Musculoskeletal Infections

BONE & JOINT INFECTIONS

 Objective of the lecture
At the end of the lecture, students must be able to:
•Describe the causative agents of osteomyelitis & septic
arthritis
•Identify the mechanisms of transmission of pathogens in
osteomyelitis & septic arthritis
•Discuss the types of osteomyelitis & septic arthritis
•Describe the pathogenesis of osteomyelitis & septic arthritis
•Describe the key risk factors for osteomyelitis & septic arthritis
•Describe the signs & symptoms of osteomyelitis & septic
arthritis
•Describe diagnosis & management of osteomyelitis & septic
arthritis
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 BONE & JOINT INFECTIONS
 Bone & joint infections are serious (life-threatening)-
lead to long-term disability & reduced quality of life.
 The word “osteomyelitis” originates from the Greek
words osteon (bone) and muelinos (marrow)
 Inflammation process of the entire bone including the
cortex and the periosteum, recognizing that the
pathological process is rarely confined to the
endosteum.
 Infections may exist separately or together.
 Both are common in infancy & childhood.
 Infections can cause growth impairments in children -
when epiphysis is involved.
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Types of bone & joint infections: 4 main diseases
1. Osteomyelitis
2. Septic Arthritis
3. Prosthetic joint infections
4. Reactive arthritis – Immunological following
infections

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 OSTEOMYELITIS
• Osteomyelitis: inflammation of the bone, bone-marrow
& surrounding soft tissue.
• It is a progressive infection that results in inflammatory
destruction followed by new bone formation.
• Bacteria & fungi can cause osteomyelitis. This painful
bone infection causes swelling that can damage bone
and lead to bone loss.
• Nelaton credited with introducing the term osteomyelitis
in 1844.
• Steomyelitis is most common in children of 3-12
years.
• Boys > girls (M: F = 3:1)
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 Osteomyelitis
• In children most often the consequence of bacteremia.
• Osteomyelitis may also be caused by numerous
endemic & opportunistic fungal agents, including
• Cocidiodes immitis (Coccidioidomycosis),
Cryptococcus, Candida, Blastomyces, Aspergillus spp.
• It may be characterized by cough, chest pain, night
sweats & anorexia, and it often is associated
with erythema nodosum or erythema multiforme.

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 PREDISPOSING FACTORS
• Fractures due to trauma & road traffic accidents
• Gun shot wounds
• Radiation damage
• Osteoporosis
• Systemic disease : Malnutrition, Acute Leukemia,
Uncontrolled diabetes, sickle cell anemia, Chronic
alcoholism
• Certain bones in the skeletal system, such as the hip &
thighbones, contain soft, spongy tissue called bone
marrow, makes stem cells that produce blood cells &
platelets.

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 Osteomyelitis
• Osteomyelitis affects about 2-5 out of every 10,000
people.
• Osteomyelitis remains extremely difficult to treat.
• The relapse rate can be as high as 20%.
Classification of osteomyelitis
• Classification based on clinical picture, pathology,
etiology & radiology: According to duration 2o major
groups:
• Acute osteomyelitis
• Chronic osteomyelitis.

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• Acute suppurative osteomyelitis
• Chronic suppurative osteomyelitis
• Chronic focal sclerosing osteomyelitis (pseudo-paget,
condensing osteomyelitis)
• Chronic diffuse sclerosing osteomyelitis
• Chronic osteomyelitis with proliferative periostitis (Garre's
chronic nonsuppurative sclerosing osteitis, ossifying
periostitis)
Specific osteomyelitis:
1. Tuberculosis osteomyelitis
2. Syphilitic osteomyelitis
3. Actinomycotic osteomyelitis
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 Osteomyelitis
 According to the type of Host response to the
infection osteomyelitis can be:
• Pyogenic: Acute & chronic osteomyelitis
• Non-Pyogenic - Granulomatous: TB, Syphilis,
Fungal, etc
 The Mechanism of infection can be:
– Exogenous
– Hematogenous

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 Osteomyelitis
1. Acute osteomyelitis
•Infection comes on suddenly. Fever, bone pain.
•Pyogenic infection of <2 weeks in duration - Symptoms
present within 2 weeks after infection
• Children have acute osteomyelitis form more often
(60-70%) than adults do, at a rate of about 1:5000.
Acute hematogenous osteomyelitis (AHO)
•Most common type of bone infection, usually seen in
children
•Bimodal distribution - younger than 2 yrs & 8-12 yrs
•More common in males
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 Osteomyelitis
Etiology of hematogeneous osteomyelitis
Acute hematogenous osteomyelitis (AHO)
1. Children:
– S. aureus (60-90%)
– Group B Streptococci (Streptococcus agalactiae)
– H. influenzae: children 6 months to 4 years old
– E. coli (in neonates)
– S. pneumoniae
– Kingella kingae are also common
– Salmonella (Children with sickle cell disease)

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 Osteomyelitis
2. Adults:
– S. aureus (55%)
– E. coli
– Klebsiella
– Pseudomonas – in patients with GUT infections or
with IV drug abusers
– Streptococci
– A. israeli (mandible)

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 Osteomyelitis
Sites of bone infection
1. Children:
• Infection generally involves the metaphyses of rapidly
growing long bones because of the relative lack of
phagocytosis activity & highly vascularized region
–Commonest are tibia & femur
–Hematogenous spread - major mechanism
2. Adults:
1. Vertebrae - it gets the richest blood supply.
2. Long bones (rarely).

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Anatomy of the bone
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 Osteomyelitis
Pathophysiology of Acute Hematogenous
osteomyelitis
•Infection initially established in the metaphyseal region
of tubular bones, as a metaphysitis → abscess
formation.
•As the abscess enlarges → compromise normal blood
flow causing cortical ischaemic necrosis, which may allow
purulent material to escape through the cortex into the
subperoisteal space.
•A subperisoteal abscess then develops
•If left untreated this process eventually results in
extensive sequetra formation and chronic osteomyelitis
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 Osteomyelitis
• Bacteremia leads to sepsis & metastatic infections –
in the heart & lungs – which may be fatal.
• Acute osteomyelitis has usually a good response to
antimicrobials and, if necessary, to surgery.
• On the opposite, chronic osteomyelitis represents a
great therapeutic challenge, becoming surgery essential
to obtain the best results

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Acute osteomyelitis - Primary site of infection usually in
the metaphysial region.
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 Osteomyelitis
2. Subacute Osteomyelitis
• More insidious onset and lacks severity of symptoms
• Duration: 2-6 weeks
• Characterized by the presence of Brodie’s abscess
(small intraosseous abscess that involves the cortex and
is walled off by reactive bone, + dead bone) at the
metaphysis
• Brodie’s abscess occurs most commonly in the long
bones of the lower extremeties

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 Osteomyelitis
Most common site:
•Tibia, distal femur, ulna
•Spine
•Ends of long bones
•Carpals & tarsals.
Its relative mildness is due to:
a.Organism being less virulent OR
b.Patient more resistant OR
c.Both

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 Osteomyelitis
Causative organisms
•S. aureus (30-60%) & S. epidermidis are predominant
organisms identified in subacute osteomyelitis
•Streptococcus
•H. influenzae
•P. aeruginosa (IV drug user)
•Salmonella (in sickle cell anemia)
•K. kingae.

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 Osteomyelitis
3. Chronic osteomyelitis
•Duration: >6 weeks; in children is uncommon. It doesn’t
go away with treatments. It causes bone pain and recurring
drainage (pus)
Types of chronic Osteomyelitis
a.Complication of acute osteomyelitis
b.Post-traumatic (Secondary to open fractures)
c.Post operative
Chronic suppurative osteomyelitis
•Common in mandible, associated with odontogenic
infections.
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 Osteomyelitis
• Polymicrobial infection, predominating anaerobes
such as Bacteriods, Porphyromonas or Provetella.
Etiology
• Primary resulting from low virulent microorganisms.
• Secondary sequelae of acute suppurative osteomyelitis
• S. aureus (commonest cause).
•S. epidermidis (commonest in surgical implants)
• S. pyogenes
• E. coli
• P. aeruginosa – forms biofilm

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 Osteomyelitis
• Salmonella spp, S. aureus cause osteomyelitis in
patients with sickle cell disease -
• S. marcescens & E. coli - isolated from contiguous
infection in another part of the body, E.g: Sinus, Ear,
Dental, Respiratory & Genitourinary infections.

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 Osteomyelitis
Non-pyogenic (granulomatous) causes of
osteomyelitis
1.Tuberculous osteomyelitis
2.Congenital/acquired syphilis (skeletal syphilis)
3.Actinomycotic (Myecetomal) osteomyelitis
4.Fungal osteomyelitis: Histoplasma, blastomycosis,
coccidioidomycosis
5.Parasitic infestation - e.g. hydatid (parasite).

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• Hematogeneous osteomyelitis of children begins in the
metaphysis of long bones: The blood-borne bacteria carried to
the marrow space by way of the nutrient artery
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 Osteomyelitis
Spread in chronic osteomyelitis
1. Hematogenous seeding:
• Usually monomicrobial, occurs in children <12 years of
age although adults can have this disease
2. Contiguous or exogenous
• From adjacent soft tissues & joints: E.g. wounds,
abscess …. Usually polymicrobial.
• Organisms: S. aureus (70%- 80%), Pseudomonas
3. Direct Inoculation Osteomyelitis
• As a result of trauma, surgery; Usually polymicrobial
• S. aureus: the most common causative organism.
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Spread
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Development of Osteomyelitis
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 Osteomyelitis

Sequestrum Involucrum

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 Osteomyelitis
Pathogenesis
•Osteomyelitis involves growing bone, particularly the
metaphyses of long bone in children → resulting in
frequent infection of the metaphysis, epiphysis.
•Femur & tibia equally& together almost half of all cases
•Adults: epiphyses & subchondral regions.
•Obstruction of flow by bacterial microemboli produces
areas of avascular necrosis & metaphyseal abscess
•The hallmark of chronic osteomyelitis is the presence of
sequestrum (dead bone).
•It also includes involucrum, local bone loss, sinus
tracts.
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 Osteomyelitis
Factors responsible for chronicity
• Local factors: Cavity, sequestrum, sinus, foreign body
• General: Diabetes Mellitus, Vascular disease, Low
immunity
• Organism: Virulence
• Treatment: inadequately treated acute osteomyelitis
• Risk factors: Trauma, prosthesis, animal bite
• Patient factors: Malnutrition, smoking.

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 Osteomyelitis
Clinical manifestation of osteomyelitis
•The signs and symptoms of bone infection are non-
specific very often. Insidious onset in subacute & chronic
cases.
•The symptoms for acute and chronic osteomyelitis are
very similar and include:
– Fever, irritability, fatigue, Nausea.
– Tenderness, redness, warmth, Swelling (edema)
around the affected bone.
– Lost range of motion.
•Difficult to diagnose, but once diagnosed, it is a curable
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 Osteomyelitis
• Treatment of osteomyelitis involves surgery &
antibiotic therapy.
• Surgery plays a key role especially in chronic
osteomyelitis.
• An aggressive debridement of all necrotic tissues (bone
and soft tissue) is essential.
• After debridement, it could be necessary to stabilize the
bone and to provide a suitable soft tissue coverage.

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 Osteomyelitis
• Reconstruction techniques provide elements to repair
the bone, adding a vascularized coverage that increases
antibiotic concentration into the bone and helps its
healing. Extended antibiotic therapy without surgery can
be curative in haematogenous and vertebral
osteomyelitis, especially in children. In the remaining
cases, it is a necessary complement to surgery.
• Usually a combination of antibiotics is necessary to avoid
bacterial resistances after extended antimicrobial
therapy

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 TB Osteomyelitis
Skeletal TB
• Dissemination of TB outside the lungs - skeletal TB.
• TB osteomyelitis is secondary to hematogenous
spread from a primary source in the lung or GI tract.
• The spinal column is involved in less than 1% of all
cases of TB
• Most common in children & young adults
• It commonly occurs in the vertebrae & long bones.
• It involves mainly vertebrae / thoracic & lumbar/(Pott’s
disease, also known as tuberculous spondylitis)
followed by long bones - knee & hip.
• Pott’s disease starts with tuberculosis (lung infection).
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 TB osteomyelitis
• There is extensive necrosis & bony destruction with
compressed fractures (with kyphosis) and extension
to soft tissues, including psoas "cold" abscess (lack
signs of inflammation).
• Psoas muscle abscess may be caused by lumbar TB
• In Pott’s disease, the infection may breaks through the
intervertebral discs and extends into the muscle
forming - Psoas abscess / inguinal mass.
• The onset of TB osteomyelitis is usually insidious.
• Potential constitutional symptoms of Pott’s disease
include fever & weight loss.

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 TB osteomyelitis
• Back pain is the earliest and most common symptom.
• The pain caused can be spinal or radicular.
• It can be associated with neurologic deficit due to
compression of adjacent neural structures and
significant spinal deformity
• Neurologic abnormalities occur in 50% of cases and
can include spinal cord compression with paraplegia,
paresis, impaired sensation, nerve root pain, and cauda
equina syndrome.
• Sequestration & formation of involucrum are uncommon
• Destruction & collapse of the vertebral bodies & discs -
– Kyphosis; Kyphoscoliosis
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 TB osteomyelitis

TB osteomyelitis - Pott’s disease

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 Syphilitic osteomyelitis
1. Congenital syphilis
• Caused by Treponema pallidum, STD.
• Transplacental spread of TP from mother to fetus
• Hematogenous spread of T. pallidum - Long bones,
such as the tibia, are mainly affected, cause 2 chief
bone lesions: Periosteitis & Osteochonditis
2. Acquired syphilis
• Bone lesions are manifestations of tertiary syphilis.
• Gummatous lesions appear as discrete punched-out
radiolucent lesions in medulla or destructive lesions
within the cortex.
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 Syphilitic osteomyelitis
• The surrounding bone is sclerotic & with no discharge
• Bones frequently affected: nose, palate, skull,
extremities, esp. the long tubular bones such as tibia.
• Histology: edematous granulation tissue containing
numerous plasma cells and necrotic bone.

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 Fungal Osteomyelitis
• Bone fungal infection is rare but potentially life
threatening condition
• Usually reported in immunocompromised hosts
• E.g. Maduromycoses

Treatment
• No effective chemotherapy –
– Amphoterecin B - IV used, but toxic
– Wide excision – amputation

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 Actinomycotic osteomyelitis
Actinomyces israelii
•Filamentous, gram-positive, non–acid-fast, anaerobic-to-
microaerophilic bacteria.
•Actinomycosis is subacute-to-chronic granulomatous
disease.
•Two-thirds of all cases occur in the cervicofacial region
•Bacteria found as normal flora of the oral cavity
•Remain localized in the soft tissues or invade the jaw
bones.
•The more aggressive lesion resembles chronic
suppurative osteomyelitis
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 Osteomyelitis
Complications of osteomyelitis especially chronic are:
1.Septic arthritis
2.Destruction of the adjacent soft tissues
3.Skeletal (bone) deformities - Limb shortening
4.Squamous cell metaplasia of the sinus tracts
5.Secondary amyloidosis - deposited in the kidney, liver
6.Pathological fractures
7.Septicemias
•Bone death (osteonecrosis): impede blood circulation
•Endocarditis
•Impaired growth
•Systemic effects such as chronic fever & fatigue
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 Osteomyelitis
Diagnostic approaches
• Physical exam: bone tenderness, swelling, redness
• Microbial etiology confirmed in 75% of osteomyelitis
Tests may include:
– Blood culture: positive in about 50% of cases
– Bone biopsy - Needle aspiration of the area around
affected bones for culture, staining or histologic exam
– Bone X-ray: in later stage – demineralization seen
– MRI or CT scanning
– CBC for Leukocytosis
– Elevated C-reactive protein, Elevated ESR
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 Osteomyelitis
Diagnosis requires 2 of the 4 following criteria:
1.Purulent material on aspiration of affected bone
2.Positive findings of bone tissue or blood culture
3.Localized classic physical findings of bony tenderness,
with overlying soft-tissue erythema or edema
4.Positive radiological imaging study
Primary treatment for osteomyelitis
•3D: Debridement, Drainage, Drugs
1.Surgical:
– Drainage of pus
– Debridement of necrotic tissues
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 Osteomyelitis
2. Bactericidal antibiotics (IV) that penetrate bone & joint
cavities for several weeks-months
– Acute osteomyelitis: for 4-6 weeks (Parenteral)
– S. aureus: Nafcillin, Ceftriaxone, Ciprofloxacin,
Cefazolin, Ceftazidime, Clindamycin, Vancomycin,
Linezolid - IV
– Fungal infection: antifungal drugs for several months

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JOINT INFECTIONS

SEPTIC ARTHRITIS

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 Septic Arthritis (SA)
Septic arthritis (Infectious arthritis):
•Inflammation of joint space due to bacteria, virus, fungi or
parasitic infections.
•It is inflammation of a synovial membrane with purulent
effusion into the joint capsule.
•Septic arthritis is a painful infection in a joint that can come
from germs that travel through bloodstream from another part
of your body.
•Septic arthritis can also occur when a penetrating injury, such
as animal bite or trauma, delivers germs directly into the joint.
•Infants & older adults are most likely to develop septic arthritis.

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 Septic Arthritis
• People who have artificial joints are also at risk of septic
arthritis.
• Knees are most commonly affected, but septic arthritis
also can affect hips, shoulders and other joints. The
infection can quickly and severely damage the cartilage
and bone within the joint, so prompt treatment is crucial.
• Treatment involves draining the joint with a needle or
during surgery. Antibiotics also are usually needed.
• Septic arthritis is most common in the young
• 30% in children <2 yrs 30% in children <2 yrs; 50% of
cases in children <5 yrs.

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 Septic Arthritis
• Joints of the lower extremity constitute 75% of all cases
• Septic Arthritis of the hip is a true orthopedic
emergency;
• Delay in diagnosis or treatment may result in
irreversible damage to the joint.

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 Septic arthritis
Etiology of septic arthritis
• Bacteria are the most significant pathogens in septic
arthritis because of their rapidly destructive nature.
S. aureus – the most common: 60-80% of cases.
Streptococcus – 2nd common - (GAS, S. viridans, S.
pneumoniae, GBS): 20%
N. gonorrhoeae: 75% among young sexually active
individuals, 3x in women than men.
Gram negative rods: E. coli in elderly, in IV drug users;
Pseudomonas

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 Septic arthritis
 Other bacterial causes: N. meningitidis, B.
burgdorferi, M tuberculosis, S. epidermidis →
Prosthetic joints; Salmonella spp in individuals with
SLE
 Brucella, mycoplasma/ureaplasma
 Fungal agents: histoplasma, sporothrix schnkii,
cocidioides imitis, blastomyces
 Viruses: HBV, Rubella.

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 Septic arthritis
Septic arthritis can be:
1.Monoarticular - Acute septic arthritis often involves a
single joint. Mortality: 4%.
2. Polyarticular
•Involving multiple joints (average 4).
•More likely to be over 60 years
•Mortality: 32% - poor prognosis
Infection sites of septic arthritis
•Infants & young children <3yrs: hip joint - 95%
•Older children: Knee joint is more common
•Adults: Knee – 40-50%, Hip – 20-25%, Elbow - 17%.
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 Septic arthritis

Septic arthritis: Knee, hip

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 Septic arthritis
Pathogenesis & transmission
• Septic arthritis develops when bacteria or other mos
gain entrance to a joint via 3 routes:
1.Hematogenous spread – common in IV drug injection
2.Direct inoculation – Injury, intra-articular injection,
arthroscopy or orthopedic surgery especially insertion of
joint prosthesis.
3.Contiguous spread from adjacent focal infections -
(e.g. penetrating trauma). More common in children.
1. Extension of osteomyelitis through epiphysis or by
lateral extension through periosteum into joint capsules.

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 Septic arthritis
• Soft tissue infections: cellulitis, abscess, bursitis,
tenosynovitis
• S. aureus has a variety of receptors, termed microbial
surface components recognizing adhesive matrix molecules
(MSCRAMMs), for host proteins that mediate adherence to
the joint extracellular matrix or implanted medical devices.
• Some of the host matrix proteins include fibronectin and
laminin (adherence proteins), elastin (imparts elastic
properties), collagen (structural support), and hyaluronic
acid (a glycosaminoglycan that is rich in the joints and
the matrix and provides cushioning through hydration of
its polysaccharides).
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 Septic Arthritis
• Complication of septicemia in pre-existing joint
disease - e.g. Rheumatoid arthritis.
• Joints of the lower extremity - most common sites -
knee & hip constitute three fourth of all cases.
• Usually affect people with underlying medical problems

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1. Hematogenous
2. Contiguous spread from
osteomyelitis
3. Contiguous spread from a
soft tissue abscess
4. Iatrogenic
5. Traumatic

Routes of joint infection

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 Risk factors for septic arthritis
1. Age >80 years
2. Chronic illness (Cancer, Rheumatoid Arthritis, SLE,
Diabetes Mellitus, HIV infection)
3. Prosthetic joint - Hip or knee prosthesis
4. Previous arthritis
5. Recent joint surgery
6. Endocarditis or Bacteremia
7. Skin infection
8. IV drug abuse
9. Alcoholism
10. Trauma
11. Sickle cell anemia
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 Acute Septic arthritis
1. Acute bacterial septic arthritis
• Synovial membrane is highly vascularized
• Acute monoarthritis is septic until proven otherwise.
• Cartilage in joints become damaged within hrs or days.
• It can affect healthy people and people at high risk.
It may develop as a result of:
• Hematogenous seeding
• Direct introduction
• Extension from contiguous focus of infection

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 Acute Septic arthritis
Causative agents
• S. aureus (50%) - Any age
• Streptococcus spp: Streptococcus viridans, S.
pneumoniae & Group B streptocci
• GNB (10%) - E. coli & pseudomonas common
• Neonates: S. aureus, GBS, GNB (E. coli, Proteus,
Klebsiella, Pseudomonas)
• 1 month- 4 yrs: H. influenzae (children <2 yrs), S.
aureus, S. pyogenes, S. pneumoniae, N. meningitidis
• 4-16 years: S. aureus
• 16-40 years:- N. gonorrhoea, S. aureus
• >40 years:- S. aureus
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 Acute Septic arthritis

Acute monoarthritis (85%) - knee

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 Acute Septic arthritis
60

50

40

30

20

10

0
Knee Hip Ankle Shoulder Wrist Elbow Other Polyart

Joints involved in SA
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 Acute Septic arthritis
• Gonococcal arthritis occurs in approximately 42-85% of
patients with disseminated gonococcal infection (DGI)
and begins with a localized mucosal infection. DGI-
producing strains are unusually sensitive to in vitro killing
by penicillin G and possess unique nutritional
requirements for arginine, hypoxanthine, and uracil.
• N. gonorrhoeae possesses a number of virulence
factors. It is the combined effects of these factors, their
phase and antigenic variation, and properties of the host
immune response that enable this pathogen to persist
and allow the localized infection to become DGI.

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 Acute Septic arthritis
Clinical Features
– Sudden onset, fever, tenderness, swelling, redness over
joint, severe pain leading to restriction of movement
– Generally single joint involvement – particularly knee
Symptoms in newborns or infants:
– Symptoms may be non-specific but local swelling,
irritability & pseudoparalysis may be the clues.
– Irritability, Cries when infected joint is moved
– Fever
– Inability to move limb with the infected joint.

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 Acute Septic arthritis
Symptoms in children & adults:
•Inability to move the limb with the infected joint
(pseudoparalysis)
•Intense joint pain
•Joint swelling
•Joint redness
•Low fever
•Chills may occur, but are uncommon
•Mortality: 7-15% despite antibiotic use

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 Chronic Septic arthritis
2. Chronic septic arthritis
 Less common: about 5% of infectious arthritis;
 Often due to fungal, mycobacterial & viral affect only
one joint or, occasionally, several joints.
 Most often affects people who are at high risk.
 Most commonly infected joints include the knee, wrist,
hip, shoulder, elbow and joints in the fingers.
Polyarticular Septic Arthritis
• More likely to be over 60 years
• Average of 4 joints - Knee, elbow, shoulder, hip
predominate
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 Chronic Septic arthritis
Etiology
• M. tuberculosis (TB)
• B. burgdorferi - Lyme disease
• T. pallidum - Syphilis
• Mycoplasmas: M. pneumoniae, M. hominis
• Fungi: C. albicans in AIDS cases; other
• Viruses: HBV, Rubella, Mumps, Varicella, Adenovirus,
Coxachie, Parvoviruses, EBV

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 Clinical presentation of
chronic septic arthritis
Signs & Symptoms:
•Low grade fever
•Pain & swelling in a single large joint
•Warmth, erythema, tenderness, loss of function

Complications of septic arthritis

•Ankylosis
•Fatal septicemia

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 Diagnosis of acute & chronic
septic arthritis
Diagnosis
•Analysis of synovial fluid for cell count, protein, glucose,
exam of crystals under microscope
This fluid will show:
– Presence of microorganisms
– Presence of Ab directed against the mos
– Turbidity
– More than 10,000 pmns/mm3
– Decreased glucose conc. (<0.6% of blood glucose)
– Increased lactic acid concentration (> 65 mg/dl)

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 Septic arthritis
• Gram stain & culture, chemical analysis.
– Blood culture (positive in 30-60%): at least 2 sets of
blood cultures to R/o a bacteremic origin of the septic
joint
– Microbial etiology confirmed in ⅔ of cases of septic
joint
– Histologic exam of tissues in granulomatous forms.
– In chronic arthritis synovial biopsy may distinguish b/n
an septic and a non-infection process.
– Serology for Lyme disease, Brucellosis

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 Septic arthritis
Other tests
– PCR: Molecular methods to detect bacterial DNA in
synovial fluid, e.g. B. burgdorferi, M. hominis, N.
gonorroheae.
– X-ray of affected joint
Treatment
•Needle aspiration/arthrocentesis of purulent exudate
•Antibiotic therapy - Prompt.
•MRSA, P. aeruginosa are MDR
•Surgical Intervention in Prosthetic Joint Infection
•Joint immobilization & Physical therapy
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 Some important Septic Arthritis
Gonococcal arthritis (N. gonorrhea)
• Neisseria gonorrhoeae is the most common cause of
septic arthritis in young sexually active adults.
• Occurs in 1-3% on patients infected with N. gonorrhea.
• Women > men.
• Complement deficiency (C5-C9); Patients with SLE.
• Arthritis: due to disseminated gonococcal infection-DGI
• A single joint - hip, knee, ankle, wrist is usually involved
Signs & Symptoms
• Tenosynovitis – (involve fingers, hand, wrist); dermatitis
• Joint pain/swelling: (knee, wrist, ankle)
• Fever, chills
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 Gonococcal arthritis
Diagnosis
•Synovial fluid contains >50,000 leucocytes/micro L
•Cervical gram stain
•Cultures of synovial fluid are positive <40%
•Blood cultures negative

Treatment Gonococcal arthritis

•Patients with gonococcal arthritis usually require initial
hospitalization for IV antibiotic therapy, later oral Rx.
•Ceftriaxone: 1gm IV or IM q24 hours
•Spectinomycin: 2gm IV or IM q12 hours
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 Mycobacterial Arthritis
• TB arthritis accounts for 1-2% of all cases of TB and
for about 10% of extrapulmonary TB.
• M. tuberculosis → chronic granulomatous monoarthritis
• Hematogenous spread after primary infection
• A long latent period without sign & symptoms

Sites:
• Large weight-bearing joints (knees, hips, ankles).
• Monoarticular involvement- 85%, knee- most common
• A draining sinus can be observed

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 Mycobacterial Arthritis
Diagnosis:
•AFB staining may be positive
•Synovial biopsy: culture of synovial tissue taken at
biopsy is more reliable.
•NAA assays can shorten the time to diagnose

Treatment
•Rest
•Anti-TB: INH, rifampicin, pyrazinamide ethambutol – 2
months (thrice weekly), and then 4 months course of INH,
ethambutol rifampicin (thrice weekly).
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 FUNGAL ARTHRITIS
• Those with chronic disease (e.g. Diabetes mellitus) or
immunocompromised individuals (e.g. HIV)
• Candida, Cryptococcus, Aspergillus spp, blastomyces,
histoplasma , coccidioides, Maduromycoses common.
• Causes granulomatous reaction leading to abscess
formation, tissue destruction and ulcer formation
Transmission
1.Haematogenous spread – in 70% of cases - e.g.
Candida, Cryptococcus
2.Penetrating trauma with foreign substance - e.g.
Sporothrix, Aspergillus
3.Contiguous spread
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 FUNGAL ARTHRITIS
Treatment
– Antifungal treatment and surgery
– Amphotericin B

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 VIRAL ARTHRITIS
• Often acute; common in younger patients
• Polyarthritis similar to acute rheumatoid arthritis (RA)
• Examples: Parvovirus B-19, Rubella, Hepatitis A, B, C;
HIV infection, EBV, mumps, Alphaviruses, Flaviviruses
In children
• Parvovirus-B19 common
• Fever, headache, rash, fatigue, Polyarthralgia
• Symmetrical joint pain
In adults
• Rubella can cause viral arthritis
• It involves small joints
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 VIRAL ARTHRITIS
Clinical manifestations
•Febrile illness due to infecting synovium or host immune -
mediated response
•Rash, malaise, headache

Diagnosis:
•Clinical: Usually begins suddenly
•Serological & PCR
•The definitive diagnosis of septic arthritis requires
examination of the synovial fluid.

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 Management of Septic arthritis
• It resolves spontaneously within 2 weeks
• No erosion on joints
1.Parenteral antimicrobial therapy for 3-6 weeks.
• Infection with MRSA or MSSA - at least 4 weeks IV
• Oxacillin or methicillin: the choice for S. aureus
• Vancomycin for MRSA
• Gram-negative - joint infections can be treated with oral
ciprofloxacin for the final 1-2 weeks of treatment.
• Linezolid with or without rifampin - for staphylococcal
prosthetic joint infection

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 Septic arthritis
2. Surgical intervention: Severe cases need surgery
–Drainage of pus: Arthrocentesis - If synovial fluid builds
up quickly due to the infection, a needle may be inserted
into the joint often to aspirate the fluid.
3. Joint Immobilization & Physical Therapy: Resting,
keeping the joint still, raising the joint, using cool
compresses may help relieve pain.
4. Exercising the affected joint helps the recovery process.

Prognosis:
•Good; Self-limited infection
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 Prosthetic Joint Infections
• Prosthetic joint infection (PJI): infection involving the
joint prosthesis & adjacent tissue.
• Between 1-5% of all prosthetic joints become infected
and is one of the leading causes of arthroplasty failure.
• 98% are hips & knees, the remaining mostly shoulder.
• PJI can be acute (<4 weeks) or chronic
Etiology of Infection
1.Early onset (<3 months):
– Organisms gain entry at the time of operation
– Organisms: S. aureus, Coliforms, mixed infections

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 Prosthetic Joint Infections
2. Delayed (3–24 months):
– Coagulase negative Staphylococci,
Propionibacterium spp

3. Late onset (>24 months):

•Spread from a distant source of infection
•S. aureus, E. coli, Coliforms
•50% have no apparent source

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 Prosthetic Joint Infections
Summary of etiologic agents
1. Gram positive: 65%
• Gram positive – CONS > S. aureus > Streptococcus >
Enterococci
a. Coagulase negative staphylococci (CoNS): 22%
b. S. aurues: 20%
c. Streptococci: 14%
d. Enterococci: 7%
2. Gr-ve cocci: 25%
• Enteric > pseudomonas
3. Anaerobes: least common - 10%
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 Prosthetic Joint Infections
Pathogenesis
• Locally introduced (60-80%)
– Operative contamination
– Wound sepsis contiguous to the prosthesis
• Haematogenous (20-40%)
– Any bacteremic episode may seed a prosthetic joint
– S. aureus bacteremia leads to 34% incidence of PJI
• Biofilms: populations of mos adhering to environmental
surfaces & bioprosthetic materials.
• These mos are usually encased in an extracellular
polysaccharide that they themselves synthesize.
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 Prosthetic Joint Infections
Risk factors Artificial joint implants
•Bacterial infection somewhere else in the body
•Chronic disease (Diabetes Mellitus, Rheumatoid Arthritis,
sickle cell disease)
•IV drug use
• Immunocompromised states
•Recent joint injury
•Recent joint arthroscopy or surgery
•Poor nutritional status
•Obesity
•Advanced age
•Smoking
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 Prosthetic Joint Infections
In Children
•Occurs most often in those younger than 3 years.
•The hip is often the site of infection in infants.
•Organisms: Group B Streptococci or H. influenzae (if
not vaccinated).
Presenting symptoms
•Joint pain: 95%
•Fever: 43%
•Periarticular swelling: 38%
•Wound / sinus drainage: 32%

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 Prosthetic Joint Infections
Diagnosis:
•Radiography: changes - Loosening of prosthesis
•Arthrocentesis: Synovial fluid leukocyte count
>1700/mm3
•Histopathology: Peri-prosthetic tissue
Management
•Goal of treating infection: pain-free, functional joint
1. Surgical
•Debridement with retention of prosthesis
•Implant removal

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 Prosthetic Joint Infections
2. Antibiotic therapy
• Antibiotics should have bactericidal activity against
surface-adhering, slow-growing & biofilm-producing mos
– Rifampin: effective within a biofilm.
– Trimethoprim–sulfamethoxazole, minocycline,
linezolid - can be combined with rifampin
– Quinolones: excellent combination agents
– Ciprofloxacin & ofloxacin
– Levofloxacin for Gram +ve bacteria

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 Reactive Arthritis (ReA)
or (Reiter syndrome)
Complication of untreated chlamydial infection
– Reactive arthritis includes the triad urethritis,
conjunctivitis & arthritis (aseptic inflammatory joint
involvement) - affecting one or more joints.
– Usually develops 2-4 weeks after a genitourinary (GU)
or gastrointestinal (GI) infection (or possibly a
chlamydial respiratory infection
– The male-to-female ratio is 5:1.
– Caused due to immunological mechanism.
– REA is a sterile inflammatory process that may result
from an extra-articular infectious process.

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 Reactive Arthritis
Forms of reactive arthritis
1. Post-sexual reactive arthritis
 Post non-gonoccal urethritis - by C. trachomatis
 Affects both men & women but more seen in men.
 Predisposing factors: HLA B 27 (50% patients)

2. Post-dysenteric reactive arthritis

•Arthritis presents after GI infection with G -ve bacilli as
Shigella, Salmonella, Campylobacter, Yersinia, etc.

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Thank You

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