Cross - Bone, Joint, and Muscle Infections

Question 1

What is native acute infectious arthritis?

Answer 1

• Typically refers to bacterial infection in a joint
• Bacterial/suppurative/pyogenic/septic arthritis: most common and most important joint infection
  1. Considered a surgical emergency due to potential for rapid joint destruction and possible loss of function
• Mycobacterial, fungal arthritis (other than Candida) usually more chronic and slowly progressive process
• Number of diverse organisms can cause infectious arthritis: bacteria, viruses, mycobacteria, fungi
• Much more common in patients with RA
• Morbidity and mortality high, esp. in those with significant comorbidity

Question 2

What are the possible sources of infection in septic arthritis?

Answer 2

• Usually hematogenously acquired during overt or occult bacteremia, incl that caused by endocarditis
  1. Normal, diseased, prosthetic joints susceptible; abnormal joint architecture INC risk substantially
  2. Synovial membrane very vascular and lacks a basement membrane, so particularly susceptible to hematogenous deposition of bacteria
• Other routes of infection:
  1. Direct inoculation in the joint via sx, trauma, bites, percutaneous puncture (nail, needle, etc)
  2. Contiguous spread from adjacent infected soft tissue or bone, e.g.: small joints of foot become infected from a diabetic foot ulcer or infection

Question 3

What are the risk factors for septic arthritis?

Answer 3

• Up to 22% of pts will NOT have identifiable risk factor
• Pre-existing abnormal joint architecture (most important), e.g.: RA, osteoarthritis, gout
• Advanced age
• Diabetes mellitus
• Previous joint surgery
• IVDU
• Endocarditis
• Immunosuppression: organ/stem cell transplants or tx w/systemic GCS or anti-TNF agents

Question 4

What is the pathophysiology of septic arthritis?

Answer 4

• Dependent on adherence of orgs to and colonization of synovial membrane, bac proliferation in synovial fluid, and synovial infection with host inflam response
  1. After entry into joint, bac adherence facilitated by vascular synovial mem w/INC adhesion factors
  2. If joint disease/injury present, INC amount or exposure of host-derived ECM proteins like fibronectin, collagen, elastin, hyaluronic acid which promote bacterial attachment
  a. This is why abnormal joint architecture increases the risk of infection

Question 5

What is the most common bug implicated in septic arthritis?

Answer 5

• S. aureus: causes 37-65% of cases
  1. RA patients: 75% of septic joints from Staph
  2. Also common in IVDU
• MRSA becoming increasingly common
  1. Esp. in the elderly, those with recent orthopedic surgery, and those colonized with or previously infected with MRSA

Question 6

How is Strep implicated in septic arthritis?

Answer 6

• 2nd most frequent cause (after Staph Aureus)
  1. Group A, Group C, Group G: usually mono-articular, but can be poly, esp. with endocarditis
  2. Group B: neonates, diabetics, malignancies, and can cause polyarticular infection
  3. S. pneumo less common
• Other gram positive causes -> coagulase negative staphylococcus (Staph Epi)

Question 7

How are G(-) bacilli implicated in septic arthritis? What are some common bug-clinical case associations?

Answer 7

• 5-20% of cases (<g> <u>at risk</u>: neonates, elderly, IVDU, immuno-compromised hosts</g>
• P. aeruginosa: IVDU and iatrogenic after surgical procedures/intra-articular injections
• Neisseria (gonorrhea and meningitidis): young adults, late complement deficiency
• Salmonella: esp in sickle cell disease and SLE
• Cat or dog bite: pasteurella multocida
• Unpasteurized milk: brucella (causes sacroiliac joint arthritis -> RARE)

Question 8

What are the clinical manifestations of septic arthritis?

Answer 8

• Mono-articular: 80-90% of cases, knee in about 50%
  1. Frequently involved: hip, shoulder, wrist, ankle
  2. Children: hip most common
• Polyarticular in 10-20% of patients (usually S. aureus)
  1. Risk factors: RA, prolonged or intense bacteremia, immunosuppression
• Most present with intense pain and loss of function of one or more joints over 1-2 week period
  1. Other symptoms: swelling, redness, increased warmth of joint -> should typically be cooler than other parts of the limb
  2. Fever and malaise common, but high fevers with shaking chills typically absent

Question 9

What are the typical PE features with septic arthritis?

Answer 9

• Focal joint tenderness
• Inflammation
• Effusion, especially knee joint
• Limited ROM (active and passive) and results in considerable pain -> most important PE finding
• Children with septic hip: hold hip in a flexed and externally rotated position, resist any ROM
• Attached image: septic knee

Question 10

What do you see here?

Answer 10

• Septic arthritis of 3rd MCP joint
• Pasteurella multocida after a cat bite

Question 11

What might this be?

Answer 11

• Sternoclavicular septic arthritis
• Uncommon, except in IVDU

Question 12

How do you diagnose septic arthritis?

Answer 12

• Non-specific findings: leukocytosis, elev. ESR, CRP
• Dx requires arthrocentesis of affected joint
  1. Synovial fluid leukocyte count >50,000 cells
  a. Lower WBC counts regularly encountered and don’t exclude the diagnosis
  b. >100,000 leukocytes: bet on it
  2. Purulent fluid seen w/elev. neutrophil count
• Look for crystals! -> will tell you if you have gout rather than a septic joint (easy to confuse the two)
• Try to tap the joint and get blood cultures prior to antibiotics (fluid culture + 80-90% of the time, gram stain + 50% of cases, blood cultures + 25-75% of time)
• Avoid puncturing skin visibly involved w/cellulitis bc if joint isn’t already infected, you could introduce it

Question 13

What might radiographs show in a case of septic arthritis?

Answer 13

• X-rays
  1. Early: peri-articular soft tissue swelling with normal osseous structures
  2. Late: joint space loss, bony erosions
• Ultrasound helpful to assess for presence of effusion and to guide needle aspiration if needed
• CT/MRI: can detect erosive bony changes, joint effusions, inflammation, cartilage destruction
• None of these are required for diagnosis, but a lot of times, at least an x-ray will be obtained initially

Question 14

What is this?

Answer 14

• Digit with septic arthritis
• Arrow shows bony erosion and soft tissue swelling

Question 15

What do you see here?

Answer 15

• CT of pubic symphysis septic arthritis
• Widening of joint space, small cortical erosions
• Iatrogenic bc patient had had a prostatectomy 2 weeks earlier -> urine culture grew P. aeruginosa

Question 16

How should you manage septic arthritis?

Answer 16

• Immediately: call ortho for drainage +/- I&D
  1. 3 procedures: needle drainage, arthroscopic drainage, or arthrotomy (open surgical drainage)
• Antibiotic therapy:
  1. GPCs: Vancomycin
  2. GNRs: Cephalosporins or Zosyn (piperacillin-tazobactam)
  3. If gram stain is negative: Vanc + Cephalosporin
  4. Tx should be narrowed or deescalated based on ID and susceptibility of bacteria identified
• Duration of therapy: 2-4 wks of IV antibiotics
  1. If S. aureus, 4 weeks of IV AB required -> some will give 2 weeks IV AB’s, then PO antibiotics for another 2 weeks (seems to work fine)

Question 17

What is gonococcal arthritis? Who gets it?

Answer 17

• 1 of 2 clinical manifestations of DGI (disseminated gonococcal infection); other being syndrome including tenosynovitis, dermatitis, & polyarthralgia/polyarthritis
  1. DGI complicates 0.5-3% of people w/ mucosal GC infection (NOT that common)
  2. Septic mono-articular or oligoarticular (few joints) arthritis in about 50% of patients with DGI
• Epi: 4x more common in women; <40 years old, lower SE status, nonwhite ethnicity, MSM, multiple sex partners, illicit drug use (i.e., high-risk sexual behavior)

Question 18

What are the risk factors for gonococcal arthritis?

Answer 18

• Women during menstruation, pregnancy, or postpartum
• SLE
• Complement deficiencies (esp. terminal components C5 to C8)

Question 19

What is the pathogenesis of gonococcal arthritis?

Answer 19

• Result of occult bacteremia (i.e., never see it in blood cultures)
  1. Immune mechs (like immune complexes) are likely involved, and may account for low yield of cultures for N. gonorrheae in synovial fluid
• Infection may have been contracted days to months before dissemination

Question 20

What are the clinical manifestations of gonococcal arthritis?

Answer 20

• Typically a triad of:
  1. Dermatitis: painless, non-pruritic, lesions in 2/3; few in number -> macules, papules, pustules
  2. Tenosynovitis: 2/3 -> hands, fingers, wrists
  3. Migratory polyarthralgia or polyarthritis: joint symptoms often severe and asymmetrical
• Fever, chills, generalized malaise present
• <50% true septic arthritis w/purulent joint effusion
• Septic GC arthritis w/o tenosynovitis or skin lesions is less common and indistinguishable from bac arthritis caused by o/bugs -> knees, wrists, ankles most comm

Question 21

What labs are used to diagnose gonococcal arthritis?

Answer 21

• Synovial fluid freq w/50,000-100,000 cells, but not always -> aspirates from pts with DGI without frank suppurative arthritis will have lower cell counts
  1. Cultures not commonly positive
• Suppurative arthritis: N. gonorrhoeae cultured from synovial fluid in 50% of cases
  1. DGI: cultures (synovial fluid) + 20-30% of cases
  2. PCR (synovial fluid) + in 80% in DGI
  3. Blood cultures + in < 30% (probably even less)

Question 22

What do you see here?

Answer 22

Examples of skin lesions in DGI (will be >=10 of these)

Question 23

What is this?

Answer 23

• Tenosynovitis in DGI -> hands usually affected
• MCP joints pretty inflamed and red

Question 24

What are the risk factors for mycobacterial arthritis?

Answer 24

• Age greater than 65
• Female sex
• Immigration from high TB regions
• Lower socioeconomic class
• Incarceration, alcohol abuse, IVDU
• Immunosuppressive therapy, HIV
• Pre-existing joint disease

Question 25

What are the pathology and clinical manifestations of MTB arthritis?

Answer 25

• Pathology: chronic granulomatous monoarthritis, usually a result of hematogenous dissemination assoc with primary pulmonary TB
  1. May be latent for long period pre-presentation
• Clinical manifestations: knee, hip and ankle usually involved (big joints)
  1. In more than half of cases, there is no sign of TB infection anywhere else
  2. Fever, constitutional symptoms absent

Question 26

How do we diagnose and treat MTB arthritis?

Answer 26

• Diagnosis: many times requires synovial biopsy (will show granulomas)
  1. PPD positive in 90%
  2. AFB culture positive 80% of the time; acid-fast stain positive minority of the time
  3. PCR on synovial fluid also is very useful
• Treatment: RIPE x 8 weeks, then INH and RIF to complete 6 months
  1. Just like typical pulmonary TB treatment

Question 27

What happened in this case?

Answer 27

• 61, pain in R foot for 5 mos, initial X-ray, CT (-) -> tx for typical bacterial septic joint, but didn’t get better
• Repeat x-rays showed possible septic arthritis in R tarsometatarsal joint, but aspiration showed no growth
• Biopsy done, and minute fragments of viable bone, no inflammation. AFB stain/culture, fungal cultures, routine cultures done -> 2 weeks later lab called saying AFB were growing in broth, later ID’d as MTB
• Treated with RIPE therapy after that -> several mos without correct diagnosis

Question 28

What is this?

Answer 28

• Erythema migrans: characteristic bullet-like rash that is about 5 cm in diameter -> seen in early infection stage I of lyme disease
• Doesn’t always have central clearing seen here
• Patients may also devo malaise, fatigue, HA, fever, chills, and regional LAD, but do not always

Question 29

What are the stages of Lyme disease and arthritis?

Answer 29

• Early infection stage I: erythema migrans (EM); pts can also devo malaise, fatigue, HA, fever, chills, and regional LAD, but do not always
• Early infection stage II (disseminated; several days to weeks of onset of EM): 2^o skin lesions similar to initial lesions, but smaller, malar rash, conjunctivitis
  1. Heart (AV block) & nervous system involvement including palsies and meningitis
  2. Joint fluid WBC counts from 500-110,000 cells/mm³, most of which are PMNs
• Late infection (stage III -> persistent infection): 60% of untreated have intermittent attacks of joint pain and swelling, mostly in lg joints, esp. knee; usually 1 or 2 joints at a time (lasting few weeks to months)
  1. Even in untreated pts, intermittent or persistent arthritis usually resolves completely in years
  2. Most respond to AB tx, but a small % have AB-refractory Lyme arthritis -> persistent joint inflam for months or years after adequate AB course
  3. Months to a few years after the onset of infection and may not be preceded by a history of early localized or disseminated Lyme disease
• US: arthritis in 1 or few joints most common feature of pts w/late Lyme disease; neuro manifestations (subtle encephalopathy or polyneuropathy) can also occur

Question 30

Prosthetic joint infections

Answer 30

• Implanted foreign material highly susceptible to local infection -> covered by host proteins favoring bacterial adherence (eg. fibronectin) after implantation
  1. Compromise granulocyte function
  2. Implant-assoc bugs growing as biofilm protected from phagocytosis and often AB’s
• Route of infection exogenous (joint inoculation of microorganisms during surgery or early post-op period); hematogenous or contiguous spread (rare)
• Microbiology: S. aureus, staph epi, streptococci, GNB, enterococci
• Diagnosis: threshold of leukocyte counts in synovial fluid much lower than for native septic joint (2,000-5000) -> (-) culture does not exclude diagnosis
• Treatment: remove the prosthesis, give prolonged course of antibiotics

Question 31

Viral arthritis

Answer 31

• Often called immune complex arthritis: virus forms immune complexes with antibody that are deposited in joints and cause inflammation.
• Clinical: arthralgias or frank arthritis
• Most cases short, and resolve spontaneously
• Small joints of hands most commonly affected; large joints can also be involved
• Causes: Rubella, Parvo B19, HCV, HBV

Question 32

What is osteomyelitis? Most common cause?

Answer 32

• Infection localized to bone: one of the most difficult infectious diseases to treat (upwards of $35,000)
• Characterized by bone destruction, formation of sequestra (dead bone)
• Contiguous spread from adjacent soft tissues and joints, hematogenous seeding, or direct inoculation of microorgs into bone as a result of trauma or surgery
• Microorganisms produce local inflammatory rxn that promotes bone necrosis and formation of sequestra
  1. S. aureus most common -> high-affinity adhesins to components of bone matrix that express fibronectin, laminin, collagen, etc.

Question 33

What are the clinical manifestations of osteomyelitis?

Answer 33

• Adults: vague symptoms with subacute-to-chronic presentation
• Non-specific pain around involved site with absence of systemic signs/symptoms
• Fever/chills, local swelling, erythema in proximity of involved bone uncommonly seen
• Draining sinus tract may be present over involved bone, usually having evolved over months and sometimes years (see attached image)

Question 34

How do you diagnose osteomyelitis?

Answer 34

IMAGING

• Radiograph: abnormalities usually seen 10-14 days after onset of infection
  1. Inexpensive, but NOT highly sensitive
• MRI (best), CT considered standard of care in dx
  1. Expensive, but very sensitive -> will show bone destruction, inflammation
• Inflammatory markers (ESR, CRP) usually elevated

FURTHER TESTING

• Organism ID important to optimize medical therapy, and is best accomplished by surgical sampling or needle aspiration under radiologic guidance to obtain tissues for pathology and culture
  1. Not done a lot of the time, but very helpful if you can get radiology or ortho to do it

Question 35

How can osteomyelitis cause this?

Answer 35

• Draining sinus tract (stump from an above the knee mutation) -> really the only sign in many cases
• Infection in bone leads to INC intramedullary pressure due to inflammatory exudates -> vascular thrombosis ensues
  1. Bone necrosis follows due to lack of blood supply, and sequestra (dead bone) and draining sinus tracts are formed

Question 36

What are the common bugs in osteomyelitis?

Answer 36

• Hematogenous long bone osteomyelitis: infection usually monobacterial
  1. Contiguous infection (soft tissue or diabetic foot ulcer, for example): usually polymicrobial
• Common (>50% of cases)
  1. S. aureus: CA-MRSA increasingly recognized as cause of acute long bone osteomyelitis in kids
  a. Infection caused by PVL-positive Staph is assoc w/multifocal, more aggressive disease compared to PVL-negative Staph
  2. Coag negative staph (S. epidermidis, etc)
• Occasionally encountered (>25% of cases):
  1. Streptococci
  2. Enterococci
  3. Gram negatives: Pseudomonas, E. coli, Serratia
  a. Pseudomonas in someone who has stepped on a nail (question favorite)
  4. Anaerobes
  5. MTB
• Rarely encountered (<5% of cases): o/mycobacteria, dimorphic fungi, candida, cryptococcus, aspergillus, brucella, salmonella

Question 37

What is the treatment for osteomyelitis?

Answer 37

• Surgical mgmt: remove hardware (if any), adequate drainage/debridement of all infected tissue (this will help AB’s work on remaining viable tissue)
• Antibiotic therapy: beta-lactams, Vanc most common
  1. Cephalosporins, penicillinase-resistant penicillin bc of low toxicity profile and spectrum of activity
  2. Linezolid: good activity against strep, staph, and VRE, and good bioavailability via oral admin, but prolonged use associated with significant pancytopenia (thrombocytopenia), peripheral neuropathy, optic neuritis, and lactic acidosis
  a. Use limited to pts w/VRE (Vanc-resistant enterococci) or who are intolerant of Vanc
  2. Daptomycin effective against gram-positive pathogens
  3. Duration of therapy: optimal duration unknown, but most recommend 4-6 weeks of IV antibiotics

Question 38

What do you see here?

Answer 38

• C5-6 vertebrae destruction and narrowed disk space

Question 39

Verterbral osteomyelitis and spondylodiskitis

Answer 39

• Infection of intervertebral disk and adjacent vertebrae -> hematogenous in origin in most cases
  1. Potential sources: skin/soft tissue infection, GU tract infection, infective endocarditis, IVDU
  2. Can also occur postop
• Clinical pres: localized insidious pain/tenderness in spine area in 90% of patients, fever present in <50%
  1. Motor/sensory deficits caused by spinal cord or nerve root compression present in 15%
• Micro: S. aureus, coag-(-) staph most common
  1. MTB and Brucella common in endemic regions (not seen that much here; TB sometimes)
• Diagnosis: need high index of suspicion in at-risk pts
  1. MRI is very useful in establishing diagnosis
  2. Image-guided percutaneous biopsy sometimes helpful
• Treatment: at least 6 weeks IV antibiotics
  1. If epidural abscess (abscess enclosed within confines of spinal column, picture next slide) is present, it should be drained, if possible

Question 40

What is this?

Answer 40

• Epidural abscess: needs to be drained because it can compress the nerves and nerve root if not
• Epidural space shown in attached image

Question 41

Osteo in DM or vascular insufficiency

Answer 41

• Typically in the foot: 15-25% of diabetics develop foot ulcers during their lifetime
  1. INC risk of foot ulcers: DM for 10+ years (or uncontrolled), poor glucose control, CV disease, retinal or renal cxs, peripheral neuropathy, evidence of INC local pressure (callus), PVD
• Diagnosis: MRI used often and very valuable
  1. Chronic ulcer with positive probe-to-bone test is associated with high PPV (bone should not be probe-able or visible)
• Treatment: combined surgical/medical therapy (want to get dead bone out)
  1. Broad-spectrum AB’s required bc surgical cultures reveal multiple microorganisms
  a. Zosyn, ertapenem, cephalosporins, flagyl; cipro or other quinolones combined with other antibiotics; use Vanc if there is MRSA
  2. Tx failure: due to lack of debridement, PVD -> - poor arterial vascular supply revascularization should be done to provide blood flow to the area
• Neuropathy, vascular insufficiency, hyperglycemia lead to variety of consequences that lead to devo of skin ulcer and osteomyelitis

Question 42

What are these?

Answer 42

• Foot ulcers: INC risk in pts with DM for 10+ years (or uncontrolled), poor glucose control, CV disease, retinal or renal cxs, peripheral neuropathy, evidence of INC local pressure (callus), PVD

Question 43

What is the pathogenesis of acute hematogenous osteomyelitis in children?

Answer 43

• Capillary ends of nutrient artery make sharp loops under the growth plate -> cap system feeds into lg venous sinusoids where blood flow becomes slow and turbulent
• Obstruction of the capillaries can lead to area of avascular necrosis
• Capillaries lack phagocytic lining cells
• Any minor trauma can lead to hematoma, vascular obstruction, bone necrosis -> can be seeded from transient bacteremia

Question 44

Where does acute hematogenous osteomyelitis most often occur in children?

Answer 44

• Involves mostly metaphyses (due to its weird anatomy) of long bones with tibia or femur affected in most cases
• Half of cases of neonatal OM also have involvement of adjacent joint with septic arthritis

Question 45

What are the most common bugs implicated in acute hematogenous osteomyelitis in children?

Answer 45

• S. aureus and S. pneumoniae; HIB used to be common but now rare due to the effective vaccine
• Neonates: GBS, E. coli

Question 46

In what types of patients does acute hematogenous osteomyelitis occur?

Answer 46

• Prepubertal children
• Elderly
• IVDU
• Patients with indwelling central lines

Question 47

How do you diagnose and treat acute hematogenous osteomyelitis?

Answer 47

• Diagnosis: clinical findings, compatible radiologic findings (MRI), and positive blood cultures
• Treatment:
  1. Most cases can be treated with antibiotics
  2. Switching from IV antibiotics to PO can be done when the patient is afebrile and able to tolerate PO
  3. Duration of therapy: 3 weeks

Question 48

What type of osteomyelitis is implicated in sickle cell disease? Why?

Answer 48

• Acute and long bone OM and septic arthritis are most commonly encountered
• Salmonella and S. aureus most common bugs
  1. Capillary occlusion 2^o to IV sickling may devitalize and infarct the gut, permitting Salmonella invasion
  2. Reduced function of the liver and spleen suppresses clearing of these organisms from the blood stream
  2. Bone is also devitalized and serves as a nidus of infection
• Most patients are children

Question 49

OM in IVDU?

Answer 49

• Common -> hematogenous or direct inoculation
• S. aureus, Pseudomonas, and Candida most commonly encountered organisms in these patients
• Unusual sites of infection common: sternoclavicular, sternochondral joint, pubic symphysis
• Eikenella corrodens, normal oral flora bacterium, can cause OM in IVDU who lick the needle tip or skin before infection (“needle licker osteomyelitis”)

Question 50

Skeletal mycobacterium infection

Answer 50

• Often spine; most hematogenous spread from pulmonary source (1-5% of TB cases)
  1. Vertebral osteo (Pott’s disease): 1 of most common osteoarticular manifestations of TB
• Suspect in: hx of (un)treated TB w/new back pain, +TB tests, young pts, ppl from endemic areas w/CXR consistent w/active or old TB, ppl w/close contacts w/TB, (-) bac cultures, granuloma biopsy specimen
• Clinical: back pain, stiffness (commonly only symptoms), swelling w/abscess & sinus formation
  1. Systemic symptoms often absent
• Significant overlap in imaging b/t TB OM and other forms -> dx should rely on MTB in culture or stain
  1. CXR abnormal in less than 50% of patients with MSK TB, but should always be obtained
  2. 50% of patients: MRI shows paravertebral soft tissue abscess in addition to bone lesion

Question 51

What is this?

Answer 51

• Pott’s disease: T12-L1 diskitis with verebral destruction

Question 52

What do you see here?

Answer 52

• Thoracic spine, Pott’s: diskitis, extensive destruction of endplates of adjacent vertebral bodies
  1. On left image, abscesses can be seen -> MRI shows paravertebral soft tissue abscess in addition to bone lesion in 50% of patients

Question 53

What is myositis?

Answer 53

• Muscle inflammation; can also indicate infection, but infection of skeletal mm uncommon
• Bacteria, mycobacteria, fungi, viruses, parasitic agents could be responsible
  1. Bacteria invade muscle from contiguous sites of infection (skin/subcu abscesses, penetrating wounds, decubitus ulcers, osteomyelitis) or by hematogenous spread from a distant focus

Question 54

What is pyomyositis?

Answer 54

• Acute bacterial infection of the skeletal muscle
  1. Most commonly: S. aureus
  2. Pus accumulates within muscles initially
• Clinically characterized by: fever, localized muscle pain, and stiffness/swelling/tenderness
• Bacteremic spread of infection to skeletal muscle extremely uncommon -> among fatal cases of staph sepsis, abscesses in skeletal muscle are found in less than 1% of patients
• Infection not usually due to 1^o infection of adjacent skin, soft tissue and bone (i.e., this infection occurs in the absence of a predisposing site of infection)
• Most cases occur in the tropics; in more temperate areas, it is very uncommon (330 reported cases in the U.S. between 1981 and 2002)

Question 55

What are the pathogenesis and clinical features of pyomyositis?

Answer 55

• Pathogenesis: previous bacteremia, commonly asymptomatic and transient along with (likely) some minor muscle trauma or injury
• Clinical: fever, distinct muscle tenderness, swelling with warm overlying skin; pus can be aspirated; If pt not diagnosed, sepsis can devo along with striking erythema, exquisite tenderness and fluctuance
• Most frequent sites of involvement: large muscle of LEs and trunk muscles including the shoulder

Question 56

What are the risk factors for pyomyositis?

Answer 56

• HIV: repeatedly reported, usually S. aureus -> predisposition relates to granulocyte dysfunction, progressive cell-mediated immuno-deficiency, and possible muscle injury (HIV myopathy, HAART side effects, myositis from parasitic disease)
• IVDU
• DM
• Alcoholic liver disease
• Corticosteroid therapy
• Hematologic malignancies (leukemia, lymphoma, multiple myeloma)
• Postpartum, postabortion and postop states are rare predisposing risk factors

Question 57

How do you diagnose and treat pyomyositis? What bugs are commonly involved?

Answer 57

• Diagnosis: prompt imaging
  1. X-ray may show swelling or gas in soft tissue
  2. Ultrasound may show focal abscess
  3. MRI the best: identifies focal muscle edema, localizes presence of focal abscesses
• Treatment: drain the abscesses -> initial AB tx should incl Vanc (covers S. Aureus and GA Strep.)
• Bugs: S. aureus causes 60-70% of cases in temperate areas, Group A Strep 1-5%

Question 58

What is gas gangrene? What causes it?

Answer 58

• Myonecrosis and necrotizing fasciitis -> caused by Clostridium perfringens, an anaerobic G+ rod (also causes food poisoning)
  1. Spores in the soil -> vegetative cells are members of normal flora of colon and vagina; transmission through wound contamination
  2. Grows in traumatized tissue (esp muslce), & produces a variety of toxins: alpha toxin (lecithinase) -> damages cell mems, including erythrocytes, causing hemolysis. Enzymes produce gas in tissues
• Trauma introduces organisms (vegetative or spore forms) directly into deep tissue -> if it compromises blood supply, an anaerobic environment forms with low oxidation-reduction potential and acidic pH, which is optimal for growth of clostridial organisms
• Necrosis progresses within 24 to 36 hours of the traumatic injury

Question 59

What are the clinical features of gas gangrene?

Answer 59

• Pain, edema, cellulitis, and gangrene (necrosis)
• Crepitus indicates presence of gas in tissues
• Hemolysis common
• Shock and death occur -> high mortality

Question 60

How do we diagnose and treat gas gangrene?

Answer 60

• Diagnosis: smears of tissue and exudate show large germination proteases (GPR’s) -> spores not usually seen
  1. Cultured anaerobically, then identified by sugar fermentation rxns and acid production
  2. Exhibit double zone of beta hemolysis on blood agar
• Treatment: penicillin G

Question 61

What do you see here?

Answer 61

• Gram stain of muscle biopsy -> large, G+ rods
• C. perfringens

Question 62

What do you see at A and B? What is this caused by?

Answer 62

• C. perfringens

A: air in external iliac vein

B: gas in buttock soft tissue