Bio 251 chapter 21

What are immune defense mechanisms of the skin; understand how they protect from microbial invasion?

Unbroken skin is an effective barrier

 Defense mechanisms:

 Salt, dry slightly acidic environment; dead

skin cells constantly shed

 Normal microbiota are adapted; less

favorable for pathogens

 Skin-associated lymphoid tissue (SALT)

Gram stain of

Staphylococcus aureus

What are the pathogens that can cause skin infections; and what are the factors that determine whether of not an infection establishes?

Staphylococcus aureus

 Staphylococcus epidermidis (often opportunistic)

 Streptococcus spp.

 Rickettsia

 Bacillus anthracis

 Virus – Varicella zoster

we know that the factors are Cuts, punctures, burns, chemical injury, and

insect or tick bites can break barrier, provide

entry for pathogens

Know the characteristics of Staphylococcus aureus

Shape: Gram-positive cocci (round-shaped bacteria)

Arrangement: Grape-like clusters (under the microscope)

Gram Stain: Positive (thick peptidoglycan wall, stains purple)

Oxygen Requirements: Facultative anaerobe (can survive with or without oxygen)

Catalase Test: Positive

(Catalase breaks down hydrogen peroxide; this helps differentiate it from Streptococcus species.)

Coagulase Test: Positive

(Produces coagulase, an enzyme that clots plasma — important for diagnosis.)

How is Staph aureus identified?

Gram +, salt tolerant

 Present in nasal environment, moist skin.

 Easily spread person to person

 Survives well in the environment

 Many strains

 Has virulence factors

Use catalase test to distinguish from Streptococcus

 S. aureus are catalase – positive; Streptotcoccus are catalase-negative

 Growth on Mannitol salt

 S. aureus are Salt tolerant and ferment mannitol (cause media to turn yellow). S.

epidermidis do not ferment mannitol

 Test isolated bacteria for antibiotic sensitivity

 E.g. Kirby-Bauer; Etest

Characteristics of Staph infections

Pus, Inflammation, Fever (systemic infection)

 Some strains cause toxic shock syndrome (high fever, muscle aches, shock, rash,

diarrhea)

What are the virulence factors of Staph aureus and what do they do

Capsule – inhibits phagocytosis

 Coagulase – produces clots; slows progress of

leukocytes to infected area

 Hyaluronidase – degrades hyaluronic acid (which holds

cells together)

 Proteases - Degrade collagen; damages host tissues

 Lipases – degrade lipids

 Alpha-toxin – makes holes in cell membranes

 Leukocidins – kill WBCs

 Hemolysins (cytotoxic to cells)

 Protein A - Binds Fc portion of antibodies; inhibits

phagocytosis

Virulence factors of S. aureus

Explain what MRSA is

Methicillin resistance in S. aureus caused by mutation of a penicillin-

binding protein

 Resistance to beta-lactam antibiotics is due to the presence of the mecA

gene

A leading cause of hospital-acquired infections

What is the MecA gene; how does it make the bacteria resistant?

MecA encodes transpeptidase PB2a

 A PBP that has lower affinity for beta-lactam antibiotics (hence making the drug

ineffective)

 Resistance is transferred between S. aureus organisms by

bacteriophages via transduction

Impetigo

(both) – superficial skin infection

 Small, fluid-filled blisters

Erysipelas

both, more often S. pyogenes)

 Affects skin and superficial tissues

Cellulitis

(both, more often S. pyogenes)

 Infects deeper layers of skin and underlying tissue

 Bacteria enter through skin breaks/wounds

Necrotizing fasciitis

(both, more often S. pyogenes)

 Highly invasive; high morbidity and mortality

 Can also be caused by Clostridium, Escherichia coli, S. aureus, and Aeromonas

Know the characteristics of Pseudomonas aeruginosa

Gram-negative rod; w/ polar flagellum

 Aerobic; biofilm formation

 Produces pigments

Where is Pseudomonas commonly found?

Widespread in the environment (soil/water).

 Grows easily on many substrates (even distilled water)

 Soaps, ointments, eye drops, contact lens solutions,

cosmetics, disinfectants, swimming pools, hot tubs,

even distilled water

 Introduced into hospitals on ornamental plants, flowers,

fruit baskets

 Not allowed in burn wards or intensive care units

 Also found on hospital equipment, soles of shoes,

illegal injectable drugs

Flagella stain of Pseudomonas

What infections can Pseudomonas cause?

Cause of some nosocomial infections.

 Lung infections; wound infections (especially burn patients);

wounds may show green pus

 Community-acquired infections.

 Frequently an opportunistic pathogen.

 Skin rashes, eye infections, foot, ear, etc.

 Characteristics

 Some strains produce biofilms, pigments (pyocyanin).

 Many strains carry antibiotic resistance

characteristics of clostridium perfringens

Gram-positive rods (bacilli)

Anaerobic (lives without oxygen)

Spore-forming (makes hardy spores that survive harsh conditions)

Non-motile (unlike many Clostridium species)

Found in soil, intestines (human and animals), sewage.

characteristics of clostridium tetani

General Characteristics:

Gram-positive rods (bacilli)

Anaerobic

Spore-forming (spores are highly resistant and found in soil, dust, rusty objects)

Motile (has flagella — "drumstick" appearance under microscope)

What are the viral pathogens that cause skin infections; and what infections?

Human Papilloma virus (HPV), HSV 1-, Roseola

Human Papilloma virus (HPV)

Cause common warts, plantar warts, flat warts, and filiform

warts. HPV can also cause sexually-transmitted genital warts

HSV 1- cold sores, fever blisters

Following initial infection, virus remains latent until

reactivation

 Virus is spread when active lesions break open

Roseola

caused by herpesvirus 6; Fith disease

caused by parvovirus b19 – cause mild skin rashes;

mostly self-limiting in children; immunocompromised

individual may experience complications

Other pathogens causing skin infections

Tineas

Caused by fungal molds called dermatophytes

 Cause cutaneous mycoses (ringworm)

Candida Albicans

Cutaneous candidiasis

 Localized on skin and nails

Tinea corporis

ringworm infecting the body

Tinea Capitis

Ringworm but on the head scalp

Tinea

pedis like athletes foot or ring worm on foot

Tinea barbae

barbers itch or Beard fungal infection

Tinea cruris

Jock itch or groin area fungal infection

Tinea ungulum

fungal infection of the nails, often leading to discoloration and thickening.

Know about Varicella virus

known as Chicken Pox

Signs and symptoms: fever, headache, malaise, rash; incubation period

10 to 21 days

• Most childhood cases mild

• Lesions on head, chest, back; perhaps on mucous membranes

• Lesions are pruritic (itchy); secondary skin infections by S. pyogenes or S.

aureus

• More severe in adults; about 20% develop pneumonia

• Damages lungs, heart, liver, kidneys, and brain in immunocompromised

individuals; death results in approximately 20%

Maybe we have to know about shingles

Reactivation of latent Varicella later in life; Shingles vaccine for people 60+;

Reduces chance of developing shingles

• Painful rash along area supplied by involved sensory nerve; No

person-person transmission Source:

causative agent of vericella

Causative agent

• Varicella-zoster virus (VZV) of

Herpesviridae: enveloped, double-stranded

DNA virus

Pathogenesis of vericella

Virus enters respiratory route; replicates in lymph nodes, travels to skin

• Virus enters nerve, travels to ganglia

• Decline in immunity poses risk of Shingles (elderly and immunocompromised)

Characteristics of streptococcus

S. aureus are catalase – positive; Streptotcoccus are catalase-negative

Streptococcus pyogenes vs. Staphylococcus aureus

For pyrogenes they produce this thing called M protein

For aureus they have this fc receptor or protein a

Streptococcus pyogenes

Chains of Gram-positive cocci

Beta-hemolytic colonies; catalase-

negative, coagulase negative, obligate

fermenter

Cell wall contains group A

polysaccharide, an Fc receptor

(protein G), and M protein. Bacterium

produces hemolysins (streptolysins O

and S), streptokinase, DNase,

hyaluronidase, and others

impetigo is caused by pyrogenes

scalded skin syndrome

Caused by the toxin exfoliatin (about 5%

strains of S. aureus.

 Risk of secondary infections