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
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”
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
3
Q
When do nits hatch?
A
8-10 days, reach maturity in 10 days
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)
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!
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
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
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
9
Q
Are lice pruritic?
A
YES!!
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
11
Q
What does scabies “imitate”?
A
- spectrum of cutaneous manifestations
- results in delayed diagnosis
- “7 year itch” described persistent, undiagnosed scabies infestations
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
13
Q
What are scybala?
A
feces: causes itchiness in scabies infestations
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
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
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
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
18
Q
What are the components of brown recluse venom?
A
8 components including enzymes, hyaluronidase, deoxyribonuclease, alkaline phosphatase, lipase
19
Q
What is responsible for most of the damage by brown recluse?
A
Sphingomyelinase D
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
- edema/ischemic bite site-erythematous halo around the lesion
- 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
Describe black widow sexual cannabalism
- 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
What is the toxin that causes lactrodectism (black widow spider bites)
Neurotoxin latrotoxin
26
How do black widow bites present itself? (3 phases)
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
What is the exacerbation phase in a black widow bite?
- 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
Describe the residual phase (black widow spider bite)
- 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
What is the treatment for black widow bites?
- pain medication
- muscle relaxants
- activenom
30
What is cellulitis?
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
What is facial cellulitis associated with in children?
H influenzae type B and S pneumoniae
| seen less so with vaccines
32
What is varicella?
- 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
What is MRSA? (cellulitis)
- 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
What are the pathogens in cellulitis?
- 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
What are the 4 main important presentations of cellulitis?
Rubor-redness
Calor-heat
Dolor-pain
Tumor-edema (swelling)
36
What are other important presentations of cellulitis?
- 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
What are human bite complications of cellulitis?
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
What are comorbid conditions of cellulitis that may place patients at higher risk for infection?
```
diabetes mellitus
chronic edema of region
prior splenectomy
liver disease
immunosuppression
presence of a prosthetic valve or joint
regional arterial or venous disease
```
39
Common treatments for cellulitis
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
Treatments with people who have severe cellulitis
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
What is empiric?
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
What is erysipelas?
bacterial infection of upper dermis extending into superficial cutaneous lympatics
43
Where is erysipelas seen on body and what causes it?
85% cases involve legs, caused by streptococcus pyogenes (st anthonys fire)-- other bacteria involved could be staph, gram-negative species
44
What is pathophysiology of erysipelas?
- 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
At what age does erysipelas occur?
60-80 years old
immunocompromised patients
lymphatic drainage problems (after mastectomy, pelvic surgery, bypass grafting)
46
How is erysipelas presented?
- 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
What is the treatment for erysipelas?
- 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
What is the presentation of impetigo?
- 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
What is the treatment for impetigo?
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!
