Bacterias Flashcards

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1
Q

STAPHYLOCOCCUS AUREUS
“The golden staff of Moses”

A

STAPHYLOCOCCUS AUREUS
“The golden staff of Moses”

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2
Q

What does Staphylococcus Aureus literally mean?

A

Staphylococcus (grape like)

Aureus (gold in color)

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3
Q

Gram type of Staphylococcus Aureus?

A

Gram Positive Cocci

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4
Q

What tests can be used to determine Staphylococcus Aureus?

A

Catalase (+)
Coagulase (+)
Beta Hemolytic (+)
Mannitol (+)

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5
Q

What is the main virulence factor on Staphylococcus Aureus and how does it work?

A

Protein A; Main virulence factor on staph aureus.

Protein A is a component of S. Aureus cell wall and
it can bind to the FC region of antibodies and this will prevent compliment from occurring.

Preventing opsonization and phagocytosis.

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6
Q

Where does Staphylococcus Aureus mainly colonize?

A

S. Aureus will colonize the nares

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7
Q

What are the 10 possible diseases that can be caused with Staphylococcus Aureus?

A
  1. Gastroenteritis
  2. Acute bacterial endocarditis
  3. Abscesses and mastitis (Humps with red cloth - Really large erythematous abscesses)
  4. Toxic shock syndrome
  5. Impetigo
  6. Scalded Skin Syndrome (SSS)
  7. Pneumonia
  8. Surgical infections
  9. Osteomyelitis
  10. Septic Arthritis
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8
Q

What causes the coughing in Staphylococcus Aureus infection?

A

Coughing - Pneumonia

Patchy infiltrate on x-ray

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9
Q

What is the shape of the capsule of the virus that will infect after a Staphylococcus Aureus infection?

A

Icosahedron shaped capsule of the virus that will infect after a S. Aureus infection.

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10
Q

What is Staphylococcus Aureus is the most common cause of in adults? (Hint: 2 diseases)

A

Septic Arthritis and Osteomyelitis.

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11
Q

In Staphylococcus Aureus acute endocarditis, what is the most common cause of it and where does it affect it in the heart?

A

IV drug use

Tricuspid valve Endocarditis

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12
Q

What mediates Scalded Skin Syndrome in a Staphylococcus Aureus infection?

A

Scalded skin syndrome mediated by a protease

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13
Q

What causes Toxic Shock Syndrome in a Staphylococcus Aureus infection?

A

Toxic Shock Syndrome, commonly caused by leaving a bandage in or a tampon which causes nonspecific binding of MHC II to T cell receptors causing over-reaction and Cytokine storm.

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14
Q

What does a Catalase test measure?

A

Turns hydrogen peroxide –> water

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15
Q

What does a Coagulase test measure?

A

Fibrinogen –> fibrin

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16
Q

What does a Beta Hemolytic test measure?

A

When looking at petri dish with B-hemolysis it looks like a glowing halo of light.

Beta-hemolysin breaks down the red blood cells and hemoglobin completely. This leaves a clear zone around the bacterial growth.

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17
Q

What does a Mannitol test measure?

A

If it CAN ferment manitol it will turn the agar to yellow.

If it CAN’T ferment manitol the agar will stay pink.

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18
Q

What is the treatment of choice for Staphylococcus aureus infection?

A

Nafcillin/oxacillin are drugs of choice because of widespread antibiotic resistance.

“Naf for Staph”

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19
Q

What is the treatment for methicillin-resistant Staphylococcus aureus (MRSA)?

A

Vancomycin

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20
Q

What is the treatment for vancomycin-resistant Staphylococcus aureus (VRSA) or vancomycin- intermediate S. aureus (VISA)?

A

quinupristin/dalfopristin

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21
Q

STAPHYLOCOCCUS EPIDERMIDIS AND STAPHYLOCOCCUS SAPROPHYTICUS
“Beauty and the Plumber”

A

STAPHYLOCOCCUS EPIDERMIDIS AND STAPHYLOCOCCUS SAPROPHYTICUS
“Beauty and the Plumber”

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22
Q

Staphylococcus epidermidis and Staphylococcus saprophyticus are what type of gram?

A

Gram (+)

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23
Q

Staphylococcus epidermidis and Staphylococcus saprophyticus are Catalase + or -?

A

Catalase Positive

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24
Q

Staphylococcus epidermidis and Staphylococcus saprophyticus are Urease Positive. What does that mean?

A

Urea –> ammonia

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25
Q

How are Staphylococcus epidermidis and Staphylococcus saprophyticus separated from staph aureus?

A

Staph epidermidis and Staph saprophyticus are coagulase negative

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26
Q

Why is Staphylococcus epidermidis considered Ortopedic’s enemy?

A
  1. Hardware - Infects hardware or orthopedic joints
  2. Tubing - Catheter tubes, Indwelling catheters are also important spots of infections
  3. Heart valves - Infection of heart implants - endocarditis of artificially implanted heart valves
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27
Q

How is Staphylococcus epidermidis able to affect tools?

A

Uses biofilms to stick to sleek metal and plastic surfaces, these are polysaccharides that protect them from antibiotics and immune cells.

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28
Q

TXT of Staphylococcus Epidermidis endocarditis?

A

Vancomycin for TXT of Staph Epidermidis endocarditis

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29
Q

Where can Staphylococcus Epidermidis be found?

A

Normal Skin Flora

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30
Q

Staphylococcus Epidermidis is sensitive or resistant to a certain drug?

A

Novobiocin Sensitive

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31
Q

What disease is mainly caused by Staphylococcus saprophyticis infection?

A

UTI’s in Sexually Active Females.

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32
Q

Staphylococcus saprophyticis is sensitive or resistant to a certain drug?

A

Novobiocin resistant

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33
Q

Who is more at risk for Staphylococcus sapropytics infection?

A

Sexual active females

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34
Q

GROUP A STREPTOCOCCUS (STREPTOCOCCUS PYOGENES)
“The Pie Genies’ Bakery”

A

GROUP A STREPTOCOCCUS (STREPTOCOCCUS PYOGENES)
“The Pie Genies’ Bakery”

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35
Q

Group A Streptococcus are:

encapsulated or no capsulated?

A

Encapsulated

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36
Q

What is the capsule of the Streptococcus Pyogenes made of?

A

Hyaluronic Acid

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37
Q

Where do we produce Hyaluronic Acid in our bodies?

A

Connective Tissue so everywhere in our body so it cannot be immunogenic or else our own immune system would constantly be attacking us.

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38
Q

What tests can be done with Streptococcus Pyogenes?

A

B-Hemolytic

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39
Q

What are the symptoms Streptococcus Pyogenes can cause?

A

Impetigo

Pharyngitis (aka Strep throat), red inflamed throat

Erysipelas (its a very superficial cellulitis infection), red lesion with well demarcated borders, S Pyogenes is the most common cause.

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40
Q

What is the toxin of the Streptococcus Pyogenes?

A

Streptococcal Pyrogenic Exotoxin (SPE)
SPE A
SPE B
SPE C

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41
Q

What are the diseases that can be caused by the Streptococcus Pyogenes toxin?

A

Scarlett Fever
Toxic Shock Like Syndrome (TSLS)
Necrotizing Fasciitis

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42
Q

What are the three main symptoms of Scarlett Fever?

A

a. “Strawberry Tongue” - reddening and swelling of the tongue
b. Pharyngitis
c. Diffuse (widespread) rash that spares the face.

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43
Q

What is Toxic Shock Like Syndrome mediated by?

A

Super Antigen SpeA, SpeC

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44
Q

What is the Necrotizing Fasciitis mediated by?

A

SpeB

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45
Q

What are the two highly tested conditions (complications) pretending to Streptococcus Pyogenes?

A

Rheumatic Fever (RF)

Post Streptococcus Glomerulonephritis (PSGN)

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46
Q

What is the main virulence factor for Rheumatic Fever and how does it function?

A

M protein in GAS (Group A Strep) is the main virulence factor for Rheumatic Fever, will interfere with opsonization, antiphagocytic, M protein will mimic antibodies in heart and cause issues with Mitral Valve in the heart.

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47
Q

How does M protein function?

A

Antiphagocytic action

Very antigenic and elicits a humoral response, creating an antibodies to a very similar antigen and in this case myosin in cardiac muscle (Molecular mimicry), thus, damages mitral valves (can cause a mitral stenosis)

Pharyngitis precipitates RF, NOT IMPETIGO

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48
Q

When does Rheumatic Fever occur?

A

AFTER Streptococcus pharyngitis infection.
Does NOT happen after skin infections.
Does NOT happen after prompt treatment of pharyngitis, which is why it happens more in young children with little access to Healthcare.

Pharyngitis precipitates RF, NOT IMPETIGO”

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49
Q

What kind of hypersensitivity reaction is Rheumatic Fever?

A

Hypersensitivity type II reaction

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50
Q

What is the criteria used for Rheumatic Fever?

A

JONES criteria

J: Joints –> polyarthritis
O: <3 : “heart problems” –> valvular damage leading to new murmurs, myocarditis, paricarditis.
N: Nodules (subcutaneous nodules): nodules on extensor surfaces (forearms, elbows, knees)
E: erythema marginatum: rash with nice thick borders
S: Sydenham’s Chorea: rapid involuntary especially of hands and face

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51
Q

What causes the Post Streptococcus Glomerulonephritis (PSGN)?

A

Our own immune system.

After a streptoccocus infection, unlike RF the damage isn’t a type2 hypersensitivity reaction, its a type 3 hypersensitivity, which means the damage is from circulating antibody antigen immune complexes that eventually deposit in the glomerulus.

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52
Q

What are the 2 main symptoms for Post Streptococcus Glomerulonephritis (PSGN)?

A

Facial edema - puffy cheeks w/ nephritis

Cola colored Urine

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53
Q

When does Post Streptococcus Glomerulonephritis (PSGN) occur?

A

Occurs 2 weeks after the onset of the initial streptococcus infection.

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54
Q

What is a way to differentiate RF and PSGN?

A

RF: can occur only after pharyngitis
PSGN: can occur after pharyngitis or superficial infection like impetigo

Treatment and complication prevention:
Early diagnosis and treatment of Strept throat can prevent RF but it cant prevent PSGN.

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55
Q

What is the treatment for Streptococcus pyogenes infection?

A

Penicillin

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56
Q

What are 3 more virulence factors for Streptococcus pyogenes?

A

a. Streptolysin O: allows Group A Streptococcus to lyse RBC to be Beta Hemolytic, we generate antibodies to Streptolysin O (called ASO antibodies).
b. Streptokinase, converts plasminogen to plasmin. Plasmin is fibrinolytic. So Streptokinase is given as medication to lyse clots to MI or Ischemic strokes.
c. DNA’ases, depolymerize DNA and really least important to know.

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57
Q

What does “kinase” mean?

A

To put a phosphate on something

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58
Q

How do we differentiate Group A Streptococcus and Group B streptococcus?

A

Group A Streptococcus is Bacitracin sensitive.

Group B Streptococcus is Bacitracin resistant.

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59
Q

How can we test if a patient recently had a Group A streptococcus infection?

A

Check ASO titers to see if there was a Group A Strep Infection since we create antibodies against it.

We generate antibodies to Streptolysin O (called ASO antibodies).

Antistreptolysin O titer

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60
Q

What is the Mnemonic for Virulence factors of Streptococcus pyogenes?

A

“SMASHED”

Streptolysins
M protein
Anti-C5a peptidase
Streptokinase
Hyaluronidase and Hyaluronic acid Capsule
Exotoxin (SPE-A, SPE-B, SPE-C)
DNAses
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61
Q

STREPTOCOCCUS AGALACTIAE
“Galactic Baby (Group B Streptococcus)”

A

STREPTOCOCCUS AGALACTIAE
“Galactic Baby (Group B Streptococcus)”

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62
Q

Streptococcus agalactiae is gram positive or negative?

A

Gram Positive (“purple plante”)

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63
Q

What tests can be done to check for Streptococcus agalactiae?

A

Hippurate Positive
CAMP test positive
B-hemolytic

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64
Q

What does a Hippurate test measure?

A

Hydrolyzes sodium hippurate.

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65
Q

What does CAMP test measure?

A

Distinguishes Streptococcus agalactiae with all other streptococcus!

Similar to staphylococcus Aureus, when GBS is plated with Staph aureus, it has increasing zone of hemolysis.

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66
Q

What kind of capsule does Streptococcus Agalactiae have?

A

Polysaccharide capsule

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67
Q

What does Bacitracin do to streptococcus agalactiae?

A

Nothing, its Bacitracin resistant.

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68
Q

What is the main concern with a streptococcus agalactiae and its also the first thing you should think about is:

A

Causes Meningitis in neonates (#1 cause of meningitis in neonates).

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69
Q

What else can streptococcus agalactiae also cause?

A

Most likely to cause meningitis sepsis and also causes pneumonia.

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70
Q

What can you see in petri dish of streptococcus agalactie?

A

a arrowhead is the arcuate that forms in the zone of hemolysis.

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71
Q

How can a neonate get a streptococcus agalactiae infection?

A

When neonates passes through the vaginal canal of the mother during delivery.

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72
Q

Part of prenatal care, how and when do we check for streptococcus agalactiae?

A

Week 35 the vagina and rectum is swabbed to see if she is colonized by streptococcus agalactie.

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73
Q

What is GBS infection?

A

Group B Strep infection

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74
Q

What is the prevention for streptococcus agalactiae?

A

Profilaxis: Penicillin will be given to mom intrapartum to prevent group B strep.

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75
Q

STREPTOCOCCUS PNEUMONIA & STREPTOCOCCUS VIRIDANS
“The Alpha Knight Tournament”

A

STREPTOCOCCUS PNEUMONIA & STREPTOCOCCUS VIRIDANS
“The Alpha Knight Tournament”

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76
Q

Is streptococcus pneumonia gram positive or gram negative?

A

Gram Positive

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77
Q

Is streptococcus pneumonia alpha or beta hemolytic?

A

a-hemolytic which means theres partial hemolysis where the surrounding zone is a green hue. This green comes from the oxidation from hemoglobin.

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78
Q

What kind of capsule does streptococcus pneumonia have and why is it important?

A

Polysaccharide capsule which is a major virulence factor.

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79
Q

Streptococcus pneumonia is sensitive to something. what is it?

A

Optochin sensitive, optochin inhibits the growth of streptococcus pneumonia

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80
Q

What does streptococcus pneumonia look like under a microscope?

A

“Double Lance” - Lancet shaped diplococci

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81
Q

Streptococcus pneumonia is soluble to what?

A

Bile soluble, meaning it does not grow in bile

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82
Q

What kind of pneumonia does streptococcus pneumonia lead to and how does the sputum look like?

A

Lobar pneumonia that generally infiltrates the lower lobes.

Rust colored sputum.

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83
Q

Streptococcus pneumonia is the number one cause of which diseases?

A

Community acquired pneumonia

"MOPS"
Meningitis
Otittis Media
Pneumonia
Sinusitis
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84
Q

Streptococcus Pneumonia has another virulence factor other than its capsule that helps it avoid our immune system. What is it?

A

IgA Protease: Protease that cleaves IgA that allows invasion of mucosa reducing host defenses.

Helps it invade and colonize our mucosa, reducing host’s defenses

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85
Q

Who is at a greater risk of getting infection of encapsulated microorganisms?

A

Spleenectomy or autospleenectomy as in the case of Sickle cell disease (asplenia). This is because the spleen plays a major role of removing encapsulated organisms from the body.

Removal of spleen leads to susceptibility of infection by encapsulated organisms like in sickle cell anemia.

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86
Q

What is the TXT for streptococcus pneumonia infection?

A

Macrolides (azithromycin)

3rd gen cefalosporin: Ceftriaxone

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87
Q

How can we prevent a streptococcus pneumonia infection?

A

Adult is a 23 valiant polysaccharide vaccine.
Children is 7 valent but conjugated to a protein.

Adults will have a T-Cell independent response creating IgM that does not last long. Adding the protein adds a more robust antigen response leading to a production of IgG in children.

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88
Q

What kind of capsule does Streptococcus viridians have?

A

its NOT encapsulated

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89
Q

Streptococcus viridians is resistant to what?

A

optochin

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90
Q

What happens to streptococcus viridians when it is put with bile?

A

it is resistant

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91
Q

What other species are part of the streptococcus viridans?

A

Streptococcus mutants

Streptococcus sanguinis

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92
Q

What can streptococcus mutants and Streptococcus sanguinis lead to?

A

dental plaque, dental carries

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93
Q

What happens if Streptococcus viridian gets in the blood?

A

subacute endocarditis in damaged heart valves most commonly mitral valve.

Strep Sanguineous adheres to fibrin platelet aggregates in damaged heart valves, most commonly occurs in mitral valve.

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94
Q

How can Streptococcus viridians do so much damage to the heart?

A

Synthesizes Dextran’s (think of it like a glue) from glucose which allows strep viridians to adhere to any fibrin from platelets that has been damaged in the heart.

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95
Q

ENTEROCOCCUS FAECALIS & ENTEROCOCCUS CAUCUS
“Protest at the Caucus”

A

ENTEROCOCCUS FAECALIS & ENTEROCOCCUS CAUCUS
“Protest at the Caucus”

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96
Q

What are the two species of the enterococcus genus?

A
Enterococcus Faecalis (California)
Enterococcus Faecium (Stop the Fees)
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97
Q

Which species of enterococcus is more common?

A

Enterococcus Faecalis (California)

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98
Q

Which species of enterococcus is more dangerous and why?

A

Enterococcus Faecium (Stop the Fees), Nosocomial infection resistant to almost every antibiotic we have.

Vancomycin resistant as well (VRE: Vancomysin Resistant Enterococcus)

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99
Q

Both enterococci can grow in mediums of?

A

Can grow in mediums up to 6.5% sodium chloride

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100
Q

What is enterococcus resistant against?

A

Bile resistant

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101
Q

What are the main symptoms of enterococcus infections?

A

DO U <3 T?

U: UTI
<3: Endocarditis
T: Infection of the Biliary Tree

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102
Q

What is the treatment for enterococcus infections?

A

“Police Line” - Linezolid

“tiger stripes” - Tigacycline

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103
Q

NEISSERIA SPECIES

“Noir Series”

A

NEISSERIA SPECIES

“Noir Series”

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104
Q

Neisseria is gram positive or gram negative?

A

Gram negative

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105
Q

neisseria: oxidase positive or negative?

A

Oxidase positive

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106
Q

What kind of shape does neisseria have?

A

Dipplicocci (“double hand cuffs”)

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107
Q

What are the agars used for neisseria?

A

Chocolate agar (its a heated blood agar).

CANT use blood agars since its inhibited by some of lipids/other elements in blood agar unless heated therefore chocolate agar.

VPN agar (Thayer Martin Agar)

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108
Q

What is a VPN agar?

A

VPN special agar enriched with vancomycin, polymixin, and nystatin

Can be used for Neisseria.

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109
Q

What is another name for VPN agar?

A

Thayer martin AKA VPN agar

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110
Q

What deficiency causes an increase susceptibility to neisseira species?

A

MAC complex deficiency due to complex c5-c9 deficiency.

MAC Deficiency unable to form the MAC complex due to complex c5-c9 being inhibited. Patients with c5-c9 deficiency are unable to form MAC complex, leading to increased infections.

MAC = Membrane Attack Complex

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111
Q

What are the virulence factors of Neisseria species?

A

Virulence Factors
a. Pilli allows attachment to surfaces and display antigenic variation which makes our immune system difficult to target neisseria and prevent any lasting immune response.

b. IgA protease will cleave IGA at its hinge point, facilitates survival along mucosal surfaces.

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112
Q

NEISSEIRA MENINGITIDES
“A SHOCKING DEATH ON CAMPUS”

A

NEISSEIRA MENINGITIDES
“A SHOCKING DEATH ON CAMPUS”

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113
Q

How does neisseria meningitis spread?

A

Easily spread in areas with a lot of people, military recruits, college dorms via respiratory droplet

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114
Q

Neissiria meningitis is gram ____________.

A

Gram negative - Red Hue

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115
Q

What does Neisseiria meningitis ferment?

A

meningitis ferments maltose and glucose.

Only meningitis ferments maltose

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116
Q

Where does neisseria meningitis first colonize?

A

Colonizes nasopharynx first, transmitted by respiratory secretions (kissing, sharing drinks, close contacts, sneezing, coughing)

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117
Q

What kind of capsule does neisseria meningitis have?

A

Polysaccharide capsule that inhibits phagocytosis and its considered its major virulence factor.

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118
Q

How can neisseria meningitis be prevented?

A

Before SDSU I had to get a shot - the Meningococcal vaccine

It was a vaccine for A,C,D polysaccharide capsules but not B.

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119
Q

Which type of neisseria meningitis accounts for most infections in USA and most developed countries?

A

Type B since theres no vaccine for it.

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120
Q

Who are more susceptible to neisseria meningitis infection?

A

Sickle cell and asplenic patients are more susceptible to Neisseria meningitides because it is encapsulated (just like Strep pneumonia!)

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121
Q

What is the physiopathology of neisseria meningitis infection?

A

N. Meningitides Invades hemotogenously leading to a massive inflammatory response generated by LOS (lipooligiosaccharides) proteins, these are Neisseria’s version of LPS, it grows so much of it that it outgrows the surface area of the bacteria and begins blabbing off.

These blebs of LOS envelope that lead to a massive inflammatory response.

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122
Q

MOST IMPORTANT QUESTION; PATHOGENOSIS:

What does the inflammatory response of neisseria meningitis lead to?

A

Inflammation leads to leaky capillaries, which leads to characteristic petechial rash leading to thrombocytopenia leading to DIC (Disseminated Intravascular Coagulation)
–> oozing at venopuncture sites, bleeding gums

Capillary leakage can lead to hypovolemia and shock.

Vasoconstriction will go to max to attempt to maintain blood pressure and adrenals can infarct and will contribute to shock (Waterhouse fritter syndrome)

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123
Q

What is the mortality rate of neisseria meningitis infection?

A

15% mortality rate even with antibiotic treatment.

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124
Q

What is the treatment for neisseria meningitis infection?

A

3rd generation cephalosporin that can penetrate the blood brain barrier like ceftriaxone

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125
Q

What is Waterhouse fritter syndrome?

A

Waterhouse fritter syndrome, characterized by hemorrhage of adrenals caused by capillary leak that leads to hypovolemia/shock.

Can be caused by neisseria meningitides.

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126
Q

What is the profilaxis treatment for someone who had close contact?

A

Rifampin.

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127
Q

Who should be given a profilaxis treatment with someone infected with neisseria mengitis?

A

Close contact is someone who had more than 8 hours with someone infected during the seven days prior to onset should be given rifampin.

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128
Q

NEISSERIA GONORRHEA
“The Violinists Last Clap”

A

NEISSERIA GONORRHEA
“The Violinists Last Clap”

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129
Q

How do you get neisseria gonorrhea infection?

A

Sexually Transmitted Disease

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130
Q

What kind of shape and gram type is neisseria gonorrhea?

A

Gram Negative Diplococci

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131
Q

what kind of cells are neisseria gonorrhea and what kind of cells do they like to invade?

A

Facultative intracellular in PMNs

The cells they like to invade are polymorphonuclear lymphocytes (PMNL)

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132
Q

What kind of capsule does neisseria gonorrhea have?

A

NOT encapsulated

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133
Q

What happens in males when they are affected with neisseria gonorrhea?

A

Urethritis
Prostatitis
Orchiditis

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134
Q

What happens in females when they are affected with neisseria gonorrhea?

A
  1. Pelvic Inflammatory Disease (PID) - can lead to scarring which leads to infertility or ectopic pregnancy.
  2. Purulent White Charge - which is characteristic of Gonorrhea (can occur to both men and women), generally more thicker and purulent in appearance than chlamydia which tends to be more thin and watery.
  3. PID can spread to the peritoneum which causes: Fitz Hugh Curtiss syndrome
  4. May cause polyarthritis in the knee and is asymmetric.
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135
Q

What is Fitz Hugh Curtiss syndrome?

A

Fitz Hugh Curtiss syndrome: A further complication of the peritoneum is that the infection of the peritoneum can lead to adhesions that form to the capsule of the liver and these long and thin adhesions are referred to as “violin string adhesions”

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136
Q

A joint tap will show purulent synovial fluid that doesnt gram stain, why is that?

A

Thats because the infection is intracellular.

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137
Q

How can a baby be infected with neisseria gonorrhea?

A

During delivery if the mother has untreated gonaccocal infection.

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138
Q

What is the first symptom seen in a newborn with neisseria gonorrhea infection?

A

Gonococcal Conjunctivitis occurs generally during within the first five days.

Chlamydia conjunctivitis occurs after a first week of birth.

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139
Q

What is the TXT of choice for neisseria gonorrhea infection?

A

Ceftriaxone but if you put that on USMLE its WRONG.

Co infections with Chlamydia are super common so treat for both: Ceftriaxone + Macrolide (such as: azithromycin or doxycycline)

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140
Q

BACILLUS ANTHRACIS + BACILLUS CEREUS
“King Anthra’s Axe”

A

BACILLUS ANTHRACIS + BACILLUS CEREUS
“King Anthra’s Axe”

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141
Q

What is characteristic symptom of bacillus anthracis infection?

A

Black Eschar with erythematous ring

Black Eschar: black necrotic cutaneous lesion with a surrounding erythematous ring

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142
Q

What is the capsule of bacillus anthracis and bacillus cereus?

A

Capsulated with Poly-D Glutamate (capsule is made up of protein instead of the usual polysaccharides)

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143
Q

What is the shape and gram type of bacillus anthracis and bacillus cereus and what disease does it create?

A

Large Gram positive rods in a chain (unusual to see them in a chain)

Bacillus anthracis, a gram positive bacterium, is the causative agent of anthrax. This organism is capsulogen and toxinogenic.

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144
Q

What does bacillus anthracis and bacillus cereus need to survive?

A

It is obligate aerobe (can only survive in the presence of oxygen)

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145
Q

How does bacillus anthracis survive?

A

Bacillus anthracis is a spore forming bacteria allowing them to survive in very poor environments. The spores hibernates without any significant metabolic activity and with a sturdy protective covering its highly resistant to temp/chemicals, so its able to survive an extremely long time in almost any environment.

Think of: 2001 anthrax attacks, also known as Amerithrax.

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146
Q

What are the two important spore forming organisms?

A

bacillus and clostridium species.

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147
Q

MOST TESTABLE QUESTIONS:

what are the two toxins of bacillus anthracis?

A

It secretes two toxins which are composed of three proteins: the protective antigen (PA), the lethal factor (LF) and the edema factor (EF).

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148
Q

How does edema factor (EF) work in bacillus anthracis?

A

EF toxin functions as adenosine cyclase.

It increases cAMP intercellularily this will cause fluid to go extracellular space leading to edema inhibiting host defenses and indirectly preventing phagocytosis

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149
Q

How does lethal factor (LF) work in bacillus anthracis?

A

LF (lethal Factor), exotoxin that acts as a protease and cleaves MAP Kinase, this is a signal transduction protein that is responsible for cell growth.

This factor (MAP Kinse) will lead to necrosis and black eschar.

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150
Q

What is wool sorter’s disease and what are its symptoms?

A

pulmonary anthrax, wool sorters disease. Spores can get into wool and hide of animals and persist there. People will inhale the spores when the animal is handled. Then germs in the lungs and cause pulmonary symptoms.

Starts with no specific pulmonary symptoms.
Dry cough.

medianstinal lymph nodes 
Hemorragic medianstinitis (looks like widen mediastinum on x-rays)
Pulmonary Hemorrhage (almost 100% mortality rate)
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151
Q

What is the TXT bacillus anthracis when caught early?

A

fluoroquinolone (drug of choice)

doxycycline (secondary treatment)

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152
Q

physical characteristics of Bacillus cereus?

A

Aerobic and spore forming

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153
Q

How can you get sick with Bacillus cereus?

A

Food poisoning

reheated fried rice and vomitting

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154
Q

CLOSTRIDIUM TETANI
“Rhesus Research Revolution”

A

CLOSTRIDIUM TETANI
“Rhesus Research Revolution”

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155
Q

Clostridium tetani: gram positive or negative?

A

gram positive

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156
Q

What kills Clostridium tetani?

A

Obligate anaerobes (cannot survive in the presence of oxygen)

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157
Q

How do Clostridium tetani survive?

A

spore forming

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158
Q

How does Clostridium tetani invade our bodies?

A

Clostridium is found in the dirt and enters the body through a puncture wound.

Rusty nails, barbed wire

Spores found in rusty nails, and in soil

Puncture wound occurs either by nail or barbed wire with tetany spores on it, spores are embedded in the flesh and the organism vegetates and stays at the wound site. It will release tetanus toxin that will cause all the symptoms

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159
Q

What are the symptoms accompanied with Clostridium tetani?

A
  1. Relentless muscle contractions: Spastic paralysis leading to rigidity
  2. Opisthosomas - exaggerated arching of the back
  3. rhesus sardonicus = evil smile, evil grin
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160
Q

IMPORTANT TEST QUESTION:

Describe pathogenesis of Clostridium tetani.

A

Tetanus toxin will travel retrograde through the motor axons to the spinal cord.

Tetanus toxin acts as a protease will cleave a protein named “snare” and will inhibit exocytosis of the neurotransmitter into the synapse (GABA and glycine) or Renshaw cells.

2 type of inhibitory neurons, GABA and glycine. If these are inhibited it will result in uncontrolled firing of the motor neurons leading to spastic paralysis.

Renshaw cells will sense over activity of nearby motor neurons and when they sense this activity they will attempt to fire and inhibit the motor neuron. So the GABA and Glycine release from these cells is inhibited leading to spasm

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161
Q

Describe to Clostridium tetani vaccine.

A

It is a toxoid Vaccine which means toxin conjugated to a protein to increase immunogenicity.

This produces an antibody response to the toxin, not to the organism.

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162
Q

CLOSTRIDIUM BOTULINUM
“Robotulism”

A

CLOSTRIDIUM BOTULINUM
“Robotulism”

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163
Q

clostridium botulinum: gram type?

A

Gram positive

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164
Q

How is clostridium botulinum transmitted?

A

Spore forming.

transmitted by improper canning of food allowing it to flourish in the anaerobic environment producing heat stable toxin.

“a family are presenting with the same neural symptoms” make the dang connection on these kind of questions!!!

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165
Q

what kills clostridium botulinum?

A

Obligate anaerobe

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166
Q

What symptoms will a patient present with clostridium botulinum infection?

A

Flaccid paralysis, descending paralysis. Opposite of Guillen barre syndrome. Multiple people is most likely botulism, not Guillen barre.

for example, multiple people who went camping showing these symptoms will be botulinum most likely, NOT Guillen barre.

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167
Q

What kind of paralysis is presented in clostridium botulinum infection?

A

descending paralysis: diplopia, ptosis

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168
Q

How is the paralysis produced in a clostridium botulinum infection??

A

to demonstrate the descending paralysis, toxin is unable to cross BBB so only peripheral nervous system is affected.

NOT the central nervous system since it cant cross BBB.

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169
Q

How does the toxin function in a clostridium botulinum infection?

A

Cleavage of SNARE protein similar to Tetany toxin, only difference is that botulism attacks motor neurons that release Ach, inhibiting motor neuron release leading to flaccid paralysis.

Toxin is a protease that cleaves SNARE proteins.

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170
Q

How do adults get infected with clostridium botulinum infection?

A

The spores must first germinate in an Anaerobic environment (canned food) and produce the toxin in that environment. Then adults ingest that PREformed toxin.

Ingestion of pre formed antigen from improperly canned foods.

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171
Q

Whats a food that can cause infantile botulism?

A

Spores in the Honey

Infantile botulism transmitted through ingestion spores in the honey.

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172
Q

How do babies get infected with clostridium botulinum infection?

A

Ingestion of spores; honey

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173
Q

What syndrome do babies get with clostridium botulinum infection and why is it caused?

A

Toxin effects similar to babies and cause flaccid paralysis “Floppy Baby Syndrome”

Babies lack robust flora of gut that can out compete Clostridium botulinum will be colonized with spores if they ingest honey. Then they will produce the toxin and have floppy baby syndrome.

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174
Q

Why don’t adults get sick from ingesting infected honey?

A

clostridium botulinum is a wimp and cant compete with our normal adult flora even though our gut is anaerobic environment, while babies lack this competition.

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175
Q

Whats more common: Adult or Infantile botulism?

A

Infantile botulism

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176
Q

CLOSTRIDIUM DIFFICILE
“Field Trip to the Chocolate Factory”

A

CLOSTRIDIUM DIFFICILE
“Field Trip to the Chocolate Factory”

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177
Q

What the street name of clostridium difficile?

A
King of Diarrhea 
Bed pan's Worst nightmare
C-Dif
Chocolate factory
pseudomembranous colitis.
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178
Q

What does clostridium difficile for?

A

Spore forming

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179
Q

What kind of diarrhea is clostridium difficile?

A

Nosocomial diarrhea (people are affected while hospitalized), spores easily transferred from patient to patient, antibiotics will wipe out normal flora making patients immunocompromised and able to be colonized then create the toxin.

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180
Q

Which is one of the main antibiotics that will cause clostridium difficile?

A

Clindamycin and poorly washed hands can cause it. Clindamycin is one of the main antibiotics that will cause this.

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181
Q

What are the 2 exotoxins that are produced by clostridium difficile?

A

Exotoxin A

Exotoxin B

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182
Q

Describe the 2 exotoxins that are produced by clostridium difficile?

A

Exotoxin A - Binds to the brush border of the intestine and causes inflammation, cell death and watery diarrhea.
“Brush border toxin causing diarrhea”

Exotoxin B - disrupts cytoskeleton integrity by
depolymerizing actin leading to enterocyte death and necrosis. Yellowish grey exudate that forms a pseudomembrane that covers the colonic mucosa. This is why clostridium difficile infection is called a pseudomembranous colitis.

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183
Q

How can you diagnose Clostridium difficile?

A

PCR: look for the toxin –> Assay to detect TOXIN (not the bacteria that is screened) in stool that will be detected downstream

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184
Q

Clostridium difficile cant survive with?

A

Obligate anaerobe

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185
Q

Clostridium difficile: Gram type?

A

Gram positive

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186
Q

What is the treatment for Clostridium difficile?

A

Oral vancomycin + Metronidazole

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187
Q

Why is oral vancomycin used for treatment?

A

IV vancomycin wont deliver to lumen of intestine. So its taken orally. Vancomycin also has poor absorption rate orally so its good for side effects minimization.

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188
Q

CLOSTRIDIUM PERFRINGENS
“Private Ringen’s Motorcycle Accident”

A

CLOSTRIDIUM PERFRINGENS
“Private Ringen’s Motorcycle Accident”

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189
Q

How does clostridium perringens spread?

A

Spores are formed in dirt and soil

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190
Q

How is one infected with clostridium perringens?

A

Classic Presentations: (deep military wounds, motorcycle accidents).

Large amounts of flesh are exposed to dirt and dust.

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191
Q

What is clostridium perringens afraid of?

A

Obligate anaerobe

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192
Q

What are the 2 diseases that clostridium perfingens create?

A
  1. clostridial myonecrosis: Causes Gas Gangrene after it enters the wound, gas produced under tissue and has a cracking sound on palpation. Gas is produced as the organism consumes carbohydrates.
  2. Slow onset diarrhea due to spores needing to reproduce in the gut then create the toxin.
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193
Q

What is the main toxin in clostridial myonecrosis?

A

This is due to Alpha toxin that effects lipid bilayer and lyses RBC’s which causes hemolysis.

Myonecrosis involves alpha toxin, which is a lecithiinase (phospholipase), which cleaves lecithin which causes damage cell membranes by damaging the lipoproteins.

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194
Q

what the heck is “Double zone of hemolysis”?

A

Lecithinase can cause red cell hemolysis both in vivo and in vitro.

So when you plate it, it has a zone of hemolysis but its unique that it forms double zone of hemolysis.

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195
Q

What is the TXT for clostridium perfingens?

A

IV penicillin G

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196
Q

CORYNEBACTERIUM DIPHTHERIAE
“Heart of the Bull Fight”

A

CORYNEBACTERIUM DIPHTHERIAE
“Heart of the Bull Fight”

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197
Q

Gram type of corynebacterium diphtheriae and its spore type and its shape?

A

Gram positive, Non-spore forming

Club shape and y or v Shape

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198
Q

What does corynebacterium diphtheriae stain with?

A

Metachromatic granules that stain with aniline dyes, Metachromatic granules will stain red and the rest of the cell will stain blue.

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199
Q

Describe the 2 exotoxins and its functions of corynebacterium diphtheriae.

A
Subunit A (active subunit)
Toxin causes Ribosylation of Elongation Factor 2 (EF-2), this will inhibit ribosome function inhibiting protein synthesis leading to cell death. This will lead to pseudomembranous exudate that will be found in the oral pharynx.

Subunit B (binding subunit)

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200
Q

Where are the pseudomembranes of corynebacterium diphtheriae found?

A

pseudomembranes Found in throat and tonsils because the infection is transmitted by respiratory droplets, Can cause airway obstruction and lymphopathy, this will cause bulls neck (thickening of the neck).

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201
Q

What happens when the corynebacterium diphtheriae toxin gets into the blood stream?

A

It can have systemic effects both on heart and nervous system:

Can cause life threatening myocarditis. Can present arrhythmia and heart block. (lethal effect of diphtheria)

Local paralysis that generally begin in posterior pharynx and can lead to cranial nerve deficits. This is because the corynebacterium diphtheriae toxin will damage the myelin of nerve fibers.

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202
Q

How can you culture test corynebacterium diphtheriae?

A

Need culturing or toxin assey.

So swab those grayish membranes and plate them on 2 special agars:

plate on Tellurite and Loeflers media

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203
Q

How can you differentiate between toxin and nontoxic strains of corynebacterium diphtheriae?

A

Eleks test - in-vitro assay on filter paper that has antitoxin on it.
So if toxin binds to it, theres a reaction and the strain is considered toxic.

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204
Q

Which vaccine is used for corynebacterium diphtheriae?

A

DTaP vaccine is used, often given with tetanus and pertussis vaccine.

Can produce a very powerful IgG response.

Toxoid Vaccine (consists of inactivated exotoxin that of protein)

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205
Q

Which type of patient are most likely to get corynebacterium diphtheriae?

A

Immigrants since USMLE thinks they dont vaccinate outside USA

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206
Q

What is the treatment for a non vaccinated corynebacterium diphtheriae infection?

A

Passive immunization (administrating antitoxoid)

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207
Q

LISTERIA MONOCYTOGENES
Santa’s List

A

LISTERIA MONOCYTOGENES
Santa’s List

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208
Q

Listeria monocytogenes: gram positive or gram negative?

A

Gram positive

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209
Q

Who are most likely to get sick from a Listeria monocytogenes infection?

A

Pregnant women are more likely (20 times more) to get listeria than anyone else.

May lead to termination or disease in the newborn

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210
Q

Which test can be done to identify Listeria monocytogenes?

A

B-hemolytic

Catalase positive

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211
Q

Describe Listeria monocytogenes physically.

A

Motile and facultative intracellular, tumbling motility extracellular

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212
Q

How does Listeria monocytogenes get around?

A

Rapidly polymerizes actin along the cell wall allowing it to move quickly in the cell.

Rocket “ Actin Rocket” intracellular movement

can even move from cell to cell

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213
Q

Where does listeria monocytogenes likes to survive and multiply?

A

Listeria survives and multiplies in near freezing temperatures

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214
Q

What does listeria monocytogenes contaminate?

A

Can contaminate food items even if they are refrigerated, like milk, cheese

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215
Q

what does listeria monocytogenes do to a new born?

A

Newborns can get meningitis from the mom, can also get in in adults over 60

Its the 3rd most common cause of meningitis, after Streptococcus B and E. Coli.

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216
Q

What should you tell a pregnant woman about listeria monocytogenes?

A

Don’t eat soft cheeses.

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217
Q

What is the TXT for listeria monocytogenes?

A

Ampicillin

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218
Q

PROTEUS MIRABILIS
“The God of the Public restroom”

A

PROTEUS MIRABILIS
“The God of the Public restroom”

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219
Q

proteus mirabilis: gram type?

A

Gram negative

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220
Q

What happens to proteus mirabilis when plated?

A

Demonstrates swarming motility

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221
Q

Is Proteus mirabilis facultative aerobe or facultative anaerobe?

A

Facultative anaerobe

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222
Q

What diseases can Proteus mirabilis cause?

A

Kidney Stones

UTI

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223
Q

Tests that can be used for Proteus mirabilis?

A

Urease positive

H2S positive

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224
Q

What kind of environment gators a struvite stone formation?

A

Alkaline environment can cause struvite stone formation.

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225
Q

Why is it to know that proteus mirabilis is urease positive?

A

may form stag horn calculi = kidney stones within pelvis

Ammonia means urease positive, this is what makes the stag horn calculi, to struvite stones causing pain and kidney stones, alkaline formation causes kidney struvite stones.

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226
Q

What kind of odor does a proteus mirabilis infection have?

A

Fishy odor

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227
Q

What is the TXT for a proteus mirabilis infection?

A

Sulfonamides

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228
Q

What are struvite stones made of?

A

Formed of ammonia, magnesium, and phosphate.

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229
Q

YERSINIA ENTEROCOLITICA & PESTIS
“YERSINS PETS”

A

YERSINIA ENTEROCOLITICA & PESTIS
“YERSINS PETS”

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230
Q

Gram type of Yersinia enterocolitica?

A

Gram Negative

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231
Q

How does yersinia enterocolitica spreads?

A

Primarily transmitterd through puppy feces

Contaminated Milk products (like Listeria)

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232
Q

Who are the most common individuals infected with yersinia enterocolitica?

A

Toddlers, Children (duh!) (since they play with puppies)

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233
Q

What is yersinia enterocolitica resistant to?

A

Resistant to cold temperatures (like listeria)

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234
Q

Whats so special about yersinia enterocolitica staining?

A

Stains Heavily on two ends

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235
Q

What is the main virulence factor of yersinia enterocolitica?

A

Encapsulated virulence factor

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236
Q

What is the main symptom of yersinia enterocolitica?

A

Bloody diarrhea (invasive)

Invasive systemic effects like fever, intestinal issues, leukocytosis, abscesses, major bowel movements

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237
Q

TEST QUESTION:

What is the main manifestation of yersinia enterocolitica?

A

Mimics appendicitis

right lower quadrant pain, fever, other classic symptoms of appendicitis like elevated WBC

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238
Q

What is another name for Yersinia Pestis?

A

Bubonic plague (25 million people dead)

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239
Q

How is Yersinia Pestis spread?

A

Transmitted through human as incidental host, usually with rats or prairie dogs.

“Rodents” with fleas, then fleas bite humans

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240
Q

What are the symptoms presented in Yersinia Pestis infection?

A

Forms Buboes (thats why its called Bubonic plague) with swollen tender lymph nodes.

Cause abscesses in organs once it gets in the blood or DIC from endotoxin and neurotoxin

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241
Q

What is the virulence factor of Yersinia Pestis?

A

Yersinia outer proteins that inhibit macrophages through a type 3 secretion system, inhibiting phagocytosis

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242
Q

What is the TXT for Yersinia Pestis?

A

?????

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243
Q

What is the prevention for Yersinia Pestis?

A

Killed vaccine is used to vaccinate

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244
Q

SHIGELLA SONHEI & SHIGELLA DYSENTERIAE
“She-Gorilla’s Circus”

A

SHIGELLA SONHEI & SHIGELLA DYSENTERIAE
“She-Gorilla’s Circus”

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245
Q

Gram type and indole for shigella?

A

Gram negative

Indole positive

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246
Q

What are the two main symptoms of shigella?

A

Gastroenteriitis

Bloody Diahrrea

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247
Q

Which type of agar is used for shigella and how does it look?

A

Green colonies on Hektoin agar (salmonella makes black colonies)

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248
Q

Special characteristic of shigella?

A

Immotile

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249
Q

What kind of state is shigella found it that makes it so dangerous?

A

It is acid stable, needs far fewer microorganisms to cause infection (salmonella needs far more)

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250
Q

What are the two types of shigella?

A

Shigella sonnei and shigella dysenteriae

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251
Q

Which of the two types of shigella is the most common in united States?

A

Shigella sonnei

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252
Q

What makes shigella lead to inflammation?

A

non-lactose, non H2S, LPS(endotoxin) leads to inflammation

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253
Q

What kind of secretion does shigella have?

A

type III secretion

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254
Q

TEST QUESTION:

describe the pathogenesis of shigella.

A

Shigella induces M Cells (they are like scouts; they sample things in the lumen and bring back antigens to immune cells on the other side of the intestinal epithelium) in peyers patches to phagocytose them and they escape from the phagolysosome to prior to destruction.

Once in the cytoplasm they will use the host cells actin cytoskeleton to create a tail it can use to propel itself from one cell to the other (like actin rockets in listeria/or like a using M cells as a trojan horse)

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255
Q

Since shigella can survive inside its own cell or in another, what is the name for that?

A

Facultative intracellular, just like salmonella

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256
Q

TEST QUESTION:

Why does bloody diarrhea occur in shigella?

A

Once shigella has invaded lymphoid tissue and enterocytes, it Damages tissue and releases cytokines that will inflame the tissues causing a large immune response, clinically we will see fecal blood and leukocytes: bloody diarrhea (underlying inflammatory diarrhea)

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257
Q

TEST QUESTION:

What is the toxin in shigella and how does it work?

A

Shiga Toxin will bind to the 60s unit of ribosomes and inhibit translation,

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258
Q

TEST QUESTION:

What is hemolytic uremic syndrome (HUS)?

A

Once shigella invades, it releases a toxin “shigatoxin”, once in blood, shigatoxin enduces endothelial damage, including in the glomerular of kidney. Activates platelets and induces their aggregation, diminishing pool of circulating platelets thus drop in platelets.

The aggregates of platelets protruding out of the endothelium, lyse RBCs they pass by, literally cutting them in half so they look like helmets or shistocytes,

This is pahotgenesis of HUS

Leads to hemolytic uremic syndrome (HUS) in younger children most commonly under 10 years of age.
Progerminal diarrhea following with acute renal failure (glomerular damage).
Form shistocytes

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259
Q

What does shigella use to cause inflammation?

A

Uses a type 3 secretion system to release inflammatory cytokines

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260
Q

What is the treatment for shigella?

A

treatment with Macrolides and Fluoroquinolones

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261
Q

ESCHERICHIA COLI & ENTEROHEMORRHAGIC E. COLI & ENTEROTOXIGENIC E. COLI
“E. Cola’s Soda Fountain”

A

ESCHERICHIA COLI & ENTEROHEMORRHAGIC E. COLI & ENTEROTOXIGENIC E. COLI
“E. Cola’s Soda Fountain”

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262
Q

Gram type of Escherichia coli?

A

Gram Negative

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263
Q

Which type of agar is used for Escherichia Coli?

A

Grow pink on MacConkey’s agar

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264
Q

One of the most defining feature of Escherichia Coli?

A

Lactose fermenter (milk)

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265
Q

What is the main virulence factor of Escherichia coli?

A

Capsular K antigen

Flagellar H antigen

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266
Q

E coli is also encapsulated with which antigen?

A

Capsular K antigen

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267
Q

Which test is positive for Escherichia coli?

A

Catalase positive
oxidase negative
Facultative anaerobic

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268
Q

What happens when Escherichia coli grows on EMB agar?

A

Eosin methylene blue (EMB, also known as “Levine’s formulation”)

Creates a green sheen

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269
Q

What is the #1 cause of UTI’s?

A

Escherichia coli (about 80%)

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270
Q

What does Escherichia coli have that allows it to cause UTI?

A

Fimbriae that will lead to UTI’s #1 cause of UTI’s

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271
Q

What else is Escherichia coli leading cause of?

A

Gram negative sepsis

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272
Q

What is the virulence factor of Escherichia coli that causes sepsis?

A

LPS endotoxin (lipopolysaccharide endotoxin) in outer cell membrane

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273
Q

How can Escherichia coli cause neonatal meningitis?

A

Causes neonatal meningitis only if it has the K antigen

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274
Q

Enterohemorrhagic Escherichia coli (EHEC) most commonly transmitted through what?

A

Undercooked meat

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275
Q

What is the main symptom of Enterohemorrhagic Escherichia coli (EHEC)?

A

Bloody diarrhea

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276
Q

Enterohemorrhagic Escherichia coli (EHEC) is the only Escherichia coli that doesn’t do what?

A

Doesn’t ferment sorbitol

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277
Q

Whats the toxin in Enterohemorrhagic Escherichia coli (EHEC) and what can it cause?

A

Toxin inhibits ribosomes at the 60s position. Shiga like toxin is the name and can cause hemolytic uretic syndrome (HUS).

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278
Q

Describe the pathogenesis of Enterohemorrhagic Escherichia coli (EHEC) toxin.

A

Shige like toxin damages endothelial cells of capillaries in the glomerulus. Damaged endothelial lining causes platelets to adhere decreasing platelet count causing thrombocytopenia and these platelets clumps will hemolysis RBC. Little to no fever but mucosal inflammation or invasion.

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279
Q

Which antigen of Enterohemorrhagic Escherichia coli (EHEC) is associated with outbreaks?

A

O157: H7

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280
Q

Enterohemorrhagic Escherichia coli (EHEC) other name?

A

Traveler’s diarrhea

Montezuma’s revenge

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281
Q

Whats the most common cause of Enterotoxigenic Escherichia coli (ETEC)?

A

Recent travel to Mexico where they drank the water.

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282
Q

What are the two toxins Enterotoxigenic Escherichia coli (ETEC) produces?

A

Heat Labile toxin produces cAMP

Heat Stable toxin produces cGMP

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283
Q

What is the main symptom of Enterotoxigenic Escherichia coli (ETEC)?

A

Watery Diarrhea

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284
Q

What is the treatment for Escherichia coli?

A

TMP/SMX or fluoroquinolones

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285
Q

What is the differences between Enterohemorrhagic Escherichia coli (EHEC) and Enterotoxigenic Escherichia coli (ETEC)?

A

EHEC bloody diarrhea

ETEC watery diarrhea

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286
Q

CAMPYLOBACTER JEJUNI
“Camping Guy and the Bears”

A

CAMPYLOBACTER JEJUNI
“Camping Guy and the Bears”

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287
Q

Gram type of campylobacter jejuni?

A

Gram negative

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288
Q

What does campylobacter jejuni look like?

A

Spiral/curved rod bacilli - enteric

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289
Q

What is the perfect environment for campylobacter jejuni to grow on?

A

Prefers warm environments around 42 degrees Celsius, thermophile (special incubator)

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290
Q

In which medium does campylobacter jejuni grow on?

A

Skirrow agar

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291
Q

What is the main reservoir of campylobacter jejuni?

A

Intestinal tract of poultry and other animals

292
Q

What is the transmission of campylobacter jejuni?

A

Fecal oral/ also contaminated water supplies or ingestion of raw milk

293
Q

TEST QUESTION:

What symptoms can be expected with campylobacter jejuni?

A

Bloody stools and diarrhea
Bacteremia, invasive
Reactive arthritis (Rider’s syndrome) sero-negative spondyloartropathies that can be precipitated by campylobacter jejuni infection
Can cause Guillen barre syndrome

294
Q

TEST QUESTION:

When does Guillen Barre syndrome occur?

A

Occurs after being infected with bacterial and viral infections.

Campylobacter being the most classic.

295
Q

TEST QUESTION:

What is the difference between botulism and Guillen barre syndrome?

A

Botulism = descending paralysis

Guillen Barre = ascending paralysis

296
Q

TEST QUESTION:

What happens in Guillen Barre syndrome?

A

Occurs after being infected with bacterial and viral infections.

Campylobacter being the most classic. The body can have an autoimmune response that causes demyelination of peripheral nerves leading to an ascending paralysis that will start at the feet and then ascend.

297
Q

Campylobacter oxidase positive or negative?

A

Oxidase positive

298
Q

TEST QUESTION:

Pathogenesis of Campylobacter jejuni?

A

Bacteria colonize intestinal mucosa and attach to epithelial cells then replicate intracellularly causing and acute PMN response, edema of the mucosa and ulcerations. Presenting with acute enteritis and diarrhea.

299
Q

TEST QUESTION:

What is the main symptom of Guillen barre syndrome?

A

Ascending paralysis

300
Q

What is the TXT for campylobacter jejuni infection?

A

Supportive care

301
Q

ENTEROBACTER CLOACAE, SERRATIA MARCESCENS, KLEBSIELLA PNEUMONIAE
“Enterodactyl, Triserratiatops, and the Kleb-Tailed Dinosaur”

A

ENTEROBACTER CLOACAE, SERRATIA MARCESCENS, KLEBSIELLA PNEUMONIAE
“Enterodactyl, Triserratiatops, and the Kleb-Tailed Dinosaur”

302
Q

Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae are considered what type of infections?

A

nosocomial infections

303
Q

What are the two most common infections caused by Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae?

A

Pneumonia, UTI

They are nosocomial infections.

304
Q

What makes Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae so hard to treat?

A

Multi Drug Resistant Carbopenam for treatment or Clindamycin

305
Q

Which agar is used on Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae?

A

MacConkey’s Agar

306
Q

What can Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae ferment?

A

All 3 ferment lactose: turns it pink along with E coli on MacConkey’s agar

307
Q

What is a special characteristic of enterobacter cloacae?

A

Very motile

308
Q

What is are special characteristic of serratia marcescens?

A

Very motile
Red pigment when cultured like a pink ring around shower or bright red
Catalase positive

309
Q

Which of the three Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae is immotile?

A

klebsiella pneumoniae

310
Q

What are the 3 “A”s of klebsiella pneumoniae?

A

Alcoholics (commonly affects them)
Abscesses (commonly creates abscesses)
Aspiration (commonly started from aspirations)

311
Q

What kind of capsule does klebsiella pneumoniae have?

A

Polysaccharide capsule

312
Q

How can you tell klebsiella pneumoniae is the cause of a patient’s pneumonia?

A

Patients cough up a current jelly like sputum that is a red color.

X-Ray - Cavatary lesion on patients right lobe “tb like”

313
Q

What klebsiella pneumoniae positive for?

A

urease positive

314
Q

What is the treatment used for Enterobacter cloacae, serratia marcescens, klebsiella pneumoniae infections?

A

3rd generation ceftriaxone, cefotaxime

315
Q

HELICOBACTER PYLORI
“The Helicopter Pilot”

A

HELICOBACTER PYLORI
“The Helicopter Pilot”

316
Q

Shape and gram type of Helicobacter pylori:

A

Curved gram negative rod

317
Q

How does Helicobacter pylori move around?

A

motile by the way of flagella

318
Q

where is Helicobacter pylori found in?

A

helical slender curved rod shape found in pylorus of the stomach

319
Q

TEST QUESTION:

What is a major virulence factor of Helicobacter pylori?

A

It is urease positive urea into ammonia and CO2 which helps reduce acidity of environment (stomach) which is absolutely necessary for Helicobacter pylori invade the stomach.

320
Q

TEST QUESTION:

What can you do to screen for Helicobacter pylori?

A
  1. Can be screened with Urea breath test where patients swallow urea with labelled with radioactive carbon, which is then split into CO2 and ammonia and this CO2 now with radioactive carbon is exhaled. Radioisotopes are detected in exhalation then that means there is a urease positive organisms in your stomach.
  2. Biopsy during endoscopy and then directly check for urease with rapid test.
321
Q

Helicobacter pylori is a curved rod. All curved rods are ________.

A

oxidase positive.

322
Q

TEST QUESTION:

What does Helicobacter pylori mainly cause?

A

Causes 95% of all duodenal ulcers.

323
Q

Why do we get ulcers with Helicobacter pylori?

A

Mechanism of Chronic infection causes increased acid production by either reducing somatostatin or increasing production of gastrin.

324
Q

What happens if you dont care about Helicobacter pylori?

A

At risk of developing gastric adenocarcinoma (almost half of gastric adenocarcinoma are linked to H. pylori).

Patient can develop lymphoma of mucous associated lymphoid tissue (MALToma)

325
Q

Whats lymphoma of mucous associated lymphoid tissue (MALToma)?

A

MALT lymphoma (MALToma) is a form of lymphoma involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted.

It is a cancer that is linked with untreated H. pylori infection.

326
Q

How do you treat a Helicobacter pylori infection?

A

Triple therapy (sometimes can be used quadruple therapy):

  1. Proton Pump Inhibitor (PPI):(to counter increased acid production caused by chronic H. pylori)
  2. Amoxicillin
  3. macrolide - Clarithromycin
327
Q

What is the transmission for Helicobacter pylori infection?

A

fecal oral or oral

328
Q

PSEUDOMONAS AERUGINOSA

“The Suiters of pseudo Mona”

A

PSEUDOMONAS AERUGINOSA

“The Suiters of pseudo Mona”

329
Q

Pseudomonas Gram type?

A

Gram Negative

330
Q

Pseudomonas shape type?

A

Rod

331
Q

In what kind of environments does pseudomonas thrive in?

A

Thrives in aquatic environments

“hot tub folliculitis” = pruritic papular pustular folliculitis

332
Q

What are tests used for pseudomonas?

A

Catalase positive

Oxidase positive

333
Q

Which disease heightens risk for pseudomonas?

A

Chronic granulomatous Disease (associated with catalase positive)

334
Q

TEST QUESTION:

What are some dead give aways for pseudomonas?

A

Produces Blue green pigment when plated, may even turn wounds blue. Its from Pyocuanin and pyoverdin that pseudomonas produce.

Fruity Grape like odor.

335
Q

Obligate _________ for pseudomonas.

A

Obligate aerobe

336
Q

Pseudomonas is the most common cause of? (2 diseases)

A

Most common Gram Neg Nosocomial Pneumonia.

Most common cause of respiratory failure in Cystic Fibrosis (CF) patients since it has a nonfunctional Chlorine ion channels in CF.

337
Q

TEST QUESTION:

What are the diseases pseudomonas can cause?

A

Gram Neg Nosocomial Pneumonia.

Respiratory failure in CF patients.

Osteomyelitis in IV drug users and Diabetics.

Skin lesions (pruritic papular pustular folliculitis - people using under chlorinated hot tubs or cutaneous necrosis “ecthyma gragrenosusm).

Ear infection (otitis externa)

338
Q

How can pseudomonas survive?

A

Encapsulated

339
Q

Who is especially susceptible for pseudomonas?

A

Burn patients are especially susceptible.

340
Q

What are some was a patient can get pneumonia infection in the hospital?

A

Indwelling catheter infections from UTI’s, chamber pot, nosocomial UTI’s.

341
Q

What are the two different types of skin lesions that can be caused by pseudomonas?

A

pruritic papular pustular folliculitis - people using under chlorinated hot tubs

cutaneous necrosis “ecthyma gangrenosum”

342
Q

What part of the head does psudomona affect?

A

Ear infection (otitis externa)

343
Q

What is the name of the pseudomonas toxin?

A

Exotoxin A

344
Q

TEST QUESTION:

Describe the pathogenicity of pseudomonas.

A

Exotoxin A - Ribosolation of elongation factor 2, leads to inhibition of protein synthesis and cell death

345
Q

pseudomonas and what other bacteria have nearly the same toxin and in what sense are they the same?

A

diphtheria - same mechanism and targets

Mechanism: ribosolated

Target: Elongation Factor 2

346
Q

What is the TXT for pseudomonas?

A

first treatment: Piperacillin (antipseudomonal penicillin) + tazobactam

Other treatment: Aminoglycosides and fluoroquinolones

347
Q

SALMONELLA TYPHI & SALMONELLA ENTERITIDIS

“The Salmon Dinner”

A

SALMONELLA TYPHI & SALMONELLA ENTERITIDIS

“The Salmon Dinner”

348
Q

Salmonella Gram type?

A

Gram positive

349
Q

Salmonella Agar type?

A

White on MacConkey

Black colonies on Hecktor on agar plate

350
Q

is salmonela motile?

A

YES

351
Q

Salmonella is H2S positive, what does that mean?

A

All motile enteric colonies stain black on Hecktor on agar plate

352
Q

Salmonella is indole negative. why?

A

Indole negative due to lack of tryptophanase

353
Q

Is salmonella capsulated?

A

Yes, positive for citrate utilization turns indicator blue due to alkaline pH

354
Q

Salmonella is acid labile, what does that mean?

A

Acid labile = easily degraded in the stomach which means it needs high doses to cause an infection

355
Q

Which kind of patients are more susceptible to infection of salmonella?

A

Patients on proton pump inhibitor more susceptible to infection since it lowers acidity of the stomach

356
Q

TEST QUESTION:

Describe pathogenicity of Salmonella.

A

Invades through the stomach, small intestine, colon and then the lymphatics.

Then taken up by the macrophages to get into the blood, it is facultative intracellular (within macrophages)

357
Q

How do we get Salmonella enteritidis infections?

A

By eating undercooked Chicken (main reservoir)

358
Q

Where do chronic Salmonella typhi carriers harbor the bacteria?

A

Gall blader, thyphoid mary

359
Q

What are the main symptoms of Salmonella enteritidis?

A

Causes:
inflammatory diarrhea
gastroenteritis

360
Q

What might you find on a physical examination on a patient with salmonella typhi?

A

rose colored macules on their stomach due to infection (only happens 25% of the time)

361
Q

Salmonella typhi is the number 1 cause of what and in which type of patients?

A

Number 1 cause of osteomyelitis in adults with sickle cell disease

362
Q

How is salmonella enteritidis able to increase infectivity?

A

Contains type 3 secretion system that detects eukaryotic cells that will increase infectivity.

This is a protein that detects eukaryotic cells and when it does it will secrete a protein that will increase infectivity.

363
Q

How is the diarrhea in salmonella typhi described?

A

“pea soup” diarrhea

364
Q

What is the name of the disease created by salmonella typhi?

A

Typhoid fever

365
Q

What is the source of Thyphoid fever?

A

ALWAYS human source, “Typhoid Mary”

Typhoid is spread by eating or drinking food or water contaminated with the feces of an infected person.

Individuals can develop typhoid fever after ingesting food or water contaminated during handling by a human carrier. The human carrier may be a healthy person who has survived a previous episode of typhoid fever yet who continues to shed the associated bacteria, Salmonella typhi, in feces and urine. Washing hands with soap before touching or preparing food, washing dishes and utensils with soap and water, and only eating cooked food are all ways to reduce the risk of typhoid infection.

366
Q

TEST QUESTION:

Which strain of salmonella has a vaccine and what kind of vaccine is it?

A

salmonella typhi: Live, attenuated vaccine

367
Q

TEST QUESTION:

You might think a patient has salmonella infection but only has gastroenteritis, which antibiotics will you prescribe?

A

gastroenteritis antibiotics not warranted, do NOT use antidiarrheal

368
Q

TEST QUESTION:

How is salmonella typhi treated and specify when to use them.

A

Antibiotics (fluoroquinolone) or a cephalosporin (cefttriaxone)

Flouroquinalones: ciprofloxacin/levofloxacin

369
Q

TEST QUESTION:

When should you use fluoroquinolone in compared with cephalosporin when dealing with salmonella typhi?

A

Ceftriaxone: for Invasive and bloody

370
Q

TEST QUESTION:

What is Salmonella septicemia and why is it important in consideration with the CDC?

A

Salmonella septicemia is a condition wherein the presence of Salmonella bacteria in the blood triggers a potentially life-threatening, whole-body inflammatory response.

Recurrent Salmonella septicemia is classified as an AIDS-defining condition by the U.S. Centers for Disease Control and Prevention (CDC).

371
Q

TEST QUESTION:

What is the TXT for Salmonella septicemia?

A

Chloraphenicol, ampicillin, amoxicillin, or TMP/SMX for 10 days

372
Q

TEST QUESTION:

What is TMP/SMX?

A

trimethoprim/sulfamethoxazole

Brand and Other Names:Bactrim, Bactrim DS, Septra, Septra DS, Cotrim, cotrimoxazole, Sulfatrim

Classes: Sulfonamides; Antibiotics, Combos

373
Q

TEST QUESTION:

What are the three phases of Salmonella Typhi?

A
  1. After sufficient bacteria have multiplied in the intestines there is a manifestation of lethargy dull frontal headache, CONSTIPATION, rise in body temp. binds to

Phase 2: Development of a bacteremia, patients have fever and are severely ill with a Dull Expressionless look, rose spots develop mainly on the trunk

Phase 3: Second Bacteremia occurs from reinfection of biliary tract, pus in stools and bleeding in peyers patches, Ileum Necrosis

374
Q

Whats the most used Proton Pump Inhibitor?

A

Omeprazol 40 mg IV

375
Q

VIBRIO CHOLERAE, VIBRIO PARAHAEMOLYTICUS, VIBRIO VULNIFICUS

“Colonel Cholera’s Base cAMP”

A

VIBRIO CHOLERAE, VIBRIO PARAHAEMOLYTICUS, VIBRIO VULNIFICUS

“Colonel Cholera’s Base cAMP”

376
Q

Gram type of vibrio cholerae?

A

Gram negative

377
Q

Shape of vibrio cholerae?

A

Comma Shaped curved rod

378
Q

Type of bacteria of vibrio cholerae?

A

Enteric Tract Bacilli

379
Q

Where is Vibrio Cholerae endemic in?

A

SouthEast Asia

380
Q

Which agar is used for Vibrio cholera?

A

TCBS agar

381
Q

Oxidase postive or negative for vibrio cholera?

A

Oxidase positive

382
Q

What is a key symptom produced by vibrio cholera?

A

Profuse watery diarrhea (10-20 liters per day)

“Rice water diarrhea”

383
Q

What kind of environment does vibrio cholera grow in?

A

Grows in alkaline environments

384
Q

whats the deal with vibrio cholera and acidity?

A

It is acid labile, dies with acid

385
Q

How is vibrio cholera transmitted?

A

Cholera is transmitted fecal oral due to poor sanitation that gets into food and is not an invasinve infection.

386
Q

Where does vibrio cholera hide in our body?

A

Found in the intestines and is found in the intestinal mucosae

387
Q

TEST QUESTION:

Describe the pathogenesis of vibrio cholera.

A

Attaches to the mucosa by fimbriae that attach to ganglioside receptors in the intestinal wall.

Then releases cholera toxin - Main Virulence Factor AB type toxin

a. Upregulates production of Gαs cAMP by binding to and increasing activating adenylate cyclase.
b. Then it will activate the GS pathway. Activates GS, upregulates cAMP, Produces watery diarrhea through an efflux if Cl and H2O

388
Q

How does vibrio cholera infect the mucosa?

A

Does NOT invade mucosa, it uses fimbriae to attach to ganglioside receptor in the intestinal wall.

389
Q

What is the TXT for a vibrio cholera infection?

A

Drinking some water - Oral rehydration therapy with electrolytes

390
Q

What type of toxin is the cholera toxin?

A

Main Virulence Factor: AB type toxin

391
Q

Vibrio Vulnificus and Vibrio paraliticus contaminates what types of food?

A

Can contaminate seafood, especially oysters

392
Q

Main symptom of Vibrio Vulnificus?

A

Acute gastroenteritis

393
Q

Main symptom of Vibrio paraliticus?

A

Fulminating septicemia leading to death.

Marked edema and necrosis

394
Q

BORDETELLA PERTUSSIS

“Board and Care”

A

BORDETELLA PERTUSSIS

“Board and Care”

395
Q

How does Bordetella pertussis spread?

A

Respiratory droplets

396
Q

How does the bordetella pertussis cause infection?

A

attaches to respiratory epithelium using pili and once attached, rather than invading, it releases toxins that cause systemic effects.

397
Q

What is the name of the pilis of the Bordetella pertussis?

A

Plus called filamentous hemagglutinin

398
Q

What are the toxin of the bordetella pertussis called?

A

Pertussis Toxin
Adenyltate cyclase toxin
Traqueal toxin

399
Q

TEST QUESTION:

How does Pertussis Toxin function?

A

Pertussis toxin ribosylates Gi thus, disabling it.

Toxic inhibits GI, disabled Gi (G inhibitor protein), Leads to a rise in cAMP.

ADP Disables Chemokine receptors for lymphocytes
leading to an overabundance of white blood cells in the blood stream, lymphocytosis

400
Q

TEST QUESTION:

How does Adenyltate cyclase toxin function?

A

Adenylate cyclase toxin acts like the anthracis toxin edema factor, increases cAMP directly,
Edema Factor, Most Virulent

401
Q

TEST QUESTION:

How does traqueal toxin function?

A

Tracheal toxin damages ciliated cells in the respiratory epithelium

402
Q

What is the name of the main disease caused by bordetella pertussis?

A

Whooping cough

403
Q

Another name for whooping cough?

A

100 day cough

404
Q

What are the three stages of whooping cough?

A

Catarrhal stage
Paroxysmal stage
Convalescent stage

405
Q

TEST QUESTION:

Describe the Catarrhal stage

A

Non specific symptoms
Most contagious
lasts 1 - 2 weeks
characterized by symptoms of an upper respiratory infection such as low-grade fever, nasal congestion and rhinorrreal

406
Q

TEST QUESTION:

Describe the Paroxysmal stage

A

Lasts 2-8 weeks
Characterized by paroxysms of coughing followed by an inspiratory whoop.
Characteristic cough “whoop”

407
Q

TEST QUESTION:

Describe the Convalescent stage

A

Lasts weeks to months
Final stage lasting 3 months with a cough, 100 day cough
Most susceptible to secondary infections

408
Q

What is the TXT for Bordetella pertussis?

A

Treatment Macrolides

409
Q

Which vaccines are available For bordetella pertussis?

A

DTaP - acellular vaccine using purified antigens (given to children with Dipthrea Toxoid, Tetanus toxoids, acellular Pertussis

Killed vaccine - no longer used in USA

410
Q

Gram type of Bordetella Pertussis?

A

Negative

411
Q

Bordetella pertussis aerobic or anaerobic?

A

aerobic

412
Q

How does bordetella pertussis move around?

A

It doesnts since its non-motile

413
Q

HAEMOPHILUS INFLUENZAE

“Phyllis’s Chocolate Covered Cherries”

A

HAEMOPHILUS INFLUENZAE

“Phyllis’s Chocolate Covered Cherries”

414
Q

Gram type of haemophilus Influenzae?

A

Gram negative bacteria

415
Q

Shape of Haemophilus Influenzae?

A

Coccobacillary shape

416
Q

In what type of agar is haemophilus influenzae grown in?

A

Chocolate agar + factor 5 (NAD, nicotinamide) + factor 10 (hemodin)

417
Q

What factor 5?

A

NAD (Nicotinamide Adenine Dinucleaotide) which needs to be added to the chocolate agar

418
Q

Whats Factor 10?

A

hemodin which needs to be added to the chocolate agar

419
Q

Haemophilus influenzae is primarily moved by what kind of transmission?

A

Aerosol transmission leading to droplets going to the respiratory tract calling pneumonia

420
Q

What is one of the most high yield manifestation of Haemophilus influenzae infection?

A

Epiglottitis - symptoms Drooling, inflamed epiglottis, inspiratory strider, drooling

“cherry red epiglottis”

As far as USMLE is concerned, epiglottis is caused by haemophilus influenzae

421
Q

Who is mostly affected by Haemophilus influenzae?

A

children

422
Q

Haemophilus influenzae also causes what?

A

otitis media (inflammation of middle ear) and meningitides

423
Q

What does haemophilus influenza need to cause meningitides?

A

Only caused by type B capsular form

424
Q

Patient without a spleen gets infected with haemophilus Influenzae, what would happen?

A

Sepsis and Septic arthritis in patients without a spleen (spleenectomized patients), hemophilic
infections, especially sickle cell disease

Since spleen is required to remove encapsulated organisms just like strep. pneumo

425
Q

There is a haemophilus influenza vaccine. Talk about it.

A

Vaccine for only the type B capsule is
conjugated with diphtheria toxoid and haemophilus type B capsule so it can prevent meningitis.

Almost all eradicated in USA.

426
Q

When is the most appropriate time to vaccinate a child with haemophilus influenza vaccine?

A

Vaccinate between 6 weeks - 18 months (polysaccharide conjugated to diphtheria toxid)

427
Q

What is the treatment for a Haemophilus influenza infection?

A

Ceftriaxone

428
Q

What is the TXT for close contacts with someone with a Haemophilus influenza infection?

A

Rifampin

429
Q

LEGIONELLA

“The SS cysteine joins the legion”

A

LEGIONELLA

“The SS cysteine joins the legion”

430
Q

Gram type of Legionella?

A

Gram negative but hard to visualize it so it needs something “special”

431
Q

What is necessary to visualize legionella?

A

silver strain to visualize

432
Q

What is the agar requirement of legionella?

A

Buffered Charcoal yeast extract in presence of cysteine and iron

433
Q

What is needed to be added to the agar to legionella?

A

Cysteine and iron need to be added to agar

434
Q

What kind of fevers can you get from legionella?

A

Pontiac Fever

Legionnaire’s Disease

435
Q

Describe Legionnaire’s Disease.

A

Atypical pneumonia patchy unilobed infiltrate

Common in smokers and elderly men.

More serious than pontiac fever

436
Q

What are the other atypical pneumonias?

A

Atypical pneumonia” is atypical in that it is caused by atypical organisms (other than Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis).

These atypical organisms include special bacteria, viruses, fungi, and protozoa. In addition, this form of pneumonia is atypical in presentation with only moderate amounts of sputum, no consolidation, only small increases in white cell counts, and no alveolar exudate.

At the time that atypical pneumonia was first described, organisms like Mycoplasma, Chlamydophila, and Legionella were not yet recognized as bacteria and instead considered viruses. Hence “atypical pneumonia” was also called “non-bacterial”

437
Q

In a question stem showing the lab results from a patient’s blood test, what should you look for?

A

Hyponatremia - excess HNO3 ammonia Na.

Look at sodium metabolic panel, If sodium is <130 (hyponatremia), smoker, headache, confusion, diahrrea, pneumonia, High fever over 104 F (40 C)

438
Q

Which lab test can be used to confirm a legionella infection?

A

rapid urine antigen test to confirm

439
Q

What is the TXT of a legionella infection?

A

Treat with macrolides and fluoroquinolones

440
Q

Legionella is oxidase positive or negative?

A

Oxidase Positive

441
Q

What is the main virulence factor of legionella and how does it work?

A

Zinc Melloprotease is the main virulence factor, its cytotoxic and inhibits PMN production,
inhibits superoxide reduction, deactivates il-1 and CD4 and TNF.

442
Q

BRUCELLA

Bruce Farms

A

BRUCELLA

Bruce Farms

443
Q

Gram type of brucella?

A

Gram negative

444
Q

Who or what can be a reservoir for brucella?

A

cows and pigs, goats, veterinarian, slaughterhouse worker, or rancher.

445
Q

How might one get infected with brucella?

A

Indirect contact with milk or cheese products that unpasteurized

446
Q

What kind of bacteria is brucella?

A

zoonotic

447
Q

Brucella bordis comes from which animal?

A

cow

448
Q

What are the initial symptoms of brucella?

A

Undulant fever (fever rises and falls)
Chills
anorexia

449
Q

Chronic infection can lead to what complication?

A

osteomyelitis

450
Q

What is the TXT of brucella?

A

tetracycline such as doxycycline along with rifampin as adjunctive therapy (blocks oxidative burst)

451
Q

TEST QUESTION:

Which cells are affected by brucella?

A

macrophages

452
Q

TEST QUESTION:

How is brucella protected from a respiratory burst?

A

Large amounts of catalase and superoxide dismutase to protect from respiratory burst

453
Q

TEST QUESTION:

Which tests are positive for brucella?

A

Urease positve

H2S positive

454
Q

TEST QUESTION:

What does brucella require to grow?

A

CO2

455
Q

TEST QUESTION:

Where does brucella live in?

A

acultative intracellular can live inside or outside of host cells ability to survive in macrophages makes it apt to travel reticular and endothelial system.

456
Q

TEST QUESTION:

What happens when brucella replicates inside a human cell?

A

Can then replicate intracellularly to the point of causing host cell lysis and then spread systemically.

457
Q

TEST QUESTION:

What happens once brucella spreads in the body?

A

Since it can spread reticular endothelial organs, it will lead to enlargement of spleen, liver, and lymph nodes.

458
Q

FRANCISELLA TULARENSIS

“Francis the Rabbit”

A

FRANCISELLA TULARENSIS

“Francis the Rabbit”

459
Q

What kind of bacteria is francisella tularensis?

A

zoonotic bacteria

460
Q

Gram type of grancisella tularensis?

A

Gram negative

461
Q

Shape of francisella telarensis?

A

Coccobaccilli

462
Q

How does francisella telarensis spread?

A

Tick vector or rabbit vector

463
Q

What is the name of the rabbit vector of francisella telarensis?

A

Dermacenter tick

464
Q

If you get a patient with francisella telarensis infection inside USA, what do you have to do and why?

A

Contact CDC since it Can be aerosolized and potential to use in bioterrorism

465
Q

Where does the francisella telarensis bacteria chill?

A

Facultative intracellular - cell mediated immunity needed to kill it

466
Q

What is the main symptom of francisella telarensis?

A

Causes painful ulcer

467
Q

TEST QUESTION:

Describe pathogenicity of francisella telarensis.

A

Enters through ulcer and into macrophages in the lymph system to reticuloendothelial organs and causes caseation necrosis

468
Q

In a physical examination of a patient with francisella telarensis, what might you find?

A

Regional lymphadenopathy

ulcer

469
Q

What is the TXT of francisella telarensis infection?

A

aminoglycoside (streptomycin)

470
Q

Why does francisella telarensis induce oxidative burst?

A

Fransciella does not induce oxidative burst

471
Q

COXIELLA BURNETII

“Curly Q the Ram”

A

COXIELLA BURNETII

“Curly Q the Ram”

472
Q

What is the main disease caused by coxiella burnetti?

A

Q fever

473
Q

Gram type of coxiella burnetti?

A

Gram negative

474
Q

What kind of rash does coxiella burnetti cause?

A

coxiella does not cause a rash, IE NO RASH

475
Q

What kind of organism is coxiella burnetti?

A

Obligate intracellular organism

zoonotic organism

476
Q

How is coxiella burnetti transmitted?

A

transmission - spore like structure that comes in animal droppings after it survives the digestive tract of animals

477
Q

How does coxiella burnetti infect humans?

A

It gets into humans through aerosol transmission -

outbreaks from farm animals to farmers or placental excretions

478
Q

Clinical presentation of coxiella burnetti?

A

Pneumonia
headache
fever

479
Q

What is a complication of coxiella burnetti?

A

hepatitis

480
Q

What antibiotics should be given to a patient with coxiella burnetti infection?

A

Antibiotics are not needed, self-limiting

481
Q

How is coxiella burnetti prevented?

A

Prevention is pasteurization of milk

482
Q

TEST QUESTION:

Literally test will give a case of: patient with pneumonia, hepatitis, and in the context of being around animals you should think:

Coxiella burnetti and Brucella

But how can you differentiate both?

A

Brucella has undulating fever while coxiella burnetti does not.

483
Q

A patient with chronic Q fever can develop what?

A

endocarditis especially if they are immunocompromised or have previous valvular damage

484
Q

How long does a Coxiella burnetti infection usually last?

A

2 weeks

485
Q

in a physical examination of a patient with Coxiella burnetti infection, what can you find?

A

Hemorrhage on fingers

486
Q

PASTUERELLA MULTOCIDIDA

“Louis Pasteur’s Lab”

A

PASTUERELLA MULTOCIDIDA

“Louis Pasteur’s Lab”

487
Q

Gram type of pastuerella multocidida?

A

Gram negative

488
Q

where is pastuerella multocidida found in?

A

respiratory tract of small mammals especially Dog and cats.

489
Q

How is pastuerella multocidida transmitted to humans?

A

Dog and cat bites

490
Q

What happens after a patient is bitten from an animal with pastuerella multocidida infection?

A

Red erythematous that happens immediately - Leads to a cellulitis after a bite

Within first 24 hours

491
Q

What are some of the complications of a pastuerella multocidida infection?

A

May lead to a necrotizing fasciitis or osteomyelitis

492
Q

Which patients can get the worst complications of a pastuerella multocidida infection?

A

Lymphadenopathy in patients with COPD or Liver disease

493
Q

Which tests are positive for pastuerella multocidida?

A

Catalase positive

Oxidase positive

494
Q

What is an important virulence factor?

A

Capsule

495
Q

On which agar does pastuerella multocidida grow on?

A

Grows on 5% sheep’s blood agar

496
Q

When observed under microscope, what does pastuerella multocidida look like and what does it resemble?

A

Bipolar / safety pin staining similar to Yersinia

497
Q

What is the TXT for pastuerella multocidida?

A

Emperic treatment is: penicillin

In addition, you might want to use Beta Lactamase inhibitor to avoid resistance such as: amoxicillin and clavulanic acid

498
Q

BARTONELLA HENSEALE

“Bart the Leopard”

A

BARTONELLA HENSEALE

“Bart the Leopard”

499
Q

Gram type of Bartonella henselae?

A

Gram negative but needs something “special”

500
Q

What is required to visualize Bartonella henselae?

A

Wartharin Starry silver Stain

501
Q

What diseases can be caused by Bartonella henselae?

A

Cat scratch fever or disease

Bacillary angiomatosis

502
Q

What happens if an immunocompromised patient gets infected with a Bartonella henselae?

A

Bacillary angiomatosis is transmitted by cat scratches to Immunocompromised individuals

503
Q

What happens if an immunocompetent patient gets infected with a Bartonella henselae?

A

Cat scratch fever: Fever and can involve regional lymph nodes in axilla in one arm, this happens in immunocompetent patient

This causes painful and large lymph nodes in axilla.

504
Q

Of the two Bartonella henselae diseases, which type of patient gets what?

A

immunocompetent - cat scratch fever

immunocompromised - Bacillary angiomatosis

505
Q

What is the main symptom of a Bartonella henselae infection in a immunocompromised patient?

A

Raised red vascular lesions in Bacillary angiomatosis all over the skin in Immunocompromised individuals (commonly HIV patients)

506
Q

What is the differential and very similar to Bacillary angiomatosis?

A

Karposi’s sarcoma is very similar and is a differential

Both have red vascular lesions on skin and happen in immunocompromised patients.

507
Q

How can you differentiate Karposi’s sarcoma and bacillary angiomatosis?

A

Skin biopsy or Wartharin starry silver stain

508
Q

What is the TXT for Bacillary angiomatosis?

A

Doxycycline or macrolide like azithromycin

509
Q

What is the TXT for cat scratch fever?

A

Usually self limiting but if there is swelling and pain and becomes severe you can use a macrolide like azithromycin

510
Q

NOCARDIA ASTEROIDES

No Card Game for Old men

A

NOCARDIA ASTEROIDES

No Card Game for Old men

511
Q

Gram type of Nocardia asteroides?

A

Gram positive

512
Q

Shape of nocardia asteroides?

A

Branching filamentous Rods

513
Q

What tests are positive for norcardia asteroides?

A

Urease positive

Catalase positive

514
Q

What does nocardia asteroides need to survive?

A

Obligate aerobe

515
Q

TEST QUESTION:

Which type of patient has an increased risk of nocardia asteroides infection?

A

Primarily affects Immunocompromised vulnerable especially those with impaired cell mediated immunity

Includes HIV, transplant patients or patients taking glucocorticoids

CGD patients have increased risk (Catalase positive)

516
Q

where is nocardia mainly found in?

A

Found in soil

517
Q

What kind of spores nocardia form?

A

Nocardia does NOT form spores as opposed to tetani and perfringens

518
Q

Although nocardia is gram positive, it weakly stains what?

A

Partially stains Acid Fast, which is carbofusion stain that stains mycolic acids in its cell wall (long chains with two tails)

519
Q

Gender wise, who is more at risk of nocardia infection?

A

men > women

520
Q

What are the three main sites of nocardia infections?

A

Pulmonary (pulmonary nocardiosis)

CNS

cutaneous (Cutaneous nocardiosis)

521
Q

Nocardia has an affinity to what kind of tissue and what is a complication it can cause from it?

A

CNS; Brain abscess formation

522
Q

What are the symptoms of pulmonary nocardiosis?

A

Pneumonia with lung abscess formation like symptoms, cavitary lesions in the lung

523
Q

What are the symptoms of cutaneous norcadriosis?

A

pyogenic response ensues that leads to indurated lesions and inflammatory reaction

524
Q

What is the treatment for nocardia infection?

A

Sulfonamides

525
Q

ACTINOMYCES ISRAAELII

“Israeli Soldier”

A

ACTINOMYCES ISRAAELII

“Israeli Soldier”

526
Q

Gram type of actinomyces israaelii?

A

Gram positive

527
Q

Shape of actinomyces israaelii?

A

Branching filamentous rods

528
Q

What does actinomyces israaelii need to survive?

A

Obligate anaerobe

529
Q

What is the main disease caused by actinomyces israaelii?

A

Cervical facies actinomyces infection

530
Q

TEST QUESTION:

Describe the course of a Cervical facies actinomyces infection

A

Slow course

Non tender lump on jaw

Forms abscess

Formation of sinus tract that drain the infection site through the skin

Thick yellow pus is formed since it forms thick yellow sulfur granules

531
Q

How is a patient infected with actinomyces israaelii?

A

Infection associated with jaw trauma due to the fact that actinomyces israeli is part of the normal flora of oral cavity

recent dental work

532
Q

How can you differentiate actinomyces israaelii and nocardia?

A

actinomyces israaelii = Obligate anaerobe

Nocardia = obligate aerobe

533
Q

What is the TXT of actinomyces israaelii?

A

penicillin G

More complicated courses: surgical drainage may also be warranted

534
Q

CHLAMYDIA TRACHOMATIS
CHLAMYDIA PNEUMONIA
CHLAMYDIA PHILAPSITTACI

“The pirates of Calam Island”

A

CHLAMYDIA TRACHOMATIS
CHLAMYDIA PNEUMONIA
CHLAMYDIA PHILAPSITTACI

“The pirates of Calam Island”

535
Q

What kind of gram type is Chlamydia?

A

Gram intermediate - does NOT gram stain

536
Q

What kind of bacteria is chlamydia?

A

Obligate intracellular bacteria

537
Q

Why is chlamydia obligate intracellular bacteria?

A

Cannot create its own ATP which is why it is intracellular

538
Q

The wall of chlamydia lacks what?

A

It lacks muramic acid that is found in the cell walls of most other bacteria.

This makes Chlamydia resistant to betalactam antibiotics such as penicillin, because such antibiotics disrupt the “typical” cell wall, which includes muramic acid.

539
Q

How is the cycle of chlamydia divided into?

A

Elementary stage
Reticular Body
Release of these newly divided cells (in elementary stage again)

540
Q

What is the 1st stage of of life cycle of chlamydia?

A

1st stage of life cycle outside of the cell aka “elementary stage”

This is the INFECTIOUS form.

Elementary enters the eukaryotic cell and are taken up by phagosomes.

“ELEMENTARY ENTERS”

541
Q

What is the 2nd stage of of life cycle of chlamydia?

A

2nd stage: “reticular body”

and is ACTIVE form and multiply, aka the DIVIDING form.

Reticular Replicates to form Inclusion Bodies seen under
microscope in cells when infected.

“RETICULATE REPLICATES”

542
Q

Under a microscope, what do you see when you’re looking at chlamydia?

A

Inclusion bodies seen when under a microscope in cells infected with chlamydia.

Inclusion bodies = bunch of reticulate bodies which are diving in the cell.

543
Q

What is the stain needed when visualizing Chlamydia?

A

Giemsa Stain since chlamydia cant be gram stained.

544
Q

How can you diagnose chlamydia?

A

NAAT Test (NAAT is just fancy word for PCR)

Nucleic Acid Amplification Test = NAAT

545
Q

Describe pathogenicity Reiter’s syndrome.

A

Maladaptive autoamune response.

The body fighting the bacteria makes antibodies that cross react and attack the body.

It has a triad of symptoms.

546
Q

What is the the Triad of symptoms Reiter’s syndrome?

A

Reactive arthritis
Uveititis
Urethritis

“can’t see, cant pee, cant climb a tree”

547
Q

Where does the reactive arthritis of Reiter’s syndrome presents itself on?

A

Sacroiliac joint and the knee but several other locations it can be presented.

548
Q

What are the three types of chlamydia?

A

Chlamydia trachomatis
Chlamydia pneumoniae (also known as Chlamydophila pneumoniae)
Chlamydia psittacci.

549
Q

How is chlamydia trachomatis divided into groups?

A

A-C: blindness
D-K: STI
L1-L3: LGV

550
Q

What is the Most common Bacterial STI in US?

A

chlamydia trachomatis D-K: STI2

551
Q

Describe chlamydia trachomatis D-K: STI.

A

Most common Bacterial STI in US

Can even remain asymptomatic.

Characterized by Watery discharge, while Ghonorrhea has a mucopurulent discharge.

Can turn into PID in women w/o symptoms.

Ectopic pregnancies as well

552
Q

Describe PID.

A

Ascending infection.
Can lead to cervicitis, salpingitis, pelvic pain, abscess formation, scarring of the tubes that can cause infertility and ectopic pregnancies later in life.

553
Q

What can happen if a mother has chlamydia trachomatis D-K: STI during delivery?

A

Baby can get infection if mother has it during delivery giving it neonatal conjunctivitis and neonatal pneumonia.

554
Q

How can you differentiate if the baby got chlamydia or gonorrhea infection during birth?

A

The key is the Time Frame!!!!!

Chlamydia: Baby will present within 1-2 weeks with a possible cough (pneumonia) or conjunctivitis.

Gonorrhea will present 2-4 days (short time frame)

555
Q

BUZZWORD:

How can you tell if a neonatal has pneumonia?

A

Staccato cough which is a really short sudden burst

556
Q

What does chlamydia trachomatis L1-L3 cause in disease?

A

Lymphogranuloma Venereum (LGV)

557
Q

How is Lymphogranuloma Venereum (LGV) characterized?

A

Tender Inguinal lymphadenopathy

558
Q

What is Lymphogranuloma Venereum (LGV)?

A

Infection of the inguinal nodes

Presents as a tender lymphadenopathy with draining lymph nodes.

Caused by chlamydia trachomatis L1-L3

sexually transmitted bacterial infection

It is caused by any of 3 different types (serovars) of the bacteria Chlamydia trachomatis.

The infection is not caused by the same bacteria that cause genital chlamydia.

559
Q

What it the leading cause of blindness of the worldwide?

A

trachoma

560
Q

Which type of chlamydia is related to blindness?

A

chlamydia trachomatis A-C

561
Q

How is chlamydia trachomatis A-C transmitted?

A

Hand to Eye contact, or formats

562
Q

What is the main disease caused by chlamydia pneumonia?

A

walking pneumonia or “seeing pneumonia”

its Atypical pneumonia (just like mycoplasma and legionella)

563
Q

Who are most likely affected by chlamydia pneumoniae?

A

More common on elderly as opposed to young adults

564
Q

How is Chlamydia Psittaci transmitted and which disease does it cause?

A

Transmitted by Birds, causes pneumonia and transmitted by bird droppings

565
Q

TEST QUESTION UWORLD EVERYWHERE!!!!!!

What is the WRONG treatment for chlamydia?

and what is the RIGHT empiric treatment?

A

WRONG TREATMENT:

  1. Macrolide (azithromycin)
  2. Tetracycline (such as doxycycline)

RIGHT TREATMENT:
Confection of Chlamydia and gonorrhea treat with
azithromycin + cephtriaxone

566
Q

TEST QUESTION UWORLD EVERYWHERE!!!!!!

What is the treatment for gonorrhea?

A

RIGHT TREATMENT:

Confection of Chlamydia and gonorrhea treat with
azithromycin + cephtriaxone

567
Q

TXT for Atypical pneumonia caused by chlamydia pneumonia?

A

1st line: Tetracycline (such as doxycycline)

2nd line: Macrolide (such as azithromycin)

568
Q

GARDNERELLA VAGINALIS

“The Fish Garden”

A

GARDNERELLA VAGINALIS

“The Fish Garden”

569
Q

What is the main buzzword of gardnerella vaginalis?

A

Fish odor

570
Q

Gram type gardnerella vaginalis?

A

Gram variable (can stain gram positive or gram negative)

571
Q

Shape of gardnerella vaginalis?

A

Rod

572
Q

What is the normal flora of the vagina?

A

Lactic bacilli

573
Q

What can get rid of the normal flora of the vagina?

A

Normal vaginal flora is lactic bacilli, an overgrowth of anaerobic flora will get disrupt the normal flora of vagina.

574
Q

What is the main symptom of gardnerella vaginalis?

A

Thin grayish white malodorous odorous discharge from the vagina.

Fishy smell.

575
Q

What is the main disease caused by gardnerella vaginalis?

A

Bacterial Vaginosis

576
Q

When does gardnerella vaginalis occur?

A

The discharge caused by bacterial vaginosis pH > 4.5 (usually pH is between 5.0 - 6.5) is when infection occurs

577
Q

How can you diagnose Bacterial Vaginosis?

A

Positive Whiff test w/ 10% KOH prep

or microscopic exam

578
Q

Describe the diagnostic microscopic exam for Bacterial Vaginosis?

A

wet mount preparation of bacterial vaginosis discharge shows these characteristic Clue cells which are epithelial cells diffusely coated with bacteria.

579
Q

What is the TXT for Bacterial Vaginosis?

A

Metronidazole

580
Q

What are clue cells?

A

Clue cells which are epithelial cells diffusely coated with bacteria.

581
Q

MYCOPLASMA PNEUMONIAE

“Walking on Thin Ice”

A

MYCOPLASMA PNEUMONIAE

“Walking on Thin Ice”

582
Q

Gram type of mycoplasma pneumoniae?

A

Gram indeterminate since it has no cell wall

583
Q

What so special about the anatomy of mycoplasma pneumoniae?

A

cell membrane with cholesterol (only bacteria that has it)

Sterols stabilize cell membrane but also allows it to be more flexible

584
Q

What is the main disease caused by mycoplasma pneumoniae?

A

Walking pneumoniae

585
Q

Why is it called “Atypical pneumoniae”?

A

Atypical pneumonia because you cant readily culture a microbe

586
Q

Why is it called “Walking pneumoniae”?

A

patients have X ray much worse than patients appear sick clinically that bad and they can even be walking around.

587
Q

What would you see in an X-ray of Walking pneumoniae?

A

Patchy infiltrate in x ray

588
Q

Who are more at risk of mycoplasma pneumoniae?

A

Young adults, commonly in military recruits living in close quarters

< than 30 year olds

589
Q

Which agar is used for mycoplasma pneumoniae?

A

Grown on eatons agar (takes about a week)

590
Q

TEST QUESTION: HIGH YIELD:

On a cellular level what happens during a mycoplasma pneumoniae infection?

A

About 1 or 2 weeks into a mycoplasma pneumonia infection, people may develop IgM molecules that agglutinate (clumping) RBC in cold temperatures (4 C).

Leads to lysis RBC.

This is called cold agglutinates.

Present in only 50-70%.

591
Q

What is the TXT of mycoplasma pneumoniae?

A

Macrolide (azithromycin) since it has no cell wall.

592
Q

RICKETSSIA SPECIES

Rickettsia Tennis

A

RICKETSSIA SPECIES

Rickettsia Tennis

593
Q

Rickettsia gram type?

A

Gram negative but don’t gram stain well aka Pleomorphic

594
Q

What kind of cell is Rickettsia?

A

Obligate intracellular

595
Q

What is the pathogenesis of Rickettsia?

A

Colonize endothelial cells and cause endothelial hyperplasia

596
Q

Why is Rickettsia is obligate intracellular?

A

Unable to produce NAD+ and CoA (which are energetic compounds) so they get it from eukaryotic cells.

Both are important for bacterial growth and replication.

597
Q

Shape of Rickettsia?

A

Coccobacillary shape that are weakly gram negative

shaped Somewhere between cocci and bacilli

598
Q

Which test can be sued to diagnose rickettsia?

A

Weil Felix agglutination test for rickettsia infections

599
Q

What are some of the symptoms of rickettsia?

A

Prodromal headache and fever in early rickettsia, along with vasculitis, a rash may be associtated

600
Q

What are the main symptom of rickettsia?

A

Vasculitis

Inflammation and destruction of blood vessels

601
Q

What is the TXT of rickettsia?

A

Doxycycline

Supportive care with vascular collapse.

602
Q

What is the TXT of a preggo with rickettsia?

A

Chloramphenicol

603
Q

RICKETTSIA PROWAZEKKI

“Pro Boot Camp”

A

RICKETTSIA PROWAZEKKI

“Pro Boot Camp”

604
Q

What kind of cell is Rickettsia prowazekki and its gram type?

A

Obligate intracelular - poor gram staining

605
Q

What is needed for Rickettsia Prowazekki to survive and grow?

A

NAD+ and CoA needed

606
Q

What is the treatment for Rickettsia Prowazekki?

A

Doxycycline treatment

607
Q

What are the symptoms of Rickettsia Prowazekki?

A
Myalgia and arthralgia
Pneumonia
Encephalitis with dizziness and confusion
Coma (if really serious)
Unremitting headache
Patchy rash that begins on the region
608
Q

What is the first symptom of Rickettsia Prowazekki?

A

Rash starts at trunk and moves toward the extremities, Rash spares the hands, feet, and head

609
Q

Who are more at risk of rickettsia Prowazekki?

A

Affects military recruits and POW’s , close contact allows for human to human spread

610
Q

How does Rickettsia Prowazekki spread?

A

Lice spread prowazeki, Louse feeds on blood and deaths near deeding sites

611
Q

What is the pathogenicity of Rickettsia Prowazekki?

A

Lice spread prowazeki, Louse feeds on blood and deaths near deeding sites

Scratching that infects from patients from the lice feces since it gets itchy on skin.

612
Q

What is the illness called cause by Rickettsia Prowazekki?

A

Illness is called epidemic typhys: widespread outbreak

613
Q

What is the difference between epidemic typhus and endemic typhus?

A

Epidemic typhus: rickettsia Prowazekki (desease thats widespread outbreak)
Endemic typhus: Rickettsia typhi (diasese localized to a region)

614
Q

RICKETTSIA RICKETTSII

“Rickett’s Rock Climbing Competition in the Dermacenter arena”

A

RICKETTSIA RICKETTSII

“Rickett’s Rock Climbing Competition in the Dermacenter arena”

615
Q

Rickettsia Rickettsii gram type?

A

Obligate intracellular - poor staining (lack of gram staining)

616
Q

Which stain can be used to vizuale rickettsia rickettsii?

A

Giemsa Stain

617
Q

What does rickettsia rickettsii need for growth and replication?

A

CoA and NAD+ are needed for growth and replication and is provided by the host

618
Q

TXT for rickettsia rickettsii?

A

Doxycycline

619
Q

How is rickettsia ricketsii transmitted?

A

Transmitted via ticks

Dermacenter Tick transmission through direct biting

620
Q

What is the incubation period of rickettsia ricketsii infection?

A

Incubation period of 2-14 days

621
Q

Describe the rash that is characteristic of a ricketsia ricketsii infection.

A

Causes a maculopapular rash that starts on ankles and wrist, then moves more centrally

Rash spreads extremities to centrally.

622
Q

Describe the symptomatology of rickettsia ricketssii infection.

A

Headache, severe fever, and muscle pains (myalgia)

623
Q

MYCOBACTERIUM TUBERCULOSIS

“Shootout at the TB corral”

A

MYCOBACTERIUM TUBERCULOSIS

“Shootout at the TB corral”

624
Q

How does mycobacterium tuberculosis stain?

A

Stains Acid fast which is represented by mycelia acids (Carbol fuschein stain)

625
Q

mycobacterium tuberculosis is obligate ______.

A

Obligate aerobe

626
Q

In which medium does mycobacterium tuberculosis grow on?

A

Lowenstein Medium

Takes 2-6 weeks

627
Q

Describe the transmission of mycobacterium tuberculosis

A

Transmission is human to human respiratory droplets

628
Q

Where does mycobacterium tuberculosis proliferate in?

A

Macrophage cage

629
Q

What is the virulence factor of mycobacterium tuberculosis.

A

Virulence factor is called cord factor.

Cell wall contains glycolipids which are responsible for clumping of bacteria into a serpentine formation.

630
Q

What is the function of the Cord factor?

A

Cord factor role is protection of bacteria from being destroyed.

Cord factor will Increases granuloma formation by increasing TNF-a activating other macrophages walling
itself off in a granuloma - this will protect the bacteria HOWEVER, it cant spread anymore

So: cord factor increases immune response (so it cant spread anymore) but protects the bacteria from walled off inside a granuloma which is created by the new activated macrophages.

631
Q

What allows TB to survive inside cells like macrophages?

A

Sulfatides - prevent phagolysosome fusion thus, sparing the microbe to lysosomal hydrolazes.

Allow TB to survive in macrophages by creating incompetent secondary lysosomes preventing fusion to hydrolyzes which are unable to fuse.

632
Q

What are the paths of progression after primary infection?

A
  1. Healed latent infection
  2. Systemic infection (Miliary TB)
  3. Reactivation of latent TB (infection was once latent but reactivates later in life)
633
Q

Describe Primary infection of TB.

A

Affects the Lungs (primarily either lower or middle lungs)

Forms the GHON complex.

634
Q

Describe the GHON complex.

A

Can occur during primary infection of TB.

After infections heals, lesion becomes fibrotic and eventually calcifies as do the nearby lymphnodes.

They are visible calcification of lung parenchyma and Heal lymph nodes that can be seen on Chest X rays.

GHON complex = Hiliar lymphadenopathy + peripheral granulomatous lesion in middle or lower lung lobe.

635
Q

What kind of necrosis forms from mycobacterium tuberculosis ifnection and why that kind of necrosis?

A

Characterized by a collection of activated macrophages (called Langerhans giant cells) and in the case of TB it is Caeseation necrosis that can cause fibrosis and scarring.

Formed in attempt to wall off an area of infection.

636
Q

Why is it called TUBERculosis?

A

Caseation Granulomas = tubers

Tuberculosis resides in broken down necrotic macrophages (Langerhans giant cells)

637
Q

What are Primary infection symptoms of mycobacterium uberculosis?

A

prolong fever and most commonly in children in areas that are endemic of TB.

Most cases of primary infection resolve and healed by fibrosis and calcification and become latent.

638
Q

How does primary infection of mycobacterium resolve?

A

Resolves by fibrosis and become latent (hibernates)

639
Q

How can you test for a mycobacterium tuberculosis.

A

Test for TB with PPD on skin

640
Q

What another name for PPD?

A

The tuberculosis skin test is also known as the tuberculin test or PPD test.

641
Q

How can you prevent a mycobacterium tuberculosis infection?

A

BCG vaccine is attenuated from mycobacterium Bovis.

Will always show positive skin test

Will show positive regardless if its active, latent or if patient received BCG vaccine.

642
Q

How effective is the BCG vaccine?

A

Effectiveness ranges from 0 - 80%

643
Q

Describe the Millciary TB.

A

Multi-organ failure (commonly affects bone, liver and lymphatics)
Potentially Lethal
Especially affects Immigrants from endemic areas.

644
Q

Describe Reactivation of latent TB.

A

Associated with immunosuppression (HIV, cancer, Old people) through down regulation of TNF alpha release (TNF alpha is a proinflamatory cytokine that causes infection to be contained but if its neutralized, then infection would spread again).

Reactivation is on the upper lungs, look for cough, night sweats, bloody cough (hemoptysis).

Only occurs in 5-10% of people

645
Q

Describe the mechanism of which immunosuppression causes reactivation.

A

Associated with immunosuppression through downregulation of TNF-a release (which is a proinflamatory cytokine that causes the infection to be contained). Therefore, if it is neutralized then the infection will spread again.

Immune system is defenseless if TNF is inhibited.

646
Q

What should you always do before using a TNF inhibitor?

A

Always screen for PPD before using a TNF inhibitor like infliximab to make sure youre not putting them at risk for reactivation of TB

647
Q

What are the 3 classic symptoms of reactivation of TB?

A

cough, night sweats, bloody cough (hemoptysis), cachexia

648
Q

Once TB reactivates, where does it primarily affects in the lungs?

A

When TB reactivates, it primarily affects upper lobes as opposed to middle and lower lobes during a primary infection.

649
Q

What other organ systems can TB affect?

A

Skeletal system and the CNS

650
Q

What is the disease called when TB affects the bones?

A

Pott’s disease is when TB has affected the spinal column.

Usually multiple vertebrae are affected.

demineralization of the bone with soft tissue pain which causes pain and can progress to abscess formation, spinal deformities and weakness.

651
Q

If TB affects the CNS, what can you expect?

A

CNS involvement can manifest as meningitis or tuberculoma (which is a cavitary lesion of the brain).

10-15% in patients with reactivation of TB

652
Q

What is the treatment for TB?

A

Combination of RIPE:

Rifampin
Isoniazid
Pyrazinamide
Ethambutol

653
Q

What is the prophylaxis of TB?

A

Prophylaxis:

Rifampin or isoniazid - 9 months

654
Q

MYCOBACTERIUM LEPRAE

“The Good, the Bad and the Lion Faced”

A

MYCOBACTERIUM LEPRAE

“The Good, the Bad and the Lion Faced”

655
Q

In what kind of environment does mycobacterium leprae thrive in?

A

Thrives in cool temperatures, explaining predilection for extremities

656
Q

Where does mycobacterium leprae like to affect our bodies?

A

prevalence of growth in extremities

657
Q

What kind of stain is used on mycobacterium leprae?

A

Acid fast bacteria (carbol fuscion stain)

658
Q

What takes up the acid fast stain?

A

Mycolic acids

659
Q

What is the major reservoir of mycobacterium leprae?

A

Armadillos are the major reservoir

660
Q

What is another name for leprocy?

A

commonly called Hanson’s Disease

661
Q

What are the two presentations of Hanson’s disease?

A

Tuberculoid

Lepromatous

662
Q

Describe the Tuberculoid presentation.

A

Helper TH1 cells stimulate macrophages to engulf the bacteria in cell mediated immunity.

Tuberculin response: able to contain bacteria within macrophages.

Mild symptoms, well demarcated hairless lesions on skin (can occur anywhere in the body)

663
Q

What kind of test can you do for the Tuberculoid leprocy presentation of mycobacterium leprae?

A

Lepermans skin test - test for immune reaction, similar to TB Test, wheel will form if positive

It is an interdermal injection of bacterial antigen to test for presence of immune reaction (just like TB)

664
Q

What does a positive lepromin skin test mean?

A

Positive Lepromin skin test demonstrates good cell mediated response.

665
Q

Describe the lepromatous prevention of mycobacterium leprae.

A

“classic leoprasy”

TH2 cells promote humoral (humorous) response

Bacteria being unable to contained in macrophages

666
Q

How is lepromatous leprocy is transmitted?

A

High chance of transmission human to human

Via respiratory droplets? Exact mode of transmission isn’t known

667
Q

Describe what lepromatous leprocy does to the human body.

A

Distal portions (its cooler in temperature) are affected in a symmetric glove and stocking pattern.

Numerous extensor surfaces are cooler and present with disease of demarcated raised lesions (can occur anywhere in body but most notably on extensor surfaces of extremities).

668
Q

What is the main clinical manifestation of lepromatous leprocy?

A

“Leonine faces” (since it makes the look like they have the face of a lion)

Causes profound facial deformity.

Thickening of the skin, loss of eyebrows and eye lashes, collapse of the nose and formation of nodular earlobes.

669
Q

What is the TXT for TH1 dominant infection?

A

multi drug therapy for long time

TH1 dominant infection: Dapsone and rifampin for 6 months

670
Q

What is the TXT for TH2 dominant infection?

A

TH2 dominant infection: Dapsone, rifampfin, and Clofazimine for 2-5 years

671
Q

BORRELIA BURGDORFERI

“the Bows and Arrows of Borrelia”

A

BORRELIA BURGDORFERI

“the Bows and Arrows of Borrelia”

672
Q

Shape of Borrelia Burgdorferi?

A

Helical and longer than Treponema

673
Q

Disease that Borrelia Burgdorferi causes?

A

Causes Lyme disease

674
Q

Primary geography of Lyme’s disease?

A

Primarily in the northeastern united states.

New Hampshire and Connecticut

675
Q

What is the vector of Lyme’s disease?

A

Transmitted by ticks, Ixodes scapularis.

676
Q

What are the three diseases that Ixodes scapularis transmits?

A

Lyme disease
erliciosis (bacterial disease)
bubesiosis (protozoan disease)

677
Q

Describe the life cycle of the Ixodes scapularis

A

Mouse - ticks larvae feed on white footed mouse, Main reservoir

Deer - adult form feeds on white tailed deer, Obligatory Host

Tick is the vector, humans are an incidental host

678
Q

What is the main reservoir of Lyme’s disease?

A

Main reservoir: White footed mouse

Mouse - ticks larvae feed on White footed mouse

679
Q

What is the Obligatory Host (Host of Adult Tick) of Lyme’s disease?

A

Obligatory Host

adult form feeds on White-tailed Deer

680
Q

Who is the incidental host of Lyme’s disease?

A

Tick is the vector, humans are an incidental host

681
Q

Gram stain of Borrelia Burgdorferi?

A

Spirochetes do not gram stain since they have thin walls

682
Q

Which stain can be sued to show Borrelia Burgdorferi?

A

Two stains that can be used, Wright and Giemsa Stain

683
Q

What is the organism that causes endemic Relapsing fever?

A

Endemic Relapsing Fever is caused by tick borne borelia hermsii and Borelia duttonii

684
Q

How many stages of Borrelia?

A

3 stages

685
Q

Describe stage 1 of Lyme’s disease.

A

Hallmark of Lyme’s disease: Erythema Chronic Migrans (“Bulls Eye” rash) Spirochete

Sweating and feverish, flu like illness

Papule will form (Ixodes tick)

686
Q

When does the Erythema Chronic Migrans (“Bulls Eye” rash) appear?

A

Usually about a month from tick bite.

687
Q

Describe stage 2 of Lyme’s disease.

A

Heart block cause by myocarditis

Bilateral facial nerve Bell’s palsy

688
Q

Describe Bell’s Palsy.

A

Bell’s palsy is a condition in which the muscles on one side of your face become weak or paralyzed. It affects only one side of the face at a time, causing it to droop or become stiff on that side.

However, in Lyme’s disease it causes BILATERAL Bell’s Palsy

689
Q

Describe stage 3 of Lyme’s disease.

A

Migratory arthritis: Joint pain arthritis of large joints, symptoms may move from joint to joint.

Memory difficulty, cognitive slowing, lymphocytic meningitis.

Suttle encephalopathy

690
Q

TXT for Lyme’s Disease?

A

Stage 1 doxycycline

Stage 2 ceftriaxone

691
Q

TREPONEMA PALLADIUM

“Pallidum Observatory”

A

TREPONEMA PALLADIUM

“Pallidum Observatory”

692
Q

What is the shape of Treponema palladium?

A

Spiral shapes - Spirochetes

693
Q

In which culture can Treponema palladium grown in?

A

Treponema palladium cannot be grown in culture, only in rabbit testes

694
Q

What disease does Treponema Palladium cause?

A

Syphilis

695
Q

What is needed for direct visualization of the organism of Treponema Palladium?

A

Dark field microscopy is needed for direct visualization of the organism.

696
Q

What is the screening test for Treponema palladium?

A

Venereal Disease Research Laboratory (VDRL)

blood screening test for Treponema but not specific aka nontreponema specific test

697
Q

What is the antigen tested in VDRL?

A

It tests antibody reactivity in patient serum to antigen: cardiolipin-cholesterol-lecithin antigen

698
Q

What is the RPR test?

A

RPR - rapid plasmin reagent

Screening tool for syphillisbut high incidence of false positives due to cross antigenicity including:

Mono
Rheumatoid Factor
Lupus
Leprocy

699
Q

What is the Confirmatory Test of syphillis?

A

FTA-ABS is a Specific test to confirm a positive screening

Much more specific than VDRL

700
Q

Describe the stages of Syphillis.

A

Early stages (occurs during 1st Year):
Primary
Secondary
Early latent

Late stages:
Terciary
Late latent

Congenital syphillus

701
Q

Clinical presentation of primary syphillis.

A

Primary: Painless genital chancre.

Syphilis locally invades small blood vessels causing ischemic necrosis and takes out nerves making it painless.

Painless: heals in 3-6 weeks

702
Q

Clinical presentation of secondary syphillis.

A

Secondary: Systemic Disease.

Maculopapular rash that occurs on palms and soles of feet weeks to months after infection.

Condoloma Latum on mucous membranes which are a lot of bumps that are flat topped.

703
Q

How can you visualize the spirochetes in the condoloma latum?

A

Can visualize the spirochetes in the condoloma lata via dark field microscopy

704
Q

Clinical presentation of tertiary syphillis.

A

Tertiary:

  1. Formations of Gummas which are soft growth with a firm necrotic center. Can appear anywhere including bone, skin, internal organs.
  2. Aortitis (particularly of the ascending aortic aorta) leading to an ascending thoracic aneurysm.
  3. Tabes dorsalis
  4. Argyle Robertson Pupils
705
Q

What happens to the aorta with syphillis?

A

Pathologically the aorta demonstrates “Tree barking” which means it will look thick and wrinkled like a tree bark

Syphillis Destroys the vasovasorum or small blood vessels that supply of the aorta.

706
Q

What is Tabes dorsalis, also known as syphilitic myelopathy?

A

Demyelination of nerves and posterior walls of the spinal cord and lead to a loss of vibration sense, proprioception and discriminative touch.

This can also accompany lancinating pain all over and a odd gait due to loss of propiocetion.

707
Q

Describe Argyle Robertson pupil.

A

Argyle Robertson: Ocular effects that make pupils that accommodate to distance but do not react to light.

“Prostitutes pupil”

708
Q

Describe Symptoms of Congenital syphillis.

A
  1. Saber Shins, an anterior bowing of tibia
  2. Saddle shaped nose
  3. Hutchinson Teeth: Notched incisors
  4. Mulberry molars: Molars will several enamel outgrowths.
  5. Deafness
709
Q

What is the TXT of Syphillis?

A

Penicillin is the treatment In every stage and in everyone

710
Q

What is the TXT of Syphillis if patient is allergic to the primary treatment?

A

If allergic - desensitize them and use penicillin

711
Q

What might occur hours after treatment with penicillin on a patient with syphillis?

A

Jarisch Herxheimer reaction

712
Q

Describe the Jarisch Herxheimer reaction.

A

Jarisch Herschimer reaction is the dying spirochetes releasing a bunch of LPS that cause and increase of cytokines that make people feel sick along with fever and chills.

Within hours of treatment.

713
Q

Jarisch Herxheimer reaction is good or bad?

A

Good indicator that the treatment is working.

714
Q

LEPTOSPIRA INTERROGANS

“The Surfer’s Oasis”

A

LEPTOSPIRA INTERROGANS

“The Surfer’s Oasis”

715
Q

What is the shape of leptospirosis interrogans?

A

Spirochetes may be question marked shaped

716
Q

leptospirosis interrogans causes what disease?

A

Leptospirosis or Leptospira

Which is the systemic leptospirosis infection

717
Q

What kind of region is endemic of leptospirosis interrogans?

A

Endemic in tropic regions

In USA highest incidence of leptosperirosis is in Hawaii.

718
Q

Which animals excrete leptospirosis interrogans and how do they do it?

A

Animals such as Rodents and dogs and is excreted in their urine

719
Q

How is leptospirosis interrogans transmitted to humans?

A

Transmitted to humans when swimming in contaminated waters such as during water sports.

720
Q

Describe clinical presentation of leptospirosis interrogans.

A
  1. Flue like symptoms such as Fever and intense headaches.

2. Conjunctival suffusion: redness around the eyes without the puss

721
Q

What is the most severe form of Leptospirosis?

A

Weil’s disease

722
Q

How does the Leptospirosis travel?

A

travels in blood stream and is able to affect multiple organs.

723
Q

Which two organs does leptospirosis interrogans like to affect when it is left untreated

A

Kidney and liver

724
Q

What are the two most severe complication that can be caused by Leptospirosis?

A

Renal dysfunction

Jaundice from live damage

725
Q

END

A

END