Micro/id Set 1

Front 1

T/F: Extracellular bacteria incite chronic inflammation +/- acute inflammation

Back 1

FALSE- extracellular bacteria incite acute inflammation with edema, with time, increasing chronic inflammation begins leading various degrees of mixed acute and chronic inflammation. Intracellular bacteria incite chronic inflammation +/- acute inflammation.

Front 2

T/F: Some intracellular bacteria may incite granulomatous inflammation

Back 2

T

Front 3

T/F: Presence of caseous necrosis is indicative of M. tuberculosis infection

Back 3

TRUE- M. tuberculosis is a type of facultative obligate intracellular bacteria. Depending upon the bacterial species, may cause necrosis including caseous necrosis.

Front 4

T/F: P. aeruginosa is associated with necrotizing pneumonia

Back 4

T

Front 5

T/F: Cytopathic changes are mainly associated with bacterial infections

Back 5

FALSE- Cytopathic changes are most typical of viral infections but may be seen with intracellular bacterial infections

Front 6

T/F: Bartonella spp. are associated with angioproliferation

Back 6

T

Front 7

T/F: Abscesses with sulfur granules are associated with Chlamydia infections

Back 7

FALSE- abcess associated with sulfur granulomas is Actinomyces

Front 8

T/F: Neutrophils in gastric mucosa are associated with H. pylori infection

Back 8

T

Front 9

T/F: Lymphocytic vasculitis is associated with Rickettsial infections

Back 9

T

Front 10

T/F: Drugs are either bactericidal or bacteriostatic independent of the infection being treated.

Back 10

FALSE- there is some variability as to whether a drug is bactericidal or bacteriostatic action, but the variability is dependent upon the infection being treated.

Front 11

T/F: Beta-lactam antibiotics tend to have bactericidal activitiy.

Back 11

T

Front 12

T/F: In general, aminglycosides are bacteriostatic

Back 12

FALSE- In general, aminoglycosides tend to be bactericidal.

Front 13

T/F: Beta-lactam antibiotics have a post antibiotic effect against gram-negative organisms

Back 13

FALSE- Beta-lactam antibiotics have PAE against Gram-positive organisms and not Gram-negative organisms (except carbapenem). Aminoglycosides and Quinolones have PAE against Gram-negative organisms.

Front 14

T/F: The dosing of aminoglycosides once every 24 hours to treat a gram-negative infection makes use of its concentration-dependent killing activity and its post antibiotic effect.

Back 14

T

Front 15

T/F: Streptococcus agalactiae is associated with rheumatic fever

Back 15

FALSE- Str. agalactiae (Group B) colonizes the vaginal tract of sexually active women, causes neonatal mortality and irreversible morbidity due to septicemia and meningitis. Str. pyogenes (Group A) is associated with causing rheumatic fever.

Front 16

T/F: Streptococcus pyogenes is the number one cause of bacterial pneumonia worldwide

Back 16

FALSE- Str. pyogenes is the number one human pathogen world-wide, but it primarily causes pharyngitis and skin infection but can cause some systemic disease including rheumatic fever and acute glomerulonephritis. Str. pneumoniae is the number one cause of bacterial pneumonia and the number one cause of meningitis worldwide.

Front 17

T/F: Streptococcus pneumoniae is beta hemolytic

Back 17

FALSE- Str. pneumoniae is alpha-hemolytic. Str. pyogenes and Str. agalactiae are beta-hemolytic.

Front 18

T/F: Gamma hemolysis means non-hemolytic

Back 18

T

Front 19

T/F: The hyaluronic capsule in Group A Streptococci is non-immunogenic and antiphagocytic

Back 19

TRUE- the hyaluronic capsule is immunologically almost identical to human connective tissue.

Front 20

T/F: The M-protein is seen in Streptococcus pyogenes

Back 20

TRUE- it is uniques to this class of bacteria and is required for virulence serving as an attachment factor, inhibitor of phagocytosis, and preventer of complement activation

Front 21

T/F: Pharyngitis caused by Groups A streptococci can be spread from person to person

Back 21

T

Front 22

T/F: Strep-throat is caused by Streptococcus pneumoniae

Back 22

FALSE- Streptococcus pyogenes causes strep-throat

Front 23

T/F: Scarlet fever is the result of pyrogenic exotoxin activity of Group A streptococci

Back 23

T

Front 24

T/F: Group A streptococcus was associated with puerperal sepsis in the pre-antibiotic era

Back 24

FALSE- Puerperal sepsis associated with Group A streptococcus was a peripartum uterine infection associated with high mortality and occurred epidemically prior to use of sterile technique due to contaminated hands. TRUE- if you consider pre-antibiotic era to be the same as pre-sterile technique. The big thing is that Group A strep is associated with puerperal sepsis. The sticky point is whether or not you want to fight about pre-antibiotic or pre-sterile technique.

Front 25

T/F: Untreated streptococcal Group A pharyngeal or skin infections can cause acute rheumatic fever

Back 25

FALSE- rheumatic fever presents 10-14 days post an actue pharyngeal infection and can be prevented by eradication of the Group A strep within 10 days of infection. But it does not present after a skin infection.

Front 26

T/F: Treating Group A streptococcus pharyngeal infection with penicillin 8 days after onset can help prevent rheumatic fever

Back 26

T

Front 27

T/F: Neonatal sepsis occurs among infants of women who are vaginally colonized with Group B streptococcus

Back 27

T

Front 28

T/F: Streptococcus agalactiae infection in infants my occur 2 months after birth

Back 28

TRUE- disease may be early disease, presenting within days of birth, or Late, one week to several months after birth.  

Front 29

T/F: The viridans group of streptococci is associated with sub-acute bacterial endocarditis

Back 29

TRUE- bacteria is shed into blood stream during chewing or dental work and is then lodged on damaged heart valves forming vegetations which prevent phagocytes and inhibits antibiotic penetration. Infection can be indolent with minimal or no evidence of inflammatory disease and slowly progressive. If untreated it is invariably fatal.

Front 30

T/F: The viridans group of streptococci are primarily located in the oral mucosa

Back 30

T

Front 31

T/F: Toxic shock syndrome can be caused by streptococci and staphylococci

Back 31

T

Front 32

T/F: The MAJOR virulence factor of Str. pneumoniae is the capsule

Back 32

T

Front 33

T/F: The Quellung reaction helps identify Staphylococcus aureus

Back 33

FALSE- the Quellung reaction (swelling with antibody) helps identify Str. pneumoniae.

Front 34

T/F: A major contribution to early death in Streptococcus pneumoniae infection is due to the effects of the pneumolysin virulence factor which is a pro-inflammatory factor.

Back 34

TRUE- pneumolysin is cytotoxic and an inhibitor of ciliary clearing. It also binds to C1 in the complement pathway and initiates inflammatory responses.

Front 35

T/F: S. pneumoniae causes a necrotizing pneumonia 

Back 35

FALSE- Str. pneumoniae does not cause necrotizing pneumonia.

Front 36

T/F: Both Staphylococcus aureus and Streptococcus pneumonia can follow an antecedent viral respiratory tract infection like the flu

Back 36

T

Front 37

T/F: The pneumococcal vaccines cover 100% of common strains

Back 37

FALSE- pneumococcal vaccines cover about 85% of common strains.

Front 38

T/F: Enterococcus faecium is associated with increasing drug resistance

Back 38

TRUE- E. faecium has the ability to acquire genetic information from other organisms and can transfer it to other species. It has developed a high level of resistance to virtually all B-lactams.

Front 39

T/F: Enterococci colonize the gastrointestinal tract and they can cause infections in both the gastrointestinal tract an the urinary tract.

Back 39

T

Front 40

T/F: Protein deficiency results in T-cell dysfunction

Back 40

TRUE- there is a minimum requirement of 40g/day of mixed protein. Additionally, organisms need all 20 amino acids available in correct proportions, and these amino acids cannot be stored.

Front 41

T/F: Groups A and Group B streptococci are increasingly becoming resistant to penicillin

Back 41

T

Front 42

T/F: Staphylococcus aureus exhibit alpha hemolysis when growing on blood agar

Back 42

FALSE- S. aureus exhibits beta hemolysis when growing on blood agar

Front 43

T/F: Protein A binds to antibiodies thereby allows Staphylococcus to escape phagocytosis

Back 43

T

Front 44

T/F: TSST-1 is a superantigen which stimulate T-cells nonspecifically and results in the release of significant pro-inflammatory cytokines/chemokines

Back 44

T

Front 45

T/F: Coagulase-negative staphylococci are the most common causes of skin and soft tissue infection in the United States

Back 45

FALSE- MRSA is the most commonly identified cause of skin and soft tissue infections in the U.S. MRSA is a type of S. aureus, which is coagulase-positive.

Front 46

T/F: T-cells are the major defense mechanism against Staphylococcus aureus

Back 46

FALSE- neutrophils and PMNs are the most important defense against Staphlococci.

Front 47

T/F: Panton Valentine leukocidin appears to be associated with enhanced virulence in Streptococcal infections

Back 47

FALSE- Panton Valentine leukocidin appears to be associated with enhanced virulence in Staphylococcus infections. It is a pore forming hemolysis that results in degranulation and lysis PMNs.

Front 48

T/F: Listeria monocytogenes is an extracellular pathogen

Back 48

FALSE- Listeria monocytogenes is an intracellular pathogen

Front 49

T/F: Listeria monocytogenes is transmitted via the inhalation route

Back 49

FALSE- the portal of entry is the GI tract.

Front 50

T/F: Listeria exhibits umbrella-like motility when grown in semi-solid agar

Back 50

T

Front 51

T/F: Anthrax can be acquired through inhalation or ingestion of spores

Back 51

T

Front 52

T/F: Inhalational anthrax causes a pneumonia

Back 52

FALSE- Inhalation anthrax initial symptoms are non-specific flu-like including malaise, fever, non-productive cough, chest discomfort. Rapid progression to dyspena, cyanosis, and shock. Hemorrhagic mediastinitis is hallmark, and meningitis may occur. Mortality approaches 100%.

Front 53

Compare the histopathology of acute inflammation and chronic inflammation

Back 53

Acute inflammation is dominated by neutrophils (purulent inflammation), with necrosis (suppuration). It is the main response to extracellular bacteria. Chronic inflammation is dominated by lymphocytes and macrophages (histiocytes). Granulomas- aggregates of lymphocytes and histiocytes, sometimes with fibroblasts and giant cells (fused histiocytes). Granulomatous- poorly aggregated infiltrated of lymphocytes and histiocytes. Chronic nonspecific inflammation- mostly infiltrates of lymphocytes with fewer histiocytes. Main response to intracellular bacteria. May occur with or without acute inflammation in this case.

Front 54

Define EXUDATIVE INFLAMMATION and list 5 organisms that cause it

Back 54

Exudative inflammation is characterized by vascular permeability, recruitment of leukocytes (especially neutrophils), and pus (necrosis). Typically caused by pyogenic, extracellular bacteria and is usually localized. Examples: Group A strep (Streptococcus pyogenes) pharyngitis, Streptococcus pneumoniae (pneumoniae and meningitis), Staphlococcus aureus, Pseudomonas aeruginosa,

Front 55

Define granulomatous inflammation

Back 55

Granulomatous inflammation is chronic inflammation and is characterized by accumulations of epithelioid histiocytes (activated macrophages). It is a response to bacteria that withstand destruction by neutrophil phagocytes. It is dependent upon intact, appropriate cytokine responses: IL-1b, IFN-g, CXCL and CCL chemokines. Does not require IL-4 or IL-10

Front 56

Which cytokines/chemokines are associated with granuloma formation?

Back 56

IL-1b, IFN-g, CXCL and CCL chemokines

Front 57

Define INTERSTITIAL INFLAMMATION

Back 57

Interstitial inflammation is characterized by nonspecific morphology (chronic nonspecific inflammation) with many monocytes and lymphocytes and only a small number of neutrophils. It is suggestive of virus, Mycoplasma, rickettsia, or spirochete infections.

Front 58

What are two reasons for a NULL reaction in a patient who is acutely infected with a bacterial organism?

Back 58

The NULL reaction is the absence of inflammatory, necrotizing, or cytopathic responses and is rare with bacterial infections. It may occur with neutropenia (no leukocytes) or immune compromise due to lack of inflammatory cells or by rapid, unrestricted bacterial growth.

Front 59

Name 3 causes of a diminished T-cell response and list 3 infections that it predisposes to

Back 59

Minimum requirement of 40g/day of mixed protein, all 20 amino acids have to be available in the correct proportions for protein synthesis to occur, and amino acids cannot be stored: unused amino acids are deaminiated and the carbon skeletons are burned. Diminished T-cell response- HIV, cancer therapy, corticosteroid therapy, immune suppressive therapy. Predisposing infections: Tuberculosis, Disseminated Herpes infections, Pneumocystis 

Front 60

List 2 infections associated with gamma-interferon deficiency

Back 60

Mycobacteria and Salmonella infections

Front 61

List 2 measures of effective cellular immunity

Back 61

Lymphocyte proliferation and IFN-g production

Front 62

Define and contrast EMPERIC therapy vs. DEFINITIVE therapy

Back 62

Empiric therapy- begins broad, probability of organism in given clinical syndrome: patient factors; geographic factors (community acquired, hospital acquired); consider lethality of possible, though less probable, pathogen; local antibiotic sensitivity pattern of organism. Often beginning treatment prior to having a clear answer of the pathogen you are dealing with. Definitive therapy- becomes narrow, culture and sensitivity- organism specific options; “best” antibiotic informed by patient characteristics; no longer as dependent upon probabilities you have a definite answer about the bug that you are dealing with and the best way to treat it.

Front 63

List 4 clinical situations when you would want to choose a bactericidal drug rather than a bacteriostatic drug. Why do you need to use a cidal drug in each of these cases?

Back 63

Endocarditis- penetration, slow growth, Meningitis- penetration, immune sanctuary, Osteomyelitis- penetration,

Front 64

List 6 factors that affect antibiotic tissue penetration

Back 64

Blood concentration, Molecular size, Protein binding in plasma, Lipid solubility, Ionic charge, Tissue binding, Inflammation, Active transport, Excretion pathways

Front 65

Vancomycin has a low CSF tissue penetration but it is a first-line agent used to treat bacterial meningitis, WHY???

Back 65

Bacterial meningitis is most often caused by S. Pneumoniae. Resistance to penicillin’s and increasingly to cephalosporins and others is rapidly compromising therapy. Though vancomycin does not penetrate the CNS well, penetration arguably increases when the meninges are inflamed.

Front 66

Which two classes of antibiotics demonstrated CONCENTRATION dependent killing?

Back 66

Aminoglycosides and Quinolones

Front 67

Define antimicrobial SYNERGY and ANTAGONISM

Back 67

Synergy- 1+1>2 the interaction of two drugs is greater then the sum of its parts. This tends to be a good thing. Antagnism- 1+1<2, the interaction of two drugs diminishes the effectivness of the individual drugs if they had been given alone. This tends to be a bad thing. Indifference- 1+1=2, the combination of drugs has not difference then if each drug would have been given by itself.

Front 68

Define the post-antibiotic effect

Back 68

PAE- suppression of bacterial growth that persists after short exposure of organisms to antibiotic agents. Effect-time relationship may differ from drug-time relationship. b-lactam antibiotics have PAE against Gram-positive organisms and no PAE against Gram-negative organisms (except carbapenem). Aminoglycosides and Quinolones have PAE against Gram- negative organisms.

Front 69

Define COMMENSAL

Back 69

Referring to organisms that reside on non-sterile body sites exposed to the outside world, providing defense to the host, who provides a hospitable living environment and nutrients

Front 70

Define the clinical manifestations of acute rheumatic fever

Back 70

Acute rheumatic fever is characterized by myocarditis, cardiac valvular disease, migratory arthritis, and arthralgias, skin rashes, and/or central nervous system disease. Patients present with fever and a subset of the above. It occurs 10-14 days post an acute pharyngeal infection and can be prevented by eradication of Group A strep within 10 days of infection.

Front 71

Know the hemolytic properties of each of the major streptococcal groups

Back 71

Str. pyogenes (Group A)- Beta-hemolytic, Str. agalactiae (Group B)- Beta-hemolytic, Str. pneumoniae- alpha-hemolytic, Viridans- alpha-hemolytic (many) or gamma-hemolytic (some)

Front 72

List all the major diseases that Streptococcus pneumoniae causes

Back 72

Number 1 cause of bacterial superinfection post influenza. Pneumonia, primary cause of bacterial meningitis worldwide, most common bacterial cause of sinusitis and otitis, bacteremia, bacterial endocarditis 

Front 73

How does advancing age influence the immune system?

Back 73

Many immunologic parameters decline with age including the thymus atrophies by age 40, primary antibody responses, skin reactivity, T cell proliferation to mitogens, number of naïve T cells, T cells make less IL-12 (immunostimulatory). Many immunologic parameters increase with age including variability or response to a new antigen, incidence of monoclonal immunoglobulin’s, incidence of auto-antibodies again DNA (anti-nuclear), immunoglobulin’s (rheumatoid factor) and organs (thyroid), increased numbers of memory T cells, T cells make more IL-10 (immunosuppressive).

Front 74

Compare and contrast the Gram-positive and Gram-negative cell wall

Back 74

Cell membrane in general does not contain sterols as in eukaryotic cells. They are important for active transport, energy generation, cell wall precursor synthesis, and secretion of enzymes and toxins. Gram-positive organisms are able to retain the crystal violet stain because of the high amount of peptidoglycan in the cell wall so they will stain dark purple. Gram-positive cell walls typically lack an outer membrane. LTA helps to anchor the peptidoglycan layer to the cell membrane. Gram-negative bacteria do not retain crystal violet dye instead they retain the safranin counterstain and appear red or pink in color. They have an outer and inner cell membrane and a small amount of peptidoglycan. They also contain LPS which gives them their pathogenic capabilities.

Front 75

List 5 properties of the Lipid A moiety of LPS

Back 75

Febrile response in the host through direct activation of the hypothalamus and induction of endogenous pyrogens such as IL-1 and prostaglandins, Activation of complement, granulocytes, and macrophages, Induction of interferon production, Induction of TNF with reduction of capillary endothelial cell permeability and development of shock, Induction of colony stimulating factor production, B-cell mitogen (chemical substance that encourages a cell to commence cell division, triggering mitosis)

Front 76

Which organism is the PRIMARY cause of bacterial meningitis worldwide?

Back 76

Str. pneumoniae

Front 77

The lab calls you and says that your patient is growing Gram-positive cocci in clusters from the blood cultures. Which SINGLE biochemical test will be the most useful to decide how best to treat the patient?

Back 77

Coagulase Test because only Staph. aureus are coagulase positive. All other Staph. infections are coagulase negative. So if it is coagulase positive you know you are dealing with Staph. aureus and if it is coagulase negative then you are dealing with some other Staph. infection.

Front 78

Why is the production of biofilms by bacteria clinically relevant?

Back 78

Biofilms are associated with the production of polsaccharide intercellular adhesin (PIA). They act like bacterial capsule to keep out antibodies, complement, and antibiotics. They also adhere to plastics which can lead to infection of hardware and other foreign material.

Front 79

Describe the clinical manifestations of a patient who presents with toxic shock syndrome

Back 79

Fever, hypotension, erythematous rash, vomiting, and diarrhea common, multisystem organ dysfunction, usually no bacteremia, initially described in women using high absorbency tampons. TSST-1 and other superantigen toxins, presence of antibody to TSST-1 is protective.

Front 80

Staphylococcus aureus is the bane of my existence (thanks for caring). Name 10 different medically important infections that it can cause (and now it is the bane of your existence!)

Back 80

Impetigo, cellulitis, cutaneous abcesses (bolis, carbuncles) wound, deep abscesses (abdominal, neck, sinus), osteomyelitis, septic arthritis, septicemia, endocarditis, toxin-mediated (toxic shock syndrome, scalded skin syndrome, food poisoning, necrotizing fascitis)

Front 81

Why are pregnant women warned against eating soft chesses and refrigerated luncheon meats (ham, salami, etc.)?

Back 81

These products are all at high risk for carrying Listeria monocytogenes. Pregnant women have mild-impairment of cell-mediated immunity so they are more susceptible to the development of the bacteremia. Lysteria may proliferate in placenta, illness occurring primarily in the third trimester. Stillborn or neonatal death may occur in up to 20% of cases. In utero infection my result in disseminated form of disease known as granulomatosis infantisepticum characterized by widespread microabscesses and granulomas. Late onset may occur two weeks post-partum and is characterized by meningitis.

Front 82

Describe the clinical manifestations of listeria infections in (a) an otherwise healthy young man

Back 82

Healthy young man- incubation period is 6-48 hours. Symptoms include diarrhea, fever, chills, headache, myalgias, and abdominal pain. The illness is self-limiting. Food Poisoning

Front 83

Describe the clinical manifestations of listeria infections in (b) a pregnant woman

Back 83

pregnant woman- pregnant women have a mild impairment of cell mediated immunity that predisposes them to Listeria infections. Listeria may proliferate into the placenta. Illness occurs in the third trimester and can be asymptomatic, mild gastrointestinal illness, bactermia characterized by fever, arthralgias, headache, GI symptoms, and backache. Stillborn or neonatal death may occur in up to 20%. Can be asx. Same sx as above +stillborn/neonatal death in 20%

Front 84

Describe the clinical manifestations of listeria infections in (c) fetus in utero

Back 84

fetus in utero- disseminated form of the disease called granulomatosis infantisepticum, sepsis of the infant with granulo inflammation.

Front 85

Describe the clinical manifestations of listeria infections in (d) 2 week old

Back 85

2 week old infant- Late onset infection can occur two weeks post-partum and is characterized by meningitis.

Front 86

Describe the clinical manifestations of listeria infections in (e) HIV+ patient with advanced immunosuppression

Back 86

HIV+ with advanced immunosuppression- most common manifestation is bacteremia without an obvious source. Can cause meningitis with a clinical presentation similar to other bacterial causes. CSF glucose is NOT low and mononuclear cells may predominate.

Front 87

Describe the clinical manifestations of listeria infections in (f) elderly patient

Back 87

elderly patient- second most common cause of meningitis in adults over the age of 50. Tx with vanc + ceftriaxone +amp!

Front 88

When treating meningitis in a 65 year old man, we usually use the following antibiotics: ceftriaxone (a cephalosporin), vancomycin, and ampicillin. Why do we use each of these antibiotics?

Back 88

Ceftriaxone – treat possible Neisseria meningitides infection Vancomycin – treat possible Strep. Pneumonia infection (primary cause of bacterial meningitis world wide) Ampicillin – treat possible Listeria infection (Listeria is 2nd most common cause of meningitis in adults >50 years old)

Front 89

Name 4 gram-positive rods

Back 89

Listeria monocytogenes, Bacillus anthracis, Bacillus cereus, Corynebacterium sp.

Front 90

Describe the virulence factors of Bacillus anthracis

Back 90

Capule- inhibits phagocytosis, Protective antigen- binds to cell membranes facilitating binding and transport of edema factor and lethal factor., Lethal factor- zinc dependent protease that cleaves protein kinases, releases oxygen radicals, and induces TNFa and Interleukin 1b. Leads to cell lysis, Edema factor- stimulates cellular camp, changes membrane permeability leading to edema, impairs neutrophil function, leads to bacterial proliferation, bacteremia, and systemic infection Inhibit PMN function + cell edema

Front 91

What is the “classical” exposure history that leads to Bacillus cereus diarrhea (in other words, the patient may tell you: “I ate XXX yesterday”)

Back 91

“Rice left sitting out.” I ate “undercooked meat” often from a bar-b-que or a fast food restaurant. Illness is usually self-limiting. Caused by heat-liable enterotoxin.

Front 92

What are the modes of spread of Corynebacterium diphtheriae?

Back 92

Modes of spread include airborne respiratory droplets, direct contact with respiratory secretions, and direct contact with exudates from infected skin lesions. Asymptomatic carriage rate is most important for spreading and maintaining epidemics.

Front 93

What is the major virulence factor of C. diphtheriae, which cells of the host body are most often affected, and as a result, what are the clinical manifestations?

Back 93

Major virulence factor is its potent exotoxin which is a 62,000 dalton polypeptide with 2 segments. B segment- binds to receptors on susceptible cells. A segment- active segement that inhibits protein synthesis in mammalian cells. Toxin effects all cells in body but heart, nerves, kidney most prominently. Toxin also contributes to pseudomembrane production.

Front 94

Streptococci are grown on this blood agar plate. Which ones are S. pneumoniae? S. pyogenes? Group A streptococci? S. agalactiae? Group B. streptococci? Enterococcus faecalis? Enterococcus faecium?

Back 94

Strep pneumonia – a-hemolysis ,Strep pyogenes – b-hemolysis, Group A strep (most common member – Strep pyogenes) – b-hemolysis, Strep agalactiae – b-hemolysis, Group B strep (most common member – Strep agalactiae) – b-hemolysis, Enterococcus faecalis – g- hemolysis (maybe a-hemolysis in some cases), Enterococcus faecium – g- hemolysis (maybe a-hemolysis in some cases)

Front 95

What organism is shown in the Gram’s stain below?

Back 95

Bacillus anthracis GPR in CHAINS

Front 96

The disc contains optochin. What organism are we likely dealing with?

Back 96

Strep. pneumonia, all other streph, staph, and enterococci are optochin resistant. STREP PNEUMONIAE IS ONLY OPTOCHIN SENSITIVE OF ALL GPC

Front 97

An alcoholic homeless man presents with this non-healing lesion; the Gram’s stain of the lesion is shown. What is the diagnosis?

Back 97

C. diptheriae CLUB-SHAPED

Front 98

Compare ‘early onset’ and ‘late onset’ neonatal infections associated with Group B Streptococci

Back 98

Early onset: (first 6 days): septicemia (60%), pneumonia (30%), meningitis (10%) Mortality 10%. Late onset: (7 days to 3 months) (mean 24 days) (Majority are due to type 3) May be culminant, with septic shock severe meningitis. Neurologic sequelae (early and late) occur in 25 – 50 % of children with meningitis.

Front 99

What infections do S. viridans cause?

Back 99

Sub Acute Endocarditis (heart valve infections); Abscesses formers: (Str. anginosis, Str. intermedius, Str. constillatus ) especially liver; Dental cares: Str. mutans; Septicemia in the immuno-compromised patient with leukemia, bone marrow transplantation; (Co-pathogens, mixed flora infections)

Front 100

What infections are associated with S. pneumoniae?

Back 100

Normal flora in 20-100% of individuals. No. 1 cause of 1) pneumonia, 2) meningitis, 3) sinusitis & 4) otitis, world wide.

Front 101

Persons infected with S. pneumoniae who are started on antibiotics have a decrease in mortality, but this decrease in mortality is only observed about 48 hours after starting antibiotics. Which virulence factor is responsible for the persistently high mortality during the first 48 hours after starting antibiotics?

Back 101

Autolysin causes suicide -> release pneumolysin -> activate complement resulting in excessive cytokine release

Front 102

Describe the emergence of antibiotic resistance in S. pneumoniae and Enterococci

Back 102

S. pneumonia: mutation of penicillin binding protein and beta-lactamase development; now encourage vaccine use. Enterococci (particularly E. faecium): Resistance to vancomycin (VRE), Readily transmits genes to other species, including staph.

Front 103

What is the #1 cause of liver abscesses in the US? (Hint: It is a streptococcus)

Back 103

Str. anginosis

Front 104

What infections do coagulase-negative staphylococci cause?

Back 104

Form biofilms, adheres to plastic, keeps out antibiotics. Virtually non pathogenic in normal people. Intravenous catheter infection, dialysis access devices, implants – artificial joints, heart valves, pacemakers and wires, vascular grafts, breast prostheses, surgical mesh, CSF shunts. Neonatal septicemia, NEC, endocarditis

Front 105

Compare the growth characteristics on blood agar of Staphylococcus aureus and S. epidermidis

Back 105

Aureus: golden yellow, beta hemolysis. Epidermidis: white, no hemolysis