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52 Cards in this Set

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  • Back
What kind of morphological appearance do the pneumococci have?
pairs or beads of elongated chains
Describe Pneumovax
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.
Why was Prevnar such a big deal?
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)
What are the epidemiological consequences of the Prevnar vaccine?
*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")
What is stronger to have: herd immunity or humoral immunity? (basis of Musher being pissed off at parents)
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.
Do antibodies produced against one serotype of pneumococcus cross-react against other serotypes?
NO, so if you are infected/colonized with one serotype you can just as easily be colonized/infected again by another serotype.
How does pneumococcus cause disease? Does it make any exotoxins?
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)
Why are PspA and PsaA considered novel and potentially beneficial vaccine targets?
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.
Explain the difference between etiology and pathogenesis?
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.
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)?
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
True or False - we all have IgG to cell wall peptidoglycan of the pneumococcus? If true, why is this IgG useless?
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)
What two things does the capsule prevent the PMN from interacting with?
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.
What happens to your risk of pneumococcal infection if you have a spleenectomy?
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
What are you thinking if you see a child with high fever, little child (under 2), high white blood cell count?
Primary bacteremia. Remember that in kids, one third of pneumococcal bacteremias are primary bacteremia.
What is a primary bactereia?
Bacteria detected in the blood with no apparent source.
How are two ways to tell apart a bacterial from a viral pneumonia/infection in general?
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).
Streptococcus pneumoniae is the major bacterial cause of ________, __________, ________, and _________ (in the absence of an outbreak of ___________)
pneumonia, otitis media, sinusitis, meningitis in the absence of an outbreak of meningococcal disease (in all age groups for meningitis except for newborns).
Name 4 major virulence factors of pneumococcus...
1) capsule
2) PspA
3) PsaA
4) Pneumolysin
Streptococcus pneumoniae are:
*gram +/-
*optochin susceptible/resistant
* ____ hemolytic
gram positive, optochin susceptible (don't grow around the optochin disk), and alpha hemolytic
Explain the hemolysin pneumococcus produces and its phenotypic appearance on the plate...
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
Peptidoglycan in the cell wall of pneumococcus is the major stimulus of ___________.
inflammation...pneumolysin also stimulates inflammation
Peptidoglycan and pneumolysin both activate the ________ complement pathway
Bacteria's major form of protection against us is their ______, while our major form of immunity against them is antibody against their _______.
capsule, capsule
Antibody to capsular polysaccharide __________ the organism for phagocytosis by PMNs.
Incidence of pneumococcal pneumonia is greatest in what age population?
the elderly
What happens to the clinical manifestations of pneumococcal infection in the elderly?
They become more subtle. You may not even see a couch, sputum, or fever in them
Describe the gram staining process
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.
Give two reasons why pneumococci may be difficult to find by gram stain or culture?
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)
Describe teichoic acid.
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.
Name two proteins that establish contact with the choline rich C polysaccharide of teichoic acid?
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)
What does autolysin do?
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.
________ (a specific protein of pneuomoccus) is capable of reproducing the changes of pneumonia in animals
Pneumococci are present in the __________ as part of the so-called normal flora
The first step of colonization is _________
adherence via (with pneumococcus their lipoteichoic/teichoic acids)
Define colonization
The presence of bacteria without any inflammatory response or symptoms of disease
Most common infectious diseases are caused by organisms taht normally colonize humans and then cause disease _____________.
when they get where they don't belong, usually with an associated underlying problem of clearance mechanisms from that region
Name two organisms who do NOT colonize humans at all, and their presence alaways indicates proliferating organisms and immune responses which = disease.
1) Mycobacterium TB
2) Treponema pallidum
What is point prevalence? And what is it for children? Adults?
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).
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)
What is the difference between aspiration and inhalation, and which one is more commonly seen with pneumococcus?
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)
5 different classes of factors predispose to Pneumococcal Infection. Name all 5 categories and each item under each.
1) Multifactorials
*extremes of age (old, young)
*previous hospitalization

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)
*Renal insufficiency
*Alcohol ingestion

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

5) Special instance: spleenectomy
What are the three most common signs of pneumococcal pneumonia?
Cough, fever, sputum production
Interpret PMN findings on both extremes, and indicate where you would expect to normally see PMN levels in a pneumococcal infection
Expect to see a leukocytosis normally, but in overwhelming infections will see reduced PMNs (ie below 6000 has a terrible prognosis)
What is the proper way to diagnostic pneumonia since an actual chest exam can lead to a number of false + or - results?
Pneumococcus is responsible for ____% of adult pneumonia
20-70% out there in the literature, Musher estimates its 50%
Peptidoglycan for the gram + bacteria has _______ like activity of the gram negative bacteria
lipoteichoic acid is to the gram positive bacteria what ______ are to the gram negatives.
fimbrae (pilli)
True or false - You can get bacteremias in pneumococcus that are usually secondary bacteremias in adults (secondary to pneumonia).
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?
During this 2-3 week period during which they will have no humoral immunity
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?
Susceptible as long as they remain colonized! Which can be weeks to months.
What is the antibiotic of choice for pneumococcus?
Explain the primary mechanism of resistance to penicillin by pneumococcus and whether it can be overcome.
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).