Pneumococcus 1 & 2

Front 1

What kind of morphological appearance do the pneumococci have?

Back 1

pairs or beads of elongated chains

Front 2

Describe Pneumovax

Back 2

This is the polysaccharide capsular vaccine that protects against 23 of the more virulent serotypes of the 90 known of pneumococcus. It offers the best level of protection in younger, healthy adults (like our age, oddly enough the population group that needs it the least). Elderly people, who need it more, are not protected well by it because they have shitty antibody production capabilities. Likewise, children under the age of 2 are not protective by Pneumovax because Pneumovax elicits a T Cell Independent Immunity, something kids under 2 are not yet capable of doing.

Front 3

Why was Prevnar such a big deal?

Back 3

Because kids under the age of 2 had immature immune responses to polysaccharides, and thus were unable to acquire any protection from the traditional Pneumovax vaccine. Prevnar changed all this by chemically conjugating the polysaccharide to a protein commonly used in other vaccines (ie diphtheria or tetanus) thus coercing the immune system to produce antibodies to the polysaccharide while providing simultaneous protection for the conjugated protein (tetanus or diphtheria)

Front 4

What are the epidemiological consequences of the Prevnar vaccine?

Back 4

*Overall frequency of all pneumococcal disease in vaccinated countries has decreased
*Infections & Colonizations by VACCINE SEROTYPES has decreased (direct effect)
*Infections & Colonizations by NON-VACCINE SEROTYPES has increased (bacterial replacement)
*Reduction in disease caused by VACCINE SEROTYPES in non-vaccinated individuals (ie "herd effect")

Front 5

What is stronger to have: herd immunity or humoral immunity? (basis of Musher being pissed off at parents)

Back 5

Having the actual humoral immunity from having the vaccination is superior to being offerred herd immunity by all the others who took on the "risks" of having the vaccination.

Front 6

Do antibodies produced against one serotype of pneumococcus cross-react against other serotypes?

Back 6

NO, so if you are infected/colonized with one serotype you can just as easily be colonized/infected again by another serotype.

Front 7

How does pneumococcus cause disease? Does it make any exotoxins?

Back 7

Pneumococcus does NOT make any toxins. It causes disease simply by the inflammatory response it elicits in the otherwise sterile spaces it gets into (ie lungs, ears, sinuses)

Front 8

Why are PspA and PsaA considered novel and potentially beneficial vaccine targets?

Back 8

Because these two virulenec factors are shared among all pneumococcus (not like the capsular polysaccharides with 90 serotypes). Therefore, one vaccination could effectively protect someone against all pneumococcus.

Front 9

Explain the difference between etiology and pathogenesis?

Back 9

etiology is the specific cause of a disease and this term is becoming more and more complex and multifactorial. Pathogenesis refers to how did someone come around to getting a disease process.

Front 10

What patient population is most likely to get nasopharyngeal contents aspirated into their lungs overnight (confirmed by radioactive test where they painted the backs of people's pharynxes)?

Back 10

Older people, also people who go into deep sleep, and people who pass out from being drunk are also more likely to aspirate contents into their lungs

Front 11

True or False - we all have IgG to cell wall peptidoglycan of the pneumococcus? If true, why is this IgG useless?

Back 11

True, its useless though because the capsule itself prevents the interaction of the PMN receptors from the IgG that diffuses across the capsule and effectively attaches to the peptidoglycan. Classical complement pathways are initiated but they only get as far as C3b anyways (gram + cells with very thick walls, not likely to die this way)

Front 12

What two things does the capsule prevent the PMN from interacting with?

Back 12

C3b (from initiation of alternative complement pathway) and IgG...both of which have diffused across the capsule and have attached onto the cell wall components of the pneumococcus.

Front 13

What happens to your risk of pneumococcal infection if you have a spleenectomy?

Back 13

NOTHING, your risk of getting a pneumococcal infection is not changed, however your risk of getting an overwhelming sepsis or shock in the case of getting a pneumococcal infection is drastically increased. Why? Because the spleen is so good at removing encapsulated bacteria from the circulation, whether antibody is bound to them or not

Front 14

What are you thinking if you see a child with high fever, little child (under 2), high white blood cell count?

Back 14

Primary bacteremia. Remember that in kids, one third of pneumococcal bacteremias are primary bacteremia.

Front 15

What is a primary bactereia?

Back 15

Bacteria detected in the blood with no apparent source.

Front 16

How are two ways to tell apart a bacterial from a viral pneumonia/infection in general?

Back 16

1) Bacterial infected patient looks SICK, viral doesn't look sick
2) In pneumococcal pneumonia, you see a mixing of blood with sputum (tends to be brownish color). This is characteristic of a bacterial pneumonia (not a viral).

Front 17

Streptococcus pneumoniae is the major bacterial cause of ________, __________, ________, and _________ (in the absence of an outbreak of ___________)

Back 17

pneumonia, otitis media, sinusitis, meningitis in the absence of an outbreak of meningococcal disease (in all age groups for meningitis except for newborns).

Front 18

Name 4 major virulence factors of pneumococcus...

Back 18

1) capsule
2) PspA
3) PsaA
4) Pneumolysin

Front 19

Streptococcus pneumoniae are:
*gram +/-
*optochin susceptible/resistant
* ____ hemolytic

Back 19

gram positive, optochin susceptible (don't grow around the optochin disk), and alpha hemolytic

Front 20

Explain the hemolysin pneumococcus produces and its phenotypic appearance on the plate...

Back 20

Pneumococcus makes an alpha hemolysin, that DOES NOT LYSE RBCs, it will only break down hemoglobin into a greenish/yellowish pigment that is the color which turns up on the agar plate

Front 21

Peptidoglycan in the cell wall of pneumococcus is the major stimulus of ___________.

Back 21

inflammation...pneumolysin also stimulates inflammation

Front 22

Peptidoglycan and pneumolysin both activate the ________ complement pathway

Back 22

alternative

Front 23

Bacteria's major form of protection against us is their ______, while our major form of immunity against them is antibody against their _______.

Back 23

capsule, capsule

Front 24

Antibody to capsular polysaccharide __________ the organism for phagocytosis by PMNs.

Back 24

opsonizes

Front 25

Incidence of pneumococcal pneumonia is greatest in what age population?

Back 25

the elderly

Front 26

What happens to the clinical manifestations of pneumococcal infection in the elderly?

Back 26

They become more subtle. You may not even see a couch, sputum, or fever in them

Front 27

Describe the gram staining process

Back 27

Stain with crystal violet (stains proteins and carbohydrates). Fix with iodine into the peptidoglycan. Wash with alcohol or acetone which removes the crystal violet from thin peptidoglycan layers (ie gram negatives) while thicker cell wall bacteria retain this purple stain (gram positive). Finally stain with Safranin which turns the entire background (and gram negatives) red.

Front 28

Give two reasons why pneumococci may be difficult to find by gram stain or culture?

Back 28

1) the organism may have already been eradicated if the patient has been on antibiotic therapy before the cultures/stain
2) May be obscured by other alpha hemolytic bacteria (ie viridans group of streptococci are the most common organism in the saliva)

Front 29

Describe teichoic acid.

Back 29

Lipoteichoic acid/teichoic acid mediates attachment to mammalian cells. It penetrates through the capsule. It contains a unique, choline rich C polysaccharide upon which CBPs bind to (choline binding proteins) PspA and PsaA.

Front 30

Name two proteins that establish contact with the choline rich C polysaccharide of teichoic acid?

Back 30

1) C reactive protein during inflammatory diseases and infections (this is a natural defense mechanism of our body)
2) the choline binding proteins (CBPs): PspA, PsaA which are virulence factors (antiphagocytic in their function)

Front 31

What does autolysin do?

Back 31

Responsible for the self-destruction (collapse from the center of the colony) of pneumococci in vitro. In vivo, release substances such as pneumolysin that causes inflammation and damages tissues.

Front 32

________ (a specific protein of pneuomoccus) is capable of reproducing the changes of pneumonia in animals

Back 32

Pneumolysin

Front 33

Pneumococci are present in the __________ as part of the so-called normal flora

Back 33

naso-pharynx

Front 34

The first step of colonization is _________

Back 34

adherence via (with pneumococcus their lipoteichoic/teichoic acids)

Front 35

Define colonization

Back 35

The presence of bacteria without any inflammatory response or symptoms of disease

Front 36

Most common infectious diseases are caused by organisms taht normally colonize humans and then cause disease _____________.

Back 36

when they get where they don't belong, usually with an associated underlying problem of clearance mechanisms from that region

Front 37

Name two organisms who do NOT colonize humans at all, and their presence alaways indicates proliferating organisms and immune responses which = disease.

Back 37

1) Mycobacterium TB
2) Treponema pallidum

Front 38

What is point prevalence? And what is it for children? Adults?

Back 38

Point prevalence is whether you have it/colonized with it on a SINGLE OCCASION. Point prevalence in toddlers is 20-40%, and 10-15% in adults in the winter (lower in summer than winter for some reason).

Front 39

True or false - pneumococcus is more likely to cause disease by being carried by secretions to a place where it doesn't belong rather than by local invasion (thruogh respiratory epithelial cells with oragnisms going directly to blood stream or lymphatics)

Back 39

TRUE

Front 40

What is the difference between aspiration and inhalation, and which one is more commonly seen with pneumococcus?

Back 40

Aspiration is the bypassing of mouth contents passed the glottis where they end up in the trachea, whereas inhalation is breathing in aerosolized oragnisms. Since, we have laminar air flow and our passageways are sticky, inhalation becomes less important for mechanisms of pneumococcal disease (we usually will catch it and cough it back up if inhaled)

Front 41

5 different classes of factors predispose to Pneumococcal Infection. Name all 5 categories and each item under each.

Back 41

1) Multifactorials
*extremes of age (old, young)
*previous hospitalization
*malnutrition
*alcoholism

2) Decreased pulmonary clearance
*alcohol, codeine, morphine (all suppress cough)
*air pollution
*cigarette smoking (damages cilia)
*viral infection (damages cilia)

3) Decreased PMN function
*Diabetes mellitus (just fucks up PMNs at every step of their path...migration, phagocytosis, killing)
*Corticosteroids
*Renal insufficiency
*Cirrhosis
*Alcohol ingestion

4) Defective IgG production
*Congenital
*Acquired (ie CVID)
*HIV Infection

5) Special instance: spleenectomy

Front 42

What are the three most common signs of pneumococcal pneumonia?

Back 42

Cough, fever, sputum production

Front 43

Interpret PMN findings on both extremes, and indicate where you would expect to normally see PMN levels in a pneumococcal infection

Back 43

Expect to see a leukocytosis normally, but in overwhelming infections will see reduced PMNs (ie below 6000 has a terrible prognosis)

Front 44

What is the proper way to diagnostic pneumonia since an actual chest exam can lead to a number of false + or - results?

Back 44

CHEST X-RAY

Front 45

Pneumococcus is responsible for ____% of adult pneumonia

Back 45

20-70% out there in the literature, Musher estimates its 50%

Front 46

Peptidoglycan for the gram + bacteria has _______ like activity of the gram negative bacteria

Back 46

endotoxin

Front 47

lipoteichoic acid is to the gram positive bacteria what ______ are to the gram negatives.

Back 47

fimbrae (pilli)

Front 48

True or false - You can get bacteremias in pneumococcus that are usually secondary bacteremias in adults (secondary to pneumonia).

Back 48

TRUE

Front 49

The normal person will make antibody within 2-3 weeks of being colonized with pneumococcus. During what time period is a person (who has been colonized) with a compromise in normal clearance mechanisms at an increased risk for acquiring pneumococcal pneumonia?

Back 49

During this 2-3 week period during which they will have no humoral immunity

Front 50

The normal person will make antibody within 2-3 weeks of being colonized with pneumococcus. During what time period is a person (who has been colonzied) who can't make IgG at risk for getting a pneumococcal pneumonia?

Back 50

Susceptible as long as they remain colonized! Which can be weeks to months.

Front 51

What is the antibiotic of choice for pneumococcus?

Back 51

penicillin

Front 52

Explain the primary mechanism of resistance to penicillin by pneumococcus and whether it can be overcome.

Back 52

The primary mechanism is an alteration in the avidity of its PBPs (trans and carboxypeptidases) to the beta lactam. This can be overcome by increasing the concentration of penicillin used. There is currently no beta-lacatamase mechanism of pneumococcal penicillin resistance (yet).