Septic arthritis characterized by

• Inflammation of a synovial membrane

with purulent effusion into joint capsule
due to bacterial infection

• Usually monoarticular joint.

Adults: commonly affected knee
Children: commonly affects the hip

• Divided into gonococcal arthritis and

non-gonococcal arthritis
Infectious agents involved:
1. In all age group except neonatal period
Staphylococcus aureus predominates.

2. Streptococcus: group A and B are the next

common bacteria. Group B streptococci have
emerged as important pathogens in the
elderly, diabetics and with neurologic diseases

3. IV drug abusers: Staph aureus and gram (-)

bacilli and fungi.
OSTEOMYELITIS: infection of bone caused by
pyogenic bacteria and mycobacteria that gain access
to bone by the:
hematogenous route via direct spread from
contiguous focus of infection
or by a penetrating wound.

In adults: vertebral bodies are most often involved

“discitis”. Infection of the vertebra and
intervertebral discs via segmental arterial
circulation of the vertebra and by extension through
the endplate into the disc or the lateral plain which
lead to vertebral abscess.
To develop septic arthritis:
• Pathogens must enter the synovial joint….via
a. blood stream because synovium is highly
vascular and lacks a protective basement
membrane.
b. Medullary infection that spread to the
epiphysis and joint cavity through capillaries
that cross the growth plate. This is in young
children with osteomyelitis.
Routes by which bacteria can reach the
joint:
1.Hematogenous route
2.Dissemination from osteomyelitis
3.Spread from an adjacent soft tissue
infection
4.Diagnostic or therapeutic measures
5.Penetrating damage by puncture or
trauma
CHARACTERISTIC OF THE INFECTING ORGANISM TO
CAUSE INFECTION:
1. Virulence of the infecting organism which depends
on
a. capsule of the organism
b. extracellular toxins and enzymes
c. components of the cell wall
d. bacterial DNA

2. Size of the bacterial inoculum

3.Resistance of the host
CLINICAL FEATURES OF SEPTIC ARTHRITIS:
• Abrupt onset of a single hot, swollen and very
painful joint (usually monoarticular)
• Polyarticular in setting of co-morbid systemic
illness
• Less than 2 weeks at presentation
• Fever
• Knee common site in adult while hip is more
common in young children.
Pseudoparalysis which is refusal to move an infected
joint, common in children.
Laboratory studies:
• Synovial fluid cell count ranges from 50,000 to
100,000
• Blood white cell count higher than 11,000
• High ESR
• Gram stain of synovial fluid
• Microbiologic testing: SF should be cultured in
solid media and blood culture bottles.
• Gonococcal arthritis: best specimen is from
infected mucosal sites. Culture & gram stain
smears of skin lesions or urethral exudates
• Ultrasonography –sensitive for detecting joint
effusion in septic arthritis
DNA-based techniques:
1. Hybridization probes
2. Polymerase chain reaction (PCR) based
detection
3. Protein based detection by mass spectroscopy

IMAGING:
1. Radiography
2. Ultrasonography to detect joint effusion in
septic arthritis.
3. MRI with gadolinium contrast
Treatment of septic arthritis
1. Daily removal of purulent synovial fluid during
the first 5 to 7 days
2. Antibiotic :
a. 2 weeks for streptococci or gram negative
cocci
b. 3 weeks for staphylococcal infection
c 4 weeks for pneumococci or gram
negative bacilli
3. Gonococcal: 3rd gen cephalosporins is the choice,
daily antibiotic 1-2 days then followed by
cefixime 400mg BID daily
PROSTHETIC JOINT INFECTION:
FACTORS ASSOCIATED WITH PROSTHETIC JOINT INFECTION:
older age
Poor nutritional status, coexistent of joint diseases, obesity, DM,
malignancies, remote infection, prior native joint infection,
prosthesis revision surgery.

Early infection (<3 months) are caused by S. Aureus, strep, g-

negative bacilli

Delayed infections: (3-24 months) caused by less virulent bacteria

such as coagulase negative staph.

Late infections: (>2 years) almost always due to hematogenous

seeding from distant foci, such as skin, dental origins, urinary tract
infection.
Diagnoses:
1. Growth of an identical organism in at least
two cultures of synovial fluid or peri-
prosthetic tissue.
2. Purulent synovial effusion
3. Presence of granulocytes on periprosthetic
tissue
4. Presence of sinus tract communication.
GONOCOCCAL ARTHRITIS:
 Sexually transmitted disease caused by Neisseria
gonorrhea. Affects the genital area but can also
infect other mucosa such as throat, anus or
conjunctiva.
 When untreated, leads to endometriosis,
salpingitis or prostatitis or DGI (disseminated
gonococcal infection).
Microbiology of Neisseria gonorrhea:
 Small, gram-negative, non-motile and non spore-forming
bacterium, grows in pairs (diplococci) and infects humans.

Factors present in Neisseria to cause and disseminate

infection:
1. Pili : role in initial attachment with host cells. Piliated
strain adhere better to epithelial cells to initiate
gonococcal transport to transcellular spaces.
2. Porin (protein I): outer membrane protein that functions
as a pore for the exchange of ions.
3. Protein II : major role in formation of intimate associations
between the plasma membrane of the host cell & the
gonococcus and promotes the invasion of epithelial cells
4. Gonococcal lipopolysaccharide contributes to local
cytotoxic effects.
Pathogenesis:
Gonococcal infection of the urethral epithelia or
upper female genital cells triggers cytokine release,
which promote neutrophil influx and inflammatory
response.

Pregnancy and menses increase the risk for DGI

because of endometrial exposure of submucosal
vessels to the gonococci.

Symptoms of DGI begins within 7 days of the onset

of menses.
Clinical manifestations of DGI:
2 stages:
A. Bacteremic form
B. suppurative form with infectious arthritis

The most common symptoms of DGI:

Fever, migratory or additive arthritis with skin lesions “acute
arthritis and dermatitis syndrome”.

Tenosynovitis especially dorsum of the wrists, fingers, toes

and ankles.
INVESTIGATION:
 Gram stain of urethral exudates
 Specimen should be collected by Dacron
or rayon swabs, and inoculated directly
into growth medium
 Bacterial culture only with pharyngeal or
rectal gonorrhea.
 Nucleic acid hybridization assays or Nucleic
acid amplification tests (NAATs): more
sensitive than bacterial culture. Good for
screening.
Management:
 DGI higher dosages and longer durations of therapy than
uncomplicated infections
 Quinolone containing regimens are no longer recommended.
 Hospitalization if diagnosis is uncertain, or if purulent
arthritis
 Cephalosporin-based IV regimen is the initial treatment of
DGI. Ceftriaxone, cefotaxime or ceftizoxime.
 Spectinomycin for allergies to B lactam drugs.
 Concomittant diagnostic test for chlamydia trachomatis
should be performed and concomittant treatment with
Azithromycin or doxycycline against Chlamydial infection
Cellulitis is an acute, spreading pyogenic inflammation
of the dermis and subcutaneous tissue, usually
complicating a wound, ulcer, or dermatosis.

The area, usually on the leg, is tender, warm,

erythematous, and swollen. It lacks sharp demarcation
from uninvolved
skin.
Types of exposure that predispose patients to cellulitis
1. Severe bacterial cellulitis has been known to occur as a complication of
liposuction.
The subcutaneous injection of illicit drugs (“skin popping”) can result in
cellulitis due to unusual bacterial species.
2. After breast surgery for cancer. Cellulitis in the ipsilateral arm has been
well described after radical mastectomy,
where it occurs because of associated lymphedema;

3. Cellulitis in the ipsilateral breast is more common now, occurring after

breast-conservation therapy

4. Cellulitis also occurs in the legs of patients whose saphenous veins

have been harvested for coronary-artery bypass.
Lymphatic disruption and edema occur on the removal of the vein.
 SYPHILITIC ARTHRITIS:
 sexually transmitted chronic systemic
infection
 Caused by Treponema pallidum
 Characterized by episodes of active disease
followed by asymptomatic periods or latency.
 Beware of concurrent syphilis and HIV
Phases of infection
 After infection, incubation period of 2 to 6 weeks, then
appearance of primary lesion at the site of inoculation.

 Secondary period appears 6 to 8 weeks after the

primary lesion has healed and is characterized by
mucocutaneous lesions and generalized
lymphadenopathy which last for 2 to 6 weeks.

 Latent stage which may last years or decades

 Tertiary period which appears in untreated cases, is

characterized by progressive mucocutaneous, vascular,
musculoskeletal or neurologic symptoms
 mucocutaneous lesions: mucous patches

This symmetric, dusky red, and

polymorphic papulosquamous rash
is consistent with secondary syphilis.
SECONDARY SYPHILIS:
the most common symptom is a rash that usually involves
the palm and soles.

Other symptoms: fever, general malaise, muscle aches,

enlarged lymph nodes, hair loss and mucous patches

TERTIARY SYPHILIS:
Neuropathy due to tabes or Charcot joint which affects the
hips or knees. This neuropathy is due to loss of deep
sensation and chronic trauma rather than by direct
infection of the joint.
INVESTIGATION:
Historically:
Screening:
Serum Rapid Plasma Reagin (RPR)
Venereal disease research laboratory test (VDRL)
…. When positive
Confirmatory:
T. pallidum hemagglutination test (TPHA)
Fluorescent treponemal antibody absorption (FTA-ABS)
New Syphilis diagnostic test:
immunochromatography strip
western blot analysis
nucleic acid amplification or molecular strain typing.
A 26-year-old man presented with a four-month history of whitish oral lesions and pain on
swallowing (Panels A and B)

Ulmer A and Fierlbeck G. N Engl J Med 2002;347:1677

CASE Presentation:

The patient had noticed lesions on the glans penis seven months
previously, but these had cleared spontaneously. Otherwise he was
afebrile and in good overall health.

Physical examination revealed pseudomembranous lesions and erosions

of the tongue, the hard and soft palate, and tonsils, as well as
generalized lymph-node enlargement.

Titers of Treponema pallidum were 1:81,920 on hemagglutination assay

(TPHA), and a fluorescent treponemal antibody absorption test (FTA-ABS)
was positive.

A serologic test for human immunodeficiency virus infection was

negative. The patient was treated with intramuscular penicillin G
benzathine (2.4 million U), with full resolution of the oral lesions within
two weeks.
MANAGEMENT:
Penicillin remain the drug of choice
Azithromycin
ceftriaxone
MYCOBACTERIAL ARTHRITIS
Key features:
 Septic arthritis of the TB: Chronic, insidious
monoarticular infection.
 TB osteomyelitis: single or multiple osteomyelitic rib
lesions
 Reactive arthritis ( Poncet’s dse) polyarthritis asst’d
with EXTRAPULMONARY TB usually the lymph node.
 Soft tissue abscess: paravertebral abscess
 TB panniculitis: non suppurative inflammation of
subcutaneous fat.
Bazin disease: lobar panniculitis associated with
vasculitis and at times associated with arthritis
around the ankle
PATHOGENESIS: Infections occur:

1. Number of organisms that survive phagocytosis and their

ability to escape host defenses such as alveolar
macrophages (pneumocytes) and delayed hypersensitivity
response.
2. Multiplication intracellularly using Toll receptor 2 and CD
14 which leads to burst of the pneumocytes.

3. Cytokine production after the released organisms are

phagocytosed by the macrophages, which then triggers
inflammatory response then hematogenous spread to
distant organs.
Skeletal TB has a tendency to involve weight-bearing joints

Clinical patterns of musculoskeletal TB:

• Spondylitis (Pott’s disease)
• Septic arthritis (peripheral joint arthritis) hips, knees and
ankle joints.
• Osteomyelitis
• Tenosynovitis and bursitis
• Soft tissue abscess
• Reactive arthritis (Poncet’s disease): reactive symmetric
arthritis affecting person with visceral or disseminated TB
Spondylitis (Pott’s disease): affects one or more
component of the spine:
vertebra, intervertebral discs, paraspinal soft
tissues and epidural space
results from secondary hematogenous spread
thoracic and lumbar regions are most frequent
sites
early stage is localized at the level of the anterior
subchondral bone of the vertebra
adjacent to the intervertebral disc.
Presents as back pain, malaise, low grade fever,
weight loss and night sweat.
Physical exams reveal gibbus or tender spinal
prominence.
gibbus or tender spinal prominence.
How do they presents to us clinically:
Majority presents as spondylitis or chronic
monoarthritis involving weight bearing joints like knees
and hips

Risk factors:
Elderly
Children in high prevalence region
On steroids and immunosuppressives
Diagnosis of musculoskeletal TB:
 Gold standard: culture BACTEC
 PCR for smear negative patients
 MRI for spondylitis
 Xrays for the joint involvement.
FUNGAL MUSCULOSKELETAL INFECTIONS:
low incidence
HIGH INDEX OF SUSPICION IS NEEDED
Risk factors if present should raise the suspicion:
1. immunocompromised hosts with HIV, SLE, RA,
malignancies
2. immunosuppressive therapy: steroids,
3. occupational-related disease
4. subacute or chronic course
5. pulmonary and cutaneous involvement
6. Definitive diagnosis needs to demonstrate fungi
PARASITIC ARTHRITIS:
Primary parasitic musculoskeletal involvement is
rare and in most cases concomitant involvement of
gastrointestinal organs and lungs is seen.

Characteristic of Parasitic Rheumatism

 Inflammatory arthropathy
Residence in or travel to an area of epidemic
parasitosis
Eosinophilia
No response to anti-rheumatic treatment
Identification of parasite
Absence of radiologic finding
Parasitic infections are grouped into 4 subsets:
Protozoan: Amoeba species, cryptosporidium parvum, cyclospora
Isospora belli, Giardia, Leishmania, Plasmodium, Pneumocystis

Cestodes: Cysticercosis (Taenia solium- Tape worm), an intestinal

tape worm. Musculoskeletal involvement is characterized by
weakness and palpable nodule.

Nematodes: Lymphatic filariasis (Wuchereria bancrofti, Brugia

malayi)

Trematodes: Toxocariasis (visceral larva migrans) and Trichinosis

(Trichinella species)
ACUTE RHEUMATIC FEVER
Systemic inflammatory disease that occurs 2 to 3 weeks
after infection with group A Beta hemolytic streptococci

Disease is mediated by an autoimmune response to

antigenic components of the organism that cross react
with similar epitopes in human tissues such as the heart,
joint, brain and skin.

One of the disease in which there is molecular mimicry

between a foreign agent (group A strep) and host tissue
(heart, brain). Components of group A strep cross react
with various human tissue.
Characteristic of Streptococcus:
 gram (+) cocci in chains
Streptococcus pyogenes also referred to as the
group A strep belongs to hemolytic strep that
produce toxins which lyse red blood cells.
 M protein plays major role in the pathogenesis of
strep infection. It inhibit complement activation
and phagocytosis.
The most common presenting manifestation of acute
rheumatic fever is ARTHRITIS

Joint pain is typically migratory : sequential involvement

of joints, with inflammation resolving in one joint and
then beginning in another joint. But sometimes, it can be
additive.

Joint pain may last for 1 to 2 weeks, before it resolves

completely. If swelling persists after 4 weeks, consider
other conditions such as JRA or SLE.
Acute form of the illness is characterized by the
following:
 fever
arthritis which is usually migratory and
predominantly affects large joints
Cardiac manifestations : pericarditis, myocarditis,
endocarditis and heart valves.
Neurologic : Syndeham chorea
Cutaneous: erythema marginatum and subcutaneous
nodules
INVESTIGATION:
Throat cultures: should be taken at presentation of
pharyngitis. Usually negative by the time with arthritis or
carditis.

Streptococcal antibody tests:

Antibody tests are directed against the extracellular products of
streptococci:
1. ASO: anti streptolysin O. High titer indicate true infection and a
significant rise in the titer on repeat testing will support the
diagnosis of recent infection.
2. Anti DNAse B (ADB)
3. Anti streptokinase
4. antihyaluronidase
RHEUMATOLOGIC ASPECTS OF VIRAL INFECTIONS:
Viral-associated rheumatic syndromes can mimic rheumatic
diseases such as RA, SLE or Sjogren’s

Viral-associated viruses can cause either

acute self-limited inflammatory polyarthritis such as Hep B
virus (HBV), parvovirus B19, rubella virus. Usually
accompanied by fever, distinctive cutaneous lesions.

chronic arthritis: HCV, HIV, Alpha viruses. Mimic other

autoimmune diseases
HIV: HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS:
Considerations of the rheumatic manifestations of
HIV infection falls into 3 sections:
A. Rheumatic manifestations in the pre-HAART era.
Highly active antiretroviral therapy (HAART).
presents with severe form of reactive arthritis, severe psoriatic
arthritis, inflammatory myopathies.

B. Rheumatic complications in global areas without

access to HAART therapy.
Unique form of large vessel vasculitis demonstrating aneurysms
leading to vascular occlusions. Involves primary branches of the
aorta such as carotid, femoral and superior mesenteric arteries.
C. Rheumatic manifestations in the HAART era:
rheumatic manifestations have diminished but replaced by the
consequence of HAART such as metabolic disorders lipodystrophy,
osteomalacia, osteonecrosis.

Immune reconstitution syndromes including rheumatoid arthritis-like

disorders, SLE, autoimmune thyroid disease, inflammaory myopathy.
In summary:
RHEUMATIC SYNDROMES IN THE SETTING OF HIV INFECTIONS:
ARTICULAR SYNDROMES:
Arthralgia
HIV associated arthritis
Spondyloarthropathies (reactive arthritis, psoriatic a,
undifferentiated spondyloarthropathy)
Septic arthritis
 osteonecrosis
Osteoporosis

Connective tissue disorders:

Sjogren’s like syndrome/diffuse infiltrative lymphocytosis syndrome
Myopathy
Vasculitis
Lupus-like syndrome
Other VIRUSES:
PARVOVIRUS B19: viral exanthem such as slapped cheek
appearance.

Hepatitis B infection: occur in 2 different setting:

a. RA-like acute, self-limiting polyarthritis in the early phase of
acute hep B
b. Arthritis accompanying HBV-associated polyarteritis nodosa
(PAN)

*In both setting, manifestation are attributed to the

deposition of immune complexes containing viral antigens
(HBsAg, HBeAg) and antibodies against these antigens (anti
HBs, anti Hbe) in the synovium or in vessel wall, resulting in
arthritis or vasculitis.
Hepatitis C Virus: it’s a chronic viral infection, transmitted
parenterally- IV drug use.
Arthritis in the setting of HCV infection:
 Coexistent arthropathy (RA, SLE, Sjogren, fibromyalgia)
 HCV associated arthritis
 Arthritis in the setting of HCV-associated mixed cryoglobulinemia,
manifested by: purpura, polyneuropathy, membranoproliferative GN
 Arthritis induced by antiviral therapy (interferon alpha)

Chikungunya (CHIKV) and other alphaviruses

Mosquito borne infection
Early phase: has macular, papular or generalized erythema located in the trunk,
conjunctivitis, myalgias, fever, polyarthritis with transaminitis and cytopenias

Late phase: arthtritis or tenosynovitis of the hand joints lasting up to 6 months

OTHER ARTHRITIDIS:
Neuropathic arthropathy:
Painless, progressive, destructive joint disease associated
with sensory loss.
Bony swelling and soft tissue enlargement, effusion, laxity,
instability and deformity occur.
Common sites involved are the midfoot, ankle and knee

Etiologies:
1. Diabetes mellitus: severe distal symmetric neuropathy
2. Tabes dorsalis: in tertiary syphilis.
3. Leprosy: alteration of the shape of the hand and feet owing
to subluxation of individual joint
Clinical Manifestation:
EARLY neuropathic arthropathy:
Acute inflammatory phase with erythema, warm, swelling and edema

In diabetes: the midtarsal joint is commonly affected , resulting in

midfoot collapse and a valgus forefoot.

Neuropathic arthropathy at the knee is usually gradual in onset,

Pseudoinflammatory in nature.
HYPERTROPHIC OSTEOARTHROPATHY (HOA)
 Digital clubbing- nail become convex
 Features: peculiar bulbous deformity of the tips of the digits
described as clubbing
 Primary HOA also known as pachydermoperiostosis.
 Secondary HOA maybe associated with pulmonary diseases,
cardiac problems, liver cirrhosis, liver carcinoma.
ENTRAPMENT NEUROPATHIES AND
COMPARTMENT SYNDROMES:

Entrapment neuropathies results

from increased pressure on a nerve
as it passes through an enclosed
space.
I.) Thoracic outlet syndrome: thoracic outlet consists of
narrow channels through which the subclavian vessels and
lower trunk of brachial plexus pass from the
thoracocervical region to the axilla.

S/Sx: paresthesias along the medial aspect of the arm

and forearm then to the 4th and 5th digit. (course of ulnar
nerve)
pain, radiating to the neck, shoulder and arm is frequent
complain.
wasting of thenar, hypothenar and intrinsic muscle of the
hand
CARPAL TUNNEL SYNDROME (CTS):
Entrapment of the median nerve.

Median nerve supplies sensory branches to the radial three fingers

and half of the ring finger, these digits may have sensory loss in CTS.

Complain of burning, pins and needles sensations, numbness and

tingling in the fingers.

Awakened at night by abnormal sensation.

PE:
Tinel’s sign: percuss the wrist in extended position, paresthesias are
reproduced

Phalen’s: both wrists in flexion for 1 minute, paresthesias are

reproduced