LECOM MMS Microbiology Lecture 12A- Derm Bacterial

what is the gram stain and morphology for Staphylococcus aureus?

gram positive cocci, grape-like clusters

What are the virulence factors of S. aureus (for skin infections)?

exfoliative toxins (ETA and ETB)- relaxed and split intracellular bridges in the epidermis

Toxic shock syndrome toxin-1 (TSST-1)- super antigen, cytokine storm (this causes symptoms)

S. aureus scalded skin syndrome (SSSS) virulence factor?

ETA and ETB -> no organisms presents

what are the symptoms of S. aureus scalded skin syndrome (SSSS)

cutaneous blisters- filled with clear fluid and covers entire body

-About 2 days, skin will peel off, painful

At risk population for S. aureus scalded skin syndrome (SSSS)

infants and children, elderly and immunocompromised

Nikolsky's sign is positive for what bacteria and disease; What does the sign mean?

S. aureus and scalded skin syndrome (SSSS); Pulls skin off by barely pulling it off

What is a localized form of S. aureus scalded skin syndrome (SSSS)

Bullous impetigo

Bullous impetigo symptoms

formation of blisters, bacteria within them

Is bullous impetigo positive or negative for Nikolsky's sign

negative

what are the toxins responsible for bullous impetigo

ETA and ETB (exfoliative toxins)

What is the at risk population for bullous impetigo

infants and children

what is S aureus folliculitis

inflammation of the hair follicles

Folliculitis presentation (S. aureus)

raised and reddened follicle base

furuncle presentation (S. aureus)

extension of folliculitis

-base of hair follicle, deep infection

-Large, painful, and raised nodules

carbuncle presentation (S. aureus)

includes multiple follicles (more than one infected follicle)

S. aureus toxic shock syndrome clinical presentation

diffuse, macular erythematous rash- includes palms/soles

-Hypotension, fever, multiorgan system involvement

Desquamation (Skin peeling off) occurs about 1-2 weeks

Virulence factor for S. aureus Toxic Shock Syndrome

Toxic shock syndrome toxin-1 (TSST-1)

S. aureus lab characteristics: Gram stain

gram positive, cocci (grape-like) cluster

S. aureus lab characteristics: Blood agar?

Beta-hemolytic (complete lyse RBCs)

S. aureus lab characteristics: Mannitol-salt agar

turns agar yellow

-S. aureus reacts with mannitol, changes pH of agar, changing the color from red to yellow

S. aureus lab characteristics: biochemical tests? (Coagulase and catalase)

Coagulase (+)

Catalase (+)

Streptococcus pyogenes (Group A) causes what disease

group A beta hemolytic strep (GAS)

Morphology of streptococcus pyogenes

gram positive short-chain cocci

what area of the body does S. pyogenes (Group A) colonize

oropharnyx

susceptible population of Group A beta-hemolytic strep (GAS)

5-15 years

virulence factors for S. pyogenes

Streptococcal pyogenic exotoxins (SPE)- different types

-is a superantigen -> toxic shock

M protein- antiphagocytotic

Scarlet fever is a complication of what disease

pharyngitis

Virulence factor for Scarlet fever

Streptococcal pyrogenic exotoxin (SPE)

clinical presentation of Scarlet fever

strawberry tongue

Diffuse erythematous rash (Sandpaper rash)

-Starts on trunk and spreads to extremities (not on palms or soles)

- 5-7 days later desquamation occurs

pyoderma (Impetigo) is caused by what bacteria

S. pyogenes

Pyoderma (Impetigo) clinical presentation

vesicles develop (bacteria within) -> progress to pustules -> rupture and crust

-Honey crusted lesion

At risk population for pyoderma

children with poor hygiene

What bacteria causes similar symptoms to pyoderma caused by S. pyogenes?

S. aureus

erysipelas is caused by what bacteria

S. pyogenes

Erysipelas clinical presentation

Acute skin infection

-red, shiny, rash with raised borders

-Legs and butterfly rash on face

-ear involvement- Milian's ear sign

-Localized pain, inflammation, fever, chills

-well demarcated rash

Milian's ear sign is distinct in what disease?

Erysipelas (S. pyogenes)

Cellulitis is caused by what bacteria?

S. pyogenes

Clinical presentation of Cellulitis

infection of deeper dermis (very painful)

-less distinction b/n infected and uninfected areas (opp. of Erysipelas)

-No raised borders (opp. erysipelas)

Necrotizing fasciitis is caused by what bacteria

S. pyogenes

How does Necrotizing fasciitis begin and progress?

Starts as Cellulitis and progresses to a deep subcutaneous tissue infection (past the muscle layer) -> destruction of muscle and fat

Clinical presentation of Necrotizing fasciitis

intense pain, swelling and pain (progress to purple, blue, then gangrene), fever, vomiting, death

how to treat Necrotizing fasciitis

surgical debridement

S. pyogenes Lab characteristics: Culture- Blood agar

beta-hemolytic

S. pyogenes Lab characteristics: Catalase

Catalase (-)

S. pyogenes Lab characteristics: Bacitracin sensitivity?

Yes it is sensitive to bacitracin

which disease is resistant to bacitracin?

Streptococcus agalactiae

Mycobacterium leprae causes

leprosy

Gram stain and morphology of Mycobacterium leprae?

No gram stain (lacks cell wall)

acid fast rods

obligate intracellular

Transmission of Mycobacterium leprae

long-term direct contact, respiratory droplets, armadillos

Leprosy (Hansen's Disease) clinical presentation

can take up to 20 years for symptoms to appear

-Severity of disease depends on host's immune response

what are the two types of leprosy

tuberculoid and lepromatous

Tuberculoid leprosy (mycobacterium leprae) type of immune response

cell-mediated immune response (T-cells)

clinical presentation of tuberculoid leprosy

less severe, hypopigmented skin macules

-Well defined and raised

-Face, trunk, and extremities

Lepromatous leprosy type of immune response

weak cell mediated response (B-cells)

Clinical presentation of Lepromatous leprosy

more severe and infectious, loss of eyebrows, thickening and enlargement of the:

-Loss nostrils, ears, cheeks

-Lion-like facial appearance

lab characteristics of M. leprae

acid-fast rod (Ziehl-Neelsen stain)

Clostridium perfringens gram stain and morphology and where is it normally found?

Gram positive rods; Soil, water, etc., Anaerobic

Clostridium perfringens how does it transmit/enter the body

enters after trauma (gunshot/knife wounds, fractures, surgery, intramuscular injection)

80-90% of gas gangrene cases

virulence factors of Clostridium perfringens

exotoxins

-Alpha toxin: Lecithinase (phospholipase C), Lyses RBCs, WBCs, platelets, and endothelial cells

-I-toxin: disrupts host cell actin filaments- loss of structural integrity (Cell rounding -> cell death)

Gas gangrene clinical presentation (clostridium perfringens)

-necrotizes the muscle (intense pain)

-Skin becomes bronze -> purple/red

-blister formation (anaerobic-> air cannot enter skin due to blisters) and foul smelling discharge

-Systemic signs- fever, shock, multiorgan failure, tachycardia, fatal

-Progresses rapidly

treatment of gas gangrene

surgical debridement

susceptible populations for

Patients with atherosclerosis and diabetes are more prone to developing gas gangrene

-Limited blood flow with these diseases, WBCs, cannot get to site of infection

lab characteristics of clostridium perfringens: Blood agar

beta-hemolytic (alpha-toxin)

Lab characteristics of clostridium perfringens: tests performed

Nagler test -> egg yolk

Litmus milk test -> stormy clot rxn

Vibrio vulnificus gram stain, morphology, characteristics

gram negative curved rod, halophile, fatal in 20% of cases (within 1-2 days)

Where is V. vulnificus found?

gulf of Mexico- warmer weather= increased organisms

-Lives in salt water and found in shellfish

Susceptible populations for V. vulnificus

alcoholics, underlying liver disease, diabetes mellitus, immunocompromising conditions

transmission of V. vulnificus

-consumption of contaminated raw shellfish (oysters)

-exposure to contaminated seawater with open wound

clinical presentation of V. vulnificus

minor cellulitis- healthy individuals

Severe symptoms

-Hemorrhagic bullae (erodes -> ulcers)

-necrotizing fasciitis, septicemia, death

V. vulnificus primary septicemia

seen after ingestion of bacteria (undercooked fish)

-GI symptoms, 33% patients with shock, 75% present with hemorrhagic bullous skin lesion (deadly in 40% of cases)

V. vulnificus lab characteristics

thiosulfate citrate bile-salt agar (TCBS)- forms blue-green colonies (yellow for V. cholera) and History

bartonella henselae gram stain and morphology, characteristics, reservoir

Gram negative rod, intracellular, cat (from cat scratch)

at risk population for bartonella henselae

children under 15 and immunocompromised

Cat scratch disease (Bartonella henselae) presentation in healthy individuals

papule at scratch location, fever, lymphadenopathy (1-3 weeks after exposure)

Bacillary angiomatosis (Bartonella henselae) presentation in immunocompromised patients

cutaneous lesions and mucosal lesions

-Red to purple papules (Kaposi's sarcoma similarity)

-Can ulcerate

B. henselae lab test diagnostics

PCR and history