Diseases of Skin and Eyes Chapter 16

Epidermis

top layer

replaced every 25-45 days

Stratum corneum

layer in epidermis

dead cells that have migrated from deeper layers

Dermis

contain sebaceous glands and hair follicles

blister formation

result of separation of epidermis and dermis

sebaceous glands

secrete sebum and are associated with hair follicles

antimicrobial peptides

positively charged chemicals in the skin that disrupt the negatively charged membranes of the bacteria

keep microbial count on skin relatively low

Sebum

low pH (acidic) makes skin inhospitable to microorganisms

high lipid concentration serve as nutrients for normal microbiota

Sweat

inhibit microorganisms due to low pH (acidic) and high salt concentration

Lysozyme

enzyme found in sweat, tears, and saliva

break down peptidoglycan

works best on Gram positive bacteria

Normal skin biota

streptococcus

staphyloccus

corynbacterium

propionibacterium

pseudomonas

lactobacillus

yeasts such as Candida

Staphylococcus sp. general info

gram positive cocci

S.aureus is main pathogenic species

white-bronze colored colonies on agar

withstands high salt, extreme pH, and high temps

Staphylococcus physiology and structure

capsules

peptidoglycan outer layer (endotoxin like effect)

Protein A (binds IgG)

Characteristics of MRSA

resistant to multiple antibiotics

Staphylococcus aureus

remains viable after air drying

signs and sx of MRSA

raised, red, tender localized lesions

pus

hot to touch

may localize around a hair follicle

fever

trasmission of MRSA

direct or indirect contact

any surface

culture/diagnosis of MRSA

PCR

isolation on SBA or MSA

positive catalase distinguishes S.aureus from other streps

MRSA prevention/treatment

good hygiene

incision of lesion and pus drainage

multiple antimicrobial treaments

MRSA toxins

Alpha, beta, gamma, delta, hemolysins

Exfoliative toxins: cause skin to blister + peel

MRSA enzymes

coagulase, catalase, hyaluronidase, fibrinolysin, nuclease, penicillinase

MRSA virulence factors

Leukocidin: kills neutrophils

Catalase: inhibits antibacterial activities

Hyaluronidase: dissolves cell-cell connection

Scalded skin syndrome (SSS): exfoliative toxin

Toxic shock syndrome (TSS)

Slime production: capsule like layer

Hemolysin: rupture RBC

Protein A: bind Fc region of IgG antibodies/ attachment

antibiotic resistance: penicillinase and beta lactimase

Scalded skin syndrome

pediatric, large bullae (blister) formed under the skin and rupture

Toxic shock syndrome sx

high fever, headache, confusion, macular rash, conjunctival injection, vomiting, diarrhea

caused by S aureus

Penicillinase

inactivates penicillin

usually associated with a plasmid

85% of S aureus are resistant to _______-

penicillin G

what is used to treat S aureus

vancomycin

starring to see VRSA

S aureus coagulase/catalase

coagulase: +

catalase: +

Characteristics of impetigo

superficial bacteria that causes the skin to flake

Bacteria that cause impetigo

Staphyloccoccus aureus or Streptococus pyogenes

which bacteria begins every case of impetigo

streptococcus pyogenes

which bacteria often takes over/ outcompetes in cases of impetigo

Staphylococcus aureus

Signs and sx of impetigo

peeling skin, honey-colored crusts

lesions around mouth, face, and extremities

Impetigo caused by Staphylococcus aureus

exfoliative toxins A and B cause blistering and spread of the bacterium

Streptococcus pyogenes differentials

Gram positive coccus

Beta hemolytic on SBA

negative catalase

Diseases caused by streptococcus pyogenes

streptococcus pharyngitis, scarlet fever, pneumonia, puerperal fever, necrotizing fasciitis, bacteremia

which organism is more likely to cause impetigo in newborns

Streptococcus pyogenes

which organism is more likely to cause impetigo in children

Staphylococcus aureus

Mupirocin

inhibits protein synthesis

Gram + and some Gram negative

Impetigo antibiotic treatments

mupirocin

Cephalosporins, Amocicillin-Clavulonic Acid

Penicillin (only if S. pyogenes)

Cephalosporins

inhibit cell wall synthesis

Amoxicillin-Clavulonic Acid

covers Beta-lactamase producing strains

Macropapular diseases

Measles, Rubella, Fifth Disease, Roseola

Measles (rubeola) signs and sx

• sore throat

• dry cough

• headache

• conjunctivitis

• lymphadenitis

• fever

• red, macropapular exanthem that begins on head and spreads to trunk and extremities

• Kopliks spots

exanthem

widespread rash from a virus or bacteria

Subacute sclerosing panencephalitis

degeneration of the cerebral cortex, white matter, and brainstem

involves a defective measles virus

measles pathogenesis and virulence factors

implant on respiratory mucosa, travel to lymphatic system and enters bloodstream which then goes to the skin

causes host cells to fuse together and not preform properly

transmission of mealses

respiratory droplets

how to test for measles

ELISA to test for IgM antigens

attenuated

modified weaker viruses in vaccines

treatment for measles

treating sx

rubella causative agent

rubivirus

Rubella virulence

stop mitosis in fetuses

apoptosis of tissue cells, causing harm to organs

damages vascular endothelium

characteristics of rubella

minor rash with few complications

serious damage in utero (teratogen)

german measles

rubella

how is rubella diagnosed

IgM antibody detection through ELISA

when is rubella virus shed

through prodromal phase and up to a week after rash appears

Fifth Disease

Parvovirus B19

Erythema infectiosum

fifth disease

how is fifth disease diagnosed

clinical presentation and ruling out rubella through testing for IgM antibodies

Fifth disease prevention and treatment

no vaccine and no treatment

Roseola causative agent

human herpesvirus 6 (HHV-6)

roseola transmission and epidemiology

it is though 100% of US population is infected by adulthood

roseola prevention and treatment

no vaccine and no treatment

Cellulitis

fast spreading infection in the dermis and subcutaneous tissue

lymphangitis

red lines leading away from the area of cellulitis

result of microbes being carries by the lymphatic system

cellulitis signs and sx

pain, tenderness, swelling, warmth

fever and swelling of the lymph nodes

cellulitis causative agents

in healthy individuals: staphylococcus aureus or streptococcus pyogenes

immunocompromised individuals: any bacteria, some fungi

infants: group B streptococci

group B strep

can naturally occur in the body

typically only cause disease in immunocompromised/infants/elderly

cellulitis transmission

introduction of bacteria into dermis, trauma ect.

cellulitis diagnosis

clinical sx

cellulitis treatment

oral or IV antibiotics

Styaphylococcal scalded skin syndrome (SSSS)

dermolytic skin condition caused by S. aureus

affects mostly newborns and babies

SSSS signs and sx

bullous lesions (fluid filled blister), widespread dequamation of skin

SSSS causative agent

staphylococcus aureus

exfoliative toxins A and B

SSSS transmission

from baby to baby or caregivers may be asymptomatic carriers

SSSS diagnosis

clinical sx

SSSS prevention and treatment

prevent contact w carriers

systemic antibiotics

Vesicular or Pustular rash diseases

chickenpox and smallpox

pox

individual lesions that contain fluid

Chickenpox causative agent

Alphaherpesvirus 3 aka Varicella-Zoster Virus

Chickenpox signs and sx

fever and rash that starts on scalp/face and trunk and radiates to extremeties

macules

flat spot

papules

raised bump

centripetal

more lesions in the center of the body than in the extremities

Shingles causative agent

Herpes zoster that enter sensory endings of spinal nerves after chickenpox

can be reactivated by stress, immunosuppressive therapy

shingles signs and sx

persistent vesicles

pain and tenderness

eye inflammation and facial paralysis

chickenpox/shingles pathogenesis

enters respiratory tract and invades bloodstream then moves to skin

virus then enters sensory nerves and remains latent

chickenpox/shingles prevention and treatment

vaccines

treat sx, no aspirin as may lead to Reye’s syndrome

smallpox signs and sx

fever, rash that starts in pharynx and then spreads to face and extremities

variola major

highly virulent

causes toxemia, shock, and intravascular coagulation

rash w bumps filled w thick, opaque fluid

variola minor

minor, less dense rash

smallpox causative agent

variola virus

smallpox transmission

droplets, contaminated bedding and clothing

smallpox prevention/treatment

vaccine, no treament

Cutaneous leishmaniasis causative agent

leishmania tropica

mucocutaneous leishmaniasis causative agent

leishmania brasiliensis

leishmaniasis transmission

female sand flies

leishmaniasis diagnosis

microscope visualisation, giemsa stain

leishmaniasis prevention/treatment

no vaccine, avoiding sand fly is the only way

leishmaniasis

parasitic disease

Cutaneous anthrax causative agent

bacillus anthracis