancylostoma braziliense- Dx method

A

Skin biopsy shows larvae, Hx of playing with dog poop

226
Q

Ancylostoma braziliense- Tx

A

Albendazole

227
Q

Who deemed the name the “fiery serpent” to Dracunculus medinesis (aka the little dragon of Medina) with the Israelites at the Red Sea?

228
Q

Dacunculus medinesis- appearance

A

Tissue-invading nematode from the Cyclops genus

229
Q

Dacunculus medinesis- life cycle

A

larve ingested in drinking water –> penetrate GI wall –> maturation and mating in retroperitoneum –> subQ tissues –> ulcer –> larvae released once water contacts them.

230
Q

Dacunculus medinesis- risky behavior to get infected

A

Drinking from “step wells”

231
Q

Dacunculus medinesis- geographical distribution

A

Asia and Africa

232
Q

Dacunculus medinesis- time until ulcer appearance

233
Q

Dacunculus medinesis- Sx

A

Pain and erythema at the ulcer site

234
Q

Dacunculus medinesis- Dx method

A

Flood the ulcer with water and wait until the worms crawl out

235
Q

Dacunculus medinesis- Ancient method of Tx

A

Slowly wrapping the worm on a twig

236
Q

Dacunculus medinesis- New Tx method

A

Surgical removal

237
Q

Black widow (L. mactans)- distribution

A

Wood piles and brush in the South

238
Q

Black widow (L. mactans)- pathogenesis

A

Sharp pain at bite –> local swelling, reness, and burning –> systemic signs like boardlike abd, chest pain, N/V –> Sx subside within 48 hours

239
Q

Black widow (L. mactans)- toxin MOA

A

↑ presynaptic release of Ach

240
Q

Black widow (L. mactans)- Tx

A

Antivenin to kids/weak people

241
Q

Brown Recluse (Loxosceles)- pathogenesis

A

painless –> hours there is itching, swelling, and soreness and bleb at the site –> 3 days there is ulceration and radiating necrosis –> possible systemic problems.

242
Q

How long does it normally take to have Sx if you’ve never been bit by scabies?

A

weeks-months

243
Q

How long does it take to have Sx if you’ve been previously exposed?

244
Q

What type of HS rxn causes the sensitization to scabies?

245
Q

Scabies- appearance

A

Oval, saclike body with claws

246
Q

Scabies- Epidemiology

A

Found everywhere

247
Q

Scabies- pathogenesis

A

Enter skin –> burrows under epidermis –> female lays eggs in skin burrows (esp folds) –> intense itching

248
Q

Scabies- Dx method

A

Skin scrapings

249
Q

Scabies- Tx

A

1% gamma benzene hexachloride (lindane)

5% permetrin cream (Enlimite) (this is better)

250
Q

Lice (P. humanus capitis)- appearance

A

Elongated, wingless, flattened insets with 3 legs and a pretty mouth.

251
Q

Lice (P. humanus capitis)- Epidemiology

252
Q

Lice (P. humanus capitis)- Sx

A

Intense itching, possible pruritic red papules around the ears, face, neck, or shoulders.

253
Q

Lice (P. humanus capitis)- Dx

A

See the lice or eggs (nits)

254
Q

Lice (P. humanus capitis)- Tx

A

Gamma benzene hexachloride (lindane)

255
Q

Bedbugs (cimex letularis)- appearance

A

Reddish brown insect, 4-5mm, short wing pads but they cant fly

256
Q

Bedbugs (cimex letularis)- epidemiology

A

all over, they feed at night

257
Q

Bedbugs (cimex letularis)- Sx

A

Small red marks to hemorrhagic bullae, they bite in a linear fashion

258
Q

Bedbugs (cimex letularis)- Dx

A

Pattern and location of bites, detecting blood spots on bedding or dead insects themselves.

259
Q

Bedbugs (cimex letularis)- Tx

A

Topical palliatives for pruritis, antihistamines if severe dermatitis.

Dermatology (4 decks)

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