BAKTERI PENYEBAB

INFEKSI TULANG DAN dr. Desy Ariani G., M. Biomed.

SENDI
OBJECTIVES

Osteomyelitis
Infeksi tulang dan
sendi
Arthritis
 OVERVIEW
 Life- threatening, long-term disability, reduced quality of life
 Spontaneous disease is uncommon, iatrogenic disease caused by infected
prosthetic
joints >>
 Usia tua: (penurunan respon imun, >> penyakit2 degenatif, fraktur pinggul, >>
operasi invasive pada sendi)
 Diagnosa pada anak sering sulit (demam; lumpuh oleh sebab yang tidak jelas
dan/atau abnormal postur/gait; enggan menggunakan atau bertumpu pada bagian
yang sakit; nyeri muskuloskletal ± nyeri pada sendi dan tulang setempat
 Trias: demam, nyeri sendi, gangguan pergerakan
BONE AND JOINT INFECTIONS:
MECHANISM
 Hematogenous seeding most common
 Seeding from a contiguous source of infection
 Direct inoculation of the bone, from surgery, trauma or
joint aspiration
RISK FACTORS FOR BONE AND
JOINT INFECTIONS:
 Diabetes mellitus
 Sickle cell disease
 AIDS
 Alcoholism
 IV drug abuse
 Chronic corticosteroid use
 Preexisting joint disease
 Other immunosuppressed states
 Postsurgical patients—especially those with prosthetic devices
 OSTEOMYELITIS
 An inflammatory process accompanied by bone destruction and caused by an infecting
microorganism
 Affects approximately 10 - 100 per 100,000 population per year.
 Often preceded by history of trauma in the affected extremity, bone surgery, or joint replacement
 Spread via the haematogenous route from a primary site of entry
 Infection may also occur by direct inoculation (open fractures, penetrating wounds), or local
extension from adjacent sites
 The infection can be limited to a single portion of the bone or can involve several regions, such as
marrow, cortex, periosteum, and the surrounding soft tissue
 Femur and tibia are most commonly affected
 Infection is usually seen in the metaphyseal region of bones
ETIOLOGY
 Usually a bacterial infection
 Staphylococcus aureus is the most common cause of osteomyelitis
 Other causes vary depending on the age of the patient
 Vagina of a pregnant woman  colonized with Streptococcus agalactiae (group B
Streptococcus) or Escherichia coli  neonate is more likely to aspirate these
organisms during labor and delivery
 Some patients are more likely to develop a particular bacterial infection of the bone
because of their predisposition to certain factors or behaviors.
 Intravenous illicit drug users  P. aeruginosa infections of the cervical vertebrae
 Athletic shoes  more likely to harbor increased numbers of P. aeruginosa
CLINICAL FEATURES
Acute osteomyelitis  several days of pain, tenderness and swelling, possibly with
signs of systemic sepsis. Concomitant septic arthritis can be the presenting feature.
Vertebral and pelvic osteomyelitis often present with pain alone (2-3 weeks
duration).

Chronic osteomyelitis  necrotic, presents over a longer period, often in adulthood

after an acute episode in childhood, or following an acutely infected open fracture.
 Sequestrum and involucrum
 A sinus tract over the infected area is pathognomonic.
PATHOPHYSIOLOGY
 First step: entry of the organism into bone
PATHOPHYSIOLOGY
 Microbes seed the tissue  adhere to the organic matrix or invade into cells 
reproduce, forming growing colonies
 Obstruct blood flow  thrombosis and infarction  creates an environment
conducive to further propagation
 Innate and adaptive immune responses  contaminated area become inundated with
fluid, fibrin, degranulated platelets, extravasated red blood cells, and inflammatory
cells  developing abscess increases intraosseous pressure
 Pus perforate the periosteum and extend into neighboring soft tissues  abscess that
can burrow to the skin surface, creating one or more sinus tracts that drain discolored
exudates and necrotic tissue
 Pus extend into the epiphysis  penetrate the articular surface or spread along
capsular and tendoligamentous insertions into the join
 Severe destruction of the articular cartilage and eventual permanent disability
PATHOLOGY AND
PATHOGENESIS
 Inflammation
 Bacterial growth
 Necrosis
 Resolution
1. INFLAMMATION
Adherence of the circulating bacteria to the bone surface, most often the richly
supplied metaphysis in growing bone, triggers a local inflammatory response.
An increase in local blood flow raises the intramedullary pressure causing acute
pain.

2. BACTERIAL GROWTH
If attachment is successful adherent growth occurs, often with the production
of a ‘biofilm’ e an exocellular polysaccharide glycocalyx. This confers
protection against phagocyte and complement clearance and is also difficult for
antibiotics to penetrate.
3. NECROSIS
Increase in intramedullary pressure causes compression of the sinuses and capillaries
in the marrow resulting in bone infarction. In addition, local prostaglandin
production enhances osteoclast activity and collagen synthesis causing bone
resorption. Spread of the inflammatory process to the subperiosteal area may cause
bone stripping, particularly in infants and children. This stripping is a potent
osteogenic stimulus and thus new bone may be laid over the underlying, sequestrated
dead cortical bone (‘sequestrum’).

4. RESOLUTION
If the local pressure is released and the infection successfully treated, the bone will
heal by this process. Uncleared sequestrum will continue to act as a nidus of
infection, however, and due to its almost absent blood supply will not be penetrated
by antibiotics .
 PATHOGENESIS S. AUREUS
 Bacterial adhesins  factors promoting attachment to extracellular matrix proteins:
MSCRAMM, microbial surface components recognising adhesive matrix molecules) on its
surface, each specifically interacting with one host protein component, such as fibrinogen,
fibronectin, collagen, vitronectin, laminin, thrombospondin, bone sialoprotein, elastin, or
von Willebrand factor
 Factors promote evasion from host defences (protein A, some toxins, capsular
polysaccharides)
 Factors promote invasion or tissue penetration by specifically attacking host cells
(exotoxins)
or degrading components of extracellular matrix (various hydrolases)
 The ability of Staph aureus to invade mammalian cells may explain its capacity to colonise
tissues and to persist after bacteraemia
 CONT..
 Staph aureus can promote its endocytic uptake by epithelial or endothelial cells  can
survive within the cells  persistence of bone infections.

 Biofilm
A biofilm is a microbial community characterised by cells that attach to substratum or
interface or to each other, embedded in a matrix of extracellular polymeric substance,
and showing an altered phenotype in terms of growth, gene expression, and protein
production. Bacteria communicate with each other in biofilms through small hormone-
like compounds, and this cell-to cell signalling system is called quorum sensing.
Biofilms can act as a diffusion barrier to slow down the penetration of antimicrobial
agents and nutrients.
SEPTIC ARTHRITIS
 Infectious arthritis of a synovial joint
 Highest in young children (first 2 years of life)
 Male : female ratio (2:1)
 Can develop from osteomyelitis (haematogenous spread of infection or by direct
inoculation)
 Risk factors include extremes of age, diabetes mellitus, immune suppression,
joint surgery or injection, intravenous drug abuse and infection of overlying skin
ETHIOLOGY
 Variety of microorganisms including viruses, fungi, and bacteria  bacteria
are the most common cause
 S. aureus is the most common cause of septic arthritis
REACTIVE ARTHRITIS
 Reactive arthritis, or Reiter syndrome, results in urethritis, conjunctivitis,
asymmetrical polyarthritis (e.g., ankles, knees, feet, and sacroiliitis), and a rash
that occurs weeks after a bacterial infection.

 Most common cause  Chlamydia trachomatis. However, Campylobacter jejuni,

Yersinia enterocolitica, Shigella or Salmonella, and Streptococcus

 More commonly in patients with human lymphocyte antigen B27 (HLA-B27).

CLINICAL FEATURES
 Presentation is with a hot, painful, swollen joint with limited range of
movement. Fever and malaise are common.
 Any joint can be affected, the knee being most common
FREQUENCY OF JOINTS
Knee : 48%
Hip : 24%
Ankle : 7%
Elbow : 11%
Wrist : 7%
Shoulder : 15%
Sternoclavicular : 8%
PROSTHETIC JOINT
INFECTION
 Over 150,000 hip and knee arthroplasty operations were performed in the UK in
2010, and over a million in the USA.
 Prosthetic material provides an ideal environment in which organisms can
flourish. A number of bacteria have the ability to form an extracellular matrix 
biofilm, in which the organisms are protected from antibiotics.
PROSTHETIC JOINT INFECTION
CRITERIA FOR THE DIAGNOSIS
 Growth of the same microorganism in two or more cultures of synovial fluid or
periprosthetic tissue
 Purulence of synovial fluid or at the implant site
 Acute inflammation on histopathological examination of periprosthetic tissue, or
 Presence of a sinus tract communicating with the prosthesis
PROSTHETIC JOINT INFECTION
ETHIOLOGY
 Coagulase-negative staphylococci ( 30 - 43 %)
 Staphylococcus aureus (12 - 23%)
 Mixed flora (10 - 11%)
 Streptococci (9 -10%)
 Gram-negative bacilli (3 – 6%)
 Enterococci (3- 7%)
 Anaerobes (2- 4%)
PATHOGENESIS
Staphylococcus aureus is
the most common cause of
septic arthritis, followed
by other gram-positive
bacteria
PATHOGENESIS
ROLE OF BIOFILM
 Within biofilms, microorganisms are enclosed in a polymeric matrix and develop into
organized, complex communities with structural and functional heterogeneity,
resembling multicellular organisms.
 When the microbial density is high, the volume of released cell-to-cell signaling
molecules is sufficient to activate genes involved in biofilm production, a
phenomenon called quorum sensing. In the biofilm, microbes are protected from
antimicrobial agents and host immune responses.
 Biofilm microorganisms have much greater resistance to antimicrobial killing than do
planktonic bacteria. This resistance may be related to the reduced growth rate of
biofilm microorganisms, which enter a stationary phase of growth, probably because
of incomplete penetration of metabolic substrates, such as glucose or oxygen.
MICROBIOLOGY AND
HISTOPATHOLOGY
 Isolate the offending organisms appropriate antimicrobial therapy
 Blood cultures, Bone biopsy , Tissue cultures
 Gram’s staining of synovial fluid and periprosthetic tissue high specificity
(>97%) but low sensitivity (<26%)
 Cultures of a superficial wound or sinus tract  false positive because from the
surrounding skin
 Swab cultures have a low sensitivity  should be avoided
THANK YOU