Module 12: Skin and Eye Infections Flashcards

1
Q

Skin Defenses

A
  • keratin
  • sloughing of skin
  • antimicrobial peptides
  • sebum
  • sweat (lysozyme)
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2
Q

Skin Infections Caused by Staphylococcus aureus

A
  • folliculitis
  • scaled skin syndrome
  • toxic shock syndrome
  • HA-MRSA and CA-MRSA
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3
Q

Folliculitis

A
  • mild superficial inflammation of the hair follicles or glands
  • can lead to an abscess
  • furuncle (boil)
  • carbuncle
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4
Q

Furuncle

A
  • single hair follicle or gland becomes inflamed and progresses into a large abscess
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5
Q

Carbuncle

A
  • cluster of furuncles that are interconnected
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6
Q

Scalded Skin Syndrome

A
  • affects mostly newborns and babies
  • sign and symptoms: large areas of skin peel off or fall away, layer of skin slips off with gentle pressure leaving wet red areas
  • pathogenesis: exfoliative toxins A and B, exotoxins enter the bloodstream, toxins cause bulls lesions, slips occurs in epidermal layers
  • direct contact and droplet contact
  • 30% of adults are asymptomatic carriers
  • treatment IV antibiotics
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7
Q

Toxic Shock Syndrome

A
  • signs and symptoms: rash which looks like severe sunburn -> peels off after a few days
  • pathogenesis: toxic shock syndrome toxin (TSST), superantigen = potent stimuli for T-cells, activates T-cells at a rate 100x greater than ordinary antigens, cause release of cytokines
  • treatment IV antibiotics
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8
Q

HA-MRSA and CA-MRSA

A
  • healthcare-acquired methicillin resistance Staphylococcus aureus
  • community-acquired methicillin resistant Staphylococcus aureus
  • encode enzyme called B-lactamase
  • virulence factors enzymes expressed: coagulase, hyaluronidase, lipases
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9
Q

HA-MRSA

A
  • associated with hospital stays on long term care facilities
  • immunocompromised
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10
Q

CA-MRSA

A
  • healthy individuals
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11
Q

MRSA

A
  • lesions are raised, red and tender
  • warm to tough, pus secretion
  • consider a serious threat by the WHO
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12
Q

Skin Infections caused by Streptococcus pyogenes

A
  • cellulitis
  • erysipelas
  • scarlet fever
  • necrotizing fasciitis
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13
Q

Cellulitis

A
  • infection in the dermis and subcutaneous layers of the skin
  • tight glossy stretched appearance of skin
  • affected area is warm to touch
  • pathogenesis: produces hyaluronidase
  • treatment: penicillin, cephalexin
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14
Q

Erysipelas

A
  • enters through a small wound in face of extremities
  • site of entry becomes redder and skin texture like orange peel
  • lesions spreads and edge is slightly elevated and warm to touch
  • treatment: penicillin
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15
Q

Scarlet Fever

A
  • red rash - sand paper texture
  • strawberry tongue - sometimes whitish coating
  • pathogenesis: erythrogenic toxin is produced, super antigen, production of rash and fever
  • treatment: penicillin or cephalexin
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16
Q

Necrotizing Fasciitis

A
  • flesh eating disease
  • centre of bump may become blackened
  • pathogenesis: Exotoxin B, bacteria spreads
  • treatment: IV antibiotics, surgery, amputation
17
Q

Viral Skin Infections

A
  • oral herpes
  • chicken pox/shingles
  • rubella
  • measles (covered in assignment)
18
Q

Oral Herpes

A
  • Herpes Simplex 1 Virus (HSV-1)
  • vesicles filled with fluid in or around mouth
  • pathogenesis: enters through oral mucosa, stays dormant in nerve cells, reactivates and travels to area of cold sore
  • very contagious
  • no prevention
  • treatment: usually self-resolved
19
Q

Chicken Pox/Shingles

A
  • Varicella-Zoster Virus (VZV), human Herpesvirus 3
  • itchy rash -> blisters filled with fluid
  • pathogenesis: enters respiratory tract and attaches to respiratory mucosa -> blood stream -> skin, causes adjacent cells to fuse and lyse
  • contagious until all lesions have crusted over
  • virus enter dorsal root ganglion and remains dormant (protect from immune system), then re-emerges as shingles
  • transmission: respiratory droplets and fluid of the skin lesions, most contagious a day or two prior to rash development
  • prevention: live attenuated vaccines
  • treatment: none
20
Q

Rubella

A
  • Rubella virus
  • mild rash, joint inflammation and pain
  • diagnosis - look for presence of rubella genetic material, or antibodies against rubella
  • congenital Rubella, mother can still transmit disease if asymptomatic, first trimester -> miscarriage or permanent defects in a newborn
  • pathogenesis: multiplies in respiratory tract -> lymph nodes -> spreads to rest of body; has ability to stop mitosis; induces apoptosis of normal tissue; damages vascular endothelium -> poor organ development
  • transmission: contact with respiratory secretions
  • prevention: MMR vaccine, live attenuated
21
Q

Skin Mycoses (fungal infections)

A
  • Ringworm
  • Tinea versicolor
  • chromoblastomycosis
22
Q

Ringworm

A
  • pathogenesis: invade and digest Keratin, can suppress the immune system which allows persistence
  • transmission: direct or indirect contact with infected humans/animals
  • treatment: topical antifungal
23
Q

Tinea versicolor

A
  • superficial mycoses, outer epidermal surface
  • caused by the yeast genus Malassezia
  • scaling of skin, discoloured skin pigmentation
  • pathogenesis: yeast feeds on the high oil content of the skin glands
  • treatment: topical antifungal
24
Q

Chromoblastomycosis

A
  • chronic fungal infection
  • subcutaneous mycoses
  • papular lesions, which appear first on the extended slowly -> nodular -> large wart-like lesions
  • treatment: difficult to treat, Itraconazole
25
Q

Bacterial Infections

A
  • Pseudomonas aeruginosa
  • Gas Gangrene
26
Q

Pseudomonas aeruginosa

A
  • most common bacteria to infect wound of burn patients
  • virulent factors: proteases (digest proteins), exotoxin A (halts synthesis of proteins), Hemolysin (break down lipids in epithelial cells, bacteria penetrate deeper and spread infection)
  • treatment: topical antimicrobial agents, wound excision
27
Q

Gas Gangrene

A
  • caused by Clostridium perferingens
  • produces gas in affected tissue (muscle tissue)
  • blisters filled with brown-red liquid
  • pathogenesis: infection requires damaged or dead tissue, alpha toxin causes RBC to rupture and destroys tissue and generates gas
  • Prevention: rigorous cweaingin and surgical repair of deep wounds
  • Treatment: antibiotics alone are not effective, excision
28
Q

Eye Infections

A
  • Conjunctivitis (pink eye)
  • Keratitis
29
Q

Eye Defenses

A
  • tears
  • immunologically privileged
30
Q

Conjunctivitis (Pink Eye)

A
  • inflammation or swelling of the conjunctiva
  • bacteria -> milky discharge
  • viral -> clear watery discharge
31
Q

Neonatal Conjunctivitis

A
  • passed from mother to child
  • treatment: antibacterial eye drops
32
Q

Keratitis

A
  • inflammation of the cornea
  • invasion of deeper eye tissues
  • can lead to complete corneal destruction
  • herpes simplex type 1 or protozoa Acanthamocba (people who wear contact lenses)
  • gritty feeling in eye
  • sharp pain
  • sensitivity to light
  • treatment: topical trifluoride +/- oral acyclovir