Module 17 LO

1. epidermis: physical barrier to pathogens

2. dermis: has ducts and points of entry to deeper tissues

3. sweat: lysozyme, salt, and other antimicrobial properties are inhibitory

4. sebum: fatty acid is inhibitory, but sebum can also be a nutrient source.

describe structures of the skin that contribute to infection: [4]

Gram-positive cocci (staphyl, entero) can survive on the skin and grow (resistant to drying and high salt)

Gram positive pleiomorphic rods (Cutibacterium acnes) are normal inhabitants of hair follicles. They feed off sebum, contributing factor in acne. Produces propionic acid, contributes to acidic skin pH

examples of normal skin microbiota: [2]

staphylococcus aureas

Folliculitis, furnucles, carbuncles causative agent:

Through natural openings in the skin (e.g., hair follicles)

Folliculitis, furnucles, carbuncles transmission:

Topical antibiotics

Folliculitis, furnucles, carbuncles treatment:

Direct contact

transmission for nonbullous impetigo

topical antibiotics

treatment for nonbullous impetigo

staphylococcus aureas

nonbullous impetigo causative agent

exfoliative toxin A (exotoxin from staphylococcus aureas)

bullous impetigo causative agent:

exfoliative exotoxin B

staphylococal scaled skin syndrome causative agent:

toxemia results from production of toxic shock syndrome toxin 1 (TSST-1)

Staphylococcal toxic shock syndrome causative agent:

fever, vomiting, sunburn-like rash, followed by shock and sometimes organ failure

Staphylococcal toxic shock syndrome S+S [5]

streptococcus pyogenes, can involves streptococcus aureas

erysipelas causative agent [2]

bright red patches with raised margins on the skin, high fever,

erysipelas S+S [2]

enters through breaks in skin (cuts, burns, bites, puncutres, surgery, ulcers)

erysipelas transmission

GAS, streptococcus pneumoniae and staphylococcus aureas

cellulitis causative agents: [3]

wounds, surgery, IV punctures, animal bites. Chronic skin contiditions can increase risk

Cellulitis transmission [5]

redness, swelling, pain, warm and tender site, fever and chills

cellulitis S+S [6]

skin assessment

Diagnosis of celulitits

bacteremia, osteomeletis, bacterial endocarditis

comlications of cellulitis [3]

oral antibiotics that target GAS

treatment for cellulitis:

GAS

streptococcal toxic shock syndrome causative agent

GAS is most common

necrotizing fasciitis causative agent:

-          red, warm, swollen, severe pain, fever

Early S+S of necrotizing fasciitis [5]

-          : Ulcers, blisters, black spots, pus, dizziness, fatigue, Nausea and diarrhea

later signs of necrotizing fasciitis [8]

Staphylococci: can be coagulase positive or negative, are only pathogenic if they have an opportunity to penetrate broken skin resulting from wounds or medical procedures (removal of catheter from vein)

             ** Can form biofilms on surfaces.

staphylococci general characteristics

-          Can survive for months on surfaces

-          the cell wall is resistant to lysozyme, and it produces proteins that neutralize antimicrobial peptides in perspiration.

-          Coagulase-induced fibrin clots protect the cells from phagocytes that are attracted to the site of infection.

-          Leukocidins produced by the bacteria can kill phagocytes that are encountered.

-          The bacteria are resistant to opsonization, a process that tags pathogens for destruction by phagocytes.

-          Cells that are phagocytized can survive within phagosomes.

-          Produces toxins that facilitate spread or cause damage to tissues

-          Some can cause sepsis or prduce enterotoxins (foodborne infections)

-          Resistant to multiple antibiotics, considered an emergent threat in hospitals and the community

Staphylococcus aureas mechanisms of pathogenicity: [9]

-          Produces different enzymes, including hemolysins.

-          they are classified as beta-hemolytic (cause complete cell lysis), alpha-hemolytic (cause partial cell lysis) or gamma-hemolytic (nonhemolytic) depending on the hemolysins produced

-          beta-hemolytis are associated frequently with disease in humans

general characteristics of streptococci

-          produces streptolysins that lyse red blood cells and are toxin to neutropils

-          surface M protein plays a role in adherence to host cell and evasion of host defensees

-          Capsule made of hyaluronic acid to protect from phagocytosis and is poorly immunogenic

-          Produces extracelllar enzymes that enable spread of bacteria through host

pathogenic properties of GAS

streptokinase, dissolves clots;

hyaluronidase, breaks down hyalurinoc acid in connective tissue;

deozyribonucleases, degrades DNA

extracellular enzymes produces by GAS [3]

-          Varicellovirus human alphaherpesvirus 3,  also known as human herpesvirus 3 (HHV-3) or the varicella-zoster virus.

chickenpox causative agent

-          enters the body via respiratory system and localizes to skin within 14 days

varicella transmission

rash, fever, tiredness, headache, anaorexia, blisters that scab

varicella S+S [6]

-          : bacterial skin and tissues infections, pneumonia, sepsis, reyes syndrome

varicella complications [4]

-          : manage S+S of illness, OTC antipyretics, calamine lotion and cold bath with oatmeal or baking soda, antivirals  for high risk

varicella treatment [4]

-          MMR vaccine (live attenuated vaccine)

varicella prevention

(same as varicella then…) Virus enters peripheral nerves and moves to dorsal nerve ganglion

shingles transmission

-          : rash similar to chickenpox or one side of the body, pain, tingling, itching, fever, headache, chills, gastrointestinal upset

shingles S+S [8]

skin assessment, history

shingles diagnosis

antivirals if rash appears

shingles treatment

vaccine (shingrix)

shingles prevention