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
What are some features of small colony variants of S. aureus?
- 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
How does mycobacterium tuberculosis spread to joints? How does this lead to vertebral destruction?
- 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
How does infection spread throughout the vertebrae?
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
What are the 4 stages of osteomyelitis?
1. medullary osteomyelitis 2. superficial 3. localized 4. diffuse
29
What imaging is the most accurate way to assess the extent of an infection in the bone?
MRI can detect osteomyelitis within 3-5 days of onset
30
What are the goals of treatment of acute osteomyelitis?
1. eradicate infection 2. restore function 3. prevent development of chronic osteomyelitis
31
What is the first line of treatment for S. aureus osteomyelitis? What is the bacteria is methicillin resistant?
beta lactam (nafcillin) (if methicillin sensitive) or cefazolin glycopeptide (vanco IV every 1 hours). (methicillin resistant) plus rifampin
32
What are some complications of chronic osteomyelitis?
-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
What does acute bacterial infection in synovial fluid appear as? How do you definitively diagnose an infection from synovial fluid?
>100, 000 WBCs >90% neutrophils diagnose with culture and PCR
34
What treatment should be used for a gonnococcal joint infection that is resistant to penicillin and quinolone?
ceftriaxone 1g IV for 7-14 days 7 days of doxycycline in case they also have chlamydia