3. OSTEOMYELITIS
2) Pathophysiology
• The most common mode by which organisms reach the
bone is by
1. Hematogenous spread (i.e., either bacteremia or
fungemia) from a distant site. Mycobacterial and fungal
osteomyelitis often arise from the initial site of infection
in the lung.
2. direct extension from an infected contiguous site such
as a skin or soft tissue infection. It also can occur
following trauma that results in an open fracture and
direct contamination of the bone.
3. Many sources are undetected.
4. OSTEOMYELITIS
Site of bone infection
In children, hematogenous spread tends to result in
osteomyelitis located at the end of long bones (at the
metaphyses) that are richly endowed with blood vessels.
In adults, hematogenous spread results most commonly
in vertebral osteomyelitis and discitis, not osteomyelitis of
the long bones.
5. OSTEOMYELITIS
Chronic osteomyelitis tends to occur in the lower
extremity, especially in diabetics who often have vascular
insufficiency. They are predisposed to skin and soft tissue
infections that extend into the bone
6. OSTEOMYELITIS
4) Clinical Manifestations
a) The most characteristic clinical manifestations are bone
pain and localized tenderness at the site of infection.
b) Most patients also have constitutional symptoms such as
fever, night sweats, and fatigue.
c) Limited range of motion of an affected site is seen.
7. Difference between acute and chronic
osteomyelitis
acute osteomyelitis chronic osteomyelitis
Onset of symptoms the symptoms occur
abruptly
and progress rapidly
the course is more
indolent
Relapses Less frequent More frequent
Necrosis of the bone,
and a sequestrum
formation (an avascular
piece of infected bone)
Less frequent More frequent
remove sequestra, is
important
to minimize the risk of
relapse
8. Fig1:Chronic osteomyelitis.. White
arrow points to draining fistula at site
of chronic osteomyelitis
Fig2: White arrow points to
necrotic bone caused by chronic
osteomyelitis
9. OSTEOMYELITIS
TABLE 1: Organisms Causing Osteomyelitis with Various Predisposing
Factors
. Viruses, protozoa, and helminths do not
cause osteomyelitis
Viruses, protozoa, and helminths do not cause osteomyelitis
10. OSTEOMYELITIS
Diagnosis
A) A microbiologic diagnosis of acute osteomyelitis is most
consistently made by
1) Culture of a specimen of the bone
lesion.
2) Blood cultures are positive in approximately half of cases.
B) Radiologic diagnosis in acute osteomyelitis
1) Defect in the bone accompanied by periosteal elevation
Early in the disease, X-rays and even computed tomography
(CT) scans may be negative.
Magnetic resonance imaging (MRI) scans are the most
sensitive radiologic tests for diagnosis of osteomyelitis
12. OSTEOMYELITIS
Treatment
Empiric therapy for acute osteomyelitis should include
drugs that are bactericidal, penetrate well into bone, and
include coverage for S. aureus. Vancomycin, nafcillin, or
cephalexin administered parenterally can be used.
Vancomycin is often used until the culture results and the
sensitivity of the organism are known.
13. OSTEOMYELITIS
If methicillin-resistant S. aureus (MRSA) is the cause then
either vancomycin, daptomycin, or linezolid can be used.
If gram-negative rods are the cause, then either
ceftriaxone, ceftazidime, or cefipime can be used. The
duration of therapy ranges from 3 to 6 weeks or longer.
Surgical debridement of chronic osteomyelitis lesions is
often necessary.
14. Prevention
1) There is no vaccine effective against the common
causes of osteomyelitis.
2) Chemoprophylaxis is typically not employed. Generally
speaking, prophylactic antibiotics are not recommended
prior to dental procedures to prevent prosthetic joint
infection.
3)Proper foot care in diabetics can prevent osteomyelitis.
15. INFECTIOUS (SEPTIC) ARTHRITIS
Definition
Infectious (septic) arthritis is an infection of the joints. The
terms infectious and septic are used to distinguish these
infections from immune-mediated arthritis, such as
rheumatoid arthritis.
16. Pathophysiology
1) Organisms typically reach the joint via the bloodstream
2) Less frequently, organisms enter the joints through
penetrating trauma, medical procedures such as
arthroscopy, or a contiguous osteomyelitis.
Patients with long-standing rheumatoid arthritis and
those with prosthetic hips and knees are predisposed to
infectious arthritis.
18. Organisms Causing Infectious Arthritis
Bacteria, especially S. aureus, cause the vast majority of
cases of infectious (septic) arthritis. Monoarticular
involvement of a large weight-bearing joint, such as the hip
or knee, is the most common presentation
19. Clinical Manifestations
• The acute onset of an inflamed joint, typically a large
weight bearing joint such as the hip or knee, is the typical
manifestation
• Fever is often present.
• On physical examination, the affected joint is red, warm,
and swollen, and a joint effusion is typically present,
limitation of joint movmenta joint, especially in a child,
may be a sign of infectious arthritis
21. 1) Lab diagnosis
• Culture of a specimen of the joint fluid.
• Blood cultures are positive in less than 30% of cases.
• Synovial Fluid Analysis
Analysis of synovial fluid aspirated from a swollen joint
plays an important role in the diagnosis of arthritis.
Diagnosis of infectious arthritis
22. • Table1 : Synovial Fluid Findings in Arthritis
23. Diagnosis of infectious arthritis
2)Radiologic diagnosis infectious arthritis :
• Soft tissue swelling.
• Evidence of joint destruction can be seen if the infection
progresses
24. Treatment
Untreated infectious arthritis can lead to joint
destruction and loss of mobility, so prompt antibiotic
treatment is required for optimal recovery.
1) Empiric therapy for infectious arthritis should include
drugs such as vancomycin, nafcillin, or cefazolin that are
bactericidal against S. aureus.
2) Ceftriaxone should be used if there is evidence that N.
gonorrhoeae is the cause.
3) Removal of joint fluid via arthrocentesis and/or
surgical drainage is an important adjunct to antibiotics.
25. VIRAL (IMMUNE COMPLEX)ARTHRITIS
Viral arthritis is often called immune complex arthritis
because the virus does not infect the joint but rather, the
virus forms immune complexes with antiviral antibody
that is deposited in joints and elicits an inflammatory
response.
26. The clinical features of viral arthritis
1) Arthralgia (painful joints but without visible inflammation)
2) Or frank arthritis in which inflammation is apparent.
3) Most cases of viral arthritis are of short duration and
resolve spontaneously, but chronic arthritis may occur.
4) The small joints of the hands are most often affected, but
large joints can also be involved.
VIRAL (IMMUNE COMPLEX)ARTHRITIS
27. Causative agents of viral arthritis
viral arthritis occurs during the course of infection by
several viruses.
Rubella virus, Parvovirus B19(is an important cause in that
the lesions resemble those of rheumatoid arthritis),
hepatitis C virus also resemble rheumatoid arthritis,
hepatitis B virus and dengue virus.
There is no antiviral treatment for viral arthritis
VIRAL (IMMUNE COMPLEX)ARTHRITIS
28. REACTIVE ARTHRITIS
Reactive arthritis: is the term used to describe arthritis that
occurs following infection by several bacteria that infect the
gastrointestinal or genitourinary tract.
The bacteria do not infect the joints. Rather, the arthritis is a
result of the immune response to the bacterial infection.
People who are HLA-B27 positive are predisposed to reactive
arthritis.
The bacteria commonly associated with this arthritis are
Campylobacter, Shigella, Salmonella, Yersinia, and
Chlamydia
29. Clinical manifestation of reactive arthritis
The main clinical manifestation is an asymmetric arthritis
of the knee or ankle accompanied by fever.
It typically resolves within a few days or weeks, but
chronic arthritis may occur.
Recurrences are common.
Culture of synovial fluid is negative.
Reactive arthritis accompanied by conjunctivitis and
urethritis is called Reiter’s syndrome.
30. Treatment of reactive arthritis
• Nonsteroidal anti-inflammatory drugs are
considered first-line therapy. Antibiotics have no
effect on reactive arthritis.
31. RHEUMATIC FEVER
• Rheumatic fever is an immune-mediated, poststreptococcal
• disease that affects the joints, heart, brain, and skin.
• It follows pharyngitis caused by Streptococcus pyogenes
• (group A Streptococcus). It typically occurs in children ages
5 to 15 years.
32. Clinical picture
• Rheumatic fever typically begins with a migratory
polyarthritis
• involving the large joints approximately 2 to 3 weeks
• after the pharyngitis.
• Carditis often occurs and is the main, life-threatening
component of rheumatic fever.
33. the diagnosis. Two major manifestations or one major
plus two minor manifestations suggest the
diagnosis(the Jones criteria)
The diagnosis. Two major manifestations or one major plus two minor
manifestations suggest the diagnosis. In addition, laboratory evidence of prior
infection by S. pyogenes is needed. This consists of either (1) a positive throat
culture or positive rapid streptococcal antigen test or (2) a rising anti–streptolysin O
antibody titer
34. Treatment
• The drug of choice is aspirin to reduce the inflammation.
• Antibiotics such as penicillin G have no effect on the
• course of the disease but can be given to reduce carriage
of streptococci in the pharynx.