Dermatologic Infections

Question 1

pityriasis rosea

Answer 1

o Maculopapular, red and scaling eruption mainly on trunk, probably caused by a virus
o 10-35 yrs
o 2% of US population
o Lesions: “Herald Patch” larger, before generalized eruption (lasts for a day or two before the eruption over the entire body
o VIRAL
o Lasts up to 8 weeks

Question 2

pityriasis rosea presentation

Answer 2

o Can be pruritic or not
o Lesions with fine scaling oval shaped macules and papules on erythematous base
o “Christmas Tree” pattern on trunk
o Herald rash + Christmas tree pattern are CLASSIC!! This is pityriasis!!
o Extends to proximal extremities
o Herald patch loves to hide under the bra
o Very fine scales. Not scaly like psoriasis or fungus

Question 3

pityriasis rosea treatment

Answer 3

o	Viral, self-limiting disease
o	Treat pruritis if present
   	UV exposure
   	Doxepin 5% cream
   	Calamine lotion (she doesn’t like it)
   	Benadryl or atarax can also work

Question 4

verruca vulgaris

Answer 4

o Raised papules and plaques caused by Human Papilloma Virus (HPV)
o Usually school-aged kids, rare after age 25
o Girls > boys
o Contagious –> you have to have some sort of genetic susceptibility, some people can touch warts and never get them and others get them right away
o These are some of the more benign strains of HPV

Question 5

verruca vulgaris presentation

Answer 5

o Lesions: firm 1-10mm hyperkeratotic, skin colored lesions
 “Cauliflower like” appearance
 Reddish brown dots in lesions
o Kids usually don’t care about them, its mom and dad that are bothered by them

Question 6

verruca vulgaris treatment

Answer 6

o Treatment is topical
 Scrape off dead tissue on top first, then treat
 Salicylic acid application
 Liquid nitrogen
 Duct tape –> keep duct tape on as long as you can (sweaty kids need to change every day but old people that don’t move can keep it on longer)
• Be careful because it will macerate the healthy skin around it as well
 Laser removal of resistant warts
 It can take anywhere from 3-10 treatments to get rid of them because the wart has roots where the virus is living and replicating

Question 7

verruca plantaris

Answer 7

o 5-25 yrs most prevalent but can occur at any age
o Females > males
o Look like verruca vulgaris, but even or flush with skin
o On soles of feet (here they are called “plantars wart”)

Question 8

verruca plantaris treatment

Answer 8

 May resolve spontaneously
 Salicylic acid and shaving
 Cryotherapy and shaving

Question 9

molluscum contagiosum

Answer 9

o Discrete, umbilicated pearly-white papules caused by poxvirus in both kids and adults
o Sexual transmission in adults
o Males > females
o IF YOU SEE “UMBILICATE” THINK MOLLUSCUM –> looks like a little belly button
o Can be a little irritating, maybe a little itchy
o She doesn’t recommend treating in kids because they will go away on their own and tx may cause a scar!

Question 10

molluscum contagiosum treatment

Answer 10

o Lesions last 2-3 months
o Tend to be pretty asymptomatic
o Can be isolated to specific area or generalized
o Neck, trunk, anogenital region, eyelids
o Treatment: self-limiting
 Can be removed with liquid nitrogen, electrocautery, curettage but may scar
• Curettage is where you scrape the lesions off
• Liquid nitrogen is the best option because its not as painful

Question 11

herpes simplex virus

Answer 11

o Herpes simplex virus infection is characterized by grouped vesicles on an erythematous base, usually recurrent
 Grouped vesicles = herpetiform
o Mostly young adults but any age
o HSV type 1 or 2
 Type 1 far more common in oral region

Question 12

herpes simplex virus primary episode

Answer 12

o Primary episode and inoculation
 Can be associated with generalized malaise, lymphadenopathy and low-grade fever, fatigue, lymphadenopathy in the location where the HSV has appeared
 Kids: gingivostomatitis most common primary symptom
• Severe, painful ulcerative stomatitis with fever, malaise, lymphadenopathy
o With recurrent disease you don’t see the viral syndrome like you do in the primary episode

Question 13

HSV recurrent episodes

Answer 13

o Recurrent episodes: prodrome of tingling, itching or burning sensation and lesions appearing 24 hours later
o Lesions: vesicles in groups, may be umbilicated, can turn into papules, can bleed and crust

Question 14

HSV oral herpes

Answer 14

o Virus lives in trigeminal nerve ganglia
 Ophthalmic branch
 Maxillary
 Mandibular
o Lesions do not cross midline –> this is helpful in the differential

Question 15

herpetic whitlow

Answer 15

	Infection of finger with herpes
	Severely painful
	Self-limiting
	Supportive treatment
	Acyclovir topical or oral
	Pain medication

Question 16

hsv treatment

Answer 16

 Cold sore eruptions self-limiting
 Treatment vs. suppression
• Topical acyclovir for occasional oral outbreaks
• Host of home remedies
• Suppression therapy is for someone who, for example, doesn’t want to give it to their partner so they take low dose every day to decrease viral shedding
 Very frequent outbreaks can be suppressed with daily oral antivirals
 She doesn’t think abreva or acyclovir are very helpful
 For a primary infection, you want to give them the highest dose and for the longest amount of time to decrease viral shedding
 For recurrent, you use lower dose for lower amount of time

Question 17

varicella

Answer 17

o Etiology varicella zoster virus
o Common in children  use Benadryl, oatmeal paste, calamine lotion, oatmeal baths, socks on hands to keep them from scratching
o Usually mild, self-limiting course confers life-long immunity
 Significant morbidity: encephalitis, pneumonia; previously 100 deaths/yr
 Low-grade fever, typical rash with intense pruritis
o Vaccine at 12-18 mos and 4-5 yrs
o This is a live virus vaccine so this may be contraindicated in pregnancy, etc. so just be aware of that
o The usual incubation period is 10-21 days. The patient is contagious from 1-2 days before the appearance of rash until the lesions crust over, usually 5-6 days after the rash first appears. The infectious particles are cell-free virus particles derived from skin lesions or the respiratory tract. Transmission occurs mainly through respiratory droplets that contain the virus, making the disease highly contagious even before the rash appears. Direct person-to-person contact with lesions also spreads the virus. Papules and vesicles, but not the crusts, have high populations of the virus. In addition, maternal varicella with viremia can transplacentally spread to the fetus. This leads to neonatal varicella.
o Wild type = getting it in the wild
o Post vaccine type = a few pox after getting the varicella vaccine

Question 18

herpes zoster

Answer 18

o Caused by varicella zoster virus
o Acute, painful bullous eruption in one dermatome
o Usually age >50
 Associated with immunosuppression, compromise, stress or age
o Contagious
o Prevented by vaccine
o VZV IS A DNA VIRUS AND IS A MEMBER OF THE HERPESVIRUS GROUP. LIKE OTHER HERPESVIRUSES, VZV HAS THE CAPACITY TO PERSIST IN THE BODY AFTER THE PRIMARY (FIRST) INFECTION AS A LATENT INFECTION. VZV PERSISTS IN SENSORY NERVE GANGLIA. PRIMARY INFECTION WITH VZV RESULTS IN CHICKENPOX. HERPES ZOSTER (SHINGLES) IS THE RESULT OF RECURRENT INFECTION. THE VIRUS IS BELIEVED TO HAVE A SHORT SURVIVAL TIME IN THE ENVIRONMENT.

Question 19

herpes zoster presentation

Answer 19

o Herpetiform lesions, beefy red base
o Turns into crusts, with or without pustules and bleeding
o Duration on lesions: 2-3 weeks
o Rash does not cross midline

Question 20

herpes zoster symptoms

Answer 20

o Symptoms: prodrome 3-5 days before eruption
 Burning, numbness, tingling in dermatome
 Pain persists with eruption then wanes over time
• Pain can linger for a long long long time –> depends on the patient and their immune system
o This is called post herpetic neuralgia
o >50% on thorax
o 10-20% trigeminal
o Trigeminal distribution
o Thoracic distribution
o Hutchinson’s sign is a clinical sign which may refer to: Vesicles on the tip of the nose, or vesicles on the side of the nose, precedes the development of ophthalmic herpes zoster.
o Associated with malaise, fever, lymphadenopathy
o 50% postherpetic neuralgia (pain that lingers in the dermatome after the lesions go away)
 Really hard to treat
 Youll see pts on opiates for this neuralgia which is BAD  it doesn’t help all that much and its chronic so using opiates is inappropriate
• Gabapentin (off label use –> used for diabetic neuropathy), lyrica, SSRIs can be helpful with nerve pain
o Treatment with oral acyclovir- high dose (800mg TID) as soon as possible
 Severe cases may need IV antivirals and hospitalization for a day or 2
 She likes VALacyclovir because its dosed less frequently
o Eye involvement warrants urgent referral to ophthalmologist!
 If they have sxs of eye involvement, it is emergent (within a couple hours)
 If they don’t have sxs of eye involvement, it is urgent (within 24 hrs)
o If you have someone with ophthalmic branch herpes, they need to be seen by an ophthalmologist regardless of current eye involvement
o Talk about treatment of postherpetic neuralgia

Question 21

cellulitis

Answer 21

o Continuum of skin infections including impetigo, folliculitis, carbuncles and abscesses
o Infection of the skin with some extension into the subcutaneous tissues
o Lower extremity is most common location –> you can see it in other places but legs most common
o Margins are generally not distinct

Question 22

cellulitis risk factors

Answer 22

o Risk factors
 Disruption of the cutaneous barrier (wound, tinea pedis, leg ulcer)
 Venous or lymphatic compromise
 Previous history of cellulitis
 Colonization of the skin with Staph aureus or β-hemolytic streptococci
o Pathogenesis is not well studied
 Typically β-hemolytic Strep and S. aureus
o Usually polymicrobial infections

Question 23

cellulitis presentation

Answer 23

o Local findings
 Confluent macular erythema; generalized swelling; warmth; tenderness
 Tender regional lymphadenopathy; lymphangitis –> usually indicates a more severe infection
• Lymphangitis = streaking of red proximally
 Associated abscess formation may be present
 Tinea, psoriasis or other dermatologic abnormality
o Systemic findings include fever, chills, and myalgias
o If the patient has a rapidly spreading cellulitis, that is concerning for necrotizing fasciitis

Question 24

cellulitis diagnosis

Answer 24

o Primarily a clinical diagnosis
o Lack of utility for culturing
 Patients with systemic toxicity, recurrent infection, unusual exposures, or those who do not respond to therapy may be cultured
 Blood and/or skin cultures may be ordered
o Look for associated dermatoses
 Tinea infections, psoriasis
o Taking a punch biopsy is more useful than getting a culture of the top of the skin. You at least want to find a spot that is oozing or broken skin

Question 25

cellulitis treatment

Answer 25

o Hospitalize patients with high fevers, rigors, mental status changes or any signs of systemic toxicity; also nontoxic patients with dramatic skin findings that have progressed quickly (in hours)
o Resolution is usually slow –> usually takes weeks even in completely healthy patients
o Local desquamation of the involved area may be seen during early convalescence
 Looks like a snake shedding its skin

Question 26

cellulitis oral treatment

Answer 26

o Cephalexin 500mg po q 6 hrs
o Clindamycin 300mg po q 6 hrs or levofloxacin 500mg po qd are alternatives
o Treat patients for 10-14 days or longer if symptoms have not resolved at the end of 2 weeks
o Special situations / populations
 IVDA, diabetics, water exposure, animal bites
o What you choose depends on if you think they have MRSA or not
o In clinical practice, just assume everyone has MRSA because it is so prevalent here
o Cephalexin or cephalosporin is good for kids

Question 27

cellulitis IV treatment

Answer 27

o	Initial empiric treatment with vancomycin (15mg/kg IV q 12 hrs) for hospitalized patients with severe infections associated with necrosis
o	Cefazolin (1-2g IV q 8 hrs) or nafcillin (2g IV q 4 hrs) are recommended for uncomplicated cellulitis
o	Clindamycin (600mg IV q 8 hrs) may be used in penicillin allergic patients

Question 28

erysipelas

Answer 28

o Cellulitis looking infection on the face –> this needs to be on your ddx for cellulitis
o Bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics
o Tender, intensely erythematous, indurated plaque with a sharply demarcated border
 well-defined margin can help differentiate it from other skin infections
o Usually Strep infection, mostly on face but some on lower extremities
o infection rapidly invades and spreads through the lymphatic vessels. This can produce overlying skin “streaking” and regional lymph node swelling and tenderness; most common complications of erysipelas include abscess, gangrene, and thrombophlebitis
o classic fiery-red plaque with raised, well-demarcated borders
o The lesion classically exhibits a sharply raised border with abrupt demarcation from healthy skin and with advancing margins. This is in opposition to the slightly deeper involvement seen in cellulitis, in which lesions present with limited edema and less well-defined borders. Local signs of inflammation, such as warmth, edema, and tenderness, are universal. Lymphatic involvement often is manifested by overlying skin streaking and regional lymphadenopathy. Erythema is irregular, with extensions that may follow lymphatic channels (lymphangitis).
o More severe infections may exhibit numerous vesicles and bullae, along with petechiae and even frank necrosis. With treatment, the lesion often desquamates and can resolve with pigmentary changes that may or may not resolve over time.
o Erysipelas is strep whereas cellulitis is more staph or strep

Question 29

predisposing factors for erysipelas

Answer 29

- same as cellulitis
o	Lymphatic obstruction or edema
o	Saphenous vein grafting in lower extremities
o	Status postradical mastectomy
o	Immunocompromise: diabetic, alcoholic, HIV 
o	Arteriovenous insufficiency
o	Paretic limbs
o	Nephrotic syndrome
o	Vagrant lifestyle

Question 30

erysipelas treatment

Answer 30

o Penicillin x 5 days (PO or IM) first line, longer if not resolved
 Macrolide if pcn allergy
o Symptomatic treatment of aches and fever
o Hydration (oral intake if possible)
o Cold compresses
o Elevation and rest of the affected limb to reduce local swelling, inflammation, and pain
o Saline wet dressings applied to ulcerated and necrotic lesions and changed every 2-12 hours, depending on the severity of the infection
 Saline wet dressing because skin gets hot and swollen

Question 31

community acquired MRSA1

Answer 31

o Methicillin-resistant Staphylococcus aureus
o THIS IS A BIG PROBLEM
o THESE ARE NOT SPIDER BITES
o Know your local resistance patterns
o Have a high index of suspicion and culture these patients readily

Question 32

MRSA risk factors

Answer 32

o Patients on sports teams such as basketball, football, rugby, wrestling
o Communities such as jail, shelters, day care centers
o Compromised skin integrity, especially in persons with inadequate personal hygiene and IV drug use
o Patients with recurrent skin infections

Question 33

MRSA treatment

Answer 33

o Bactrim (+ rifampin to decrease development of resistance)
 Aka septra
 Rifampin and linezolid are very good against MRSA, but they CANNOT BE USED ON ITS OWN
o Clindamycin (+/- rifampin or linezolid)
 Inducible resistance in some areas
o Tetracyclines (minocycline, doxycycline) + rifampin
o Vancomycin remains the standard of care
o Linezolid and rifampin are good drugs but should never be used alone

Question 34

Impetigo

Answer 34

o Superficial vesiculopapular skin infection occurring predominantly on exposed areas of the face and extremities
o Usually a secondary infection
o HONEY CRUST = IMPETIGO
o See it a lot in the face, hands, etc where you would get a scrape
o Usually multiple lesions without systemic symptoms
o Occur in a traumatized area of the skin
o Typically vesiculopustules form which rupture leading to crusting with a characteristic golden “honey crust” appearance

Question 35

impetigo treatments

Answer 35

o Staph aureus and Group A Strep are the primary etiologies
o Topical mupirocin (Bactroban) ointment tid recommended for localized impetigo
o Oral therapy for extensive disease or in young children involving the hands or face
 Erythromycin 250mg po qid
 Dicloxacillin 250mg po qid
 Not appropriate if MRSA is a concern
o Kids may need more help because of the weak immune system

Question 36

impetigo prevention of spread

Answer 36

o Prevention of spread
 Frequent hand washing or disinfection
 Daily shower with soap
 Cover wounds
 Avoid sharing personal items such as towels, razors, or clothing

Question 37

folliculitis

Answer 37

o Pyoderma localized to hair follicles –> basically pustules, looks like acne, folliculitis is usually more localized than acne
o Multiple lesions that are erythematous, pruritic, measure ≤5mm and usually cluster in groups
o Most common pathogens are S. aureus, P. aeruginosa, and Candida spp.
 Pseudomonas folliculitis is also called pseudomonas folliculitis
• Can be a little itchy
o No systemic symptoms
o Lesions may drain or resolve spontaneously

Question 38

folliculitis treatment

Answer 38

o First line tx = warm water and soap. If that’s not working, THEN you can use antibioitics or antifungals
o Risk factors: nasal carriage of Staph aureus; exposure to whirlpools, swimming pools and hot tubs; antibiotic use; steroid therapy
o Treatment: warm compresses and topical antibiotics or antifungals as indicated
o Avoid shaving over involved areas

Question 39

pseudofolliculitis barbae

Answer 39

o Pseudofolliculitis barbae, often referred to as “razor bumps” or “shave bumps,” is a common cutaneous condition affecting the bearded area of the face, particularly in black men. In addition to the negative cosmetic appearance of this condition, the lesions often itch, and scratching can lead to bacterial superinfection. Other potential complications include postinflammatory hyperpigmentation, permanent scarring, and keloid formation. Pseudofolliculitis barbae occurs when the free ends of tightly coiled hairs reenter the skin, causing a “pseudofolliculitis” or a foreign-body-like inflammatory reaction. Inflammation around the embedded hairs results in the formation of firm, skin-colored, erythematous or hyperpigmented papules that become repeatedly irritated by shaving. Pustules may develop secondarily. Pseudofolliculitis barbae should be distinguished from true folliculitis which tends to be more of an acute problem with more localized inflammation. Avoiding close shaving or permanently removing hair cures pseudofolliculitis barbae. Shaving is discontinued for a minimum of one month in patients with mild pseudofolliculitis barbae; moderate and severe cases require longer shave-free periods. Shaving should not resume until all inflammatory lesions have resolved and there are no visible ingrown hairs. Warm compresses are applied to the lesions for ten minutes, three times per day. Patients should use a magnifying mirror to search for ingrown hairs each day and release them gently using a sterilized needle or tweezers. The hairs should not be plucked because regrowth may exacerbate symptoms. Hydrocortisone 1% cream can be applied as necessary following application of compresses to relieve inflammation. Topical erythromycin is indicated twice daily for patients with mild pustular involvement. Oral erythromycin or tetracycline 500 mg twice daily should be used for patients with evidence of more severe secondary inflammation.
o Not actually folliculitis
 its from shaving, happens with people with thick, curly hair, causes inflammatory nodule in the skin –> not filled with pus, they are just inflammatory
o Tx = warm compresses and stop shaving

Question 40

keratosis pilaris

Answer 40

o Keratosis pilaris, while often asymptomatic, may produce pruritic and pustular lesions of the lateral face, trunk, upper > lower arms, thigh, and buttocks. It is caused by plugging of the follicle by keratin that has failed to exfoliate, leading to a sterile papular or pustular eruption. Prepubertal children can have significant involvement of the lateral cheeks.
o Treatment includes chronic use of exfoliating moisturizers such as lactic acid or urea containing creams. Topical tretinoin gel or cream may be used in recalcitrant cases. Chronic erythromycin or tetracycline-based antibiotics can be helpful in conjunction with topical therapies when the lesions are pruritic/inflammatory.
o Has a dry, rough appearance to it
o Usually on upper outer arms

Question 41

furuncles and carbuncles

Answer 41

o Furunculosis is an inflammatory nodule involving the hair follicle
 Usually follows an episode of folliculitis
o Carbuncles are a series of abscesses in the subcutaneous tissue that drain via hair follicles
o Most commonly caused by S. aureus

Question 42

furuncles and carbuncles treatment

Answer 42

o Most patients can be treated with warm compresses to promote spontaneous drainage
o Surgical incision & drainage (I&D) may be required in some cases
o Patients with systemic symptoms (fever) should be treated with oral antibiotics
 Dicloxacillin 500mg po q 6 hrs
 Cephalexin (Keflex) 250mg po qid

Question 43

recurrent furunculosis

Answer 43

o Nasal mupirocin ointment
 Apply ointment intranasally bid x 5 days
 Nasal carriers of S. aureus
 Bactroban ointment (mupirocin) good for staph aureus
 Vitamin c to prevent recurrence
o Empiric trial of vitamin C
 1g/day po x 4-6 weeks
 Can prevent recurrence in patients with impaired neutrophil function
o Low dose clindamycin suppressive therapy
 150mg po qd x 3 months

Question 44

abscess

Answer 44

o Infection tracks in from the skin surface deeper than carbuncles
o Localized accumulation of PMN leukocytes with tissue necrosis involving the dermis and subcutaneous tissue
o Large numbers of microorganisms are present in the purulent material
 Polymicrobial
o Not associated with hair follicles
o Start as a carbuncle or furuncle and develop into an abscess

Question 45

Abscess risk factors

Answer 45

o Can be due to a variety of microorganisms and may be polymicrobial
o Most common single organism is S. aureus
o Risk factors:
 Minor local skin trauma (insect bite, abrasion)
 IVDU especially with skin popping
 Nasal colonization with S. aureus
 Diabetes or other immunosuppressive disorders

Question 46

abscess presentation

Answer 46

o Local pain, swelling, erythema, fluctuance, warmth
 Fluctuance = balloon filled with pudding
o Cellulitis around the abscess often occurs
o Regional adenopathy may occur
o Spontaneous drainage of purulent material
 Some people have spontaneous drainage, some don’t
o Fever, chills and systemic toxicity unusual
 Usually have a low grade fever, if they have a higher fever, may not be as simple as you thought
o Single or multiple skin abscesses

Question 47

Necrotizing fasciitis

Answer 47

o Necrotizing infections of the skin and fascia include necrotizing forms of cellulitis and fasciitis types I and II. Necrotizing fasciitis is a deep seated infection of the subcutaneous tissue that results in progressive destruction of fascia and fat, but may spare the skin. These infections are characterized clinically by fulminant destruction of tissue, systemic signs of toxicity, and a high rate of mortality. Common pathologic features are extensive tissue destruction, thrombosis of blood vessels, abundant bacteria spreading along fascial planes, and an unimpressive infiltration of acute inflammatory cells. Accurate diagnosis and appropriate treatment must include early surgical intervention. Among patients with soft tissue infection, there are a number of clinical features that raise the likelihood of necrotizing infection. These include systemic findings, such as fever, tachycardia, and hypotension, and typical signs and symptoms such as tense edema outside the involved skin, disproportionate pain, blisters/bullae, crepitus, and subcutaneous gas. These findings, although fairly specific, have a low sensitivity of 10 to 40 percent. Therapy consists of antibiotics and early and complete surgical debridement. Antibiotic therapy alone is associated with a mortality rate approaching 100 percent. Early recognition of necrotizing fasciitis is important since there may be a remarkably rapid progression from an inapparent process to one associated with extensive destruction of tissue, systemic toxicity, loss of limb or death. Necrotizing fasciitis should be considered in patients with fever, toxicity, soft tissue involvement with pain out of proportion to skin findings, and elevated CPK. When necrotizing fasciitis is suspected, surgical exploration is the only way to be certain whether this is the correct diagnosis. Prompt surgical exploration both facilitates early debridement and obtaining material for appropriate cultures. Treatment of necrotizing fasciitis consists of early and aggressive surgical exploration and debridement of necrotic tissue, antibiotic therapy, and hemodynamic support as needed. The best indication for surgical intervention is severe pain, toxicity, fever and elevated CPK with or without radiographic findings. In addition, the various types of infection require some specific modalities. Empiric antibiotics should cover aerobic and anaerobic organisms. Ampicillin or ampicillin-sulbactam plus clindamycin or metronidazole are good first choices. For patients who have been hospitalized previously, gram-negative coverage should be improved by substituting ticarcillin-clavulanate, piperacillin-tazobactam, a third generation cephalosporin, a carbapenem, a fluoroquinolone, or an aminoglycoside for the ampicillin or ampicillin-sulbactam. If group A streptococcal infection is suspected, we recommend the combination of clindamycin and penicillin. Antibiotic therapy should be narrowed based upon operative culture results and susceptibility patterns when these become available. We do not currently recommend adding IVIG to the treatment of necrotizing fasciitis, but this recommendation could change if a randomized, double blind trial is performed.
o PAIN OUT OF PROPORTION IS KEY!!!
o Symptoms progress over a very short amount of time
o Usually you give vancomycin to cover MRSA
o This is a medical emergency

Question 48

Fournier’s gangrene

Answer 48

o Necrotizing fasciitis of the perineum (Fournier’s gangrene) can involve the scrotum. The infection can begin abruptly with severe pain and may spread rapidly.
o In the perineal area, penetration of the gastrointestinal or urethral mucosa by enteric organisms can cause Fournier’s gangrene, an aggressive infection. These infections begin abruptly with severe pain and may spread rapidly onto the anterior abdominal wall, into the gluteal muscles and, in males, onto the scrotum and penis. These infections are induced by a mixture of aerobic and anaerobic organisms and are therefore classified as type I infections.

Question 49

Abscess I and D

Answer 49

o I&D if there is fluctuance or the abscess has “pointed”
 Not necessary if spontaneous drainage
o Send the purulent drainage for culture and sensitivty testing
o Oral antibiotic therapy is secondary to I&D
 Often begin treatment if the abscess is not ready for I&D, systemic symptoms, or concern about MRSA

Question 50

abscess treatment

Answer 50

o Dicloxacillin 500mg po qid
o Cephalexin (Keflex) 250mg po qid
o Clindamycin 150mg po qid
 600mg IV q 8 hrs in toxic patients
o Oral, perirectal, vulvovaginal abscesses:
 Amoxacillin-clavulanate (Augmentin) 875/125mg po bid
 Clindamycin 150mg po qid + ciprofloxacin 500mg po bid
o If you think they MRSA, then you use clinda
o DON’T NEED TO KNOW DOSES

Question 51

abscess prevention

Answer 51

o Patients with recurrent abscesses should be evaluated further
 Screening for diabetes and immunologic diseases (IgA deficiency)
• Especially in kids this is something to think about
 Ask about IVDA
 Look for hidradenitis suppurativa
 Screen for nasal carriage of S. aureus
• Mupirocin nasal ointment bid x 5 days
• Anyone who has their second abscess or skin infection, you want a nasal swab
 Discuss good skin hygiene (bathing, etc.)
• Consider bleach baths?

Question 52

hidradenitis suppurativa

Answer 52

o HS is a chronic follicular occlusive disease involving the intertriginous skin of the axillary, groin, perianal, perineal, and inframammary regions. HS affects more women than men: the sex ratio is 3:1. The onset of symptoms usually occurs between puberty and age 40. The primary pathologic event is terminal follicular obstruction leading to rupture of the follicle and subsequent inflammation. Bacterial infection occurs secondarily. The disease affects the axillae most commonly; genitofemoral region; gluteal folds and perianal region; infraumbilical midline, inframammary and periareolar areas. The usual presentation is of small painful subcutaneous nodules, but early symptoms consisting of pruritus, erythema, burning, and local hyperhidrosis have been reported. Nodules develop and may rupture, discharging purulent, sometimes malodorous material and forming sinus tracts. Unruptured nodules eventually turn into indurated inflammatory masses. Hyperpigmentation, scars, and pitting of the skin occur over time. The diagnosis of HS is based upon characteristic clinical manifestations. Biopsy is neither diagnostic nor required unless there is suspicion of malignancy. The clinician should have a high index of suspicion for the disease in individuals with recurrent “boils” in intertriginous areas after puberty, despite antibiotic therapy. There is no cure for hidradenitis suppurativa (HS), but medical and surgical strategies can help to eliminate existing lesions and prevent development of new lesions. counsel patients to use antiperspirants (not deodorants) regularly; avoid tight, synthetic clothing over affected areas; and avoid prolonged exposure to hot, humid environments. However, antiperspirants and deodorants, as well as shaving and depilation, should be avoided if they cause irritation in affected areas. Weight reduction and smoking cessation can also be helpful. In addition to these general measures, medical therapy with or without surgical therapy may be indicated. For patients with mild disease, we suggest use of topical antibiotics and intralesional steroids to suppress inflammation. For resistant cases, we suggest a trial of oral systemic antibiotics. We suggest concurrent therapy with an anti-androgen for women. Zinc gluconate (50 to 90 mg orally daily) is given to help prevent development of new or recurrent lesions. We suggest wide surgical unroofing and debriding of all cysts and sinuses and fistulous tissue by an experienced surgeon.

Question 53

dermatophytosis

Answer 53

o Superficial fungal infection of skin, hair and/or nails
o 3 most common dermatophytes affecting humans are Trichophyton, Microsporum, Epidermophyton sp.
 T. rubrum most common industrialized world
o Described as tinea (meaning fungus) followed by affected body part
 Tinea corporis = body; tinea pedis = foot; tinea cruris = groin; tinea capitis = head

Question 54

presentation of dermatophytosis

Answer 54

o Presents as erythematous, annular patch with distinct borders and central clearing; fine scale usually covers patch
o Pts c/o itching, stinging and/or burning; maceration or peeling fissures common btw digits
o Nails present with thickening discoloration, onychomycosis or nail bed and plate
o Kerion = inflammatory reaction causing indurated, boggy papule with pustules
 Need to be treated with oral abx, TOPICALS DON’T WORK
o Rolled peripheral borders

Question 55

diagnosis of tinea

Answer 55

o	KOH prep of tinea corporis
   	FOR EXAM PURPOSES 
    spaghetti and meatballs appearance 
o	Dermoscopy of tinea capitis
   	Looking for broken hairs and curly Q growth

Question 56

treatment of tinea

Answer 56

o Keep skin clean, dry, allow to breathe
o Avoid steroids
o Topical antifungals BID x 4 wks or more
o Powders may help macerated/wet areas
o Chronic or resistant infections, nail infections, scalp infections (kerion) require oral meds for up to 3 mos
 Monitor LFT’s, starting with baseline
o Oral antifungals: griseofulvin, itraconazole, terbinafine, ketoconazole
 The downside is that these medications are hepatotoxic!! You have to be careful with people that have decreased liver function
o AVOID STEROIDS!!! FUNGUS LOVES STEROIDS!
 For the most part, if you put steroids on stuff, it gets better. If it gets worse, IT’S A FUNGUS
o Use griseofulvin for kids
o Terbinafine is good because its short term

Question 57

tinea (pityriasis) versicolor

Answer 57

o Superficial fungal infection
 Malassezia yeast
o Extremely common esp summer or in tropical regions; not contagious
 Adolescents, young adults most commonly
o Hypopigmented, hyperpigmented or erythematous macules, usually upper trunk and proximal upper extremities
o KOH prep confirms dx; not Wood’s lamp

Question 58

treatment of tinea versicolor

Answer 58

o Topical antifungal shampoo or creams daily x 2 wks should be effective
 Selenium sulfide or ketoconazole
o Single oral dose itraconazole 400mg if resistant, extensive dz or recurrent
o Monthly antifungal shampoo for prevention or multiple recurrences

Question 59

candidal intertrigo

Answer 59

o Superficial yeast infection of intertriginous areas (skin folds)
o Common in people who get their hands wet a lot
o Extremely common  will see all the time
o Risks include obesity, occlusive clothing, incontinence, hyperhidrosis, DM, steroid use, antibiotics, other medications
o Erythematous macerated plaques and erosions with delicate peripheral scaling and erythematous satellite papulopustules
o SATALITE LESIONS = CANDIDA

Question 60

how to tell the difference between eczema vs candida

Answer 60

 In candida you usually see masceration
 Eczema is less burning and more uncomfortable
 KOH PREP IS KEY!!

Question 61

treatment of candidal intertrigo

Answer 61

o Remove exacerbating factors, treat underlying illness
o Keep area clean and dry
o Antifungal creams and/or powders BID x 1-2 wks or until resolved
o Severe or recalcitrant infxns give oral fluconazole 50-100mg daily or 150mg weekly x 2-6 wks
o Powders can be extremely helpful to keep the skin dry

Question 62

scabies

Answer 62

o Infestation with Sarcoptes scabeii, an 8 legged mite
o Transmitted via direct contact
o Most common on hands, genitalia, axilla; web spaces, belt line, edges of socks
o Extremely pruritic burrows, vesicles or nodules with excoriations and crusting
 Can become secondarily infected by GAS
o Rare in babies <3 mos
o Dermoscopy: the dark triangular shape in this image represents the head of the scabies mite. This mite is located at the end of a burrow

Question 63

treatment of scabies

Answer 63

o Control transmission, treat direct contacts
 Wash all clothing/bedding hot water
 Bag soft toys 2-3 days
o Topical permethrin 5% cream
 Apply to entire body below neck, wait 8-12 hrs then wash off; repeat in 1 week
o Alternative: oral ivermectin 200 mcg/kg once then repeat in 2 wks
o Antihistamines or topical steroids for itching

Question 64

pediculosis

Answer 64

o Types of lice causing human infection
o Pediculosis corporis, chronic with hyperpigmentation and excoriation
o The three varieties of ice specifically parasitic for humans are Phithirus pubis (picture A, crab louse), Pediculosis humanus capitis (picture B, head louse), and Pediculosis humanus corporis (picture C, body louse).

Question 65

treatment of pediculosis

Answer 65

o Prevention is key; treat all direct contacts
o Topical insecticides such as permethrin, pyrethrins, malathion as 1st line therapy; lindane or ivermectin as alternatives
o Special combs help remove nits; occlusive dressing with petroleum to suffocate lice
o Retreat 7-10 days to kill any newly hatched lice