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INFECTIONS IN ORTHOPAEDICS 1865: Lister open fracture with

carbolic acid World War II: Prophylactic antibiotics,

leaving wounds open Approach infections benign tumor

rarely is fatal, but recur if not adequately treated

the chemotherapy is antibiotics tumor surgery principles

millions of bacteria populate skin and body cavities

Microorganisms biofilm slime layer colonizing surfaces: resistant to antagonists

Colonization of surfaces: not always synonymous with infection

TABLE 18-1 Bacteria Commonly Found on the Surfaces of the Human Body

Bacterium SkinConjunctiva Nose

Pharynx Mouth

Staphylococcus epidermidis (1)

++ + ++ ++ ++

Staphylococcus aureus* (2) + +/- + + +Streptococcus mitis + ++Streptococcus salivarius ++ ++Streptococcus mutans* (3) + ++Enterococcus faecalis* (4) +/- +Streptococcus pneumoniae* (5)

+/- +/- + +

Streptococcus pyogenes* (6) +/- +/- + +Neisseria sp. (7) + + ++ +Neisseria meningitidis* (8) + ++ +Veillonellae sp. +Enterobacteriaceae* (Escherichia coli) (9)

+/- +/- +/- +

Proteus sp. +/- + + +Pseudomonas aeruginosa* (10)

+/- +/-

Haemophilus influenzae* (11) +/- + + +Bacteroides sp.*Bifidobacterium bifidum (12)Lactobacillus sp. (13) + ++Clostridium sp.* (14) +/-Clostridium tetani (15)++ = nearly 100 percent, + = common, +/- = rare, * = potential pathogen.

Pathogenesis

Planktonic state: bacteria / small clusters that are not colonized metabolically active susceptible to the body's host defense

systems / antibiotics Bacterial colonization: bacteria adhere

to a surface resists host and extrinsic efforts at eradication

Inert surface: glycoproteinaceous film

early stages of colonization: bacteria can be killed or contained by host defenses

bacteria can remain the inoculum is larger than threshold levels host defense mechanisms are impaired the tissue on which the bacteria colonize is

traumatized (or necrotic), a foreign body is present, the surface (or tissue) is acellular or inanimate

(e.g., dead bone, cartilage, and biomaterials) Colonization alone is not enough for

infection, but rather a necessary antecedent

Bacteria bone surface or biomaterial surface: direct contamination contiguous spreading hematogenous seeding

van der Waals forces bacteria to develop “irreversible” cross-links with the surface (adhesin receptor interaction)

Adhesion: time-dependent specific protein adhesion-receptor

interactions carbohydrate polymer synthesis charge and physical forces: surface is anionic and

initially repels bacteria (which are also anionic) anchorage to the surface polysaccharide slime

layer, “biofilm-enclosed” colony of bacteria forms

biofilm bacterial colonization process1.the bacteria need to find an inert surface (e.g., implant or dead tissue)2.Implants or dead tissue that have been integrated by the host with some type of surface are not inert and will resist colonization3.colonization process will continue until mature colonies are formed4.Once mature, the colonies can change based on environmental signals or signals between colonies

Biofilm: a community of sessile bacteria, surrounded by a glycocalyx of extracellular matrix only form on inert or nonviable surfaces antibiotics penetrate this film

Biofilm (or slime): extracapsular exopolysaccharides bind to surfaces / cell-to-cell aggregation

Inert surface (dead tissue, implants, or debris): area for bacteria to colonize and form biofilm escape the host defense, antibiotic treatments

Body control the bacterial colonization abscess or involucrum is formed

sinus: method to dispel the detritus and bacteria

equilibrium chronic infection history of intermittent symptoms and

drainage that responds to an antibiotic Bacteria numbers / weakening of the systemic

host: infection develop, spread, and persist Small electric fields, low pH, as well as acidic

and negatively charged surfaces: resistant to biofilms adjunctive treatments

Adherence to Bone and Biomaterials Damaged bone: bacterial

colonization Bone relatively acellular No normal periosteum presents a

collagen matrix bacteria can bind bone sialoprotein: a ligand for

bacterial binding to bone

Biomaterials / foreign bodies: bacterial colonization

outer surface atomic layer glycoproteins prokaryotic and eukaryotic cells Stainless steel and cobalt-chromium

and titanium resistant to corrosion Elemental composition, crystalline

homogeneity, and the surface oxide passivates

Antibiotic Resistance

resistance ~~ depend on the type of surface hydrocarbon polymers: extremely resistant to

antibiotics Metals: resist antibiotic therapy ↓

bacteria within biofilms decreased metabolic rate and undergo phenotypic changes resistance and virulence

bacteria adherent to surfaces: more resistant to antibiotics

within the biofilm: antibiotic concentrations of greater than 1,500 times normal

most antimicrobials work via interference with cell wall synthesis or reproduction and require metabolically active bacteria biofilm appear dormant resistant

Acute Posttraumatic Osteomyelitis Traumatized soft tissue and bone

exposes Traumatized tissue compromised

blood supply, tissue and bone necrosis infection

Fixation devices hypotension, inadequate debridement

of the fracture site, malnutrition, alcoholism, and smoking

Tissue injury or bacteria:A. activation of the complement cascade

local vasodilationB. tissue edemaC. migration of polymorphonuclear leukocytesD. enhanced ability of phagocytes to ingest

bacteria Trauma

A. delay the inflammatory response to bacteriaB. depress cell-mediated immunityC. impair function of polymorphonuclear

leukocytes (chemotaxis, superoxide production, and microbial killing)

Chronic Osteomyelitis

degree of bone necrosis, nutrition, infecting organism, age, comorbidity, and drug abuse

acute osteomyelitis Staphylococcus aureus

after a fracture polymicrobial (although in most cases, it is S. aureus)

IV drug users Pseudomonas / S. aureus infections

Gram-negative organisms: 50% of all cases of chronic osteomyelitis

fractures or surgical procedures: enter the bone directly

A surgical or traumatic insult: no longer perfused adequately

collagen protein matrix and acellular crystal regions

devascularization of bone necrotic material seclusion from systemic antibiotic therapy

Sequestrum wall off with a reactive and inflammatory (involucrum)

Involucrum: highly vascular and potentially viable and structural

Classification

acute or chronic based on the etiology of the

osteomyelitis type I (hematogenous) type II (osteomyelitis with fracture

union) type III (osteomyelitis without fracture

union) type IV (postoperative or posttraumatic

osteomyelitis without fracture)

1984, based on the nature of the bony involvement: Weiland et al: type I (open, exposed bone without soft tissue infection) type II (circumferential cortical and endosteal infection) type III (associated with a segmental defect).

1989, based on the nature of the bone after soft tissue and bony debridement: May et al: type I (intact tibia and fibula able to withstand functional loads

with no reconstruction needed) type II (intact tibia unable to withstand functional loads

requiring bone grafting; type III (<6 cm tibial defect with an intact fibula requiring

cancellous bone grant, tibiofibular synostosis, or distraction histogenesis)

type IV (<6 cm tibial defect and intact fibula requiring distraction histogenesis, tibiofibular synostosis, or a vascularized bone graft)

type V (>6 cm tibial defect without an intact fibula requiring a possible early amputation

Cierny and Mader

based on four factors: the degree of osseous involvement, the site of involvement, the degree of impairment caused by the disease, and the host's general condition

Type I: medullary osteomyelitis (examples of which include hematogenous osteomyelitis and infections of intramedullary rods).

Type II: superficial osteomyelitis confined to the bone surface.

Type III: localized osteomyelitis involving the full thickness of the cortex but without the loss of axial stability.

Type IV: diffuse osteomyelitis involving the circumference of the cortex and loss of axial stability.

Cierny and Mader's types of osteomyelitis.

Cierny-Mader Staging System for Osteomyelitis Anatomic Type

Stage 1: Medullary osteomyelitisStage 2: Superficial osteomyelitisStage 3: Localized osteomyelitisStage 4: Diffuse osteomyelitis

Physiologic ClassA host: HealthyB host:   Bs: Systemic compromise   Bl: Local compromise   Bls: Local and systemic compromiseC host: Treatment worse than the disease

Factors Affecting Immune Surveillance, Metabolism, and Local VascularitySystemic factors (Bs): Malnutrition, renal or hepatic failure, diabetes mellitus, chronic hypoxia, immune disease, extremesof age, immunosuppression or immune deficiencyLocal factors (Bl): Chronic lymphedema, venous stasis, majorvessel compromise, arteritis, extensive scarring, radiation fibrosis, small-vessel disease, neuropathy, tobacco abuse Reprinted with permission from Cierny G, Mader JT, Pennick H. A clinical staging system of adult osteomyelitis. Contemp Orthop 1985;10:17–37.

Class A patients have normal systemic defenses, metabolic capabilities, and vascular supply to the limb.

Class B patients have a local (trauma, prior surgery, local inflammation) or systemic (immunosuppressed, on corticosteroids, peripheral vascular disease) deficiency

Class C patients are those in whom the treatment of the disease (the infection) is worse than the infection itself

success rates of 98% were achieved, even in type IV osteomyelitis

class B hosts: anatomic type, success ranged from 79% to 92%.