Microbiology Flashcards

1
Q

Osteomyelitis

A

Inflammation of the bone or bone marrow usually due to infection

Caused most commonly by staphylococcus aureus or TB

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2
Q

Risk factors for osteomyelitis

A

Diabetes

Kidney failure

Smoking and/or IV drug use

Traumatic wounds

Joint replacement/fixation devices

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3
Q

TB specific osteomyelitis is also known as what?

A

Pott Disease

Osteomyelitis that Moves to the spine specifically.

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4
Q

Possible pathogens that cause osteomyelitis outside of TB or S. Aureus

A

Salmonella: Sickle cell patients

S. Epidermidis: prosthetics patients

P. Multocida: cat and dog bite patients

Gonorrhea: STI

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5
Q

Osteomyelitis treatment

A

Antibiotic beads that surround the bone and/or joint.

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6
Q

Staphylococcus aureus osteomyelitis specific risk factors

A

Prosthetic joints

Sickle cell

IV drug use

Trauma of the spine

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7
Q

Quick characteristics of S. Aureus

A

Gram positive cocci that tends to cluster

Aerobic pathogen

B-hemolytic: complete hemolysis

Coagulase and catalase positive

Has protein A

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8
Q

Protein A

A

Binds to host antibodies to prevent antibody-mediated clearance of bacteria

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9
Q

Why is Staph Aureus such a good pathogen?

A

Produces its own unique virulence factors all the time and controls up and down regulation of them.

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10
Q

Examples of S. Aureus structural virulence factors

A

Capsule: inhibits proliferation of mononuclear cells

Slime layer: facilitates adherence to foreign bodies

Peptidoglycan wall: increases osmotic stability, enables release of endogenous endotoxins and inhibits phagocytosis

Teichoic acid: binds to fibronectin

Protein A: inhibits antibody-mediated clearance by binding to antibodies.

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11
Q

Examples of S. Aureus enzymatic virulence factors

A

Coagulate: converts fibroids to fibrin and promotes clots

Hyalurnidase: hydrolysis hyaluronic acids promoting spread deep in connective tissue

Fibrinolysin: dissolves fibrin clots

Lipase: Hydrolysis lipids

Nuclease: hydrolysis DNA

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12
Q

Biofilms

A

Colonies of bacteria that enable bacteria to survive better and make it much harder to kill the bacteria.

Slime layers are present in order to form biofilms

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13
Q

Examples of S. Aureus toxin virulence factors

A

Cytotoxins

Exfoliating toxins: scalded skin syndrome

Enterotoxins: food poisoning

Toxic Shock Syndrome Toxin: TSS

Superantigens

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14
Q

MRSA commonly affected areas

A

Out in Community: 50%

Health care-acquired places outside of hospitals: 42%

Hospital acquired: 8%

Most common symptoms of MRSA infection =

  • cellulitis and skin ulcers
  • Pneumonia
  • Septicemia
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15
Q

Endocarditis, myocarditis and pericarditis

A

Infections in the heart muscle most commonly caused by S. Aureus

  • most common in the endocardium
  • often cause valve replacement or worse
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16
Q

Infective myositis

A

Pretty rare infection of deep skeletal muscle around the spine

  • almost always caused by S. Aureus
  • usually asymptomatic until actually having it
17
Q

Septic arthritis

A

Infection moves to joint caused by trauma to the joints

Common causative agents
- S. Aureus (most common overall)

  • Strep A and B: (most common in children)
  • haemophillus influenza: (not common)
  • N. Gonorrhoeae: (often causative agent if multiple joints affected)

Borrelia burgdorferi: (often causative agent in conjunction with Lyme disease patients

  • sporothrix schencii: (fungal infection via rose thorns. Increased likelihood with HIV positive patients)
18
Q

Viral arthritis

A

Same as septic arthritis but viral instead of bacterial

Common causative agents:
- Hep B: (often caused in prodromal period)

  • rubella: (common in young women and via live viral vaccination)
  • mumps: ( rare and only in men)
  • paravovirus: (follows adult infection)

Ross river (follows mosquito infections)

19
Q

Prodromal period

A

Period before diagnosis

20
Q

Myonecrosis gangrene

A

C. Perfringens causes deep muscle infections

Often caused by fecal contamination

21
Q

Pathogenesis of myonecrosis Gangrene

A

C. Perfringens pathogen reaches anaerobic environment and begins anaerobic multiplication

  • causes anaerobic cellulitis
  • invades muscle and produces gas and necrosis of muscle cells
  • may or may not get into blood. If enters blood often fatal via hemolysis and renal failure*
22
Q

C. Perfringens characteristics

A

Game positive rod

Spore forming anaerobe

Toxins can hemolysis if in blood and food poisoning in GI

Treated via hyperbaric chambers (flood with oxygen and suffocates C. Perfringens

23
Q

Types of toxins produced by C. Perfringens

A

Perfringolysin O: Forms pores in cells

Alpha toxin (AKA lecithinase or PPC): destroys cell membranes via phospholipase C activity 
- antitoxin not affective since alpha toxin destroys pathways for it to get there. 

ALL toxins cause clumping of leukocytes in blood vessels and prevents immune system from getting to primary site of infection