MUSCULOSKELETAL SYSTEM Flashcards
What is the MUSCULOSKELETAL SYSTEM
what does it consist of
Skeleton (bone & joints) and muscles: support, movement and to maintain body shape
Connective tissues
Ligaments bind bone to bone.
Tendons bind muscles to bone.
Cartilage - found in many places like in joints between bones - cant regenerate
Synovial fluid - in between bones - lubrication
Fascia - thin sheet of collagen binding tissue and organs
How is osteomyelitis caused and ways it is spread
by bacteria , mycobacteria or fungi
Hematogenous- seeded through bloodstream , mostly in long bones in children
direct inoculation - directly inoculated in bone from trauma, fracture or surgery
continous spread- org spreads from infected soft tissue or contaminated prosthetic joint at surgery
What is kind of contiguous spread of osteomyelitis
Vascular insufficiency osteomyelitis.
spreads from neary soft tissue infection caused by poor circulation because of diabetic infection
Acute osteomyelitis:
Sudden fast progressing infection often in long bones in children).
-fever
-area over bone is sore , warm and swollen
Chronic osteomyelitis:
-bone infection that wont go away with treatment
-in adults after injury, surgery or prosthetic infection
-slower to progress and intermittent
-bone pain and abscess with pus
the abscess disrupts blood flow creating necrotic bone called sequestrum which reduces access to immune system or ABs
-pus can drain into sinuses
VERTEBRAL OSTEOMYELITIS
Infection of vertebrae
-elderly, sickle cell, kidney dialysis, or those who inject drugs.
-gets in spine via hematogenous spread or following spinal surgery/epidural injection
-Affects nerve roots, epidural & intradural space & bones of spine.
-Causes soft tissue & bone destruction.
-S. aureus is most common bacterial cause followed by E. coli .
COMMON PATHOGENS IN OSTEOMYELITIS
-any org in bone is pathogenic
-Staphylococcus aureus : MRSA
-Coagulase-negative staphylococci (S. epidermidis, S. lugdunensis) & Propionibacterium species: chronic osteomyelitis in immunocompromised or PPL with prosthetics.
-Enterobacterales or Pseudomonas aeruginosa
BHS & Enterococcus
Anaerobes
-Salmonella species: in ppl with sickle which breakdown intestinal lining causing salmonella to get into bloodstream
LESS COMMON CAUSES OF BONE INFECTION
-pathogens in immunocomp or ppl who work with animals or tropical climates BSL3 orgs in CL3 facility
Fungi-Dimorphic fungi like Histoplasma capsulatum & Paracoccidioides brasiliensis -BSL3
-Candida spp., Aspergillus spp. (BSL2).
-Mycobacteria (TB) BSL3- when affects spine =Potts disease
-Actinomyces – GPB infects cervical facial area but can spread to bone thru blood.
-Bartonella henselae (cat scratch disease), Brucella spp. (cattle & other farm animals BSL3 )Coxiella burnetii (sheep/goat & other farm animals BSL3)
Parasites: Leishmania spp. (sandfly), Malaria (mosquito)
Types of stains for mycobacteria
Acid fast due to waxy cell wall with mycolic acids
-makes orgs resistant to decolorization by concentrated alcohol
types of acid fast stains
Ziehl–Neelsen (ZN) stain: Carbol fuchsin (heated on the slide)
3% acid alcohol
Methylene blue
Kinyoun stain (cold):
Carbol fuchsin (higher concentration of phenol)
3% acid alcohol
Methylene blue
Modified acid fast: uses lower conc of acid alcohol 0.5 – 1.0%
AURAMINE RHODAMINE FOR MYCOBACTERIA
-stain for acid fast bacilli using florescence micro
-fluorescent dyes with high affinity for mycolic acid
-Stains cell wall bright yellow or orange, with dark background
Reagents
-Auramine-Rhodamine dyes (Primary stain)
-Distilled Water
Acid-alcohol (decolorizer)
-Potassium permanganate (counterstain
DIMORPHIC FUNGI
blastomyces
coccidioides
histoplasma
paracoccidiodes
sporothrix
-start as lung infections spreading to skin, bone or can be systemic causing infection in immunocomps
blastomyces- inhaling fungus in soil at 25(in vitro)- mold at 37(in vivo)yeast
coccidioides- inhaling arthroconidia in soil at 25(in vitro)- mold at 37(in vivo) spherule
histoplasma- inhaling microcondia/hyphe in bat and bird feces at 25(in vitro)- mold at 37(in vivo)yeast
paracoccidiodes-inhaling fungus in soil where coffee is grown at 25(in vitro)- mold at 37(in vivo)yeast
sporothrix inhaling fungus in soil where roses, rose thorns or plants at 25(in vitro)- mold at 37(in vivo)yeast
LAB DIAGNOSIS OF DIMORPHIC FUNGUS
-risk 3 orgs only in CL3 lab
-PPE and Class 2 bio safety cabinet
-Ag or AB detection
-PCR for dimorphs
-Direct specimen microscopy - detect yeast form in body
-culture on fungal media at 25 and 25- takes a long time to grow
-Lactophenol cotton blue (LPCB) stain from the culture - dimorphic yeast or mold structures
SPECIMENS FOR DIAGNOSIS OF BONE INFECTIONS
-Bone biopsy: Gold standard- needle aspirate with Na heparin
-Bone piece- 2nd best
-Pus fluid from sinus/abscess needle aspirate only if biopsy cant be done
-Blood cultures only pos in 50% of osteomy cases
-if delay in testing keep at 4 deg
SWAB IS NOT APPROPRITAE can be contaminated with skin flora and wont see any pathogens or anaerobes
SPECIMEN PROCESSING
STERILE SAMPLES
At hospital
-bone piece or marrow biopsied via needle put directly in THIO broth or culture bottles (subbed to solid media after 48hrs or if cloudy)
AT school
bone sample is put right on agar +thio
-all bone samples EXCEPT bone piece needs direct gram with call to dr
-culture for O2 and ANO2 orgs
-mycology or virology requests - sent off
-mycobacteria - PHL
MYOSITIS
MUSCLE TISSUE INFECTION
Infectious myositis:
-muscle infection from bacteria, fungus, parasite or virus
-Direct infection by injury, object penetration or surgery
-2ndary infection by contiguous spread (infection in nearby tissue) or by hematogenous spread via organism in bloodstream.
Specific types of myositis:
Gas gangrene, necrtoic infection = c perfringens or Clostridia
-Synergistic myositis, non-clostridial necrotic infection caused by mixed aerobes, anaerobes
-Pyomyositis a bacterial infection of skeletal muscle that leads to abscess formation
NECROTIZING FASCIITIS
-Rare serious, infection of muscles, subcutaneous fat & superficial fascia overlying soft tissues
-quick and deadly
-can happen after minor injury, pox lesion or post op
-classified by # of bacteria and type causing an infection
types of NECROTIZING FASCIITIS
Type I : Caused by a polymicrobial mix of GAS, S. aureus, Enterobacteriales & anaerobes.
Type II: Caused by GAS alone or 2nd most commonly by S. aureus alone or very rarely, by both together
Type III: due to marine bacteria Vibrio vulnificans
Gas Gangrene: due to Clostridium spp.
MOST COMMON PATHOGENS IN MUSCLE INFECTIONS
-Staphylococcus aureus (most common)
-BHS (GAS may cause necrotizing fasciitis)
-Streptococcus pneumoniae
-Enterobacterales
-Pseudomonas & other GNB
-Many anaerobes (C. perfringens causes gas gangrene)
LESS COMMON CAUSES OF MUSCLE INFECTIONS
Rhabdomyolysis:
-muscle fiber death which releases toxic end products into bloodstream
-muscle proteins are seen in urine = kidney failure
-from traumatic crush injury, muscle exertion or alcohol abuse
-or inflammatory bacterial or viral infection.
Streptococcus, Salmonella, Legionella, Staphyloccus & Listeria (also many viruses)
LESS COMMON CAUSES OF MUSCLE INFECTIONS
Mycetoma:
-Chronic destruction of skin, subcutaneous tissue, muscle and bone - mostly in foot Madur foot
-tropical areas after puncture
-caused by Nocardia or fungus
-results in abscesses with draining sinuses with black granules (if due to fungus) & red granules (if due to Nocardia).
LESS COMMON CAUSES OF MUSCLE INFECTIONS
Actinomycosis:
-Chronic infection of muscle, bone, joints around jaw, chest or abdomen
-bacteria classified as Actinomycetes.
- branching beaded GPB.
-A. israelii causes actinomycosis = emits yellow “Sulphur granules”
-Actinomyces is anaerobic and is NOT acid fast
LESS COMMON CAUSES OF MUSCLE INFECTIONS
Viruses:
mostly in immunocomp
Influenzae virus (most common virus), Adenovirus, Cytomegalovirus
what is NOCARDIA
-beaded, branching GPB classified in Actinomycetes group
-found in standing water, decaying plants, & soil
-infection via inhalation of organism or by direct inoculation of skin thru a cut/trauma
-different from Actinomyces because it is a strict aerobe and partially acid fast.
-Modified acid-fast stain - has lower concentration of acid alcohol decolorizer
LESS COMMON CAUSES OF MUSCLE INFECTIONS
Fungi
mostly in immunocomp
Candida spp (most common), Cryptococcus, Aspergillus.
Dimorphs like Blastomyces dermatitidis, H. capsulatum
LESS COMMON CAUSES OF MUSCLE INFECTIONS
Parasites:
mostly in immunocomp
Trichinella-eating larvae in undercooked wild game meat.
Taenia solium- eating eggs on unwashed food or self- inoculation -causes Cysticercosis
Toxoplasma gondii: contact with cat feces, eating undercooked meat with parasite in tissue cysts, or from mother to baby
MYOSTIS LAB SPECIMENS
-Muscle/tissue biopsy or needle biopsy of tissue (all sterile)– placed in sterile container
-Abscess aspirate (Semi sterile) in sterile container
-Abscess or muscle swab – (not sterile & least appropriate) contaminated by normal skin flora the transport media should maintain aerobic and anaero orgs
-Blood cultures (sterile) not postive often since bacteremia is transient
SPECIMEN PROCESSING of MYOSTIS LAB SPECIMENS
-Grind or homogenize tissue specimen with, sterile tissue grinder -with small volume of sterile, filtered water.
-Direct gram stain done on all specimens except blood culture (automated testing).
-Specimens other than blood are cultured onto BA, CHOC, CNA, MAC, BRUC & THIO.
JOINT INFECTIONS
Infectious (Septic) Arthritis:
-Infection of fluid & tissues of joint mostly by bacteria
-Orgs spread by hematogenous route (bloodstream).
- direct injury puncture wounds.
-from a nearby infection (contiguous).
JOINT INFECTIONS
Acute infectious arthritis:
-starts quick and tissue destructs in hours or days even in healthy people
JOINT INFECTIONS
Chronic infectious arthritis:
-gradual & often affects people who have predisposing risk factors - less pain and swelling
MAIN BACTERIAL CAUSES OF INFECTIVE/SEPTIC ARTHRITIS
children <3 years of age
-H. influenzae – < 2yrs old, less common now that babies are vaccinated against H. influenzae type B.
-Kingella kingae (gram neg coccobacillus) - most common GN bacterial cause in this group
MAIN BACTERIAL CAUSES OF INFECTIVE/SEPTIC ARTHRITIS
Pathogens that affect any age:
-Staphylococcus aureus most common 70 % - all ages
-MRSA
-N. gonorrhoeae – most frequent in young adults <30 yrs.
-GAS & other BHS
-S. pneumoniae
-Enterobacterales & Pseudomonas aeruginosa
-Anaerobes
GONOCOCCAL ARTHRITIS
-untreated GC spreads from genitals through body - disseminated gonococcal infection -can also spread to joints from blood stream
symp-Fever, chills, skin rash, pain & swelling due to pus inside joint = purulent arthritis
Add selective media for GC (NYC or TM) for Joint fluid specimens:
if requested from dr or if you see gndc in direct specimen gram
THAYER MARTIN
-selectively enriched for NG
-MHA with 5% sheeps blood
-Vancomycin kills most GP.
-Colistin kills all GN except Neisseria.
-Nystatin kills fungi.
-Trimethoprim Inhibits swarming by Proteus
PROSTHETIC JOINT INFECTION
-post surgery infection in people with artificial joints
-wound wont heal and the bacteria spreads to bloodstream
-happens in early recovery -1st 2 months
-bacteria will adhere to artificial joint and form a biofilm which acts like a shield so the bacteria is hidden from immune system & AB
-bacterial metabolism is slowed making it harder to culture, ID & treat
tough in ppl with 2nd joint replacement, prior prosthetic infection, immunosupp, diabt, RA
PATHOGENS IN PROSTHETIC JOINT INFECTIONS
Early onset
Delayed onset
Late onset
Early onset (< than three months after surgery):
Staph aureus
Anaerobes
Polymicrobial infection
Delayed onset (3-12 months after surgery):
Coagulase-negative staphylococci
Propionibacteriumsp
Enterococci spp.
Late onset (< than twelve months after surgery)
Staph aureus
Gram-negative bacilli
BHS
REACTIVE ARTHRITIS
-inflammatory arthritis due to autoimmune response triggered by infection in intestines, genitals or urinary tract.
Orgs that infect Genitourinary tract that can cause RA
-Chlamydia trachomatis, Neisseria gonorrhea, Mycoplasma hominis, and Ureaplasma urealyticum
Orgs that infect Gastrointestinal tract that can cause RA
Salmonella enteritidis, Shigella flexneri, and dysenteriae, Yersinia enterocolitica, Campylobacter jejuni, Clostridium difficile.
OTHER CONSIDERATIONS FOR JOINT INFECTION SPECIMENS
Specimens from genitourinary tract, respiratory tract, CSF, & blood should also be tested for bacteria to help determine original source of infection.
Blood cultures are especially important since bacteria from joint infections often initially came from the bloodstream
LAB JOINT FLUID PROCESSING
-volume, color, turbidity, viscosity.
-If clotted, break apart with sterile swab or loop
-If too thick digest with hyaluronidase – releases trapped bacteria
-If >1 mL received, centrifuge first use sediment for slides and culture media
-if <1 mL received, do NOT centrifuge prep slides and culture directly
JOINT FLUID TESTING
Hematology or Chemistry tests:
-WBC with diff
-MIC for crystals under polarized light , TP, GLU
Micro lab tests
-Direct Gram stain, culture for aerobes and anaerobes
-BA, CHOC, *TM, CNA MAC, BRUC & THIO (THIO only indicated not actually done).
-NYC or TM only if requested
-Culture is the most definitive diagnosis of infective arthritis
MUSCULOSKELETAL SPECIMENS AT THE MICHENER
Joint(synovial) fluid, Bone/bone marrow or Muscle Biopsy - are all sterile specimens.
Direct specimen gram:
Performed on all MS specimens except if piece of bone is received
Presence/absence of pus cells with quantity
Presence/absence of epithelial cells with quantity
Presence/absence of organisms with quantity
For fluids: do not report epithelial cells
Gram result must be phoned to physician on Day 1
ADDED PROCEDURE FOR JOINT FLUIDS WITH GC INVESTIGATION
Perform oxidase on any colonies growing on either CHOC or TM to rule out GC.
If oxidase neg, it is not GC, re-incubate both CHOC & TM for up to 72 hours
If oxidase positive, perform Gram stain. (ALL NEISSERIA ARE OX POS)
If GNDC then perform Identification tests.
ID of this organism must be by 2 different principles before you can report it to doctor i.e., Biochemical, mass spectrophotometry, molecular, immunological.
At the Michener we will be using MALDI (first - if neg just stop there and reincubate choc and TM- 72 hrs) & Bacticard (after pos maldi ONLY FROM selective media TM/NYC)
-if colonies are too scant because you need 2 mcfar you should subculture to choc and then do test on D3 from the choc
-if both pos then do a b lactamase test -the only susceptibility test
-note youll reincubate CHOC/TM if GC by D3
What are other tests for NG
rapid carb fermentation
PIP or PRO
ID Tubes
NAAT (org doesnt have to be alive)
Rapid carbohydrate fermentation:
Glucose, maltose, sucrose and lactose – GC ferments only glucose.
Other enzymatic tests for PIP OR PRO:
We use Bacticard for this
Biochemical ID: Vitek NH, rapid NH or API NH
Nucleic acid amplification (NAAT):
Amplify & detect nucleic acid sequences specific for GC.
Don’t require viable organisms – test right from urine.
-very sensitive only need one strand of target DNA or RNA
gon needs to be sent to PHL
all positive GC reports will remain preliminary until PH sends the AST results back.
