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. Diagnosis of infectious arthritis
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.
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. VIRAL (IMMUNE COMPLEX) ARTHRITIS
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.
27. VIRAL (IMMUNE COMPLEX) ARTHRITIS
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
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.