exam 4 Flashcards

1
Q

HA-MRSA

A

Hospital-associated MRSA

  • Resistant to all antibiotics but Vancomycin (only treatment) only treatment
  • Methacilin resistant, so it has mec A gene
  • Way more problematic and CA-MRSA
  • No PVL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CA-MRSA

A

Community-associated MRSA

  • Resistant Methcillin, but sensitive to most other antibiotics including Vancomycin
  • Do not have to treat with vancomycin so you have other choices to treat with
  • mec A gene
  • Contains PVL (Panton-Valentine Leukocidin) gene
  • All skin infections

–> CA has mec A gene AND PVL gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Scalded Skin Syndrome

A
  • bacteria colonize in the intesting of newborn and children <2
  • adults can get it after toxic shock
  • toxins enter bloodstream, goes to skin cells and the toxins affect the epidermis.

EXAMPLE OF TOXEMIA

Happens when a baby born (sterile), if they come across S. aureus before normal gut flora gets established, they can get S. aureus colonized in gut

If that s. aureus can make the toxin, they they will have scaled skin syndrome
The bacteria are multiplying in intestine but seeing affect on skin

THE TOXIN IS Exfoliative toxin A & B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Virulence factors of scalded skin

A

Exfoliative toxin A & B

  • destruction of intracellular CT
  • skin peels off in sheets
  • must do histological testing to rule out other causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Toxic shock syndrome

A

a. Colonization elsewhere
b. Toxin enters bloodstream
c, Body-wide effects
1) fever, vomiting
2) sunburn-like rash
3) Leads to peeling skin
(looks like scalded skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Staphylococcal Toxic shock syndrome

A
  • S. aureus usually remains localized but may become systemic; all give rise to systemic superantigens (usually TSST-1, SEB, or SEC)
  • Massive cytokine production: IL1-β (fever), TNF-αβ (hypotension), interferon-γ and IL-2 (rash and other symptoms)
  • Menstrual TSS occurs primarily in association with tampons; incidence rises with increases in absorbency (oxygen) – the air lets S. aureus grow really well
    Can grow in nasal sinuses with you get surgery and they pack sinuses
  • Must rule out other causes
  • Culture on blood agar must Verify TSST-1 toxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute glomerulonephritis (AGN)

A

Glomeruli – sterile water comes in, picks up trash from blood and you pass it as urine the antigen-antibody complexes get stuck in here; land on tissue, activate compliment against the tissue, and the complement then puts holes on kidney and causes kidney damage AKA ACUTE GLOMERULONEPHRITIS

Immune response to strep antigens where the antibodies are reacting with you own antigens after the antigen is gone
- Antigen is gone but you are still seeing effects; I THINK THIS IS CALLED late sequele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Necrotizing fasciitis

A
  • Flesh-eating Streptococcus
  • Have proven that S. aureus also causes it
  • Rapid disease course
  • Destroys tissue as quickly as it is removed
  • has ability to travel through tissues
  • this is a TOXEMIA OF S. PYROGENES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Epidemiology of necrotizing fasciitis

A
  • can cause death

- loss of limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Virulence factors of necrotizing fasciitis

A

a) Pyrogenic exotoxin A (SPE A) - strepococcal
1) Superantigen (SPE A is superantigen –> cytokine storm)

b) Streptolysin O (SLO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diagnosis of necrotizing fasciitis

A
  • culture on blood agar
  • beta-hemolytic, Group A
  • immunological assays for toxin
  • catalase negative
  • SPE A and SLO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment of necrotizing fasciitis

A
  • antibiotics-penicillins still drug of choice

- wound debridement necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Strep Toxic Shock Syndrome

A
  • similar symptoms as staph toxic shock
    • less frequent rash
    • more frequent bacteremia
    • shock and organ damage
  • Toxin called strep TSS-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pathogens attack in 3 ways

A

breach of intact skin
skin manifestation of a systemic infection
toxin-mediated skin damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Subacute Schlerosing Panencephalitis (SSPE)

A
Rare event 1/million male children and young adults infected
- 1-10 years after measles infection
- fatal
- subacute (no sign of it)
LATE SEQUELAE OF MEASLES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

herpes encephalitis

A
Rare spread of herpes to the brain
- latent infections in nerve ganglion
- relapse
  --> reactivation = stress, UV
Nerve stores DNA – can come down and cause cold sore during stress (sometimes on same part of lip because its coming from the same nerve)
17
Q

Explain Chlamydias odd lifecycle

A

Obligate intracellular bacteria
-To complete life cycle, HAS to be inside cell

Complex life cycle
a) Elementary body is infectious form of chlamydia

b) Reticulate body-noninfectious, but metabolically active in this form
c) Replicate in cytoplasm of host cells

What you get from infectious agent (fly, kid, dirty clothes, etc.) is elementary body which is the infectious form
Elementary body enters the host cells and then it transforms into RETICULATE BODY
Reticulate body is non infectious BUT its METABOLICALLY active; it duplicates (it’s a bacteria so it undergoes binary fission as a reticulate body)
The host cell fills up with reticulate bodies and ends up changing back into elementary bodies and then the cell bursts and lyses
The reticulate body can not survive outside cell, but elementary bodies can survive on surfaces for a long time, and that is how its spread

18
Q

Describe the Lymphatic System

A
Lymphatic system very permeable
Fixed Macrophages clear bacteria
both types Lymphs
T cells and B cells
RES links circulatory and lymphatic
(Reticuloendotheial system)
19
Q

Anatomy of cardiovascular and lymphatic systems

A

Lymph nodes are were APC present to helper cells and activate B cells

Some concentrations of immune systems associated with lymphatic system
GALD (gut associated lymphoid tissue)
Bald (lungs)
Malt (skin)

20
Q

Exposure to bacteria that stick; how do you get endocarditis?

A

– Major dental treatment oral dental flora sticks to teeth, if you get dental treatment and get oral flora in blood, can go to heart and cause endocarditis

– Open heart surgery/Genitourinary procedure

    • Body piercing
    • IV Drug use
    • Scar tissue on valve –> thickening –> valve cant move correctly
21
Q

Puerperal Sepsis

A

Childbed Fever

a) Nosocomial infection of uterus
b) Transmitted by hands/instruments or physicians

Historical disease

a) prevented by hand washing
b) rare disease now

22
Q

Lemierre’s syndrome

A

Abscess secondary to strep throat infection

  • After strep throat
    • caused by anaerobe Fusobacterium necroforum found in respiratory system
  • Virulence factors- Streptolysins, hyaluronidase

Cause infected clot in jugular

Can travel to lung or heart FATAL.

Used to be high in prevalence until we started treating people with antibiotics for strep throat

23
Q

Rheumatic Fever

A

Original Pharyngitis infection (strep throat)
- autoimmune complication of strep throat

The organism that causes strep throat has a certain M protein; that M protein looks like heart muscle tissue; you make antibodies against those M proteins, you clear the strep throat, But you have all those antibodies and now they are attacking your heart antibodies bind to heart, a bound antibody activates compliment, and your compliment system and your immune cells are destroying your heart tissue

TYPE 2 HYPERSENSITIVITY because it is acting on a cell (heart muscle cells)

What happens after a strep infection where you make antibodies?  you get memory; so when you get strep throat again, you have a stronger, more damaging immune response

Once you have been diagnosed with rheumatic fever, it is very important that you never get strep throat again

24
Q

Rheumatic Fever Symptoms

A

a) Arthritis, fever
b) Due to misdirected immune response
c) M protein self-like
d) Leads to heart damage

25
Q

Rheumatic Fever Epidemiology

A

a. early century killed children
b. declining due to loss of virulence
c. reemergence of virulent serotypes seen in US
d. Re-infection renews immune attack

26
Q

Rheumatic Fever treatment

A
  • High risk patients get long-acting Benzathine Penecillin G (shot in butt)
  • Anyone with a history of rheumatic fever with be on profalactic antibiotics so they will not get strep throat
27
Q

Rheumatic Fever prevention

A

hand washing

treat strep throat

28
Q

You just need to know the LIST of hemorrhagic fever viruses:

A
Yellow fever
Dengue fever
Chikungunya
Ebola and/or marburg
Lassa fever