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clinical medicine > Derm: Insects, Bacterial, Viral > Flashcards

Derm: Insects, Bacterial, Viral Flashcards

0
Q

What are lice?

A

-ectoparasites that live on body & feed on human blood after piercing skin and injecting saliva

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1
Q

What is another word for lice infestation?

A
  • pediculosis (louse infestation)–prehistorical
  • oldest known fossils of louse eggs: 10,000 years old

-lousy, nit-picking, “going over things w/ a fine-tooth comb”

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2
Q

How do lice survive?

A
  • survive away from their host, die of starvation within 10 days of removal from their human host
  • female louse lays 3-6 eggs/nits a day
  • nits white and less than 1mm long
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3
Q

When do nits hatch?

A

8-10 days, reach maturity in 10 days

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4
Q

Which types of lice feed on which parts of the body?

A

Pediculosis capitis: head lice
Pediculosis corporis: body lice
Pthirus pubic: pubic lice (crabs)

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5
Q

How do lice spread?

A
  • person to person by close physical contact
  • through fomites (combs, clothes, hats, linens)
  • LICE DO NOT JUMP!
  • overcrowding encourages spread of lice
  • body louse is vector of typhus, trench fever, and relapsing fever
  • human lice have been used as a forensic tool!
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6
Q

What is the workup for lice?

A

Distance of the nits from the scalp determines duration of infestation (if several mm from scalp, they are nonviable empty egg cases)
~hair grows 10mm/mo
-cellulose tape picks up lice in infested area
-wood lamp exam shows yellow-green fluorescence of lice and nits

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7
Q

What are the treatments for lice?

A

-topical pediculicidal agents:
pyrethrin shampoos & permethrin 1% rinse OTC
permethrin 5%- wide margin of safety
malathion- more ovicidal than permethrin, more lethal, less reinfestation
lindane- not with defective cutaneous barrier, seizures
ivermectin topical- single dose, 10 min application, no nit combing needed
spinosad- must be >4 yrs old, cream rinse for 10 min, then shampoo out, ovicidal activity (combing nits unnecessary

-oral anthelmintics, ivermectin, levamisole, albendazole effective against head louse infestation, repeat 7-10 days to kill lice emerging from nits that have survived the 1st treatment

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8
Q

What are “treatment failures” in the treatment of lice?

A
  • effective in killing nymphs/mature lice, but LESS effective in killing eggs- cure in >90% of cases w/ appropriate Rx
  • kids can return to school after treatment, but require repeat therapy in 7-10 days
  • causes of therapeutic failure: misdiagnosis, inappropriate treatment, noncompliance, insufficient application of pediculicide, lack of ovicidal activity of pediculicide and failure to re-treat in 7-10 days, lack of removal of live nits, lack of environmental eradication, reinfestation, resistance to pediculicide
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9
Q

Are lice pruritic?

A

YES!!

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10
Q

What are scabies?

A
  • very pruritic
  • skin infestation
  • host-specific mite: Sarcoptes scabiei var hominis (obligate human parasite)
  • source of human infestation >2500 years
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11
Q

What does scabies “imitate”?

A
  • spectrum of cutaneous manifestations
  • results in delayed diagnosis
  • “7 year itch” described persistent, undiagnosed scabies infestations
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12
Q

What is the pathophysiology of scabies?

A
  • life cycle 30 days within human epidermis
  • after mating, male mite dies & female mite burrowns into superficial skin
  • lays 60-90 eggs (<10% mature)
  • ova require 10 days for larval-nymph-adult maturation
  • move through top layers of skin by secreting proteases that degrade the stratum corneum
  • feed on dissolved tissue but do not ingest blood
  • scybala (feces) left during their travels through the epidermis creating linear lesions/BURROWS
  • 300,000,000 cases of scabies are reported worldwide each yr
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13
Q

What are scybala?

A

feces: causes itchiness in scabies infestations

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14
Q

What are the requirements for treatment of scabies?

A

scabicidal agent
antipruritic agent (sedating antihistamine)
antimicrobial agent if secondarily infected
-verbal + written instructions for compliance, family/close contacts may need treatment even if asymptomatic, pets DO NOT require treatment, carpets and upholstered furniture vacuumed, launder clothing/bed linens used within the last week in hot water and again in 1 week

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15
Q

What are the treatments for scabies?

A
  • permethrin (lyclear, elimite)- 5% cream drug of choice (esp >2 months old and small children), better efficacy than crotamiton–postscabietic nodules and pruritus may persist for months
  • lindane (kwell)- 1% lotion or cream, stimulates nervous system of parasite, causing seizures and death- 2nd line after other Rx fail due to neurotoxicity in children/infants
  • sulfur topical- creams/ointments (6% preferred), oldest known treatment, safe, effective, 1st choice Rx in infants <2 months & in pregnant/lactating women— 2nd odor and mess
  • crotamiton (eurax)- 10% cream or lotion, method of action unknown
  • ivermectin (stromectol)- binds with glutamate-gated chloride ion channels in invertebrate nerve/muscle cells, causing cell death; 1/2 life is 6
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16
Q

Describe brown recluse spider

A
  • 13 species in US
  • at least 5 associated with necrotic arachnidism
  • called Loxosceles reclusa
  • have dorsal violin shape
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17
Q

Describe brown recluse pathophysiology

A
  • Dermonecrotic arachnidism- local skin/tissue injury resulting from envenomation
  • Loxoscelism: systematic clinical syndrome caused by envenomation from the brown spiders
  • venom cytotoxic and hemolytic
  • sphingomyelinase D- protein component responsible for most of the tissue destruction and hemolysis
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18
Q

What are the components of brown recluse venom?

A

8 components including enzymes, hyaluronidase, deoxyribonuclease, alkaline phosphatase, lipase

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19
Q

What is responsible for most of the damage by brown recluse?

A

Sphingomyelinase D

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20
Q

Where on body does scabies usually occur?

A

intertriginous areas, wrists, belt area

intensely pruritic-takes 1.5 week for itch to stop

21
Q

How does brown recluse bite present itself? (2 main steps)

A
  1. edema/ischemic bite site-erythematous halo around the lesion
  2. margin enlarges peripherally, 2nd gravitational spread of venom into the tissues
    - 24-72 hours: single clear or hemorrhagic vesicle develops at the site, then forms a dark eschar (dead tissue)
    - necrosis most common in fatty spots–butt, thigh, abdominal wall
22
Q

What is the treatment for brown recluse bites?

A
  • directed by severity of injury
  • local debridement, elevation, loose immobilization of affected area
  • sphingomyelinase D activity is temp dependent–apply cool compresses until necrosis stops
  • dapsone (leukocyte inhibiting properties)
  • hyperbaric oxygen therapy might reduce skin lesion size but there are limited studies on humans
23
Q

What is the name for black widow spider?

A

Lactrodectus, 32 species

24
Q

Describe black widow sexual cannabalism

A
  • female eats male after mating
  • female black widow has unusually large venom glands, bite harmful to humans
  • female venom 3x more potent than males, making male’s self defense bite ineffective
25
Q

What is the toxin that causes lactrodectism (black widow spider bites)

A

Neurotoxin latrotoxin

26
Q

How do black widow bites present itself? (3 phases)

A
  1. Exacerbation phase: 1st 24 hours after bite
  2. Dissipation phase: 1-3 days after bite symptoms start to decline
  3. Residual phase: weeks or months after
27
Q

What is the exacerbation phase in a black widow bite?

A
  • severe muscle pain in muscle groups near bite
  • muscle cramping in abs, back, thighs
  • headache, dizziness, tremors, salivation, diaphoresis (lots of sweating), nausea, vomiting
  • anxiety, fatigue, insomnia
  • lacrimation (tearing of eyes)
  • migratory arthralgia (joint pain)
  • tachycardia, bradycardia, restlessness, hypertension, tachypnea (hyperventilation)
28
Q

Describe the residual phase (black widow spider bite)

A
  • muscle spasm, tingling, nervousness, weakness, potential risk of paralysis
  • complications rare, death rarer, progression may be rapid
  • changes in heartbeat, breathing or blood pressure
29
Q

What is the treatment for black widow bites?

A
  • pain medication
  • muscle relaxants
  • activenom
30
Q

What is cellulitis?

A

Infection without formation of abscess and without purulent drainage or ulceration

  • majority of cases are caused by streptococcus pyogenes or staphylococcus aureus
  • metastatic seeding seen with S. pneumoniae and marine vibrios, Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species
31
Q

What is facial cellulitis associated with in children?

A

H influenzae type B and S pneumoniae

seen less so with vaccines

32
Q

What is varicella?

A
  • invasive gas
  • onset 4th day of varicella
  • sometimes progresses to severe necrotizing soft-tissue infections requiring surgical debridement
  • concern about association with ibuprofen and superinfections
33
Q

What is MRSA? (cellulitis)

A
  • HA-MRSA: increased risk with recent hospitalization, surgery, renal dialysis, residence in long-term-care facilities, or IV drug use
  • CA-MRSA: 1st seen in 1968
34
Q

What are the pathogens in cellulitis?

A
  • animal bites (dogs more common in boy and cats in girls)
  • puncture wounds; through bottom of athletic shoes, may cause pseudomonas osteomyelitis and/or cellulitis
  • aquatic lacerations and puncture wounds-pathogens not found in land-based injuries—-aeromonas hydrophila, pseudomonas and plesiomonas species, vibrio species, erysipelothrix rhusiopathiae, mycobacterium marinum
35
Q

What are the 4 main important presentations of cellulitis?

A

Rubor-redness
Calor-heat
Dolor-pain
Tumor-edema (swelling)

36
Q

What are other important presentations of cellulitis?

A
  • UNLIKE erysipelas, the borders are not elevated or sharply demarcated
  • most common site is leg
  • regional lymphadenopathy may be present
  • malaise, chills, fever, and toxicity
  • skin infection WITHOUT underlying drainage, penetrating trauma, eschar, or abscess most likely caused by strep
  • S aureus, MRSA most likely with drainage or abscess formation
  • perianal cellulitis seen with perianal fissures (perianal erythema, pruritus, purulent secretions, painful defecation, bleeding in stools)
  • violaceous color and bullae suggests systemic infection with organisms such as V vulnificus or S pneumoniae
  • Lymphangitis (red lines streaking away from area of infection)-crepitus (creaking) indicates more systemic infection
  • circumferential cellulitis or pain disproportional to exam findings may indicate more severe soft-tissue infection
37
Q

What are human bite complications of cellulitis?

A

before antibiotics, up to 20% of hand bites required amputation of finger
permanent hand disability after stiffness and/or chronic pain
infectious tenosynovitis
septic arthritis
abscess formation
transmission of disease (hep B or C, HIV)
osteomyelitis
necrotizing fasciitis

38
Q

What are comorbid conditions of cellulitis that may place patients at higher risk for infection?

A 
diabetes mellitus
chronic edema of region
prior splenectomy
liver disease
immunosuppression
presence of a prosthetic valve or joint
regional arterial or venous disease
39
Q

Common treatments for cellulitis

A

In cases WITHOUT draining wounds or abscess, STREP is most likely cause—–beta lactam antibiotics are appropriate therapy:

  • mild cases: dicloxacillin, amoxicillin, cephalexin
  • patients allergic to penicillin: clindamycin or a macrolide (clarithromycin or azithromycin)
  • Levofloxacin - there are resistant strains
  • some clinicians prefer parenteral antibiotics with a long half life (ceftriaxone then oral agent)
40
Q

Treatments with people who have severe cellulitis

A

parenteral therapy:

  • if due to staph or strep, treat with cefazolin, cefuroxime, ceftriaxone, nafcillin, or oxacillin
  • antimicrobial options in patients who are allergic to penicillin: clindamycin or vancomycin
  • patients with diabetic ulcers: infections polymicrobial–EMPIRIC coverage in this setting (broad coverage of gram positive, gram negative, anaerobic organisms)
41
Q

What is empiric?

A

person who depends upon experience or observation alone, without using scientific method or theory

**strep most common when skin is in tact, staph is the opposite

42
Q

What is erysipelas?

A

bacterial infection of upper dermis extending into superficial cutaneous lympatics

43
Q

Where is erysipelas seen on body and what causes it?

A

85% cases involve legs, caused by streptococcus pyogenes (st anthonys fire)– other bacteria involved could be staph, gram-negative species

44
Q

What is pathophysiology of erysipelas?

A
  • preexisting lymphedema a risk factor
  • infection rapidly invades, spreads through the lymphatic vessels, producing overlying skin streaking and regional lymph node swelling and tenderness
45
Q

At what age does erysipelas occur?

A

60-80 years old
immunocompromised patients
lymphatic drainage problems (after mastectomy, pelvic surgery, bypass grafting)

46
Q

How is erysipelas presented?

A
  • small, erythematous patch–>fiery red tense, shiny plaque
  • well-demarcated borders
  • lymphatic involvement evident by overlying skin streaking and regional lymphadenopathy (abnormal number of lymph nodes)
  • lesion desquamates with treatment, resolves with pigmentary changes
47
Q

What is the treatment for erysipelas?

A
  • elevation, rest to reduce local swelling, inflammation, and pain
  • saline wet dressings applied to ulcerated and necrotic lesions
  • strep most common cause
  • penicillin FIRST, orally or intramuscularly for 10-20 days
  • 1st generation cephalosporin or macrolide if allergic to penicillin
  • cephalosporins can cross-react with penicillin; avoid in patients with a history of anaphylaxis to PCN
  • hospitalization for monitoring & IV antibiotics recommended in severe cases and infants, elderly patients and immunocompromised
  • coverage for Staph aureus not necessary in typical infections
  • most common complications of erysipelas: gangrene, thrombophlebitis, abscess
  • uncommon complications: (<1%)-acute glomerulonephritis, endocarditis, septicemia, streptococcal toxic shock syndrome
48
Q

What is the presentation of impetigo?

A
  • nonbullous impetigo (caused by GABHS), S aureus–appears later in infection; produces bacteriotoxins toxic to strep
  • most common form
  • caused by staph
  • affects skin on face/extremities that has been affected by bites, cuts, abrasions, or diseases like varicella
  • vesicles, pustules, sharply demarcated honey-colored crusts
  • bullous impetigo: coagulase-positive S aureus predominates, strain produces exfoliating toxin causing subcorneal epidermal cleavage, MRSA isolated in 20%
  • epidermal layer sloughs, lots of skin loss
  • may present as folliculitis: impetigo of hair follicles caused by S. aureus
  • GABHS skin infection or carrier-minor trauma may cause impetigo lesions within 1-2 weeks
  • 30% colonized in anterior nares by S aureus (60-70% patients with eczema)
  • impetigo seldom progresses to systemic infection, but poststreptococcal glomerulonephritis is a rare complication with GABHS infection only
49
Q

What is the treatment for impetigo?

A

topical mupirocin (2-3x a day for 7 days) for single lesions of nonbullous impetigo

systemic antibiotics for bullous impetigo/extensive involvement:

  • beta-lactamase resistant antibiotics (cephalosporins, amoxicillin-clavulanate, cloxacillin, dicloxacillin)
  • cephalexin for oral antimicrobial therapy in children
  • community-acquired MRSA covered by alternative antibiotics - clindamycin, trimethoprim-sulfamethoxazole & vancomycin
  • erythromycin and clindamycin alternatives with penicillin hypersensitivity
  • ANTIHISTAMINES!

clinical medicine (12 decks)

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