Infeksi Pada Sistem

Muskuloskeletal
Gangguan Sistem Muskuloskeletal
dr. Dewi Klarita Furtuna, M.Ked.Klin.,Sp.MK
Fakultas Kedokteran Universitas Palangka Raya
2018
Kelainan Muskuloskeletal

1. Kelainan kongenital

2. Inflamasi / Infeksi

3. Trauma muskoloskeletal

4. Keganasan

5. Kelainan metabolik
Description
Infection in the bones, joints, or muscles may occur at any age.
Infections can spread quickly through a young child’s blood and
bones.
Inflamasi / Infeksi
1. Inflamasi

Reaksi lokal jaringan hidup (tissue respon) terhadap adanya

iritant (rangsangan)

2. Iritant
a. Dari luar tubuh (External)
b. Dari dalam tubuh  Misal Auto imune

3. Infeksi
Inflamasi yang iritantnya kuman (mikro-organisme)
Inflamasi :
a. Galen

Rubor  Respon vaskuler (Dilatasi)

Tumor (Bengkak)   exudate , krn permeabilitas kapiler.

Calor (Panas,)  aliran darah   energi dan panas 

Dolor (nyeri, pain)  Tertekannya saraf

Functio laesa (Ggn fungsi) krn perusakan jaringan

b. Celsus  Rubor, Tumor Calor, Dolor

Pembagian Inflamasi / Radang
- Inflamasi Spesifik  Penyebab diketahui

Inf . Pyogenik (pus) Arthritis & Osteomyelitis,

Inf. Granulomatous (granuloma)  tbc

- Inf . Non spesifik (idiopatik) (Rematik disease)

Rhematic fever, Rh/ Artritis , Transient sinovitis dll

- Inf . karena iritasi chemis  Mis Gout (Metabolik Arthritis)

- Inf karena trauma yang berulang

Bursitis & Tenovaginitis stenosans

Definitions:
Abscess - a collection of pus. This can occur in the skin,
soft tissue, muscle, or even bones.

Osteomyelitis – infection of the bone caused by bacteria

Myositis– infection of the muscle caused by bacteria

Pyomyositis – myositis that also has an abscess in

the muscle.

Septic arthritis – infection of the joint caused by

bacteria.

Antibiotics – medicine that fights infection

Symptoms

Pain, swelling, fever, not being able move the arm or

leg, or being unable to put weight on a leg are all
possible signs of infection.
These signs are worrying when there has not been a
recent accident or fall.
Most frequent agents were MSSA (30,2%) and MRSA (21,8%), followed by
Streptococcus species (8,9%) and Pseudomonas aeruginosas (7,1%).
Although most patients were infected by a single agent, 18,6% had two or
more causative agents isolated in cultures. Of those, 69,7% had either
MSSA or MRSA as one of the isolated agents.
GENUS: STAPHYLOCOCCUS

• Genus Features : Gram-positive cocci in clusters

• Catalase positive (streptococci are catalase negative)
• Species of Medical Importance : S. aureus , S. epidermidis,
S. saprophyticus
 Staphylococcus aureus

Distinguishing Features
• Small, yellow Staphylococcus aureus colonies on blood agar
• ß-hemolytic
• Coagulase positive (all other Staphylococcus species are negative
• Ferments mannitol on mannitol salt agar
Reservoir
Normal flora
– Nasal mucosa (25% of population are carriers)
– Skin
Transmission

• Hands
• Sneezing
• Surgical wounds
• Contaminated food
– Custard pastries
– Potato salad
– Canned meats
Predisposing Factors for Infection

• Surgery/wounds
• Foreign body (tampons, surgical packing, sutures)
• Severe neutropenia (<500/µL)
• Intravenous drug abuse
• Chronic granulomatous disease
• Cystic fibrosis
 Pathogenesis
• Protein A binds Fc component of IgG, inhibits phagocytosis
• Enterotoxins: fast acting, heat stable
• Toxic shock syndrome toxin-1 (TSST-1): superantigen
• Coagulase: converts fibrinogen to fibrin clot
• Cytolytic toxin (a toxin): pore-forming toxin, Panton-Valentine leukocidin (PVL),
forms pores in infected cells and is acquired by bacteriophage; associated with
increased virulence, MRSA strains
• Exfoliatins: skin-exfoliating toxins (involved in scalded skin syndrome [SSS])
and bullous impetigo
Treatment
•Gastroenteritis is self-limiting.
•Nafcillin/oxacillin are drugs of choice because of
widespread penicillinase-producing strains.
•Mupirocin for topical treatment.
•For methicillin-resistant Staphylococcus aureus
(MRSA): vancomycin
•For vancomycin-resistant Staphylococcus aureus
(VRSA) or vancomycin-intermediate S. aureus
(VISA): quinupristin/dalfopristin
GENUS: STREPTOCOCCUS
• Genus Features
• Gram-positive cocci in chains
• Catalase negative
• Sero grouped using known antibodies to the cell wall carbohydrates
• (Lancefield groups A–O): S. pneumoniae serotyped via capsule; S.
pyogenes serotyped via M protein

• Species of Medical Importance : S. pyogenes, S. agalactiae (group B

streptococci; GBS), S. pneumoniae, Viridans streptococci: S.
mutans; S. sanguinis; S. gallolyticus (bovis)
 Streptococcus pyogenes
(Group Enterococcus Streptococcus; GAS)
Distinguishing Features
• ß hemolytic
• Bacitracin sensitive
• Pyrrolidonyl arylamidase (PYR) positive

• Reservoir: human throat; skin

• Transmission: direct contact; respiratory droplets

Pathogenesis

• Hyaluronic acid: is non-immunogenic

• M-protein: antiphagocytic, associated wit acute glomerulonephritis,
rheumatic fever

• Streptolysin O: immunogenic, hemolysin/cytolysin

• Streptolysin S: not immunogenic, hemolysin/cytolysin

Spreading Factors
• Streptokinase: breaks down fibrin clot
• Streptococcal DNAse: liquefies pus, extension of lesion
• Hyaluronidase: hydrolyzes the ground substances of the connective
tissues
• Exotoxins A–C (pyrogenic or erythrogenic exotoxins)
– Phage-coded (i.e., the cells are lysogenized by a phage)
• – Cause fever and rash of scarlet fever: superantigens
Diseases
Laboratory Diagnosis

• Rapid strep test (ELISA-based) misses approximately 25% of

infections. Culture all negatives.

• Antibodies to streptolysin O (ASO) titer of >200 is significant for

rheumatic fever.

• Anti-DNAse B and antihyaluronidase titers for AGN

 Treatment:
beta lactam drugs, macrolides in the case of penicillin allergy
• rheumatic fever; beta lactams and macrolides

Prevention
possible prophylactic antibiotics for at least 5 years post-acute
rheumatic fever; beta lactams and macrolides
 Streptococcus agalactiae
(Group B Streptococci; GBS)
Distinguishing Features
• ß hemolytic
• Bacitracin resistant
• Hydrolyze hippurate
• CAMP test positive (CAMP factor is a polypeptide
which “complements” the sphingomyelinase of S.
aureus to create an enhanced hemolytic pattern in
shape of an arrowhead)
• Reservoir: human vagina (15-20% of women); GI tract

• Transmission: newborn infected during birth (increased risk with

prolonged labor after rupture of membranes)

• Pathogenesis: capsule; ß hemolysin and CAMP factor

• Diseases: neonatal septicemia and meningitis; most common causal

agent
• Treatment: ampicillin with an aminoglycoside or a cephalosporin
Prevention

• Prophylaxis during delivery in women with positive

vaginal/rectal culture of GBS, history of recent infection
with GBS, or prolonged labors after membrane rupture

• Ampicillin or penicillin drugs of choice

• Clindamycin or erythromycin for penicillin allergies

 Streptococcus pneumoniae
Distinguishing Features
• a hemolytic
• Optochin sensitive
• Lancet-shaped diplococci
• Lysed by bile (bile soluble)

Reservoir: human upper respiratory tract

Transmission: respiratory droplets (not considered highly communicable;
often colonize the nasopharynx without causing disease)
Predisposing Factors

• Antecedent influenza or measles infection

• Chronic obstructive pulmonary disease (COPD)
• Congestive heart failure (CHF)
• Alcoholism
• Asplenia predisposes to septicemia
Pathogenesis

• Polysaccharide capsule is the major virulence factor

• IgA protease
• Teichoic acid
• Pneumolysin O: hemolysin/cytolysin: damages respiratory epithelium;
• inhibits leukocyte respiratory burst and inhibits classical complement
fixation
Diseases

• Typical pneumonia: most common cause (especially in decade 6 of

life); shaking chills, high fever, lobar consolidation, blood-tinged,
“rusty” sputum
• Adult meningitis: most common cause; peptidoglycan and teichoic
acids are highly inflammatory in CNS; CSF reveals high WBCs
(neutrophils) and low glucose, high protein
• Otitis media and sinusitis in children most common cause
Laboratory Diagnosis

• Gram stain and culture of CSF or sputum

• Quellung reaction: positive (swelling of the capsule with the addition
of type-specific antiserum, no longer used but still tested!)
• Latex particle agglutination: test for capsular antigen in CSF
• Urinary antigen test
Treatment:
• beta lactams for bacterial pneumonia; ceftriaxone or cefotaxime for
adult meningitis (add vancomycin if penicillin-resistant S. pneumoniae
has been reported in community); amoxicillin for otitis media and
sinusitis in children (erythromycin in cases of allergy)
Prevention

• Antibody to capsule (>80 capsular serotypes) provides type-specific

immunity
• Vaccine
– Pediatric (PCV, pneumococcal conjugate vaccine): 13 of most
common serotypes; conjugated to diphtheria toxoid; prevents invasive
disease
– Adult (PPV, pneumococcal polysaccharide vaccine): 23 of most
common capsular serotypes; recommended for all adults age =65 plus
at-risk individuals
 Viridans Streptococci (S. sanguis, S. mutans)
Distinguishing Features
• a hemolytic
• Optochin resistant
• PYR-negative
• Bile insoluble
Reservoir: normal flora of human oropharynx (S. mutans, S. sanguinis),
human colon (S. gallolyticus)
Transmission: endogenous
Pathogenesis: dextran (biofilm)-mediated adherence onto tooth
enamel or damaged heart valve and to each other (vegetation); growth
in vegetation protects organism from immune system
Diseases

• Dental caries: S. mutans dextran-mediated adherence glues oral flora

onto teeth, forming plaque and causing dental caries
• Infective endocarditis (subacute): m
– Malaise, fatigue, anorexia, night sweats, weight loss, splinter
hemorrhages
– Predisposing conditions: damaged (or prosthetic) heart valve and
dental work without prophylactic antibiotics or extremely poor oral
hygiene
– S. gallolyticus associated with colon cancer
• Treatment:
penicillin G with aminoglycosides for endocarditis

• Prevention:
prophylactic antibiotics prior to dental work for individuals with
damaged heart valve
GENUS: ENTEROCOCCUS
Genus Features
• Catalase negative
• PYR+

• Species of Medical Importance

• Enterococcus faecalis
• Enterococcus faecium
 Enterococcus faecalis/faecium
Distinguishing Features
• Group D gram-positive cocci in chains
• PYR test positive
• Catalase-negative, varied hemolysis
• Hydrolyze esculin in 40% bile and 6.5% NaCl (bile esculin agar turns
black)

• Reservoir: human colon, urethra ± and female genital tract

• Transmission: endogenous
Pathogenesis
• Bile/salt tolerance allows survival in bowel and gall bladder.
• During medical procedures on GI or GU tract: E. faecalis →
bloodstream → previously damaged heart valves → endocarditis

• Diseases: urinary and biliary tract infection; infective (subacute)

endocarditis in persons (often elderly) with damaged heart valves

• Diagnosis
• Culture on blood agar
• Antibiotic sensitivities
Treatment: all strains carry some drug resistance
• Some vancomycin-resistant strains of Enterococcus faecium or E.
• faecalis have no reliably effective treatment; or low-level resistance
use ampicillin, gentamicin, or streptomycin
• VanA strains have UDP-N-acetylmuramyl pentapeptide with terminal
d-alanyl-d-alanine replaced with d-alanyl-d-lactate, which functions in
cell wall synthesis but does not bind to vancomycin

• Prevention: prophylactic use of penicillin and gentamicin for

patients with damaged heart valves prior to intestinal or urinary tract
manipulation
Osteomyelitis
The key to successful management is early diagnosis and appropriate
surgical and antimicrobial treatment.
History : ??
• Osteomyelitis is an ancient disease, which has been present for the
last 250 million years and was first described in humans by
Hippocrates

• Nelaton is credited with introducing the term “osteomyelitis” in 1844

• The first paper on osteomyelitis in the Journal in February 1948, was

from the Royal Hospital for Sick Children in Glasgow

benefits of penicillin which had gradually become available in

the 1940s
Definition : ??
Introduction

Osteomyelitis
osteon (bone) ; myelo (marrow) ; itis (inflammation)

Infection in bone

differ from another (duration, etiology,

pathogenesis, bone involvement) & type
Osteomyelitis
of patient (infant, child, adult, or
in long bones
immunocompromised)
Osteomyelitis :
• Osteomyelitis adalah infeksi dari jaringan tulang yang mencakup sumsum dan
atau kortek tulang dapat berupa eksogen (infeksi masuk dari luar tubuh) atau
hematogen (infeksi yang berasal dari dalam tubuh). (Reeves,2001:257).

• Osteomyelitis adalah infeksi substansi tulang oleh bakteri piogenik (Overdoff,

2002:571).

• Osteomyelitis adalah infeksi pada tulang yang disebabkan oleh mikroorganisme.

Osteomyelitis biasanya merupakan infeksi bakteri dan jamur yang dapat
menyebabkan osteomyelitis jika mereka menginvasi tulang (Ros, 1997:90).

• Osteomyelitis adalah infeksi jaringan tulang (Price, 1995:1200)

• Osteomyelitis akut adalah infeksi tulang panjang yang disebabkan oleh infeksi
lokal akut atau trauma tulang, biasanya disebabkan oleh Escherichia coli,
staphylococcus aureus, atau streptococcus pyogenes (Tucker, 1998:429).
Classification :
1. Waldvogel et al.

2. Cierny et al
The Waldvogel system :
• Duration : Acute and chronic

• Source infection : hematogenous and contiguous focus

• vascular insufficiency
Cierny-Mader Staging System
Osteomyelitis Classification :
• Duration : Acute, Subacute or Chronic
• Route of infection : Hematogenous or Exogenous

• Host response : Pyogenic or non pyogenic

ETIOLOGY
Acute hematogenous
osteomyelitis
• distribution- younger than 2 years, and 8-12 years
• More common in males
• Caused by a bacteraemia
• Bacteriological seeding of bone generally is associated with other
factors such as localized trauma, chronic illness, malnutrition or an
inadequate immune system.
• In children the infection generally involves the metaphyses of rapidly
growing long bones

• Bacterial seeding leads to an inflammatory reaction which can cause

local ischaemic necrosis of bone and subsequent abscess formation

• As the abscess enlarges, intramedullary pressure increases causing

cortical ischaemia, which may allow purulent material to escape
through the cortex into the subperoisteal space
Sign : pain of affected area (localized pain) and loss of function,
fever, Localized erythema, swelling, inability to bear weight
Diagnosa : Diagnosa Banding :
• Lab Studies : leukosit, Marker - Osteosarkoma
Infection
• Imaging : Rontgen, CT Scan, MRI
- Ewing Sarkoma
• Microbiologic Data :
- Blood cultures,
- Bone biopsy, debridement,
- Abscess drainage
Radiograph
• Soft tissue swelling

• Periosteal reaction

• Bony destruction
(10-12 days)
Treatment :
• Surgery and antibiotic treatment are complementary, in some cases
antibiotics alone may cure the disease.

• Choice of antibiotics is based on the highest bacteriocidal activity, the

least toxicity and the lowest cost
• The two main indications for surgery in acute hematogenous
osteomyelitis are:

1. The presence of an abscess requiring drainage

2. Failure of the patient to improve despite appropriate
intravenous antibiotic treatment
SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
• More insidious onset and lacks severity of symptoms
• More than two weeks.
• The indolent course of subacute osteomyelitis is due to:
• increased host resistance
• decreased bacterial virulence
• administration of antibiotics before the onset of symptoms
• Systemic signs and symptoms are minimal
• Temperature is only mildly elevated
• Mild to moderate pain
BRODIE ABSCESS
• an intraosseous abscess related to a focus of subacute
pyogenic osteomyelitis
• patients are younger than 25 years of age and present with joint pain
and localized swelling.
• Signs and symptoms of systemic disease are frequently absent.
• Staphylococcus aureus (30%–60%), Pseudomonas (5%), Klebsiella
(5%) and coagulase negative Staphylococcus (5%) are causative
organisms.
• 20% of cultures are negative for these organisms.
• Radiographically, an intramedullary area of central lucency with
sclerotic margins is characteristic.
Chronic Osteomyelitis
• “ A severe, persistent and incapacitating infection of bone and bone
marrow”

• surrounded by sclerotic, relatively avascular bone

Types

• A complication of acute Osteomyelitis

• Post traumatic

• Post operative
Clinical manifestations
• Hematogenous osteomylitis usually involves a single bone.
• The most common presenting complaints are focal pain, warmth,
erythema, swelling, and decreased use of the affected extremity.
• Fever, anorexia, irritability, and lethargy may accompany the focal
findings.
Factors responsible for chronicity

• Local factors: Cavity, Sequestrum, Sinus, Foreign body, Degree of

bone necrosis
• General: Nutritional status of the involved tissues, vascular disease,
DM, low immunity
• Organism: Virulence
• Treatment: Appropriateness and compliance
• Risk factors: Penetrating trauma, prosthesis, Animal bite
Treatment
• Antibiotics
• Surgical treatment
Preoperative assessment & preparation
Derbridement
Sequestrectomy
Local antibiotics
Stability
Treatment of bone cavity
Complications

• “Recurrence & Recurrence & Recurrence”

• Pathological fractures
• Growth disturbance
• Amyloid disease
• Epidermoid carcinoma of the fistula
• surgical drainage may be appropriate at earlier time if :
1. sequestrum is present
2. disease is chronic
3. the hip joint is involved
4. Presence of spinal cord compression
75-year-old man with acute recurrence of chronic post-
traumatic femoral osteitis which had been dormant for 17
years (Necrotizing soft tissue infections)
Treatmen Therapy :

Treatment algorithm of Cierny-Mader stage 1, or

hematogenous, long bone osteomyelitis.
Treatment algorithm of Cierny-Mader stage 2 long bone osteomyelitis
Initial Antibiotic Therapy for Treatment of Osteomyelitis in Adults
 Local Antibiotic Therapy
(Antibiotic Impregnated Beads)

• Antibiotic Impregnated beads & self-setting bone cement

have used to treat chronic osteomyelitis allowing the local
delivery of high concentrations of antibiotics, while avoiding
potential systemic side effects.
• Antibiotic usually used Vancomycin, Gentamycin, Tobra
• The beads are usually removed within 2-4 weeks and
replaced with cancellous bone graft
Kegagalan pemberian antibiotika dapat
disebabkan oleh :

• Pemberian antibiotik yang tidak sesuai dengan mikroorganisme

penyebab
• Dosis tidak adekuat
• Lama pemberian tidak cukup
• Kesalahan hasil biakan
• Antibiotik antagonis
• Pemberian pengobatan suportif yang buruk
• Kesalahan diagnostik
Sumber :