Infectious Diseases

Question 1

Double-stranded DNA virus that infects skin and mucosal epithelial cells which is species-specific and require fully differentiated squamous epithelia for their life cycle

Answer 1

Human Papilloma Virus

Question 2

HPV early proteins (E1-E7)

Answer 2

Responsible for DNA replication and kertinocyte immortalization

Question 3

HPV late proteins (L1-L2)

Answer 3

Expressed in superficial epidermis and encode structural proteins required for virion formation

Question 4

HPV Capsid

Answer 4

Contains DNA
Composed of L1 (major structural protein) and L2 (minor structural protein) – important for binding/entering epithelial cells

Question 5

First to be expressed at strata basale and spinosum – control transcription of other genes + replication of viral DNA (using host cell machinery)

Answer 5

E1 and E2 genes

Question 6

Disrupts cytokeratin network → koilocytosis

Answer 6

E4 protein

Question 7

Allow viral replication above stratum basale → amplification

Answer 7

E5, E6, and E7 genes

Question 8

Decrease host immune response; in high-risk mucosal subtypes are oncoproteins

Answer 8

E6 and E7 genes
E6 → ubiquitin-mediated p53 destruction →↓apoptosis/↑replication/↑mutations
E7 binds RB → loss of inhibition of E2F transcription factor → ↑expression of genes important for DNA replication

Question 9

Genus that account for most known types

Answer 9

α - most of the mucosal and cutaneous HPV types

β - epidermodysplasia verruciformis (EV)-associated HPV types

Question 10

Common warts

Answer 10

HPV-1, HPV-2, HPV-4, HPV-27, and HPV-57 (can cause 10 nail dystrophy)
Hyperkeratotic papules with pinpoint black dots (thrombosed capillaries), most commonly on fingers, dorsal hands/elbows/knees

Question 11

Palmar/plantar warts

Answer 11

HPV-1, HPV-2, HPV-4, HPV-27, and HPV-57

Thick/deep endophytic papules with black dots on palms/soles

Question 12

Flat/plane warts

Answer 12

HPV-3, HPV-10, HPV-28, and HPV-41
Light pink/brown, soft/smooth, slightly raised, occ. linear flat-topped papules on dorsal hands/face; more common in children; adult women ≫ adult men

Question 13

Butchers warts

Answer 13

HPV-7 and HPV-2

Extensive lesions on hands in meat/fish-handlers

Question 14

Epidermodysplasia verruciformis

Answer 14

Genetic disorder in which host has susceptibility to genus β HPV types (HPV-3, HPV-5, HPV-8, HPV-9, HPV-12, HPV-14, HPV-15, HPV-17, HPV-19, HPV-25, HPV-36, and HPV-38)

Question 15

Generalized polymorphic papules (generally flat wart-like appearance (dorsal hands, neck, face, and extremities), but also scaly, pink macules or hypopigmented, guttate macules/patches, and seborrheic keratosis-like lesions on forehead/neck/trunk) with AD inheritance – mutations in TMC6 (EVER1) and TMC8 (EVER2); acquired form may be seen in HIV
HPV types 5 and 8 can → AKs and SCC (generally patients ≥30 years old in sun-exposed areas; >30% of pts will develop SCC)

Answer 15

Epidermodysplasia verruciformis

Question 16

WHIM syndrome

Answer 16

AD 1° immunodeficiency caused by a CXCR4 mutation – Warts, Hypogammaglobinemia, Infections (bacterial), and neutropenia (2° to Myelokathexis)

Question 17

WILD syndrome

Answer 17

Warts, Immunodeficiency, Lymphedema, and Dysplasia (anogenital)

Question 18

Most common STD which occur on external genitals/perineum/perianal/groin/mons/vagina/urethra/anal canal; smooth, sessile, raised, skin-colored to brown lobulated papules
Most cases resolve spontaneously within 2 years
RFs: sexual intercourse at young age, # of sexual partners, and MSM
Circumcision →↓risk HPV transmission
May → cervical cancer

Answer 18

Condylomata acuminata (Genital warts)
HPV-6, HPV-11, HPV-16, HPV-18, HPV-31, HPV-33, and HPV-45

Question 19

HPV type of Condylomata acuminata with highest risk for cancer

Answer 19

HPV-16, HPV-18, HPV-31, HPV-33, and HPV-45

Question 20

Multiple brown papules/smooth plaques on genitals/perineum/perianal that are high-grade squamous intraepithelial lesions (HSIL) or SCCIS; progression to invasive SCC is very rare; a/w high-risk HPV types

Answer 20

Bowenoid papulosis

Question 21

Red smooth plaque on glabrous penis/vulva that is HSIL or SCCIS; increased risk of progression to invasive SCC; has high-risk HPV types

Answer 21

Erythroplasia of Queyrat

Question 22

Part of a group of verrucous carcinomas (slow growing and locally destructive) that includes oral florid papillomatosis (HPV-6, HPV-11; RFs: smoking, radiation, and inflammation), epithelioma cuniculatum (HPV-2, HPV-11, and HPV-16), and papillomatis cutis carcinoides
HPV-6 and HPV-11
Cauliflower-like tumors that infiltrate deeply on external genitals and perianally

Answer 22

Buschke-Lowenstein tumor

Question 23

Histology: papillomatous acanthotic epidermis with bulbous (“pushing”) downward-extending rete ridges; no cellular atypia/basement membrane penetration

Answer 23

Buschke-Lowenstein tumor

Question 24

Histology: flat wart-like architecture + cells w/ perinuclear halos and blue-gray granular cytoplasm

Answer 24

Epidermodysplasia verruciformis

Question 25

Multiple flat wart-like papules on gingival/buccal/labial mucosa in children (esp. South American); HPV-13 and HPV-32

Answer 25

Focal epithelial hyperplasia (Heck’s disease)

Question 26

Papillomas of airways due to HPV-6 and HPV-11; #1 benign tumor of larynx; hoarseness + stridor + respiratory distress; childhood (2° to vertical transmission) and adulthood (2° to genital-to-oral contact) onsets; can → SCC, esp. in smokers

Answer 26

Recurrent respiratory papillomatosis

Question 27

Characterized by an icosahedral capsid containing linear double-stranded DNA, surrounded by a glycoprotein-containing envelope; replicate in host nucleus

Answer 27

Human herpes viruses

Question 28

HSV-1/HHV-1

Answer 28

Orolabial 1° HSV can be severe (gingivostomatitis in children; pharyngitis/mononucleosis-like in adults) Mouth (esp. buccal mucosa and gingivae; favors anterior mouth unlike herpangina) and lips (recurrent lesions prefer vermilion border) affected

Question 29

HSV-2/HHV-2

Answer 29

Genital 1° infection often asymptomatic, but can → painful/tender erosions on external genitalia, vagina, cervix, buttocks, and perineum (women) +/− lymphadenopathy/dysuria (women mainly) Recurrent – mildly symptomatic with few vesicles lasting about 1 week; frequency of outbreaks usually decreases over time

Question 30

Latent HSV infection

Answer 30

virus lies dormant in sensory (dorsal root) ganglia

Question 31

Pathogenesis: Herpes simplex virus

Answer 31

Infection can occur without clinical lesions (and often does), and virus may still be shed HSV-1 spread by saliva/secretions and HSV-2 spread by sexual contact → viral replication at skin/mucous membrane → retrograde axonal flow to dorsal root ganglia → latency and subsequent reactivation HSV can evade host immune system (e.g., ↓expression of CD1a by APCs, ↓TLR signaling) Reactivation triggers: stress, UV (UVB > UVA), fever, injury (e.g., chemical peel or fractionated laser), and immunosuppression

Question 32

Grouped/clustered vesicles on a red base and Can become pustules, erosions (with classic scalloped borders due to coalescence), and ulcers, ultimately crusting over and healing within 6 weeks

Answer 32

Herpes simplex virus

Question 33

Widespread, sometimes severe HSV infection in areas of atopic dermatitis, Hailey-Hailey, or Darier’s disease (Fig. 5-2) +/− systemic symptoms, lymphadenopathy, may be life-threatening; ↑in children Increased with filaggrin mutations Usually HSV-1; associated with Th2 shift in immune system Increased in patients with severe atopic dermatitis w/ onset <5 years old, ↑IgE levels, ↑eosinophils, and food/environmental allergies Have been associated with topical calcineurin inhibitors

Answer 33

Eczema herpeticum

Question 34

Infection of digits (HSV-1 in children and HSV-2 in adults) w/ vesiculation/pain/swelling; recurrence seen; bimodal peaks at <10 years old and 20 to 40 years old

Answer 34

Herpetic whitlow

Question 35

HSV-1 infection 2° to athletic contact (classically on lateral neck/side of face and forearm)

Answer 35

Herpes gladiators

Question 36

Follicle-based vesicles/pustules in beard-area (HSV-1)

Answer 36

HSV folliculitis (herpetic sycosis)

Question 37

Keratoconjunctivitis w/ lymphadenopathy and branching dendritic corneal ulcer; blindness may occur (HSV-2 in newborns; HSV-1 otherwise)

Answer 37

Ocular HSV

Question 38

Most common fatal viral encephalitis in the United States (>70% die without tx); can be associated with mutations in TLR-3 or UNC-93B; usually HSV-1; fever/altered mentation/strange behavior; temporal lobe #1 site

Answer 38

HSV encephalitis

Question 39

Histology: intraepidermal vesicle + slate-gray enlarged keratinocytes (ballooning degeneration) which are multinucleated with margination of chromatin +/− Cowdry A inclusions (eosinophilic inclusion bodies) within nucleus, epidermal necrosis, multicellular dermal infiltrate, and perivascular cuffing

Answer 39

Herpes simplex virus

Question 40

Most common cause of EM minor

Answer 40

HSV-1

Question 41

Varicella zoster virus (HHV-3)

Answer 41

Varicella is the 1° infection and herpes zoster is the reactivation of the latent infection (more common in immunosuppressed and elderly and can → death

Question 42

Pathogenesis: Varicella zoster virus

Answer 42

Transmitted via aerosolized droplets and direct contact with lesional fluid Contagious from 1 to 2 days before lesion develops in varicella until all lesions crusted over After primary varicella infection, VZV travels to dorsal root ganglion and stays dormant – if reactivated later will replicate, travel down sensory nerve to the skin, and present as herpes zoster

Question 43

More severe disease in adolescents and adults Prodromal symptoms: fever, fatigue, and myalgias Cephalocaudal progression of classic lesions described as “dew drops on rose petal:” vesicles on an erythematous base that become pustular, then crust over Crops of lesions in various stages Vaccine-associated varicella zoster may rarely develop after the vaccine is administered – represents mild case of chickenpox that may start at injection site

Answer 43

Primary Varicella

Question 44

Cutaneous scarring; CNS/ocular/limb anomalies; risk greatest if infection occurs during first 20 weeks of gestation; exposed fetus may develop reactivation (herpes zoster) in childhood

Answer 44

Congenital varicella syndrome

Question 45

Perinatal varicella transmission (within 5 days before delivery until 2 days postdelivery); disease is severe (up to 30% mortality) because of the lack of protective maternal antibodies

Answer 45

Neonatal varicella

Question 46

Prodrome (itch, tingling, hyperesthesia, and pain) → painful grouped vesicles on red base in a dermatomal pattern; Trunk = most common location

Answer 46

Herpes zoster

Question 47

Oain, potentially chronic, after lesions have cleared in Herpes zoster; more common, severe and chronic in elderly

Answer 47

Postherpetic neuralgia

Question 48

Dermatomal disease + >20 lesions outside of dermatome +/− visceral involvement; almost exclusively seen in immunosuppressed (AIDS, lymphoreticular malignancy, long-term immunosuppressive medication use, etc.); increased risk of life-threatening pneumonitis and encephalitis

Answer 48

Disseminated Herpes zoster

Question 49

Disease of geniculate ganglion of facial nerve (CN-VII) may → ear pain, vesicles on tympanic membrane and EAM; ipsilateral facial nerve paralysis, dry mouth/eyes, anterior 2/3 tongue taste loss, and auditory (e.g., deafness and tinnitus) and equilibrium issues (vestibulocochlear nerve)

Answer 49

Ramsay-Hunt syndrome

Question 50

Ivolvement of the side and tip of nose: indicates disease of the external division of the V1 nasociliary branch; may → to ocular involvement (e.g., keratitis, uveitis, acute retinal necrosis, and visual loss) 3/4 of time

Answer 50

Hutchinson’s sign

Question 51

Treatment: Primary varicella

Answer 51

Treatment with systemic acyclovir or valacyclovir within 3 days of lesion onset → ↓severity/duration disease Oral administration appropriate in healthy children/adults IV acyclovir in immunocompromised patients

Question 52

Post-exposure prophylaxis: Varicella

Answer 52

Varicella vaccine may be given within 72 to 120 hours of exposure in nonimmune, immunocompetent individuals >12 months VZIg (Varicella zoster immunoglobulin) should be administered within 96 hours of exposure in immunocompromised, pregnant females, and neonates IVIg may alternatively be administered Oral acyclovir can be administered within 7 to 10 days of exposure

Question 53

Varicella vaccination

Answer 53

Live attenuated virus recommended as a 2 dose vaccination series; part of primary immunization series Initial dose at 12 to 15 months, booster dose at 4 to 6 years Contraindicated in pregnancy and in immunocompromised patients

Question 54

Treatment: Herpes zoster

Answer 54

Antiviral treatment with acyclovir (IV form in immunosuppressed), famciclovir, or valacyclovir is best given within 72 hours; prednisone helps with acute pain but has no effect on course or development of PHN ↓duration of lesions/pain ↓rate of postherpetic neuralgia (PHN) in patients >50 years old Valacyclovir and famciclovir preferable to acyclovir

Question 55

Causes infectious mononucleosis plus many other disorders (e.g., oral hairy leukoplakia, hydroa vacciniforme, Gianotti-Crosti syndrome, genital ulcers, and various hematologic disorders/malignancies (e.g., Burkitt’s lymphoma, NK/T-cell lymphoma, post-transplant lymphoproliferative disorder, and nasopharyngeal carcinoma)

Answer 55

Epstein-Barr virus (HHV-4)

Question 56

Pathogenesis: Epstein-Barr virus (HHV-4)

Answer 56

transmission via saliva/blood → infects mucosal epithelial cells initially → B-cells (where virus can lay dormant and evade immune system via production of EBNA-1 protein and latent membrane protein-2) Incubation period of 1 to 2 months; symptoms develop with viral replication In patients with ↓cell-mediated immunity, infected B-cells may continue to replicate → lymphoproliferative disorders (cell-mediated immunity appears to be more important than humoral, conferring immunity after first mononucleosis episode)

Question 57

Typically young adults w/ pharyngitis, fever, and cervical lymphadenopathy Splenomegaly (and possible rupture) +/− hepatomegaly ↑LFTs in subset of patients Lymphocytosis (up to 40% atypical lymphocytes) May have nondistinct polymorphous (e.g., urticarial, morbilliform) eruption in 5% to 10% occurring within first week of illness Centrifugal spread Petechial lesions on eyelid and hard/soft palate junction +/− genital ulcers (esp. females) Ampicillin/amoxicillin → “hypersensitivity” skin reaction (itchy generalized morbilliform eruption → desquamation)

Answer 57

Infectious Mononucleosis

Question 58

Corrugated white plaque typically on lateral tongue, with strong HIV association; more common in smokers

Answer 58

Oral hairy leukoplakia

Question 59

Nonspecific, confirms presence of IgM heterophilic antibodies which are often present in EBV infection and may persist for months after infection; 85% of older children/adults are positive during second week of infection, but is often negative in younger children

Answer 59

Monospot test

Question 60

Higher sensitivity in younger children; can be useful in determining current vs prior infection for diagnosis of EBV

Answer 60

EBV-specific antibodies

Question 61

Treatment: Epstein-Barr virus (HHV-4)

Answer 61

Supportive care Oral corticosteroids may be considered for severe cases of tonsillitis Avoid contact sports until splenomegaly resolves (risk for splenic rupture) Rare sequelae: upper airway obstruction, aseptic meningitis, meningoencephalopathy, myocarditis, pericarditis, and renal failure

Question 62

Transmitted via body fluids, fomites, vertical transmission, transplanted organs, and hematopoietic stem cells

Answer 62

Cytomegalovirus (HHV-5)

Question 63

Pathogenesis: Cytomegalovirus (HHV-5)

Answer 63

Infects leukocytes → dissemination → various organs → latency Most infections are asymptomatic in healthy adults; however, can cause severe disease in utero (TORCH), or in immunosuppressed/transplant patients (CMV retinitis/blindness, meningoencephalitis, pneumonitis, GI ulcers) After the 1° infection, very low risk of reactivation, except for immunocompromised patients

Question 64

Mononucleosis-like presentation (e.g., sore throat, fever, lymphadenopathy, and hepatosplenomegaly) may be associated with nonspecific exanthem (e.g., morbilliform) If ampicillin given → eruption (as in infectious mononucleosis) Recalcitrant ulcers of perineum or leg in HIV patients; these patients may also get verrucous plaques, vesicles, and/or nodules

Answer 64

Cytomegalovirus (HHV-5)

Question 65

Histology of ulcers may show enlargement of endothelial cells with pathognomonic “owl’s eye” (intranuclear) inclusions

Answer 65

Cytomegalovirus (HHV-5)

Question 66

One of the most common viral exanthems of childhood; up to 15% of infants may develop febrile seizures, but otherwise follows a generally benign course in healthy patients, 95% are between 6 months to 3 years of age

Answer 66

HHV-6 (Roseola infantum, exanthem subitum, sixth disease)

Question 67

Virus remains latent in T cells for life → reactivation has been a/w pityriasis rosea (along with HHV-7) and DRESS syndrome (along with EBV, CMV and HHV-7)

Answer 67

HHV-6 (Roseola infantum, exanthem subitum, sixth disease)

Question 68

Lymphotropic virus that shares significant homology with HHV-6 and may participate in co-infection w/HHV-6 Although not definitively causative of any disease, it has been a/w pityriasis rosea (along with HHV-6), and a subset of exanthem subitum cases (co-infection with HHV-6; unique clinical presentation)

Answer 68

HHV-7

Question 69

Etiologic factor for Kaposi sarcoma – discussed in Neoplastic Dermatology chapter Also associated with multicentric Castleman disease, primary effusion lymphoma (PEL), and paraneoplastic pemphigus

Answer 69

HHV-8

Question 70

Infection via respiratory tract → 7 to 17 days incubation period → 1 to 4 days prodromal period (fever, headache, myalgias, and malaise) → centrifugal (face/arms/legs > trunk) vesiculopustular eruption and may involve hands/feet (lesions in any given anatomic region will be in same stage) w/ lethargic/“toxic” appearance Rash: macule → papule → vesicle → pustules; typically scarring Lesions first appear on palms/soles Patients infectious from eruption onset till 7 to 10 days posteruption Oral lesions (tongue, mouth, and oropharynx) often appear before cutaneous by lesions 1 day

Answer 70

Smallpox (Variola virus; Orthopox genus)

Question 71

Used for live smallpox vaccine SEs: lymphadenopathy, ocular vaccinia, generalized vaccinia, vesiculopustular/urticarial/morbilliform eruption, eczema vaccinatum (in patients with atopic dermatitis, Darier’s, or Hailey-Hailey disease), erythema multiforme, postvaccinial CNS disease, and progressive vaccinia (immunosuppressed patients; can → death)

Answer 71

Vaccinia (Vaccinia virus; genus = Orthopox)

Question 72

Can spread via cutaneous inoculation or inhalation (hosts are monkeys, rodents, or humans) Prodrome (fever/sweating/chills) → smallpox-like lesions, but usually milder/fewer lesions Lesions may present in various stages and favor face and extremities (esp. palms/soles), with centrifugal spread; may scar May have systemic symptoms (respiratory, fever, and LAD in 67%) Central/western Africa, though United States outbreak from prairie dogs

Answer 72

Monkeypox (Monkeypox virus; genus = Orthopox)

Question 73

Spread via cutaneous contact (hands and face) with infected animal (usually cats) Incubates 7 days → painful red papule at contact site → vesicular → pustular → hemorrhagic → ulcer w/ eschar Lesions usually solitary and occur on hands/fingers Can have LAD, and fever Europe and Asia

Answer 73

Cowpox (Cowpox virus; genus = Orthopox)

Question 74

Develop one to few lesions at contact site (usually hands) as a result of contact with infected animals (sheep, goats, or reindeer; usually on udders/perioral areas of ewes) RFs: certain jobs (shepherds, butchers, and veterinarians) Self-resolves Diagnosis via histology (depends on stage) or PCR

Answer 74

Orf (ecthyma contagiosum; Orf virus; genus = Parapox)

Question 75

Papules at site of contact (usually muzzles of calves and teats of cows) on distal upper extremities usually with single lesion(s), which look like orf Most common in farmers/ranchers, veterinarians, and butchers Diagnosis via histology or PCR

Answer 75

Milker’s nodules (“Pseduocowpox;” Paravaccinia virus; genus = Parapox)

Question 76

Common infection in school-aged children; may be sexually transmitted in adolescents/adults; spread by contact with infected skin or fomites, or possibly via water Cause by molluscipox infection with two subtypes: MCV-I and MCV-II Prototypical lesion is an umbilicated, pink, and pearly papule most common on intertriginous areas, torso, lower extremities, and buttocks Lesions can become widespread in patients with impaired skin barrier (atopic dermatitis or ichthyosis) or immunodeficiency (chemotherapy-induced or HIV; may also see giant molluscum lesions)

Answer 76

Molluscum contagiosum (Molluscum contagiosum virus [MCV]; genus = Molluscipox

Question 77

Six lesion stages of Orf

Answer 77

maculopapular (umbilicated) → targetoid → acute (weeping nodule) → regenerative (nodule w/ thin crust and black dots) → papillomatous → regressive (crust overlying resolving lesion)

Question 78

Histology: Henderson-Patterson bodies within dermis

Answer 78

Molluscum contagiosum

Question 79

Treatment: Molluscum contagiosum

Answer 79

Cryotherapy, cantharidin, extraction/curettage, cimetidine, candida antigen immunotherapy, topical retinoids, and imiquimod Self-limited with resolution after weeks to years of infection

Question 80

≤50% of newly infected patients; presents in conjunction with classic mononucleosis-like syndrome of primary HIV infection, typically within 6 weeks of transmission Rash may be limited or widespread, is often asymptomatic, and is typically characterized by ill-defined erythematous maculopapules

Answer 80

Acute exanthem of primary HIV infection

Question 81

Characterized by eosinophil-rich inflammatory infiltrate in or around hair follicles Intensely pruritic, erythematous, and follicularly based papules located on the upper trunk, face, neck, and scalp

Answer 81

Eosinophilic folliculitis

Question 82

Lesions most often occur on mobile, nonkeratinized oral mucosal surfaces, but esophageal and anogenital aphthae are not uncommon in HIV patients Treatments: topical anesthetics, potent topical steroids, intralesional steroids, systemic corticosteroids, and thalidomide (severe or refractory disease)

Answer 82

Aphthous stomatitis

Question 83

In HIV, often associated with β-hemolytic strep infection Dapsone = treatment of choice Oral antibiotics indicated for Streptococcus-associated cases

Answer 83

Erythema elevatum diutinum

Question 84

Intensely pruritic condition commonly seen in patients with advanced HIV in developing world May represent aberrant immunologic response to insect bites or reactivation of prior bites Patients present with extensive, skin-colored-to-hyperpigmented, excoriated papules

Answer 84

Pruritic papular eruption

Question 85

Group of photodistributed rashes with multiple clinical manifestations including lichenoid (most common), eczematous, hyperpigmented, and vitiliginous Exposure to certain photosensitizing medications, particularly trimethoprim-sulfamethoxazole, can increase risk Treatment difficult; strict photoprotection and topical steroids; thalidomide in refractory cases

Answer 85

HIV photodermatitis

Question 86

Pathologic inflammatory response to preexisting antigen that develops soon after initiation of antiretroviral therapy in the setting of decreasing viral load, +/− corresponding increase in CD4+ counts; Most commonly occurs 2 weeks to 3 months after initiation of antiretroviral therapy; rarely require discontinuation of antiretroviral therapy – findings typically improve/resolve after several months

Answer 86

Immune reconstitution inflammatory syndrome (IRIS)

Question 87

HIV-Associated Dermatoses >500 cells/mm3

Answer 87

Acute exanthema of primary HIV infection Seborrheic dermatitis Oral hairy leukoplakia Vaginal candidiasis

Question 88

HIV-Associated Dermatoses <500 cells/mm3

Answer 88

``` Psoriasis Herpes zoster HPV HSV Staphylococcal infections Oropharyngeal candidiasis ```

Question 89

HIV-Associated Dermatoses <200 cells/mm3

Answer 89

``` Kaposi sarcoma Eosinophilic folliculitis Molluscum contagiosum Major aphthae (<100) Bacillary angiomatosis Disseminated coccidiomycosis, histoplasmosis; Cryptococcus (<100) Xerosis, eczematous dermatitis, acquired ichthyosis Crusted scabies ```

Question 90

HIV-Associated Dermatoses <50 cells/mm3

Answer 90

Large, nonhealing herpes simplex related ulcerations Giant molluscum Pruritic papular eruption HIV photodermatitis

Question 91

Caused by protease inhibitors, nucleoside reverse transcriptase inhibitors, and to lesser extent, nonnucleoside reverse transcriptase inhibitors; manifest as lipoatrophy (loss of fat in face, extremities, and buttocks) or lipohypertrophy (accumulation and redistribution of fat to upper back, neck, or abdomen); typically seen ≤2 years of starting therapy; associated with metabolic abnormalities (e.g., hyperlipidemia and insulin resistance)

Answer 91

Antiretroviral-associated lipodystrophy

Question 92

Approved for treatment of antiretroviral-associated facial lipoatrophy

Answer 92

Poly-L-lactic acid and calcium hydroxylapatite

Question 93

Can cause nail and mucocutaneous hyperpigmentation (longitudinal streaks or diffuse hyperpigmentation of fingernails/toenails)

Answer 93

Zidovudine

Question 94

Most common antiretroviral to cause DIHS/DRESS (up to 8% patients; can be fatal); HLA-B*5701 linked

Answer 94

Abacavir

Question 95

Most common bacterial infection in children

Answer 95

Impetigo

Question 96

How many are carriers of S. aureus?

Answer 96

35% of population carry S. aureus (anterior nares>perineum>axilla, toe webs) → ↑risk impetigo

Question 97

Non-bullous impetigo

Answer 97

70%): S. aureus (>Streptococcus pyogenes); children > adults Most commonly see erosion + “honey-colored” crust; affects traumatized, abraded, or eczematous skin; most commonly face (perioral/perinasal); self-resolves in 2 weeks Histology: neutrophilic microvesiculopustules, spongiosis, and Gram(+) cocci

Question 98

Bullous impetigo

Answer 98

(30%): phage group II (types 55 and 71) S. aureus → produce exfoliatoxins A and B (ETA and ETB) → cleaves desmoglein 1 → subcorneal/intragranular acantholysis Children > adults; presents with (p/w) flaccid bullae + erosions w/ collarette of scale, minimal surrounding erythema; affects intact skin, has more generalized distribution Histology: subcorneal/intragranular acantholysis, neutrophils in blister cavity, Gram(+) cocci

Question 99

Treatment: Impetigo

Answer 99

Localized: topical Mupirocin, retapamulin, or fusidic acid Widespread: oral β-lactamase resistant PCN or first generation CSN or clindamycin Complicated: IV ceftriaxone

Question 100

Used for patients w/ recurrent infections; topical mupirocin BID to nares for 7 to 10 days +/− skin decolonization w/ mupirocin ointment or chlorhexidine washes

Answer 100

Decolonization

Question 101

Most common form of bacterial folliculitis; most commonly on face (beard area typically)

Answer 101

S. aureus folliculitis

Question 102

S. aureus folliculitis - Superficial form (Bockhart’s impetigo)

Answer 102

small papulopustules on erythematous background

Question 103

S. aureus folliculitis - Deep form (“sycosis barbae”)

Answer 103

large red papulopustules +/− plaques with small pustules

Question 104

Bacterial folliculitis seen in acne patients on long-term ABX

Answer 104

Gram(-) folliculitis

Question 105

Bacterial folliculitis a/w poorly chlorinated hot tubs/whirlpools

Answer 105

Pseudomonal folliculitis

Question 106

T/F: No risk of rheumatic fever from streptococcal impetigo

Answer 106

True

Question 107

Collections of pus, most commonly from S. aureus (often MRSA); may be complicated by surrounding cellulitis/phlebitis

Answer 107

Abscesses/Furuncles/Carbuncles

Question 108

Inflamed and fluctuant nodule; arises on any site

Answer 108

Abscess

Question 109

Only occurs in a/w hair follicles/on hair-bearing sites (“FURuncle = FURry sites”); head/neck (#1 site) >intertriginous zones, thighs, other sites of friction

Answer 109

Furuncle

Question 110

Collection of furuncles, often deeper w/ multiple draining sinuses; most often affects thick skin of posterior neck, back, and thighs; systemic symptoms typically present

Answer 110

Carbuncle

Question 111

Most common cause of purulent infections presenting to ED; most commonly p/w furunculosis mistaken clinically for “spider bite”; may be a/w cellulitis, and necrotic plaques (>necrotizing fasciitis and toxic shock syndrome)

Answer 111

MRSA

Question 112

Pathogenesis: MRSA

Answer 112

Resistance because of mecA gene (encodes penicillin-binding protein, PBP2a) →↓affinity for β-lactams

Question 113

Pathogenesis: CA-MRSA

Answer 113

Also has Panton-Valentine leukocidin (PVL) virulence factor; a/w increased virulence, leading to more severe necrosis of skin and other tissues

Question 114

Most commonly infants/young children (low mortality, <5%) who lack neutralizing antibodies and have ↓renal clearance Also seen in adults w/ CRF (high mortality, >50%); M > F (2–4 : 1) p/w febrile prodrome, widespread skin tenderness; skin eruption begins on face (periorificial radial fissuring) and intertriginous zones → generalizes within 48 hours as wrinkled-appearing skin w/ flaccid bullae and (+)Nikolsky sign → desquamation continues for up to 1 week, then heals without scarring

Answer 114

Staphylococcal scalded skin syndrome (SSSS)

Question 115

Pathogenesis: Staphylococcal scalded skin syndrome (SSSS)

Answer 115

Infection by phage group II (types 55 and 71) S. aureus at a different/distant site → production of exfoliatoxins A & B (ETA, ETB)→exfoliatoxins disseminate via bloodstream→widespread cleavage of Dsg1 → subcorneal/intragranular acantholysis

Question 116

Histology: Staphylococcal scalded skin syndrome (SSSS)

Answer 116

Resembles P. foliaceus; lacks inflammatory cells and bacteria in blisters (vs bullous impetigo)

Question 117

Treatment: Staphylococcal scalded skin syndrome (SSSS)

Answer 117

Mild disease: β-lactamase resistant PCN (dicloxacillin) or first generation CSN (cephalexin) Severe disease: hospitalization + IV ABX

Question 118

T/F: Most common primary sites of infection in children = nasopharynx or conjunctivae

Answer 118

True

Question 119

Severe multisystem disease with cutaneous and internal involvement (renal > GI, MSK, CNS, hepatic, hematologic, and mucosal); typically affects young, healthy adults; occult primary site of infection; p/w high fever (>102°F) + rash + systemic symptoms + hypotension (100%)

Answer 119

Staphylococcal toxic shock syndrome (S-TSS)

Question 120

Menstrual TSS

Answer 120

<50% of cases; young women w/ superabsorbent tampons; mortality rate less than 5%

Question 121

Nonmenstrual TSS

Answer 121

>50%; M = F; a/w nasal packing, surgery, skin, or internal infections; mortality rate <20%

Question 122

Mucocutaneous eruption classically starts w/ scarlantiniform eruption (initially on trunk → becomes generalized), redness and edema of palms/soles, “red strawberry tongue,” conjunctival hyperemia → palmoplantar desquamation (1 to 3 weeks later), Beau’s lines, onychomadesis; usually negative blood cultures (<15% positive); low mortality

Answer 122

Staphylococcal toxic shock syndrome (S-TSS)

Question 123

Pathogenesis: Staphylococcal toxic shock syndrome (S-TSS)

Answer 123

Production of toxic shock syndrome toxin-1 (TSST-1) by certain strains of S. aureus → TSST-1 acts as superantigen, binding to Vβ region of TCR and class II MHC on APCs → nonspecific activation of T-cells + cytokine storm (↑TNF-α, IL-1, IL-6, TLR2, and TLR4)

Question 124

Treatment: Staphylococcal toxic shock syndrome (S-TSS)

Answer 124

β-lactamase resistant ABX, clindamycin (suppresses toxin production) +/− IVIG; IV fluids for hypotension

Question 125

T/F: Staph-TSS has lower mortality (3%–20% vs 30%–60%) vs Strep-TSS

Answer 125

True

Question 126

S. aureus infection of skeletal muscle; usually have predisposing factors (immunosuppression, diabetes, trauma, and IVDA); p/w 1 to 2 week febrile prodrome, muscle pain, and a soft tissue mass w/ surrounding woody induration → muscle abscess +/− septicemia

Answer 126

Pyomyositis

Question 127

Best diagnostic tool for S aureus Pyomyositis

Answer 127

MRI

Question 128

Deep granulomatous and suppurative infection most frequently caused by S. aureus; may extend to skeletal muscle and bone; affects all ages; a/w ↓T-cell counts and other defects in cellular immunity; 70% have skin-limited disease (rarely visceral in severely immunosuppressed patients; lung most common); p/w deep, ulcerative plaques/nodules with multiple draining sinuses that drain yellow granules

Answer 128

Botromycosis

Question 129

Histology: Botromycosis

Answer 129

Large granules w/ basophilic center (nonfilamentous bacteria) and eosinophilic/hyaline periphery (Splendore-Hoeppli phenomenon; comprised of IgG and C3 deposits), granules are surrounded by abscess and granulomatous inflammation; granules are PAS(+), Giemsa(+), and Gram(+)

Question 130

Treatment: Botromycosis

Answer 130

Surgical debridement + antistaphylococcal antibiotics

Question 131

Deep variant of impetigo; most common in children; caused by Streptococcus pyogenes; p/w few vesicopustules, most commonly on legs → develop into “punched-out” ulcers with purulent base and hemorrhagic crust → slowly self-resolves w/ scarring; frequently as a result of scratching bug bites

Answer 131

Ecthyma

Question 132

Histology: Ecthyma

Answer 132

Well-circumscribed ulcer w/ overlying impetiginized scale crust and dense underlying dermal neutrophilic inflammation

Question 133

Treatment: Ecthyma

Answer 133

β-lactamase resistant PCN (dicloxacillin) or first generation CSN (cephalexin)

Question 134

More superficial variant of cellulitis (upper-mid dermis vs deep dermis/SQ) with sharply defined (“ridge-like”) borders, fiery-red color, and pain or burning sensation; prominent lymphatic involvement; most common sites = lower extremity (#1 site) > face; lymphedema is major risk factor; caused by group A β-hemolytic strep

Answer 134

Erysipelas (“St. Anthony’s Fire”)

Question 135

Diagnosis: Erysipelas

Answer 135

Wound/blood cultures usually negative; best confirmatory tests = ↑DNase B and ASO titers

Question 136

Treatment: Erysipelas

Answer 136

Penicillin (treatment of choice) for 10 to 14 days; erythromycin if PCN-allergic

Question 137

Classically boys >4 years old; p/w sharply defined red plaques spreading up to 3 cm from anus; a/w pain upon defecation, blood in stool, guttate psoriasis outbreak Labs: skin culture confirmatory

Answer 137

Perianal streptococcal skin infection

Question 138

Treatment: Perianal streptococcal skin infection

Answer 138

Oral cefuroxime (treatment of choice) or penicillin (slightly less effective)

Question 139

Initially p/w darkening of skin of distal finger (>toe) volar fat pad → progresses to purulent vesicle/bulla on erythematous background within 1 week; affects children; as a result of picking of nose or local skin trauma; S. pyogenes > S. aureus

Answer 139

Blistering distal dactylitis

Question 140

Treatment: Blistering distal dactylitis

Answer 140

I&D + 10-day course oral β-lactam

Question 141

Affects young children (1–10 years old); caused by group A β-hemolytic streptococcus → produces streptococcal pyrogenic toxins A, B, and C (SPE-A, B, and C); most commonly in setting of streptococcal pharyngitis/tonsillitis; p/w sore throat, high fevers, and systemic symptoms → 1 to 2 days later, macular erythema on upper trunk/neck → soon develop classic “sandpaper-like” papular eruption, Pastia’s lines (linear petechiae; favors flexural sites), flushed cheeks with circumoral pallor, and “white strawberry tongue” (white background + red papillae) → later “red strawberry tongue,” purulent exudate from throat → 1 to 2 weeks later, palmoplantar desquamation

Answer 141

Scarlet Fever

Question 142

Treatment: Scarlet Fever

Answer 142

PCN (treatment of choice), amoxicillin, or erythromycin (if PCN allergic)

Question 143

Complications: Scarlet Fever

Answer 143

Acute glomerulonephritis | Rheumatic fever

Question 144

Affects young/healthy adults, is more severe w/ higher mortality (30%–60%), usually a/w florid skin/soft-tissue infections (often necrotizing fasciitis vs occult infections in Staph-TSS), much less frequent generalized macular erythematous rash, and far more frequent blood culture positivity (>50%)

Answer 144

Streptococcal toxic shock syndrome

Question 145

Most common primary source of Streptococcal toxic shock syndrome

Answer 145

Skin infection from skin barrier breakdown (excoriation, bug bite, and infected surgical site)

Question 146

Classically p/w severe localized pain in extremity w/ redness, swelling or necrotizing fasciitis → within 24 to 48 hours, systemic symptoms (hypotension [100%])

Answer 146

Streptococcal toxic shock syndrome

Question 147

Pathogenesis: Streptococcal toxic shock syndrome

Answer 147

Group A β-hemolytic strep (M types 1 and 3) produce various toxins: SPE A, B, and C Streptococcal mitogenic toxin Z (SMEZ) Streptolysin O Toxins act as superantigens, binding to Vβ region of TCR and class II MHC on APCs → nonspecific activation of T-cells + cytokine storm (↑TNF-α, IL-1, IL-6, TLR2, and TLR4)

Question 148

Treatment: Streptococcal toxic shock syndrome

Answer 148

Most cases severe, requiring hospitalization + surgical debridement of soft-tissue infection (possibly fasciotomy or amputation) + clindamycin (inhibits toxin production) + PCN +/− IVIG

Question 149

Infection of deep dermis/SQ most commonly affecting adults w/ skin barrier disruption; p/w tender/red/warm, ill-defined plaques w/ fever/chills/lymphangitis, in severe cases, may see necrosis, bullae, vesicles; most commonly caused by group A β-hemolytic strep > S. aureus (most common cause in children); most common sites: head/neck (children), lower extremities (adults), and IV injection sites on arms (IVDA)

Answer 149

Cellulitis

Question 150

Treatment: Cellulitis

Answer 150

Uncomplicated cases: oral dicloxacillin, cephalexin, or clindamycin for 10 days (must empirically cover for Staph and Strep) Cellulitis a/w diabetic/decubitus ulcers: piperacillin/tazobactam, or ciprofloxacin + metronidazole Severe cases: hospitalize and IV antibiotics MRSA cellulitis: TMP/SMX, minocycline/doxycycline, and clindamycin

Question 151

Rapidly progressive, life-threatening (up to 50% mortality) necrotizing infection of skin, SQ, and fascia; most common site = extremities (>trunk); caused by group A β-hemolytic strep M types 1 and 3 (#1 cause in children) or polymicrobial (#1 cause in adults; mixture of Streptococci, S. aureus, E. coli, Clostridium, and Bacteroides)

Answer 151

Necrotizing fasciitis

Question 152

Initially p/w severely painful indurated/”woody” plaque (“pain out of proportion to visible skin changes”) → over 1 to 2 days and rapidly progresses → color changes from erythematous → dusky purple/gray +/− hemorrhagic bullae/ulceration, crepitus, foul-smelling discharge; patients always severely toxic-appearing (fever, tachycardia, and septic shock) → late in course and skin becomes anesthetic (nerves destroyed)

Answer 152

Necrotizing fasciitis

Question 153

Necrotizing fasciitis of genitalia/perineum/lower abdominal wall

Answer 153

Fournier’s gangrene

Question 154

Polymicrobial Necrotizing fasciitis arising as a postoperative complication

Answer 154

Meleney’s gangrene

Question 155

Treatment: Necrotizing fasciitis

Answer 155

Fasciotomy + IV abx (piperacillin/tazobactam + clindamycin + ciprofloxacin)

Question 156

Risk factors: Necrotizing fasciitis

Answer 156

``` Diabetes Immunosuppression PVD CRF Trauma IVDA Recent surgery ```

Question 157

Prognostic factors a/w ↑mortality: Necrotizing fasciitis

Answer 157

``` Older age ↑time to first debridement ↑extent of infection Females ↑lactic acid ↑creatinine ```

Question 158

Caused by C. minutissimum (Gram(+) filamentous rod) Affects stratum corneum of moist, intertriginous zones (groin and toe webs (particularly fourth) > axillae, inframammary, umbilicus, and intergluteal) Fluoresces “coral red” w/ Wood lamp (bacterial coproporphyrin III production) Groin: light red-pink slightly scaly patches w/ thin scale Toe webs: chronic, asymptomatic fissuring and maceration Histology: filamentous Gram(+) rods within stratum corneum

Answer 158

Erythrasma

Question 159

Treatment: Erythrasma

Answer 159

Localized: 20% aluminum chloride, topical clindamycin/erythromycin Widespread/recalcitrant: oral erythromycin and tetracyclines

Question 160

Caused by Kytococcus sedentarius, which digests keratin in stratum corneum Noninflammatory infection of weight-bearing areas of plantar (>palmar) skin p/w small crateriform pits and foul odor → may coalesce into arciform pits RFs: hyperhidrosis and occlusion Histology: sharply demarcated, deep pits in stratum corneum with Gram(+) bacteria at base of pits

Answer 160

Pitted Keratolysis

Question 161

Treatment: Pitted Keratolysis

Answer 161

Topical erythromycin (or clindamycin, mupirocin, and azole antifungals) +/− 20% aluminum chloride, or botulinum toxin for hyperhidrosis

Question 162

Asymptomatic, adherent yellow-red concretions on axillary hair shafts; fluoresces with Wood lamp; caused by Corynebacterium tenuis

Answer 162

Trichomycosis axillaris

Question 163

Treatment: Trichomycosis axillaris

Answer 163

Shaving of axillary hair (treatment of choice); may use topical erythromycin/clindamycin

Question 164

Very rapid, potentially fatal necrotizing soft tissue infection with localized gas production (“gas gangrene”); caused by Clostridium perfringens (Gram(+), spore-forming rod) - obligate anaerobe (only reproduces in hypoxic tissues)

Answer 164

Clostridial anaerobic cellulitis and myonecrosis

Question 165

Due to traumatic inoculation (surgery or crush/penetrating injuries) of C. perfringens into oxygen-poor deep tissues; bacteria produces two pathogenic toxins: α-toxin (cleaves lipids) and perfringolysin (induces vascular clots and worsens tissue hypoxia) → bacteria proliferates freely in anaerobic environment, producing CO2 and cleaving lipids → clinically p/w crepitus, foul-smelling brown exudate (“dirty dishwater” color), w/ variable skin changes RFs: diabetes, PVD

Answer 165

Clostridial anaerobic cellulitis and myonecrosis

Question 166

Treatment: Clostridial anaerobic cellulitis and myonecrosis

Answer 166

Immediate aggressive surgical debridement (most important) + clindamycin and third gen CSN +/− hyperbaric oxygen

Question 167

Agent: Actinomycosis

Answer 167

Actinomyces israelii

Question 168

Caused by gram(+), nonacid fast, and anaerobic/microaerophilic filamentous bacteria which are part of normal flora of mouth, GI/GU tracts → infection arises after trauma (dental procedures or surgical interventions); subacute-chronic granulomatous lesions with suppurating abscesses + sinus tracts

Answer 168

Actinomycosis

Question 169

Most common form of Actinomycosis, accounts for 70%): “lumpy jaw disease,” red-brown nodules with fistulous abscesses draining characteristic yellow sulfur

Answer 169

Cervicofacial Actinomycosis

Question 170

Histology: Actinomycosis

Answer 170

Dense granulomatous and suppurative inflammation with “granules” with basophilic center (Gram(+) branching filaments of Actinomyces) and eosinophilic rim (Splendore-Hoeppli phenomenon)

Question 171

Treatment: Actinomycosis

Answer 171

Penicillin G or ampicillin Chronic or deep-seated infections: 2 to 6 weeks of IV abx followed by 3 to 12 months of oral PCN Acute infections: 2 to 3 weeks of oral PCN + I&D of abscesses + surgical excision of sinus tracts

Question 172

Half of all cases are caused by the Gram(+), weakly acid-fast, filamentous bacteria; traumatic inoculation causes a painless nodule that enlarges, suppurates, and drains via the sinus tracts; purulent discharge contains sulfur granules; foot is the usual site of involvement but may involve underlying muscle and bone

Answer 172

Nocardiosis

Question 173

Histology: Nocardiosis

Answer 173

Intense neutrophilic infiltrate + sulfur granules (only seen in actinomycotic mycetoma form); branching filaments are Gram(+), AFB+ (Fite > Ziehl-Neelsen), and GMS+

Question 174

Treatment: Nocardiosis

Answer 174

Sulfonamides (treatment of choice) +/− surgical drainage

Question 175

Agent: Bacillus anthracis - Gram(+), spore-forming rod

Answer 175

Anthrax

Question 176

Arises via occupational exposure (“Woolsorter’s disease”) from direct contact w/ infected animals/carcasses and presents 1 week postexposure with purpuric papulovesicle (“malignant pustule”) that drains serosanguinous fluid → vesicle ulcerates to form painless/black/necrotic eschar w/ satellite vesicles and edema; most common and least lethal form

Answer 176

Cutaneous anthrax

Question 177

Treatment: Anthrax

Answer 177

First line (cutaneous anthrax): quinolone or doxycycline ×2 weeks (treat for 60 days if suspect bioterrorism or possible inhalation exposure)

Question 178

Virulence factors: Anthrax

Answer 178

1. Poly-D-glutamic acid capsule (resists phagocytosis) 2. Lethal toxin = protective antigen + lethal factor (↑TNF-α and IL-1β → septic shock, death) 3. Edema toxin = protective antigen + edema factor (↑cAMP → edema)

Question 179

Acute, self-limited infection; occupational disease of fisherman or poultry/fish handlers; as a result of traumatic inoculation of Erysipelothrix rhusiopathiae (Gram(+) rod); most commonly p/w localized form: red-violaceous nonsuppurative cellulitis +/− hemorrhagic vesicles; classically affects finger web spaces w/ sparing of terminal phalanges

Answer 179

Erysipeloid

Question 180

Treatment: Erysipeloid

Answer 180

Penicillin (treatment of choice), ciprofloxacin (if PCN allergic)

Question 181

Most commonly affects pregnant women, elderly, and the immunosuppressed as GI illness caused by the ingestion of Listeria monocytogenes (motile Gram(+) rod) → fever, bacteremia, and meningitis; rarely see skin lesions – mostly occurs in setting of neonatal septicemia (from vertical transmission), which p/w disseminated papules/pustules/vesicles

Answer 181

Listeria

Question 182

Treatment: Listeria

Answer 182

First line: ampicillin | Second line: TMP/SMX

Question 183

Green/blue-black nail discoloration; a/w excessive water exposure, nail trauma; from P.aeuruginosa pyocyanin pigment production

Answer 183

Green nail syndrome

Question 184

Treatment: Green nail syndrome

Answer 184

Topical quinolone, vinegar soaks, or aminoglycoside solution × 4 months

Question 185

Superficial erosive infection w/ blue-green purulent exudate, “moth-eaten” appearance to skin surface, with “mousy” or “grape-like” odor; may arise at burn sites, in mixed toe web infections, and other chronic wounds

Answer 185

Pseudomonal pyoderma

Question 186

Treatment: Pseudomonal pyoderma

Answer 186

Systemic antipseudomonal antibiotics, topical antiseptics, debridement, and drying agents

Question 187

P. aeuruginosa infection of external auditory canal; p/w edema, skin maceration, and purulent green exudate; tympanic membrane intact; classically severe pain upon pinna manipulation

Answer 187

Otitis externa (“swimmer’s ear”)

Question 188

Severe variant of otitis externa usually only in diabetics or immunosuppressed; persistent drainage w/ excessive granulation tissue extending to bony portion of ear → may result in osteomyelitis of skull base

Answer 188

Malignant otitis externa

Question 189

Self-resolving P. aeuruginosa infection arising from poorly chlorinated hot tubs/whirlpools; p/w red, perifollicular papulopustules 1 to 2 days postexposure; commonly affects areas covered by bathing suit; spontaneously resolves within 2 weeks

Answer 189

Pseudomonal folliculitis (“hot tub folliculitis”)

Question 190

Self-resolving P. aeuruginosa infection arising from wading in pools w/ high concentrations of Pseudomonas; p/w painful, red-violaceous plaques/nodules on weight-bearing areas of plantar surface Histology: identical to idiopathic palmoplantar hidradenitis

Answer 190

Pseudomonas hot-foot syndrome

Question 191

Cutaneous lesion indicative of P. aeuruginosa septicemia; most commonly occurs in immunosuppressed patients w/ severe neutropenia (often BMT patients); p/w a small number of purpuric macules → progresses to hemorrhagic bullae → bullae rupture → ulcer w/ necrotic black eschar and tender, red skin surrounding eschar; most common sites = anogenital region and extremities Histology: sharply demarcated epidermal necrosis w/ hemorrhagic crust, and underlying dermal infarction w/ septic vasculitis (Gram(-) rods in vessel walls)

Answer 191

Ecthyma Gangrenosum

Question 192

Treatment: Ecthyma Gangrenosum

Answer 192

IV aminoglycoside + antipseudomonal PCN

Question 193

Prognostic factors a/w poor outcome in Ecthyma Gangrenosum

Answer 193

↑# lesions Delay in diagnosis Prolonged neutropenia

Question 194

Small, facultative intracellular Gram(-) bacilli that cause that can cause cat scratch disease, bacillary angiomatosis, peliosis hepatitis, trench fever, and Carrion’s disease/Oroya fever/verruga peruana

Answer 194

Bartonella

Question 195

Bartonellosis (Carrion’s disease, Oroya fever, and verruga peruana)

Answer 195

Bartonella bacilliformis

Question 196

Vector: Bartonellosis

Answer 196

Phlebotomine sand fly (Lutzomyia verrucarum)

Question 197

Reservoir/host: Bartonellosis

Answer 197

Human

Question 198

Treatment: Oroya fever (acute phase)

Answer 198

1st line - Chloramphenicol* plus β-lactam antibiotic Quinolone (norfloxacin and ciprofloxacin) (>6 years of age and not pregnant) 2nd line - Trimethoprim–sulfamethoxazole Macrolide Doxycycline

Question 199

Treatment: Verruga peruana (chronic phase)

Answer 199

1st line - Rifampin + streptomycin (traditional) | 2nd line - Ciprofloxacin Azithromycin

Question 200

Cat scratch disease

Answer 200

Bartonella henselae

Question 201

Vector: Cat scratch disease

Answer 201

Cat flea (Ctenocephalides felis)

Question 202

Reservoir/host: Cat scratch disease

Answer 202

Cat

Question 203

Treatment: Cat scratch disease

Answer 203

Mild to moderate, uncomplicated - Supportive care (analgesics) only Azithromycin Doxycycline plus rifampin Azithromycin (2nd line) Severe, complicated - Doxycycline plus rifampin

Question 204

Bacillary angiomatosis

Answer 204

Bartonella henselae | Bartonella quintana

Question 205

Trench fever “Five day fever” | “Urban trench fever”

Answer 205

Bartonella quintana

Question 206

Vector: Trench fever

Answer 206

Human body louse (Pediculosis humanus)

Question 207

Reservoir/host: Trench fever

Answer 207

Human

Question 208

Treatment: Trench fever

Answer 208

Doxycycline plus aminoglycoside

Question 209

Mostly occurs in HIV + patients w/ CD4 count <200; only 20% recall cat bite/scratch (vs 90% w/ cat scratch disease); vascular proliferation caused by bacterial angiogenic factor; can involve lymph nodes, bone, and viscera; lesions are dome-shaped, vascular papulonodules but more developed lesions can have a friable eroded appearance, resembling pyogenic granulomas

Answer 209

Bacillary angiomatosis

Question 210

Histopathology: resembles pyogenic granuloma (lobular capillary proliferation), but has dense neutrophilic infiltrate, and extra- and intracellular organisms (within endothelial cells) seen w/ Warthin-Starry stain

Answer 210

Verruga peruana | Bacillary angiomatosis

Question 211

Small, obligate intracellular Gram(-) organisms; transmitted by arthropod host/vector (ticks, fleas, lice, and mites); target = endothelial cells

Answer 211

Rickettsia

Question 212

Transmitted from arthropod (tick, flea, mite, and louse) via saliva or feces → bacteria enter dermis via bite or scratching → bacteria attach to endothelial cells → spread hematogenously and destroy infected vessels via reactive oxygen species formation → ↑vascular permeability → vascular skin findings (petechiae, purpura, and vasculitis = “spotted fever”) and life-threatening end organ damage (meningoencephalitis and pulmonary edema/pneumonitis most important causes of mortality), thrombocytopenia, hypovolemia, and hypotension

Answer 212

Rickettsia

Question 213

Gram(-) diplococcus (strains A, B, C, Y, and W-135); Most commonly affects children/young adults living in close quarters (military recruits and college students); M > F (4 : 1); humans are only reservoir; 10% to 15% population are asymptomatic carriers (in nasopharynx); disease transmitted via respiratory secretions

Answer 213

Neisseria meningitidis

Question 214

1 to 10 days postexposure, p/w fever, chills, headache, petechial rash (30%–50%), retiform purpura w/ classic “gunmetal gray” color, or hemorrhagic bullae on legs and trunk; may progress to septic shock with DIC (purpura fulminans)

Answer 214

Acute meningococcemia

Question 215

Less common; p/w recurrent fevers, arthralgias, and macular/papular eruption; condition self-resolves, only to recur days to weeks later

Answer 215

Chronic meningococcemia

Question 216

Treatment: Meningococcemia

Answer 216

First line: high-dose IV penicillin (treatment of choice) Second line: quinolones or chloramphenicol (if PCN-allergic); third generation CSN (resistant disease) Prophylactically treat all close contacts w/ ciprofloxacin, rifampin, azithromycin

Question 217

Main virulence factor of Meningococcemia

Answer 217

Polysaccharide capsule

Question 218

Caused by Gram(-) coccobacillus, Brucella spp.; endemic in Middle East (consuming unpasteurized goat milk/cheese). In the United States, occupational disease (farmers, butchers, and veterinarians) from direct contact or inhalationvp/w undulating fevers, arthralgias, lymphadenopathy, hepatosplenomegaly, and rare (<10%) skin findings (disseminated violaceous papules, EN)

Answer 218

Brucellosis (Malta fever, “undulant fever”)

Question 219

Treatment: Brucellosis

Answer 219

Multidrug regimens of doxycycline + other antibiotics (streptomycin, rifampin, TMP/SMX, quinolones, and aminoglycosides)

Question 220

Gram(-) bacillus, Burkholderia mallei caused by contact w/ infected horses or donkeys

Answer 220

Glanders

Question 221

Forms: Glanders

Answer 221

Localized—hemorrhagic, ulcerative papulopustule at inoculation site Chronic—multiple soft tissue nodules (“farcy buds”) on skin overlying lymphatics Septicemic form—mortality rate >95% without treatment and 50% w/ treatment Pulmonary form—mortality similar to septicemic form

Question 222

Treatment: Glanders

Answer 222

Localized disease: 60- to 150-day course of amoxicillin/clavulanate, doxycycline, or TMP/SMX Septicemic: IV carbapenems + ciprofloxacin or doxycycline

Question 223

Gram(-) bacillus Burkholderia pseudomallei caused by direct contact w/ contaminated water or soil RFs: diabetes, alcoholism, immunosuppression, and IVDA Clinical presentation and mortality rates ~same as glanders

Answer 223

Melioidosis

Question 224

Chronic granulomatous infection as a result of the inability of macrophages to kill phagocytosed E. coli Most commonly affects immunosuppressed (BMT > HIV/AIDS) Most commonly affects GU tract; may affect skin of perianal/genital region (ulcerated abscesses and soft polypoid lesions)

Answer 224

Malakoplakia (malacoplakia)

Question 225

Histology: dense granulomatous infiltrate comprised of von Hansemann cells (large macrophages w/ eosinophilic cytoplasm) containing Michaelis-Gutmann bodies (round, laminated, calcified basophilic intracytoplasmic inclusions; comprised of incompletely killed bacteria within calcified phagolysosomes; stain w/ von Kossa, PAS, Perls, Giemsa)

Answer 225

Malakoplakia (malacoplakia)

Question 226

Treatment: Malakoplakia (malacoplakia)

Answer 226

Localized: surgical excision | Nonsurgical candidates: difficult to treat; may try long courses of ciprofloxacin, TMP/SMX, or clofazimine

Question 227

Gram(-) coccobacillus, Francisella tularensis transmitted through contact w/ rabbit carcasses (classic!), deer flies, and ticks; increased risk in hunters and animal handlers; most common presentation is ulceroglandular = 80% which p/w necrotic, punched-out ulcer at inoculation site w/ suppurative lymphadenopathy

Answer 227

Tularemia (rabbit fever and deer fly fever)

Question 228

Treatment: Tularemia

Answer 228

Streptomycin (treatment of choice)

Question 229

Gram(-) coccobacillus which classically affects infants, p/w deep red-violaceous/blue facial cellulitis (most commonly periorbital or buccal) following a URI-like illness; usually positive blood cultures

Answer 229

H. influenzae cellulitis

Question 230

Treatment: H. influenzae cellulitis

Answer 230

Third generation CSN

Question 231

Chronic granulomatous infection of nose and upper respiratory tract which affects adults, mainly in tropical locations; transmitted by inhalation of Klebsiella rhinoscleromatis; a/w cellular immune defects: inability of macrophages to kill phagocytosed bacteria → Mikulicz cells (large, vacuolated histiocytes containing bacteria)

Answer 231

Rhinoscleroma

Question 232

Three clinical phases: Rhinoscleroma

Answer 232

1. Catarrhal phase (rhinitis, obstruction from soft tissue edema) 2. Granulomatous/infiltrative phase (granulomatous nodules in nose/URT, epistaxis, dysphonia, anesthesia of soft palate, and Hebra nose) 3. Sclerotic phase (extensive scarring requires tracheotomy and nasal reconstruction)

Question 233

Histology: dense pan-dermal infiltrate of Mikulicz cells containing bacteria (seen w/ Warthin-Starry, Giemsa) and Russell bodies

Answer 233

Rhinoscleroma

Question 234

Treatment: Rhinoscleroma

Answer 234

Tetracycline (treatment of choice) for 6 months along with surgical correction of airway; ciprofloxacin is second line

Question 235

Enteric infection caused by Salmonella typhi; spread by direct contact w/ infected individuals or carriers; p/w fever, nausea/vomiting, diarrhea, headache, and characteristic “rose spots” of skin (2- to 8-mm pink, grouped papules on trunk); bacteria can be cultured from rose spots

Answer 235

Salmonellosis (typhoid fever)

Question 236

Treatment: Salmonellosis (typhoid fever)

Answer 236

Quinolones (treatment of choice); use third gen CSN in children

Question 237

Caused by Streptobacillus moniliformis as a result of a rat bite (“rat bite fever”), or occasionally, ingestion of contaminated food (“Haverhill fever”); ↑incidence in urban areas w/ high rat concentration; p/w redness, edema, and ulceration at bite site → paroxysmal fever w/ systemic symptoms → 2 to 4 days later, migratory polyarthritis + acral eruption (palms and soles most common) of petechial red macules/papules, vesicles, or pustules; up to 15% mortality

Answer 237

Rat-bite fever (“Haverhill fever”)

Question 238

Treatment: Rat-bite fever (“Haverhill fever”)

Answer 238

Penicillin (treatment of choice) for 1 week (6 weeks if septicemic)

Question 239

Classic triad of Rat-bite fever (“Haverhill fever”)

Answer 239

1. paroxysmal fever 2. migratory polyarthritis 3. acral rash

Question 240

Caused by Yersinia pestis, a Gram(-) bipolar bacillus with characteristic “safety pin” appearance of bacteria on gram or Giemsa stain

Answer 240

Plague

Question 241

Present with pustule or ulcer at inoculation site (10%) + painful, suppurative regional lymphadenopathy = “buboes” (groin, axillae most common); 25% to 50% mortality rate if untreated; most common form

Answer 241

Bubonic Plague

Question 242

Treatment: Plague

Answer 242

First line: aminoglycosides (streptomycin and gentamicin) Plague meningoencephalitis: chloramphenicol (high penetration of blood-brain barrier) Postexposure prophylaxis: doxycycline or ciprofloxacin ×7 days (highly effective)

Question 243

Most commonly affects men >40 years old who have predisposing factors: liver disease (hemochromatosis, cirrhosis, or alcoholism), diabetes (peripheral neuropathy/vasculopathy predisposes to wound infections), GI disease, immunosuppression, and ESRD Reservoir = shellfish

Answer 243

Vibrio vulnificus

Question 244

Two modes of infection: Vibrio vulnificus

Answer 244

1. Cutaneous exposure to contaminated seawater/shellfish: affects shellfish handlers; trauma → primary skin infection, or superinfection of preexisting wound → may progress to necrotizing fasciitis, myositis, or septicemia 2 .Consumption of raw/undercooked shellfish: most commonly from raw oysters; septicemia, abdominal cramps, and hypotension; 75% have skin findings – red-purple macules/vesicles → progress to hemorrhagic bullae and necrotic plaques

Question 245

Treatment: Vibrio vulnificus

Answer 245

Doxycycline + third gen CSN

Question 246

Dog bite

Answer 246

Pasteurella multocida, Pasteurella canis, or Capnocytophaga canimorsus (potentially fatal in asplenic or immunosuppressed patients)

Question 247

Cat bite

Answer 247

Pasteurella multocida >Streptococcal spp.

Question 248

Human bite

Answer 248

Eikenella corrodens (a/w chronic infections), S. aureus (a/w severe infections), Peptostreptococcus, Enterococcus, and Bacteroides

Question 249

Treatment: Bite-induced infections

Answer 249

Amoxicillin/clavulanate (treatment of choice)

Question 250

Pathogenesis: Lyme disease

Answer 250

Ixodes tick feeds on infected animal reservoir → spirochetes stored in tick’s salivary glands → tick bites human and releases Borrelia spirochetes into dermis → erythema migrans develops at bite site 1 to 2 weeks later → if untreated, hematogenous dissemination + systemic symptoms

Question 251

Three clinical stages of Lyme disease

Answer 251

1. Early localized 2. Early disseminated 3. Chronic

Question 252

Initial cutaneous manifestation; develops 7 to 14 days posttick attachment; p/w expanding annular plaque w/ central clearing (“bull’s eye” appearance) → reaches >5 cm diameter; favors trunk (#1 site in children), legs (#1 site in adults), and intertriginous areas; lesion self-resolves in 4 weeks if untreated

Answer 252

Erythema migrant

Question 253

Multiple smaller annular lesions; arise days to weeks after primary erythema migrans lesion

Answer 253

Disseminated erythema migrans

Question 254

Strongly a/w B. afzelii and B. garinii; p/w firm, plum-colored tender nodule/plaque on earlobes (children), or nipple/areola (adults)

Answer 254

Borrelial lymphocytoma

Question 255

Strongly a/w B. afzelii and B. garinii; occurs months to years after initial infection; two clinical phases: erythematous plaques with “doughy”/swollen skin on distal extremities (early phase; easily treated/reversible) → progresses to atrophic “cigarette-paper” skin w/ telangiectasias (chronic phase; recalcitrant to treatment) and subcutaneous fibrous nodules overlying joints

Answer 255

Acrodermatitis chronica atrophicans

Question 256

Treatment: Lyme disease

Answer 256

First line: doxycycline | In pregnancy or children <8 years old → amoxicillin is treatment of choice

Question 257

T/F: Tick must be attached for >24 hours to transmit Lyme

Answer 257

True

Question 258

Yaws

Answer 258

T. pallidum pertenue

Question 259

Pinta

Answer 259

T. pallidum carateum

Question 260

Endemic Syphilis/“Bejel”

Answer 260

T. pallidum endemicum

Question 261

1° stage: legs most commonly affected; p/w indurated, red, painless papule that enlarges to 1–5 cm, then ulcerates (“Mother”); occurs at site of inoculation; may have hypomelanotic macules on dorsal wrists/hands 2° stage: multiple smaller widespread “daughter” 3° stage: necrotic and ulcerative abscesses that heal with severe/deforming scars + bony damage

Answer 261

Yaws

Question 262

Skin-only disease 1° stage: legs most commonly affected; p/w papules surrounded by red halo; enlarges over months up to 12 cm 2° stage: smaller scaly papules and psoriasiform plaques erupt (“pintids”) and change in color from red → blue → brown → gray/black 3° stage: symmetric vitiligo-like lesions over bony prominences w/atrophic epidermis. Histology shows lichenoid interface + complete loss of melanocytes + epidermal atrophy

Answer 262

Pinta

Question 263

1° stage: rarely noticed; p/w inconspicuous papule or ulcer in mouth or on nipples of breastfeeding women; may have hypomelanotic macules on extremities, genitalia, areolae, and trunk 2° stage: mucous membrane lesions (mucosal patches, condyloma lata, and angular stomatitis) + generalized lymphadenopathy +/− skin lesions 3° stage: Gumma formation of mucous membranes, skin, and bones

Answer 263

Endemic Syphilis/“Bejel”

Question 264

Treatment: Nonvenereal (endemic) treponematoses

Answer 264

Benzathine PCN

Question 265

Early congenital (<2 years old) syphilis

Answer 265

``` Snuffles Dactylitis Parrot’s pseudoparalysis Epiphysitis Hepatitis ```

Question 266

Late congenital (>2 years old) syphilis

Answer 266

keratitis, mulberry molars, Hutchinson’s teeth (notched/peg-shaped incisors), rhagades (linear scars at angles of mouth) saddle nose, Higoumenakis syndrome, Clutton’s joints, optic atrophy, corneal opacities, and eighth nerve deafness

Question 267

Incubation: Primary chancre

Answer 267

10-90 days

Question 268

Painless, well-defined, and indurated ulcer) w/ enlarged lymph nodes

Answer 268

Primary syphilis

Question 269

Prodromal signs (e.g., malaise, fever, lymph node enlargement, and arthralgia) Papulosquamous/maculopapular generalized rash (“copper colored”) w/ papules/plaques on palms/soles “Moth eaten” alopecia Split papules (syphilitic perlèche) Mucous patches in oropharynx (condyloma lata-like lesions of the mouth) Hypopigmented macules on neck (“necklace of Venus”) Condyloma lata

Answer 269

Secondary syphilis

Question 270

``` Gummas (skin, bones, liver, and organs) Cardiovascular syphilis (e.g. aortitis) Neurosyphilis (e.g., paresis, meningitis, ataxia, tabes dorsalis, optic atrophy, gummas, and Argyll-Robertson pupil (accommodates to light, but does not react) ```

Answer 270

Tertiary syphilis

Question 271

Treatment: Syphilis

Answer 271

IM benzathine PCN (2.4M IU ×1 dose for primary/secondary/early latent disease; 7.2M IU total for late latent disease)

Question 272

Most sensitive and specific tests for Syphilis

Answer 272

FTA-ABS and MHA-TP

Question 273

First serologic test to become positive for Syphilis (within 1-2 weeks)

Answer 273

RPR and VDRL

Question 274

Used to monitor response to therapy as titers decrease and then become negative after successful treatment

Answer 274

RPR and VDRL

Question 275

Stain identifies spirochetes

Answer 275

Warthin-Starry

Question 276

Overall most sensitive and specific test for diagnosis of primary syphilis

Answer 276

Positive darkfield examination

Question 277

Histology: slender, elongated psoriasiform epidermal hyperplasia + lichenoid interface changes + “dirty” dermal inflammatory infiltrate (neutrophils, cell debris, and abundant plasma cells)

Answer 277

Secondary syphilis

Question 278

Chancroid

Answer 278

Hemophilus ducreyi (Gram(-) coccobacilli)

Question 279

Painful, purulent ulcers with ragged/undermined borders and fibrinous base (may get ’kissing ulcers’ from apposition of skin with initial ulcer) Prepuce/coronal sulcus/frenulum are common sites Painful inguinal lymphadenitis (40%)

Answer 279

Chancroid

Question 280

Treatment: Chancroid

Answer 280

Azithromycin 1 gm PO × 1 dose

Question 281

Gonorrhea

Answer 281

Neisseria gonorrhoeae (Gram (-) diplococci)

Question 282

Most findings are not cutaneous, but can get hemorrhagic acral pustules w/arthritis (of larger joints), and fever (arthritis-dermatosis syndrome) if hematogenous dissemination occurs

Answer 282

Gonorrhea

Question 283

Treatment: Gonorrhea

Answer 283

Dual therapy: Ceftriaxone 250 mg IM ×1 dose + Azithromycin 1 gm PO × 1 dose

Question 284

Lymphogranuloma venereum

Answer 284

Chlamydia trachomatis (serotypes L1–3)

Question 285

``` Stage 1 (after 3–12d incubation period): painless ulcer which resolves (transient) +/− lymphangitis Stage 2 (10–30 days, up to 6 months after stage 1): buboes (unilateral, painful, erythematous, and enlarged inguinal lymph nodes) w/ ’groove sign’ (enlarged nodes above and below Poupart ligament); buboes may rupture → pus drainage and sinus tracts Stage 3 (months-years after stage 2; aka ano-genito-rectal syndrome): proctocolitis w/ perirectal abscesses, fistulas, strictures/stenoses, and ’lymphorrhoids’ (perirectal/intestinal lymphatic hyperplasia) ```

Answer 285

Lymphogranuloma venereum

Question 286

Treatment: Lymphogranuloma venereum

Answer 286

Doxycycline 100 mg PO BID × 21 days

Question 287

Granuloma inguinale

Answer 287

Klebsiella granulomatis (Gram-negative bacillus)

Question 288

Enlarging chronic painless ulcer with ’beefy red,’ friable, hypertrophic granulation tissue (avg incubation = 17 days) Get ’pseudobuboes’ (nodules), genital swelling, and secondary infections (→ bad odor) Most common sites: prepuce/glans/frenulum/coronal sulcus (men); vulvar area (women) May get extragenital lesions as a result of dissemination or autoinoculation (skin, bones, oral, and abdominal)

Answer 288

Granuloma inguinale

Question 289

Treatment: Granuloma inguinale

Answer 289

Azithromycin 1 gm PO once weekly (or 500 mg daily) for at least 3 weeks AND until all lesions have resolved

Question 290

Safety pin’ Donovan bodies on Wright or Giemsa stain of smears

Answer 290

Granuloma inguinale

Question 291

’Gamma-Favre bodies’ in macrophages on Giemsa stain

Answer 291

Lymphogranuloma venereum

Question 292

Culture for Neisseria gonnorheae

Answer 292

Thayer-Martin media

Question 293

'School of fish’ sign on Giemsa stain of exudate smear

Answer 293

Chancre

Question 294

Acid-fast, alcohol-fast, aerobic bacillus, and ↑risk in HIV

Answer 294

Mycobacterium tuberculosis

Question 295

Test better for patients who have had BCG (live, attenuated M. bovis) vaccination (false (+) with skin test)

Answer 295

Interferon-γ release assays (QuantiFERON® Gold)

Question 296

In patients w/o previous infection (hence no immunity against TB); 2 to 4 week inoculation period; painless, red, and indurated papule that ulcerates – heals after 3 to 12 months; may spread to lymph nodes

Answer 296

Tuberculous chancre

Question 297

Reinfection via inoculation, in patients w/ previous infection w/ moderate-to-high immunity; #1 form of cutaneous TB; warty/verrucous, growing papule may heal over years

Answer 297

Tuberculosis verruca cutis

Question 298

Contiguous spread or hematogenous/lymphatic; red-brown, sometimes annular, papules/plaques (with “apple jelly” color on diascopy) that → scarring centrally; head/neck #1 site; moderate-to-high immunity

Answer 298

Lupus vulgaris

Question 299

Result of contiguous spread of infection to skin from underlying disease (usually cervical lymph nodes and bones); fluctuant nodules that develop sinus tracts, draining to skin, with tethered appearance; low immunity

Answer 299

Scrofuloderma

Question 300

Patients with advanced TB and poor cell-mediated immunity; autoinoculation of mucosa/skin close to anatomic orifice draining active systemic TB infection → ulceration/drainage

Answer 300

Orificial tuberculosis

Question 301

Hematogenous dissemination from lung, most often in immunosuppressed pts; pinpoint blue-red crusty papules → small scars

Answer 301

Acute miliary tuberculosis

Question 302

Hematogenous dissemination → deep nodule that ulcerates/drains; immunosuppressed pts

Answer 302

Tuberculous gumma

Question 303

Obligate intracellular, weakly acid-fast bacillus that parasitizes macrophages and Schwann cells which requires cool temperatures (30°C–35°C) for growth → predilection for cooler areas of skin (nose, testes, and ear lobes) and peripheral nerves that lie close to skin surface; transmitted primarily by nasal/oral droplets; also 9-banded armadillos in the southeast United States; cannot be cultured in vitro → must be cultivated in mouse footpads or in armadillos

Answer 303

Mycobacterium leprae

Question 304

Chronic, deforming disease characterized by skin and nerve involvement; characterized by granulomas and neurotropism, both within skin and peripheral nerves

Answer 304

Leprosy (Hansen’s disease)

Question 305

Incubation period of Leprosy (Hansen’s disease)

Answer 305

Average 4–10 years, but up to 30 years

Question 306

T/F: Peripheral nerves are enlarged in all forms

Answer 306

False | except Indeterminate

Question 307

Earliest stage of leprosy p/w solitary, ill-defined hypopigmented macule, without enlargement of peripheral nerves; disease will either self-resolve, or evolve into one of five leprosy forms (LL, BL, BB, BT, or TT)

Answer 307

Indeterminate leprosy

Question 308

Result of change in cell-mediated (Th1) immunity against M. leprae. May either be downgrading (borderline leprosy pt who “downgrades” toward lepromatous pole) or upgrading (increase in cell-mediated immunity). Both may p/w ulceration of existing lesions and preferential targeting of nerves, resulting in dangerous neuritis (= emergency!); generally lacks systemic symptoms; highest risk with Borderline forms (BL > BB, BT); Treatment = prednisone

Answer 308

Type 1 (reversal reaction)

Question 309

Th2 (humoral)-mediated formation of immune complexes, resulting in multisystem vasculitis and EN-like lesions scattered at previously unaffected skin sites (medial thighs and extensor forearms are #1 sites); prominent systemic symptoms; highest risk with LL and BL forms; Treatment = thalidomide

Answer 309

Type 2 (erythema nodosum leprosum)

Question 310

Severe necrotizing vasculitis w/ thrombosis; only occurs in patients from western Mexico with diffuse lepromatous leprosy; p/w purpuric macules and ulcerative bullous lesions below the knees; Treatment = prednisone

Answer 310

Lucio phenomenon

Question 311

Histology: Grenz zone, diffuse infiltrate of parasitized foamy histiocytes (Virchow cells), free-floating clumps of bacilli (globi) in dermis, and “onion-skin” pattern around nerves; lacks well-formed granulomas

Answer 311

Lepromatous Leprosy (LL)

Question 312

Histology: Well-formed sarcoidal granulomas w/linear arrangement (East-West) along nerves, numerous Langhans giant cells, fragmented nerve fibers, lacks organisms (no globi or Virchow cells), and Grenz zone

Answer 312

Tuberculoid (TT) Leprosy

Question 313

Small hypopigmented macules, papulonodules, and diffuse infiltration (→ leonine facies, elongated earlobes, and madarosis)

Answer 313

Lepromatous Leprosy (LL)

Question 314

Plaques and dome-shaped lesions

Answer 314

Borderline Leprosy

Question 315

Dry, scaly, hypopigmented, and anesthetic plaques with raised peripheral rim and central atrophy +/− alopecia and anhidrosis

Answer 315

Tuberculoid (TT) Leprosy

Question 316

Highest risk for type 1 reactions

Answer 316

Borderline Leprosy

Question 317

High risk for type 2 reaction | Lesions do not have anhidrosis or alopecia

Answer 317

Lepromatous Leprosy (LL)

Question 318

Treatment (WHO recommendations): Multibacillary

Answer 318

rifampicin 600 mg Qmonth + dapsone 100 mg QD + clofazimine 300 mg once a month and 50 mg daily 12 months

Question 319

Treatment (WHO recommendations): Paucibacillary

Answer 319

rifampicin: 600 mg Qmonth + dapsone 100 mg QD | 6 months

Question 320

More commonly seen in AIDS patients; found in environment (water, soil, and animals); pulmonary infection is most common finding; skin findings w/ primary inoculation or via dissemination (pustules, ulcers on legs, and nodules); ↑alkaline phosphatase; clarithromycin/azithromycin + ethambutol +/− rifampin

Answer 320

Mycobacterium avium complex

Question 321

Acquired via cutaneous contact (usually hands w/ abrasions) with aquatic environments (e.g., fish tanks and swimming pools) → erythematous/blue ulcerating nodules in a sporotrichoid pattern; Diagnosis is confirmed with culture: grows best at 31 degrees Celsius (~3 weeks required for growth), as opposed to the usual 37 degrees for most other mycobacteria; Treatment: clarithromycin +/− rifampin/ethambutol, minocycline, and TMP-SMX

Answer 321

Mycobacterium marinum

Question 322

Usually in Africa, in areas close to water bodies; nodule → ulcer on extremities; can become >15 cm and extend to bones; tx: excision (treatment of choice), local heating, rifampin + streptomycin, and amputation

Answer 322

Mycobacterium ulcerans aka Buruli ulcer

Question 323

Rapid growing mycobacteria; saprophytic organisms; can get infections posttrauma/surgery or medical treatments (e.g., implant placement, liposuction, and botulinum toxin)/tattoo/nail salon footbaths; skin presentations vary, but most common is inflamed subcutaneous nodules in sporotrichoid pattern; clarithromycin is treatment of choice, but surgical treatment may be needed

Answer 323

Mycobacterium fortuitum, chelonae, and abscessus

Question 324

Tinea capitis

Answer 324

Trichophyton tonsurans (#1 cause in United States), Microsporum canis (#1 cause worldwide; more inflammatory), and T. violaceum (East Africa)

Question 325

Endothrix (black dot; arthroconidia within hair shaft)

Answer 325

T. rubrum, T. tonsurans, T. schoenleinii, T. yaounde, T. violaceum, T. gourvilli, and T. soudanense (Mnemonic: “Ringo Gave Yoko Two Squeaky Violins”)

Question 326

Ectothrix (arthrospores around hair shaft)

Answer 326

Fluorescent (via Wood lamp – pteridine): M. canis, M. audouinii (formerly #1 cause in children), M. gypseum, M. ferrugineum, M. distortum, and T. schoenleinii (Mnemonic: “Cats And Dogs Fight and Growl Sometimes”) Nonfluorescent: T. mentagrophytes, T. rubrum, M. nanum, T. megninii, T. gypseum, and T. verrucosum

Question 327

Favus

Answer 327

T. schoenleinii > M. gypseum, T. violaceum

Question 328

Kerion

Answer 328

M. canis, T. verrucosum, T. mentagrophytes, and T. tonsurans

Question 329

Majocchi granuloma

Answer 329

T. rubrum most common

Question 330

Tinea corporis

Answer 330

T. rubrum most common

Question 331

Tinea imbricatum

Answer 331

T. concentricum

Question 332

Tinea barbae

Answer 332

T. verrucosum, T. mentagrophytes, T. tonsurans, and T. rubrum

Question 333

Tinea faceii

Answer 333

Usually zoophilic species (M. canis and T. metagrophytes) > T. rubrum; most commonly in kids after visiting rural areas

Question 334

Tinea cruris

Answer 334

T. rubrum >E.floccosum and T.interdigitale

Question 335

Moccasin and interdigital Tinea pedis

Answer 335

T. rubrum > E. floccosum (mocassin), T.interdigitale (interdigital)

Question 336

Vesicular/bullous Tinea pedis

Answer 336

T. mentagrophytes

Question 337

Distal subungual onychomycosis

Answer 337

T. rubrum, T.interdigitale, and E. floccosum

Question 338

Proximal white subungual onychomycosis

Answer 338

T. rubrum | ↑risk in HIV

Question 339

White superficial onychomycosis

Answer 339

T. mentagrophytes (adults) vs T. rubrum (children)

Question 340

Restricted to humans and cause a chronic, mild inflammatory response; includes all Trichophyton spp. (except T.mentagrophytes and T.verrucosum), E.floccosum, M.audouinii, and M.ferrugineum

Answer 340

Anthropophilic

Question 341

Primarily affect animals; cause massive inflammatory response in humans; includes M.canis (cats and dogs), M.nanum (pigs), T.verrucosum (cattle), and T.mentagrophytes (rodents)

Answer 341

Zoophilic

Question 342

Found in soil; cause severe inflammatory response and scarring in humans; M.gypseum (soil) is the only common species in this class

Answer 342

Geophilic

Question 343

Histology - Dermatophytes

Answer 343

septate hyphae in stratum corneum or nail plate, brisk dermal inflammation (vs minimal in tinea versicolor) +/− neutrophilic microabscesses in epidermis or corneum/nail plate PAS (red) and GMS (black)

Question 344

Chlorazol black E

Answer 344

Chitin stain – hyphae will be green

Question 345

Calcofluor white

Answer 345

Chitin stain – blue or green with fluorescence microscopy

Question 346

Pathogenesis - Dermatophytes

Answer 346

virulence factors (hydrolases and keratinases) allow penetration into stratum corneum and the released enzymes induce inflammation (Th1 response)

Question 347

Yellow cup-shaped crusts (scutula) that cluster together, resulting in a honeycomb appearance and can → scarring

Answer 347

Favus

Question 348

Boggy inflamed nodule/abscess with pustules and possible lymphadenopathy which may → scarring

Answer 348

Kerion

Question 349

Concentric and polycyclic rings of scale

Answer 349

Tinea imbricatum

Question 350

Erythematous papules/nodules around hair follicles, particularly lower legs (may arise from tinea pedis); systemic antifungals needed for treatment

Answer 350

Majocchi’s granuloma

Question 351

Erythematous follicular-based papules, often in an annular distribution most common in kids; treat with systemic antifungals

Answer 351

Tinea faciei

Question 352

Histology: hyphae and spores (“spaghetti and meatballs”) seen in stratum corneum (also on KOH)

Answer 352

Pityriasis versicolor

Question 353

Hyper- or hypopigmented finely scaling circular/oval macules/patches in sebaceous distribution (scalp, face, neck, upper chest, and upper back); more common in darker skin/adolescents/summer

Answer 353

Pityriasis versicolor

Question 354

Pathogenesis: Pityriasis versicolor

Answer 354

Overgrowth of normal flora, which is ubiquitous (esp. with warmth and humidity in the right host); hypopigmentation due to melanocyte inhibition by azelaic acid (dicarboxylic acid byproduct of Malassezia)

Question 355

Treatment: Pityriasis versicolor

Answer 355

Topical or systemic azole-antifungals, selenium sulfide shampoo, or topical ciclopirox

Question 356

Black Piedra

Answer 356

Piedra hortae

Question 357

White Piedra

Answer 357

Trichosporon asahii (most strongly linked to white piedra; formerly, T. beigelii; may cause disseminated disease in immunocompromised pts), T. ovoides, T. inkin, and T. cutaneum

Question 358

Microscopy: Piedra

Answer 358

Black or white concretions along hair (encircle hairs, unlike the sac-like appearance of lice) White piedra with soft mobile nodules; black piedra with hard nonmobile nodules

Question 359

Treatment: Piedra

Answer 359

Hair shaving/cutting and antifungal shampoos; systemic antifungals if recalcitrant

Question 360

Tinea nigra

Answer 360

Hortaea werneckii

Question 361

Microscopy: Tinea nigra

Answer 361

Dark brown septate hyphae with budding yeast in thickened stratum corneum

Question 362

Dark-brown/black macule or small patch on palms/soles, limited to stratum corneum

Answer 362

Tinea nigra

Question 363

Treatment: Tinea nigra

Answer 363

Azole creams, Whitfield’s ointment; oral terbinafine if recalcitrant

Question 364

Sporothricosis

Answer 364

Sporothrix schenckii (ubiquitous saprophyte; endemic to Central/South America and Africa)

Question 365

Microscopy: Sporothricosis

Answer 365

usually not well-visualized with stains; granulomatous inflammation with plasma cells and asteroid corpuscles (Splendore-Hoeppli phenomenon); organisms are cigar-shaped budding yeast

Question 366

Pathogenesis: Sporothricosis

Answer 366

Traumatic inoculation from soil via plant thorns, wood splinters, and sphagnum moss ≫ cats/rodents/armadillo bites; inhalation of spores

Question 367

Multiple ascending ulcerated nodules or subcutaneous abscesses, most frequently in gardeners, agriculture/farm workers, and veterinarians; may lead to erythema nodosum

Answer 367

Sporothricosis

Question 368

Treatment: Sporothricosis

Answer 368

Obtain fungal culture (difficult to find in tissue samples), itraconazole (treatment of choice), SSKI, and amphotericin B in disseminated disease

Question 369

Lobomycosis

Answer 369

Lacazia (Loboa loboi) - infects freshwater dolphins in South American Rivers

Question 370

Keloid-like verrucous fibrotic nodules that can ulcerate; men ≫ women; rural areas

Answer 370

Lobomycosis

Question 371

Microscopy: thick-walled yeast with tubular connections between cells – “pop bead” or “chain of coins” appearance

Answer 371

Lobomycosis

Question 372

Madurella spp. Pseudallescheria boydii (most common), Exophiala jeanselmei, and Acremonium spp.

Answer 372

Eumycetoma (fungus)

Question 373

Nocardia (N. brasiliensis [#1 bacterial cause] and N. asteroides both have white grains), Actinomadura spp. (A. pelletieri = red grains; A. madurae = cream or pink grains), and Streptomyces somaliensis (yellow-brown grains)

Answer 373

Actinomycetoma (bacteria)

Question 374

Slow progression of tumors with sinus tracts draining grains, which are fungal or bacterial aggregates; most common on feet/lower legs; long-standing lesions → bone and visceral involvement

Answer 374

Mycetoma

Question 375

Treatment: Mycetoma

Answer 375

Actinomycetoma: sulfonamides and other antibacterial agents Eumycetoma: surgical debridement and several month courses of azole antifungals

Question 376

Chromoblastomycosis

Answer 376

Fonsecaea pedrosoi

Question 377

Microscopy: pseudoepitheliomatous hyperplasia, granulomatous dermal inflammation with medlar bodies (pigmented muriform cells, “copper pennies”)

Answer 377

Chromoblastomycosis

Question 378

Weeks to months after inoculation, pruritic papules/nodules that expand and become verrucous with black dots; does not invade muscle or bone; chronic lesions can → SCC

Answer 378

Chromoblastomycosis

Question 379

Pathogenesis: Chromoblastomycosis

Answer 379

Traumatic inoculation by thorns or splinters

Question 380

Histoplasmosis

Answer 380

Histoplasma capsulatum var. capsulatum | Ohio and Mississippi River valley

Question 381

Microscopy: tuberculoid granuloma with intracellular 2–4 μm yeast in histiocytes (looks like leishmaniasis, but see yeast have surrounding halo and are more evenly distributed throughout histiocyte cytoplasm; lacks “marquee sign” and kinetoplast)

Answer 381

Histoplasmosis

Question 382

Pathogenesis: Histoplasmosis

Answer 382

Inhalation (esp. bird and bat feces) with hematogenous spread (can go to liver, spleen, bone marrow, and brain; skin involvement more common in HIV, often p/w umbilicated or “molluscoid” papules)

Question 383

Primary cutaneous chancre with lymphangitis and lymphadenitis (rare); more commonly, secondary cutaneous molluscoid nodules, cellulitis, ulcers, panniculitis, and oral lesions Pulmonary manifestations = most common presentation

Answer 383

Histoplasmosis

Question 384

Treatment: Histoplasmosis

Answer 384

Itraconazole (mild-moderate disease), or amphotericin B (severe disease)

Question 385

Blastomycosis

Answer 385

Blastomyces dermatitidis | Eastern United States Great Lakes, Ohio, and Mississippi River valleys

Question 386

Microscopy: pseudoepitheliomatous hyperplasia, granulomatous dermal inflammation with unipolar budding yeast (8–18 µm) (broad-based buds)

Answer 386

Blastomycosis

Question 387

Pathogenesis: Blastomycosis

Answer 387

Inhalation with subsequent hematogenous spread to skin (>75% of cases), bones, and genitourinary tract (e.g., prostate, spleen, liver, and brain)

Question 388

Primary cutaneous form (rare) presents with lymphangitis and lymphadenitis at injury site Secondary cutaneous form (more common; due to hematogenous dissemination from lungs to skin), presents with verrucous nodules, abscesses, and ulcers (can occur orally as well) Pulmonary manifestations = most common presentation

Answer 388

Blastomycosis

Question 389

Treatment: Blastomycosis

Answer 389

Polyene and azole antifungals (mainly itraconazole) and amphotericin B (severe disease)

Question 390

Coccidioidomycosis

Answer 390

Coccidioides immitis | Desert Southwest United States, Mexico, and Central/South America

Question 391

Microscopy: large (up to 100 µm) spherules containing endospores; also has PEH and granulomatous inflammation

Answer 391

Coccidioidomycosis

Question 392

Pathogenesis: Coccidioidomycosis

Answer 392

Inhalation with hematogenous spread to skin (as well as CNS and bone); very rarely primary cutaneous infection

Question 393

Verrucous nodules/papules, pustules, abscesses, or ulcerative lesions Pulmonary manifestations = most common presentation

Answer 393

Coccidioidomycosis

Question 394

Treatment: Coccidioidomycosis

Answer 394

Limited and cutaneous: itraconazole Severe: amphotericin B Meningeal: amphotericin B and fluconazole

Question 395

Paracoccidioidomycosis

Answer 395

Paracoccidioides brasiliensis | Southern United States, Mexico, and Central/South America

Question 396

Microscopy: Pseudoepitheliomatous hyperplasia, granulomatous dermal inflammation with multipolar budding yeast (mariner’s wheel)

Answer 396

Paracoccidioidomycosis

Question 397

Pathogenesis: Paracoccidioidomycosis

Answer 397

Inhalation of infected soil (can disseminate to skin, liver, adrenal glands, lymph nodes, gastrointestinal tract, and spleen); rarely may arise from direct inoculation in skin

Question 398

``` Granulomatous ulcerative oropharyngeal and perioral involvement in 70% of adults; cutaneous lesions can be contiguous, hematogenous, or via inoculation; clinical appearance of ulcers with infiltrated borders and hemorrhagic dots, and associated lymphadenopathy (can be massive) Men >>> women Pulmonary disease (granulomatous and chronic) most common presentation ```

Answer 398

Paracoccidioidomycosis

Question 399

Treatment: Paracoccidioidomycosis

Answer 399

Mild: TMP/SMX Moderate: itraconazole Meningeal: fluconazole or voriconazole Severe: amphotericin B

Question 400

Microscopy: KOH = yeast and pseudohyphae

Answer 400

Candidiasis

Question 401

Pathogenesis: Candidiasis

Answer 401

Candida species form biofilm on plastic medical devices SAPs (secretory aspartyl proteinases) and phospholipases aid in fungal adhesion and tissue invasion Chitin, mannoprotein and glucan may function as adhesins, which allow candida to adhere to mucosal surfaces C. albicans exists in normal flora of skin and digestive/genitourinary tracts with pathologic state with immunosuppression, and debilitation and imbalances in microbiome

Question 402

Usually starts in GI tract; 10% of bloodstream infections; 30% mortality in systemic candidiasis despite antifungal therapy usually in immunosuppressed patients who are neutropenic; scattered papules/nodules, occ. hemorrhagic and ecthyma gangrenosum-like; also infect muscles, retina, internal organs, and heart valves

Answer 402

Deep-seated candidiasis

Question 403

Third web space of fingers; also 4th web space of toes

Answer 403

Erosio interdigitalis blastomycetica

Question 404

Central smooth erythema of tongue

Answer 404

Median rhomboid glossitis

Question 405

Typically see beefy red color + satellite pustules +/− erosions

Answer 405

Candidal intertrigo

Question 406

Perlèche; RFs: edentulous, elderly, atopic dermatitis, and vitamin deficiencies

Answer 406

Angular cheilitis

Question 407

Treatment: Candidiasis

Answer 407

Mucocutaneous: polyenes (e.g., Nystatin) and azole preparations (e.g., clotrimazole and fluconazole) Systemic: amphotericin B, azoles, and echinocandins

Question 408

Cryptococcosis

Answer 408

C. neoformans and C. gattii (In bird droppings particularly pigeons and bark/fruit of tropical trees; C. neoformans – ubiquitous, C. gattii – tropical, subtropical)

Question 409

Microscopy: single-celled sphere with a double cell wall and thick capsule (“halo” appearance), may have one or more buds (blastoconidia); collections of organisms look like soap bubbles

Answer 409

Cryptococcosis | Stains: India ink, PAS, mucicarmine, GMS, and Fontana-Masson

Question 410

Pathogenesis: Cryptococcosis

Answer 410

Inhalation → lungs (1° pulmonary infection, usually mild) → hematogenous spread (CNS, bones, and skin); can also arise from primary inoculation of skin (rare) More common in immunosuppressed individuals (esp. in HIV/AIDS, but also associated with sarcoidosis and pregnancy) Glucuronoxylomannan polysaccharide capsule is a virulence factor

Question 411

Papules/nodules (often molluscum-like) that can be umbilicated and/or ulcerated, and prefer head/ neck, mouth, and nose Patients with 2° cutaneous lesions have high mortality rate Nodular lymphangitic syndrome – nodule at inoculation site, nodular lymphangitis, and adenopathy Meningoencephalitis is a serious and common manifestation

Answer 411

Cryptococcosis

Question 412

Treatment: Cryptococcosis

Answer 412

Mild: oral fluconazole CNS: amphotericin B and flucytosine

Question 413

Aspergillosis

Answer 413

Aspergillus fumigatus (most common)

Question 414

Microscopy: septate hyphae with 45° angle branching

Answer 414

Aspergillosis

Question 415

Pathogenesis: Aspergillosis

Answer 415

Can be 1° cutaneous disease (most commonly A. flavus) via direct inoculation (e.g., IV catheter, trauma sites, burn sites, and disturbed skin under dressings) vs 2° cutaneous disease (most commonly A. fumigatus; more common, typically in immunosuppressed, esp. neutropenic) via inhalation → pulmonary aspergillosis → disseminated disease Both can → hematogenous spread with a tendency for vascular invasion causing thrombus and necrosis

Question 416

Six clinical forms including erythematous edematous plaques, nodules with necrotic centers, hemorrhagic bullae, and necrotic ulcers Can involve CNS, heart, kidneys, bone, and GI tract

Answer 416

Aspergillosis

Question 417

Treatment: Aspergillosis

Answer 417

Azoles, echinocandins, and amphotericin B

Question 418

Fusarium

Answer 418

Fusarium solani most common

Question 419

Microscopy: 45° angle branching, similar to Aspergillus

Answer 419

Fusarium

Question 420

Pathogenesis: Fusarium

Answer 420

More common in immunosuppressed; severe burns (most common fungus cultured in burn patients); cutaneous disease via direct inoculation and hematogenous spread with a tendency for vascular invasion causing thrombus/necrosis

Question 421

Erythematous; edematous plaques more common than subcutaneous nodules (purpuric or ecthyma gangrenosum-like); panniculitis

Answer 421

Fusarium

Question 422

Penicilliosis

Answer 422

Penicillium marneffei | Southeast Asia

Question 423

Zygomycosis (mucormycosis)

Answer 423

Order Mucorales, genera Rhizopus, Rhizomucor, Mucor, Absidia, and others – systemic and cutaneous disease

Question 424

Microscopy: broad ribbon-like nonseptate hyphae with 90° angle branching, angioinvasive with thrombosis

Answer 424

Zygomycosis (mucormycosis)

Question 425

Pathogenesis: Zygomycosis (mucormycosis)

Answer 425

Most commonly enter via respiratory tract (though there are other portals of entry like skin), and can invade blood vessels → thrombosis/infarction/ necrosis More common in immunosuppressed patients, but also nonimmunodeficient (e.g., severe diabetes and severe burns)

Question 426

``` Forms: rhinocerebral pulmonary, gastrointestinal, primary cutaneous, and disseminated All forms are rapidly progressing and commonly fatal Cutaneous lesions (can be primary or secondary) typically indurated, necrotic black plaques/eschars most commonly seen on face (nasal and oral in rhinocerebral type); from surgery, catheterization, or burns Rhinocerebral type most common, usually in diabetes patients with DKA, may have epistaxis, facial pain, periorbital cellulitis, proptosis, and loss of extraocular muscle movement (2° to cranial nerve palsies) ```

Answer 426

Zygomycosis (mucormycosis)

Question 427

Treatment: Zygomycosis (mucormycosis)

Answer 427

Aggressive surgical resection of all necrotic areas (crucial to survival of patient) and amphotericin B (lipid formulation); posaconazole may be alternative

Question 428

Due to dematiaceous (pigmented) fungi: Exophiala jeanselmei (#1 cause), Wangiella dermatitidis, Alternaria, bipolaris, Phialophora, and Curvularia

Answer 428

Phaeohyphomycosis

Question 429

Subcutaneous, possibly draining, inflammatory abscesses/cysts (may mimic Baker cysts) Microscopy: cyst composed of macrophages and short hyphae, with a fibrous capsule Hyphae are pigmented/brown, and stain (+) with Fontana-Masson

Answer 429

Phaeohyphomycosis

Question 430

Slow-growing friable, red-purple, soft, lobulated, mucosal polyps, particularly on nose (associated with epistaxis), and conjunctivae; young men most commonly Microscopy: Very large (up to 300 µm sporangia containing trophozoites in dermis

Answer 430

Rhinosporidiosis | Rhinosporidium seeberi

Question 431

Nodules/ulcers/plaques and/or olecranon bursitis introduced into skin via trauma in contaminated water Microscopy: organisms have a morula-like appearance on H&E

Answer 431

Protothecosis | Prototheca wickerhamii

Question 432

Most consistent factor associated with scabies

Answer 432

Overcrowding

Question 433

Scabies

Answer 433

Sarcoptes scabies var. hominis

Question 434

Most common complication of Scabies

Answer 434

Secondary bacterial infections

Question 435

Scabies in immunosuppressed patients

Answer 435

Crusted (Norwegian) scabies

Question 436

Host-species restricted with 30-day life-cycle within stratum corneum; 1 week survival off human; classically affects interdigital webspaces, wrists, genitals (a/w chronic, reactive inflammatory nodules), and trunk; mineral oil scraping demonstrates scabies mite

Answer 436

Scabies

Question 437

Treatment of choice: Scabies

Answer 437

Permethrin 5% cream

Question 438

Head louse

Answer 438

Pediculus humanus capitis

Question 439

Body louse

Answer 439

Pediculus humanus corporis

Question 440

Pubic louse

Answer 440

Pthirus pubis

Question 441

Active infection only if within 5 mm from scalp; most commonly located in occipital and postauricular areas Mites can survive 36 hours w/o blood meal; nits are strongly adherent to hair shaft and can survive 10 days w/o blood meal

Answer 441

Head louse

Question 442

Larger, but similar shape to head louse Vector in epidemic typhus (R. prowazekii), louseborne relapsing fever (B. recurrentis), and trench fever (B. quintana) Live and lay eggs on clothing; more common in homeless population (since unable to change/wash clothes regularly)

Answer 442

Body louse

Question 443

``` Identify by four frontal crab-like appendages and short/broad body Maculae ceruleae (blue-gray macules due to bites) may be seen on surrounding skin ```

Answer 443

Pubic louse

Question 444

Female burrows head-first into skin (usually feet/toes) and extrudes eggs from punctum before dying and being sloughed with epidermis; can → gangrene

Answer 444

Tungiasis | Burrowing flea – Tunga penetrans

Question 445

Larvae cannot penetrate intact skin; once laid within open wound, penetrate subcutaneous structures and can continue to penetrate through cartilage and bone (leading to cranial penetration if developing near nose)

Answer 445

Wound myiasis

Question 446

Chronic infection due to obligate intracellular protozoan Exist in 2 forms: promastigote and amastigote Vector: Sandflies (Phlebotomus or Lutzomyia) Reservoirs: mainly canines and rodents

Answer 446

Leishmaniasis

Question 447

Pathogenesis: Leishmaniasis

Answer 447

Within gut of sandfly, organisms proliferate into flagellated promastigotes → migrate to sandfly proboscis → sandfly bites human and transfers promastigotes → histiocytes engulf promastigotes, which then transform into amastigotes and multiply → develop clinical manifestations within weeks (cutaneous leishmaniasis) or many months-years later (mucocutaneous and visceral leishmaniasis)

Question 448

Old world Leishmaniasis

Answer 448

L. major, L. tropica > L. aethiopica, L. infantum, and others Vector: Phlebotomus sand flies

Question 449

New world Leishmaniasis

Answer 449

L. mexicana, L. braziliensis, L. amazonensis, and others Vector: Lutzomyia sand flies (also the vector of B. bacilliformis → verruga peruana, Carrion disease, bartonellosis, Oroya fever

Question 450

Most common agents: L. major, L. tropica (>L. infantum) Begins as a solitary, small, erythematous edematous nodule at bite site (usually exposed skin sites—arms, face, legs) that ulcerates or becomes verrucous (Fig. 5-20) → may later develop sporotrichoid spread with satellite lymphatic nodules and lymphangitis → heals with scarring over months to years

Answer 450

Old world cutaneous Leishmaniasis

Question 451

Most common agents: L. mexicana (> L. braziliensis) More varied presentation: ulcerations (Chiclero ulcer = ear lesion in workers who harvest chicle gum in forest), impetigo-like, lichenoid, sarcoid-like, nodular, vegetating, and miliary

Answer 451

New world cutaneous Leishmaniasis

Question 452

More widespread cutaneous lesions; usually arises in immunosuppressed pts Most common agent: L. amazonensis (Americas), L. aethiopica (Africa) Multiple keloidal lesions of face (esp. nose) and extremities

Answer 452

Diffuse Cutaneous Leishmaniasis

Question 453

Affects skin and mucous membranes; almost always in New World; Predominantly New world subspecies: L. braziliensis (> L. amazonensis, L. panamensis, and L. guyanensis); Present with lip, nose and oropharyngeal infiltration and ulceration; Progressive nasopharyngeal destruction → airway obstruction, mutilation of mouth and perforation of nasal septum (aka “tapir face” or espundia)

Answer 453

Mucocutaneous Leishmaniasis

Question 454

Most severe form; due to systemic infection of bone marrow liver, spleen; Old World > New World; long incubation time months-years Most common agents: L. donovani (India, Sudan, Bangladesh; most common cause in adults), L. infantum (Europe; often a/w HIV), L. chagasi Present with fever, weight loss, diarrhea, abdominal tenderness, lymphadenopathy, hepatosplenomegaly, nephritis, intestinal hemorrhage, and death within 2 years (if not treated) Skin changes: Specific: papules, ulcers at bite site; Non-specific: purpura, hyperpigmentation, kwashiorkor changes (brittle hair)

Answer 454

Visceral (Kala-azar, “black fever”)

Question 455

New-onset cutaneous leishmaniasis lesions that arise up to 20 years after presumed recovery from untreated visceral leishmaniasis

Answer 455

Post-kala-azar dermal leishmaniasis

Question 456

Culture: Leishmaniasis

Answer 456

Novy-McNeal-Nicolle medium

Question 457

Histology: amastigotes with kinetoplasts are arrayed around periphery of parasitized histiocyte cytoplasm (“Marquee sign”); organisms are best seen on Giemsa

Answer 457

Leishmaniasis

Question 458

Most sensitive and specific test for Leishmaniasis

Answer 458

PCR

Question 459

Treatment: Cutaneous and mucocutaneous leishmaniasis

Answer 459

Pentavalent antimony (ToC)

Question 460

Treatment: Visceral leishmaniasis

Answer 460

Amphotericin B (ToC)

Question 461

African trypanosomiasis (sleeping sickness)

Answer 461

T. brucei gambiense (West Africa)/T. brucei rhodesiense (East Africa)

Question 462

Vector: African trypanosomiasis (sleeping sickness)

Answer 462

Tsetse fly (Glossina)

Question 463

Earliest sign: local pruritic inflammatory reaction at site of inoculation [48 hours]) → local lymphadenopathy and ulcerates → eschar with fever, headache, and joint pain at irregular intervals Winterbottom’s sign (posterior cervical LAD) (2 to 3 weeks) → trypanids (erythematous, urticarial or macular diffuse eruptions [6 to 8 weeks]) → neurologic changes and Kerandel’s deep delayed hyperesthesia, daytime sleepiness (late stage)

Answer 463

African trypanosomiasis

Question 464

Treatment: African trypanosomiasis

Answer 464

suramin or pentamidine (early) | melarsoprol, or eflornithine (CNS involvement)

Question 465

American trypanosomiasis (Chagas disease)

Answer 465

T. cruzi

Question 466

Vector: American trypanosomiasis (Chagas disease)

Answer 466

``` Triatomine bug (Reduviidae) Central/South America ```

Question 467

Clinical presentation: local inflammatory lesion (often on face) at site of entry (Chagoma) → Romanña’s sign (unilateral eyelid edema and conjunctivitis at site of inoculation) → rapid unilateral painless bipalpebral edema → late heart, esophagus, and intestinal enlargement (megacolon)

Answer 467

American trypanosomiasis (Chagas disease)

Question 468

Treatment: American trypanosomiasis (Chagas disease)

Answer 468

benznidazole and nifurtimox

Question 469

Toxoplasmosis

Answer 469

Toxoplasma gondii

Question 470

Vector: intestinal parasite of cats, but also infects dogs and rabbits Hemorrhagic or necrotic papules Acquired cutaneous disease occurs in pregnant women and immunocompromised patients Congenital disease (TORCH syndrome)

Answer 470

Toxoplasmosis

Question 471

Most common tropical parasite dermatosis; found in animal feces Species – Ancylostoma brasiliense (most common)

Answer 471

Cutaneous larva migrans

Question 472

Erythematous serpiginous cutaneous eruption (usually on feet) as a result of larva penetrating intact epidermis, but unable to penetrate human basement membrane zone (therefore unable to cause systemic disease) Moves 2–10 mm/hr

Answer 472

Cutaneous larva migrans

Question 473

Treatment: Cutaneous larva migrans

Answer 473

Albendazole, ivermectin, topical/oral thiabendazole, and liquid nitrogen

Question 474

Moves faster (5–10 cm/hr) Strongyloides stercoralis Often indurated serpiginous papule on buttocks/groin If disseminated, may get periumbilical (thumbprint) purpura and petechiae on trunk/proximal extremities Loeffler’s syndrome = chronic strongyloidiasis (affects lungs and GI tract; eosinophilia) Caused by contact with contaminated soil (e.g., sitting on beach)

Answer 474

Larva currens

Question 475

Onchocerciasis

Answer 475

Onchocerca volvulus

Question 476

Vector: Onchocerciasis

Answer 476

Simulium fly (black fly; also vector for tularemia; has also been implicated in Fogo selvagem form of pemphigus; present near fast-flowing rivers)

Question 477

``` Pruritic papules (can be acute, chronic, or lichenified) → leopard skin (depigmentation and atrophy); nodules (onchocercomas) over bony prominences; may develop Mazzotti reaction if given diethylcarbamazine Nodules of female microfilariae; male microfilariae migrate between nodules to mate ```

Answer 477

Onchocerciasis

Question 478

Treatment: Onchocerciasis

Answer 478

Ivermectin (treatment of choice) | Newer trials with doxycycline (kills symbiotic Wolbachia bacteria); surgical excision of onchocercomas

Question 479

Vector: Loa loa

Answer 479

Chrysops (Mango/deer flies; also transmit tularemia)

Question 480

Calabar swellings (recurrent migratory focal angioedema on limbs); visible migration of adult worm across eyes

Answer 480

Loiasis

Question 481

Treatment: Loiasis

Answer 481

Diethylcarbamazine

Question 482

Filariasis

Answer 482

Brugia malayi/timori and Wuchereria bancrofti

Question 483

Vector: Filariasis

Answer 483

multiple mosquito spp. of Culex (also West Nile virus vector), Aedes (also vector of chikungunya fever, Dengue fever, and yellow fever), and Anopheles (also vector of malaria and yellow fever) mosquitoes

Question 484

Treatment: Filariasis

Answer 484

Diethylcarbamazine (ToC)

Question 485

Species: Schistosoma, during the cercarial stage (snails are a vector) ■ ○ Northern United States and Canada fresh water Clinical presentation: papules and papulovesicles on uncovered skin 10 to 15 hours post exposure, lasts 5 to 7 days

Answer 485

Swimmer’s itch (“cercarial dermatitis”)

Question 486

Species: Edwardsiella lineata (sea anemone) and Linuche unguiculata (thimble jellyfish) during larval stage Southern United States and Caribbean salt water Clinical presentation: pruritic papules and wheals in covered areas within hours with new lesions for days

Answer 486

Seabather’s eruption

Question 487

Nitrophorin is one of its salivary products responsible for human immune reaction; p/w grouped “breakfast, lunch and dinner” urticarial papules at bite sites

Answer 487

Bed bugs | Cimex lectularius

Question 488

Direct contact with hairs and toxin-mediated reactions (not allergy) Train-track appearance of urticaria or hemorrhage Ophthalmia nodosa are ocular reactions as hairs tend to migrate inward

Answer 488

Lepidopterism

Question 489

Overall the most effective insect repellant

Answer 489

DEET (N,N-diethyl-3-methylbenzamide)

Question 490

Live in hair follicles of humans | Possible association with rosacea/perioral dermatitis

Answer 490

Demodex (Demodicidae)

Question 491

Involved in indoor allergies in atopic patients

Answer 491

Dust mite (Dermatophagoides)

Question 492

Has characteristic red hourglass on body Acute pain and edema at site Systemic symptoms: chills, abdominal pain/ rigidity, rhabdomyolysis, chest pain, sweating, hypertension, and shock α-Lactotoxin depolarizes neurons

Answer 492

Black widow spider - Latrodectus mactans

Question 493

Characteristic dark brown-black violin/fiddle shaped marking Necrosis with eschar formation at site of bite (which is painless; erythema → ischemia → thrombosis) Toxins: sphingomyelinase D and hyaluronidase (allows eschars to spread)

Answer 493

Brown recluse spider - Loxosceles reclusa