Semester 3: Microbiology - Mini 3

Front 1

What two components make up the LPS?

Back 1

* Lipid A = hydrophobic lipid component
* Carbohydrate component

Front 2

What two components make up the hydrophilic carbohydrate portion of LPS?

Back 2

* O-polysaccharide
* Core oligosaccharide

Front 3

Of the two components of the hydrophilic carbohydrate, which is utilized to differentiate between the serological diversity of gram bacteria?

Back 3

O-polysaccharide

Front 4

When during its development cycle will N. meningitidis shed endotoxin? By which method?

How does that compare to Enterobacteriacae?

Back 4

N. meningitidis sheds endotoxin while still growing via a process of BLEBBING.

Enterobacteriacae only release endotoxin at the death of the organism.

Front 5

Are all of the LPS components immunogenic?

Are they all useful for differentiating between strains or species?

Back 5

Yes

No

Front 6

Which of the two components of the LPS activate the complement pathways:

* Lipid A
* Carbohydrate

Back 6

* Lipid A = classical
* Carbohydrate = alternative

Front 7

How are the major effects of Lipid A derived? Through which interaction?

Back 7

Through its interaction with MACROPHAGES

Front 8

Describe the major effects of Lipid A and its interaction between macrophages.

Back 8

1. Lipid A enters the bloodstream, bound by LPS binding protein (LPS-BP)

2. LPS-BP + Lipid A = bound to soluble CD14 (sCD14)

3. LPS-BP + Lipid A + sCD14 are transferred to TLR4 on a MACROPHAGE

4. TLR4 (has signal transduction capabilities) when bound to Lipid A results in CYTOKINE gene activation

5. Production of TNF-α, IL-1, IL-6, and IL-8

Front 9

Of the cytokines given here, which activate the "acute phase reaction" and which "recruit neutrophils"?

TNF-α, IL-1, IL-6, IL-8

Back 9

acute phase reaction = TNF-α, IL-1, IL-6

neutrophil recruitment = IL-8

Front 10

Of the known cytokines, which has systemic effects and is thought to cause extreme morbidity?

Back 10

TNF-α

Front 11

Clinically, what five effects are seen with the activation of TNF?

These effects will lead to what two events?

Back 11

1. High fever
2. Vasodilation
3. Capillary leakage
4. DIC
5. Cardiodepression

*** These will all lead to SHOCK and ultimately MULTIPLE ORGAN FAILURE

Front 12

Describe N. meningitidis based on the following:

* Type of bacteria
* Which two -ASEs?
* Ferments what? Does not ferment what?
* What is its only natural host?

Back 12

Type: encapsulated gram (-) diplococcus

ASEs: oxidase, catalase

Ferments: glucose, maltose but NOT sucrose, lactose

Host: humans

Front 13

What are the three (3) important virulence factors for N. meningitidis?

Back 13

1. Polysaccharide capsule resisting phagocytosis

2. LPS that sheds by blebbing

3. IgA protease to cleave IgA

Front 14

Describe N. meningitidis in terms of transmission, attachment, and spread?

Back 14

Transmitted: airborne droplets where infection is preceded by colonization of the nasopharynx

Attachment: to nasopharyngeal epithelial cells aided by fimbraiae

Spread: by fimbriae allowing it to enter the bloodstream and spread to other sites

Front 15

The N. meningitidis organism is serologically divided into which groups?

Back 15

A, B, C, W135, X, Y, Z

Front 16

Which of the groups cause the most disease?

A vaccine is available against these groups?

Which of the groups is NOT strongly immunogenic?

Back 16

Disease: A, B, C

Vaccine: A, C, Y, W135

NOT immunogenic: B

Front 17

What "drug" is recommend for those in close contact with patients with meningococcal disease?

Back 17

Antimicrobial chemoprophylaxis

Front 18

Patients with acute meningococcal infections can present with 1 of 3 syndromes. What are they?

Back 18

1. Uncomplicated bacteremic process

2. Metastatic infection that involves the meninges

3. Overwhelming systemic infection with circulatory collapse and evidence of DIC

Front 19

Meningococcal septicemia is produced by four basic process.

What are they?

Back 19

1. Capillary leak
2. Coagulpathy
3. Metabolic derangement
4. Myocardial failure

Front 20

What is the associated with each of the four process of septicemia?

Back 20

CAPILLARY LEAK
loss of albumin into urine & extravascular space -> hypovolemia & decreased venous return

COAGULOPATHY
severe bleeding tendency with severe thrombosis in (microvasculature of skin) -> amputation of digits or limbs

METABOLIC DERANGEMENT
Profound acidosis w/ severe metabolic abnormalities:

Hypo-(kalemia, calcemia, magnesemia, phosphatemia)

MYOCARDIAL FAILURE
skin lesions often contain meningococci being phagocytosed by neutrophils

skin rash is characteristic manifestation w/ widespread petechial eruption

Front 21

Fulminant meningococcemia has a mortalityrate that can exceed what percentage DESPITE appropriate antibiotic therapy?

Back 21

50%

Front 22

N. meningitidis is found to replicat where?

Back 22

Upon entering the meninges, it multiples in the CSF and pia arachnoid

Front 23

The neurological damage is a consequence of which three process?

Back 23

* Direct bacterial toxicity

* Indirect inflammatory processes (cytokines, edema)

* Systemic effects (shock, seizures, cerebral hypoperfusion)

Front 24

What are the major symptoms of N. meningitidis?

Back 24

* Headache, stiff neck
* Lethary and drowsiness
* Coma (ominous sign)
* Kernig and Brudzinski sign

NOTE: Children may exhibit projectile vomiting

Front 25

How is a diagnosis of N. meningitidis made?

Back 25

CULTURES
blood (+ in 60-80% of untreated patients)
CSF (+ in 70% of untreated patients)

FINDINGS
Incr. PMNs
Incr. Thrombocytopenia
Incr. CSF pressure
Incr. proteins (breakdown of enzymes)
Decr. glucose (bacteria utilize glucose)

Front 26

What immunity is there against N. meningitidis?

What about immunity for newborns?

What about immunity for those in their teens or 20s?

Back 26

Immunity due to protective IgG antibody but it REQUIRES complement (classical) for protection

Newborns receive mother's IgG through milk

The colonization of non-pathogenic strains may give protection against disease

Front 27

What are two important factors that predispose us to meningococcemia?

Back 27

1. Inability to activate MAC
2. Patients with anatomic or functional asplenia

Front 28

What is the treatment for N. meningitidis?

Back 28

Pencillin G is recommended therapy

Rifampin is recommended for chemoprophylaxis after contact with patient

Front 29

This bacteria is responsible for 80% of pus forming infections

Back 29

S. aureus

Front 30

Define the following words:

Suppuration (pyesis)
Abscess

Back 30

Suppuration (pyesis): the formation of pus

Abscess: well circumscribed collection of pus associated with infection

Front 31

An abscess is relatively inaccessible to ____________ and _____________

It may have to be __________ to relive pressure or resolve infection

Back 31

antibodies, antibiotics

drained

Front 32

What is the most frequent cause of septicemia following surgical procedures?

Back 32

S. aureus

Front 33

Non-specific activation of macrophages and other cells of the innate immune system are brought about by which receptor?

Back 33

TLR-2

Front 34

Describe S. aureus based on the following:

* Type
* ASEs
* Motility
* Spore forming capability
* Resistance

Back 34

Type: gram + coccus (irregular grapelike clusters)

ASEs: catalase and caogulase positive

Motility: none

Spore-forming: none

Resistance:
1. high temp
2. high salt concentrations
3. drying

Front 35

S. aureus when grown on a mannitol salt agar produces this type of a halo

Back 35

yellow halo

Front 36

Colonies of S. aureus are this color __________

S. aureus is known to be ____________________ on blood agar

Back 36

Golden

strongly hemolytic (beta hemolytic)

Front 37

Which groups of individuals have higher rates of S. aureus colonization?

Back 37

Health care workers, diabetic patients, dialysis patients, alcoholics, and those that inject drugs (legal or illicit)

Front 38

What are some of the major sites of colonization for S. aureus?

Back 38

Anterior nares (major)
Axilla, rectum, perineum (minor)

Front 39

The colonization rate in this location (low then high) varies depending on blood loss.

When will this happen?

Back 39

Vagina

Higher colonization rate during menses

Front 40

TRUE or FALSE

S. aureus can escape from the abscess and can disseminate hematogenously

Back 40

TRUE

Front 41

If S. aureus is able to spread beyond the local site, what conditions can a patient suffer?

Back 41

* Pneumonia
* Bone and joint infection
* Heart valve infection

Front 42

Untreated S. aureus septicemia has a mortality rate exceeding _________ %

Mortality rate for toxic shock syndrome is _______ %

Back 42

S. aureus: 80%

TSS: 3-5%

Front 43

Define the following words:

Folliculitis
Furuncle
Carbuncle

Back 43

Folliculitis: appearance of a tender pustule involve a hair follicle (ZIT)

Furuncle: an apparent small abscess that exudes purulent material from a single openin (BOIL)

Carbuncle: an aggregate of furuncles with several openings

Front 44

What is impetigo?

Back 44

Small area of erythema, then bullae (blister like lesions filled with cloudy fluid)

As it heals, a honey-colored crust develops

Front 45

Describe septic arthritis

Back 45

* warmth, erythema, tenderness of joints

* infection is often unilateral

Front 46

Describe osteomyelitis

Back 46

* bone infections indicated by fever, bony tenderness, and limp

Front 47

Describe endocarditis

Back 47

* highly variable as it involves multiple organs

* high fever, chills, sweats, and murmurs
* Janeway lesions, Roth's spots

Front 48

Catherer associated infection are often due to ________________

UTIs in sexually active young girls are often due to ________________

Back 48

Staph. epidermis

Staph. saprophyticus

Front 49

What are four virulence factors associated with S. aureus?

Back 49

1. Capsule
2. Protein A
3. Coagulase and fibrinogen binding
4. Toxins

Front 50

What is the function of the capsule?

What is the function of Protein A?

Back 50

Capsule: inhibit phagocytosis

Protein A: binds to H chain of antibody and inhibits Ab opsonization -> inhibit phagocytosis

Front 51

What is the function of coagulase and fibrinogen binding?

Back 51

coagulase allows S. aureus to coagulate plasma and form a fibrin barrier around infectious loci

staphylokinase aids the bacteria in breaking down fibrin and blood clots

Front 52

These four S. aureus toxins are know to by cytotoxic to blood cells

Back 52

αβγδ-toxin

Front 53

This toxin consists of two _______________ factors that act synergistically with α-toxin to kill leukocytes

Is this toxin an endotoxin or exotoxin?

Back 53

Leukocidin

Panton-Valentine (P-V)

Exotoxin

Front 54

Exofoliatin consists of these two factors.

Back 54

ETA, ETB

Front 55

ETA and ETB result in this blister-like syndrome

Back 55

SSSS (s. aureus scalded skin syndrome)

Front 56

The initial features of SSSS are:

Back 56

* Fever
* Erythema
* Blisters -> rupture, leave red base
* NIKOLSKY SIGN: +

Front 57

What is the Nikolsky sign?

In which other disease is Nikolsky sign (+) ?

Back 57

It is when you can push a blister up and down the skin without damaging the intact dermis

Pemphigus vulgaris

Front 58

This range of enterotoxins is responsible for different types of common food poisoning.

Back 58

Enterotoxin A-E, G-I

Front 59

Enterotoxins A-E, G-I stimulate T cell by binding to ____________

This causes the production of which cytokines?

Back 59

TCR Vβ chain

INF-γ and TNF-β

Front 60

What is the most common presentation of food poisoning?

Back 60

* Acute onset of vomiting
* Watery diarrhea 2-6 hours AFTER INGESTION

Front 61

TSS is caused by _____________

It is most frequently associated with the use of ________________ during menstruation

Back 61

Tampons

Front 62

TSS is mostly associated with S. aureus strains that produce _____________

However, strains that produce ________________ and ________________ can cause 50% of non-menstrual TSS

Back 62

Exotoxin TSST-1

Enterotoxin B, C

Front 63

TSS can be identified based on these symptoms:

Back 63

* Fever
* Diffuse macular erythema -- sunburn rash, petichae
* Hypotension

Front 64

Tampon use is associated with 50% of TSS cases. Which other situation is considered high risk for this condition?

Back 64

Injuries to the nose

Front 65

What is Bullous Impetigo?

Back 65

* Localized form of SSSS
* Bullae are culture +
* Nikolsk sign -
* Occurs in infants and children

HIGHLY COMMUNICABLE

Front 66

How do you diagnose S. aureus?

Back 66

1. Obtain cultures WITH SUSCEPTIBILITIES appropriate for site of infection

2. Blood cultures (repeat if + as it could be contaminated)

Front 67

TRUE or FALSE

Most purulent infections are going to be caused by S. aureus

Back 67

True

Front 68

The most important defense against S. aureus is ___________________

Back 68

Neutrophils

Front 69

_____________ patients are much more susceptibile to serious infections

Back 69

Neutropenic

Front 70

These two innate immunte system process are also involved in defense

Back 70

* Opsonization by Ab
* Complement activation

Front 71

What part of the complement pathway is NOT involved in defense against S. aureus?

Back 71

MAC

Front 72

What is the most common Coagulase Negative Staphylococcus (CoNS) bacteria?

Back 72

S. epidermis

Front 73

Does S. epidermis have virulence factors?

Back 73

No

Front 74

S. epidermis can cause problems in _____________ and _____________

Back 74

Heart valves, catheters