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MSK final > Infections of MSK system -Saviola > Flashcards

Infections of MSK system -Saviola Flashcards

1
Q

What is bacterial arthritis?

A

invasion of the synovial membrane by micoorganisms, usually with extension into the joint space

closed space infection

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2
Q

What are the 3 mechanisms by which microorganisms can be brought to the joints?

A
  1. blood (hematogenous): most common.
  2. direct implantation (needle or prick of plant or bite)
  3. Extension from adjacent infections. (least common)
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3
Q

What makes synovial tissue susceptible to infection?

A

highly vascularized and no basement membrane

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4
Q

What do monocytes do when there is an infection of the synovial tissue? When will this take place?

A
  • macrophages respond and produce pro-inflammatory cytokines
  • arthritic symptoms develop after 2 hours due to the presence of monocytes
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5
Q

What are polymorphonuclear cells responsible for producing in response to bacteria? What does this cause?

A

TNF-alpha, IL-1 and IL-6 (proinflammatory cytokines that have been involved in septic shock)

-accumulate in order to control growth of bacteria –> can trigger arthritis.

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6
Q

Are infections of the bone more likely to extend into the joint space in kids or adults? Why?

A

adults

-kids have their growth plates still and it contains the infection because growth plates are avascular cartilage

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7
Q

What are the most likely causes of nongonococcal septic arthritis in children less than 1 month? Children under 2 years? Children 3-15 yo? Adults?

A

< 1 month: Group B Strept (S. agalactiae), gram - organisms and S. aureus

<2 years: S. aureus is common but Kingella kingae also common

3-15: S. aureus and Streptococcus pyogenes

adults: S. aureus is common

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8
Q

When bacteria is most common after a prosthetic joint infection ?

A

coagulase negative staphylococci» S. aureus

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9
Q

What are some virulence factors of S. aureus?

A
  • bacteria bind to bone tissue receptors (fibrinogen, fibronectin and collagen)
  • peptidoglycan in it’s cell wall–> potent stimulator of monocytes–> destruction of the cartilage
  • induces production of MMPs (metalloproteinases) and inflammatory cells by the host–> degrade collagen (host cell does most destruction)
  • produces TSST-1 and enterotoxin ==> arthritis
  • produces leukocidins and hemolysins–> destroy leukocytes–> create pores
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10
Q

What typically causes gonoccocal arthritis in sexually active adults? What type of bacteria is this?

A

Neisseria Gonorhea

gram - diplococcus

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11
Q

What normally allows for N. gonorrhea to be invasive?

A

defects in the host innate immune system (resident macrophages)

these normally contain the bacteria to the site of infection (mucosa)

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12
Q

What are some virulence factors of N. gonorrhea?

A
  • pili allow for initial mucosal attachment to epithelial cells
  • Protein IA–> binds to host protein which inactivates a key factor for complement –> invasive
  • invasive tend to lack Opa and are transparent (possible down regulation after used to attach to mucosa)
  • LOS–> host sialic acid attached to this and prevents complement from killing
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13
Q

What are the 2 manifestations of disseminated gonnococcal infections? Will the joint fluid be + or - for organism in these?

A
  1. triad of tenosynovitis, dermatitis, and polyarthralgias without purulent arthritis. Synocial fluid usually - for organism –> Immune complex mediated
  2. purulent arthritis (more common): without associated skin lesions and with recovery of organisms from joint fluid–> LOS
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14
Q

What are some features of viral arthritis? some causes of viral arthritis?

A
  • normally temporary self-limited arthritis
  • usually involve >1 joint
  • Hepatitis B –> tissue deposit of HBsAg-antiHBBsAg complexes
  • Rubella virus and vaccine: virus and immune complexes
  • Parvovirus B19
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15
Q

Why are joint replacements susceptible to any bacteria that can enter the blood stream?

A
  • no immune system on the joint replacement

- biofilm formation* often leads to inflammation and tissue damage and even failure of the prosthesis

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16
Q

What is a biofilm?

A
  • complex aggregation of microorganisms that may contain one or more species of bacteria (often on joint replacements)
  • communicate via quarum sensing and induce cells to either adapt a biofilm lifestyle or to enter a stationary phase
  • extracellular polymer aids adhesion by the bacteria and protects them from external stresses
  • 15% cells and 85% matrix
  • resistant to antibiotics (can’t penetrate and bacteria in a different metabolic state)
  • hard to culture
  • MOST defensive life strategy that prokaryotic cells have
17
Q

What is a sonicate?

A

removal of part of a prosthetic joint tat allows for culturing that is not normally successful due to biofilm presence

18
Q

What is Infectious Osteomyelitis? What are the most common aerobic and anaerobic causes?

A

-a purulent inflammation of bone caused primarily by bacteria but occasionally by other microrganisms.

  • aerobic: S. aureus and coagulase negative staphlococci
  • anaerobic: Bacteroides spp.

-M>F

19
Q

What are some virulence factors of S. aureus?

A

an antiphagocytic capsule allows it to survive in blood

proteins on bacteria surface can bind to fibronectin, fibrinogen and collagen –> allow for colonization of bone (bacteria without collagen binding proteins were NOT as virulent)

-produces leukocidins and hemolysins–> destroy WBCs and create pores

20
Q

Where does hematogenic spread of infection normally take place in bone? Why?

A
  • metaphyses of long bones
  • capilllary ends make sharp loops under the growth plate and enter large veinous sinusoids where blood becomes slow and lacks active phagocytic cells
  • trauma can also cause focal hemorrhage and allow bacteria into bone tissue
  • blocking of blood flow can impair the immune system
21
Q

What is the host response to in response to bacteria in the bone?

A

inflammation, edema, increased vascularity, influx of PMNs and decreased pH

22
Q

What can happen due to pyogenic osteomyelitis?

A
  • pus forming bacteria can increase the pressure confined within rigid bone –> cut off blood supply–> necrosis
  • can also spread to the sinuses and soft tissue (penetration of the periostieum in adults but NOT in kids–> doesn’t reach soft tissue in kids)
  • can also spread from bone to joint in adults (not in kids because of growth plate being avascular)
23
Q

What is often found in people with chronic osteomyelitis?

A

micro colonies with biofilms (resistant to antibiotics and host defenses)

(often S. aureus)

24
Q

What is another more invasive way that S. aureus can affect cells?

A

can survive intracellularly in osteoblasts (contains capsule)

  • elaboration of the capsule w/in host increases survival
  • induce apoptosis–> increasing damage and inflammation of the area.
  • further increase resistance to antibiotics
25
Q

What are some features of small colony variants of S. aureus?

A
  • isolated from pts with chronic infectious osteomyelitis (not the same as the micro colonies in biofilm because they will grow ex-vivo)
  • auxotrophic–> lack key enzymes for things–> deficient in Electron transport chain and energy production
  • grow slowly
  • increased antibiotic resistance
  • more likely to cause persistent infections
  • in vitro, phagocytosed by human cells.–> do NOT lyse the cells because lack alpha toxin (intracellular= protected)
26
Q

How does mycobacterium tuberculosis spread to joints? How does this lead to vertebral destruction?

A
  • hematogenous spread to joints. –> bones are highly vascularized
  • arrive within infected macrophages
  • additional macrophages and T-cells attempt to control infection
  • TH-1 cell produces TNF and IFN gamma ==> inflammation ==> increase bone resorption ==> bone destruction
27
Q

How does infection spread throughout the vertebrae?

A

segmental arteries bifurcate to adascent vertebrae and affect both.

Initian infection=anterior inferior vertebral body (entrance from the anterior spinal A). Spread of infection normally occurs through the anastomosing venous channels draining the vertebral bodies.

28
Q

What are the 4 stages of osteomyelitis?

A
  1. medullary osteomyelitis
  2. superficial
  3. localized
  4. diffuse
29
Q

What imaging is the most accurate way to assess the extent of an infection in the bone?

A

MRI

can detect osteomyelitis within 3-5 days of onset

30
Q

What are the goals of treatment of acute osteomyelitis?

A
  1. eradicate infection
  2. restore function
  3. prevent development of chronic osteomyelitis
31
Q

What is the first line of treatment for S. aureus osteomyelitis? What is the bacteria is methicillin resistant?

A

beta lactam (nafcillin) (if methicillin sensitive) or cefazolin

glycopeptide (vanco IV every 1 hours). (methicillin resistant) plus rifampin

32
Q

What are some complications of chronic osteomyelitis?

A

-May harbor small colony variants (SCV) of S. aureus
-Medically-incurable–> Lifelong antibiotic suppression
-
Risk for developing:
pathologic fractures,
osteogenic sarcoma,
squamous cell CA at sinus tract,
amyloidosis

33
Q

What does acute bacterial infection in synovial fluid appear as? How do you definitively diagnose an infection from synovial fluid?

A

> 100, 000 WBCs

> 90% neutrophils

diagnose with culture and PCR

34
Q

What treatment should be used for a gonnococcal joint infection that is resistant to penicillin and quinolone?

A

ceftriaxone 1g IV for 7-14 days

7 days of doxycycline in case they also have chlamydia

MSK final (21 decks)

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