Microorganisms And Skin

Front 1

What are the three basic layers to the skin?

Back 1

-Epigermis-living layer of epithelias cells, producting and covered by a dead layer of keratin
-Dermis- an underlying layer of connective tissue, rich in sweat and oil glands, along with nerves and blood vessels
- subcutaneous tissue (fat and muscle)

Front 2

Abscess

Back 2

localized collection of pus and associated inflammation

Front 3

Vesicle

Back 3

a fluid filled blister (thin-walled sac)

Front 4

rash

Back 4

an area of irritated skin

Front 5

erythema

Back 5

reddening of the skin due to capillary congestion

Front 6

cellulitis

Back 6

acute inflammation of the connective tissue of the dermis

Front 7

wart

Back 7

a rough area of hyperplasia due to the action of a papillomavirus

Front 8

when a patient presenting with skin lesions comes into a docotors office, what are they evaluation based on?

Back 8

-the pertinent medical history
-the appearance of the lesion
- culture or histopathology of the lesion
-diagnostic testing for the presence of particular agents

Front 9

(varicella-Zoster virus) VZV characteristics

Back 9

- a herpesvirus with a tropism for nerve cells
-ubiquitous
-dual life cycle: can be in replicative or latent stage
-forms giant multinucleated cells
> presented as chicken pox (varicella) in children and presented as shingles (zoster) in adults upon the reactivation of a latent chickenpox infection

Front 10

varicella pathogenisis

Back 10

-primary chickenpox is a systematic disease
-symptoms: rash (vesticular lesions), ffever, malaise, self limited
-replicates int he oropharygeal region, then disseminates systematically via lymphocytes
-complications
>secondary bacterial infections of the viral skin lesions
> encephalitis
>viral pneumonitis
>Reye's syndrome

Front 11

zoster (shingles)

Back 11

-reactivation of latnet varicella infection
-latent state int eh dorsal root, latently infected nerve cells have avoided alerting CMI surveillance, since neurons can't present antigen
> pathogenesis directly related to replication during lytic cycle

Front 12

(varicella-Zoster virus) VZV epidemiology & treatment

Back 12

> chickenpox deisseminatin to the respiratory mucosa is responsible for the transmission of the virus to others
>highly contagious
> spread through repiratory droplet
> late winter/early spring
> vaccines available
> individual with primary chickenpox infection cannot cause shingles in other individuals; people with shingles cannot caue shingles in other individuals. people with singles can cause primary chickenpox in susceptible individuals

Front 13

Tinea unguium

Back 13

-due to dermatophyte T. rubrum
-hydrolyzes keratin (infections of hair skina nd nails)
-tinea refers to a fungal disease of the skin

Front 14

Tinea epidemiology

Back 14

-can be spread form infected person or fomite
-can be diagnosed macroscopically or microscopically

Front 15

tinea treatment

Back 15

-since fungi are eukaryotes, treatment target at unique structures is essential in order to avoid toxic side effects
-polyenes (amphotericin)-binds to ergosterol a molecule unique to fungal membranes but similar to mammalian sterols
-azoles (flucanazole)- that inhibit ergosterol synthesis

Front 16

tinea- pathogenisis

Back 16

-dermatophytes possess keratinases, allowing them to hydrolyze keratin containing material
- rarely invade/ penetrate into deeper tissues
ringworm is due to the expanding circle of inflammatory response as the fungal hyphe grow outward from the original site of infection
the host causes the expanding rings (inflammatory response)

Front 17

Staphylococcus aureus

Back 17

-associated with CA and HA (nosocomial) infections
-can be acquired from endogenous and exogenous
sources
-MDR strains are becoming a problem; resistant to beta lactams, aminoglycosides, tetracyclines, macrolides, and fluoroquinolones
-indigenous microflora part of the anterior nails, skin, and GU tract
- some S aureus strains are resistant to methicillin (MRSA)

Front 18

infections due to S. aureus

Back 18

-Folliculitis – inflammation around hair shaft
-Furuncles and carbuncles – localized skin abscesses, starting as folliculitis
-Impetigo - Superficial infection of the skin usually seen in children:
-Wound infection- frequently post-surgical
-Foreign body infection- usually associated with medical devices.
-Mastitis- infected milk gland
-Staphylococcal food poisoning
-Osteomyelitis – infection of bone
-Necrotizing pneumonia- frequently secondary to influenza infection
-Bacteremia – organisms multiplying in the bloodstream (potential for endocarditis)
-Erysipelas – superficial cellulitis

Front 19

S. aureus virulence factors

Back 19

• Adhesins- fibronectin-binding proteins- important in adherence to endothelial surfaces and foreign objects such as intravascular devices; also key in endocarditis
• Hyaluronidase - degrades acellular matrix of connective tissue; important in spread of organism through tissue
• Hemolysins – membrane damaging toxins – five have been recognized, including Panton-Valentine leukocidin - creates lytic pores in the membrane of leukocytes, releasing cytokines that contribute to skin/soft tissue infections as well as pneumonia
• Epidermolytic toxins- superantigens, cause exfoliation of skin
• Enterotoxins - produced by half of Staphylococcus aureus strains - heat stable proteins – act as superantigens, including Toxic Shock Syndrome Toxin (TSST)
• Protein A - binds the Fc portion of IgG coating the bacteria so it may not be seen as “foreign” by phagocytes; may have a role in immune evasion
• Inhibition of opsonization/phagocytosis – various molecules involved

Front 20

S. aureus antimicrobial resistance

Back 20

• Penicillin and cephalosporin resistance - due to the production of multiple beta-lactamases.
• Oxacillin (methicillin) resistance - due to modification of penicillin binding protein resulting in decreased binding of all beta-lactam drugs to the bacteria.
o MRSA first arises in hospital settings
o Community acquired MRSA (CA-MRSA)
• Multi-drug resistant strains of S. aureus are resistant to other classes of antimicrobials including aminoglycosides, tetracyclines, macrolides, and fluoroquinolones.
• Vancomycin resistant Staphylococcus aureus (VRSA) - first seen in US in 2002 - vanA gene from Enterococcus faecilis was transferred to Staphylococcus aureus