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Greg J. Beilman and David L.

Dunn

Historical background
Knowledge of surgical infectious disease was derived from the evolution of germ theory and antisepsis. The development of modalities to effectively prevent and treat infection has occurred only within the last several decades.

Historical background
1846:Ignaz Semmelweis hypothesized that puerperal fever was cause by putrid material dying of this disease by carriage on the examination fingers of medical students and physician . Latter part of the nineteenth century: Louis Pasteur provided germ theory that contagious disease are cause by specific microbes that these microbes are foreign to the infected organism.

Historical background
1859:Joseph Lister used carbolic acid to dressing wound resulted in improving wound outcome. 1879:Robert Koch develop technique to culture Bacillus anthracis and proved the ability to cause anthrax in healthy animals.

Historical background
He developed four postulates
The suspected pathogenic organism should by present in all cases of the disease The suspected pathogen should be isolated from a diseased host and grow in a pure culture in vitro Cell from a pure culture of suspected organism should cause disease in a healthy animal The organism should be reisolated from the newly diseased animal.

Historical background
1889:Charles McBurney pioneered appendectomy. 20 th century : Sir Alexander Fleming discover peicillin. Frank Meleney ,Willium Altemeier proposed concept that resident microbes were non pathologic until they entered a sterile body cavity at the time of surgery.

William Osler : Except on few occasions ,the patient appears to die from the bodys response to infection rather than from it

Pathogenesis of infection
Host defense prevent microbial invasion ,limit proliferation of microbe within the host and contain or eradicate invading microbes. include site specific defense and systemic host defense

Host defense
Barriers surface(epithelial or mucosa) Barrier cells may secrete substance that limit microbial proliferation or prevent invasion Resident or commensal microbes(colonization resistance) Most extensive physical barrier is the integumant or skin

skin
Skin
Chemical that secreted by sebaceous gland. Constant shedding of epithelial cell Endogenous microflora : gram positive aerobic microbes(Staphylococus and Streptococus) ,Corynebacterium and Propionibacterium species Infraumbilical region: Enterococus faecalis and faecium,Escherichia coli,enterobacteriacae,yeast(Candida albican) Diseases of the skin are associated with overgrowth of skin commensal organisms and barrier breaches.

Respiratory system
The respiratory tract
Upper respiratory tract:respiratory mucus trap larger particles then passed into upper airways and oropharynx by ciliated epithelial cells,where the mucus is cleared by coughing. Smaller particles arriving in lower respiratory tract are cleared via phagocytosis by pulmonary alveolar macrophages.

GI tract
Urogenital ,biliary,pancreatic ductal,and distal respiratory tract do not possess resident microflora. Microbe may present in barrier affected by disease or introduce from an external source. Significant number of microbe are found in GI tract.

GI tract
Organisms are routinely killed in highly acidic,low mitility envirolment of the stomach. Small numbers of microbes populate the gastric the gastric mucosa(10 2-3 CFU/ml) This organism expands in the presence of drug or disease states the diminish gastric acidity. Microbe that not destroyed enter the small intestine,which proliferation takes place(10 5-8 in terminal CFU/ml in terminal ileum)

GI tract
Relatively low oxygen ,static environment of the colon is accompanied by the exponential growth of microbes. Anaerobic outnumber of aerobic species approximately 100:1 10 11-12 CFU/g are present in feces. Facultative and strict anaerobes (Bacteroides fragalis,distasonis,thetaiotaoicron,Bifidobacterium,Clostri dium,Eubacterium,Fusobacterium,Lactobacillus,Paptostre ptococus) fewer aerobic microbe(E. coli,enterobacteriacae,E. faecalis and faecium,C. albican)

GI tract
Characterized host microflora effectively prevents invasion of enteric pathogens but cause of infection if GI perforation has occurred.

GI tract
Once microbe enter a sterile body compartment or tissue. Initially primitive and relative non specific host defense
Physical barrier of the tissue Capacity of proteins such as lactoferrin and tranferrin sequester the critical microbial growth factor iron Fibrinogen trap the microbe during process polymerized into fibrin

GI tract
Peritoneal cavity:

diaphragmatic pumping mechaism omentum ,act as gatekeeper Intestinal ileus :serve to wall off infection(also combine with fibrin trapping to cause intra abdominal absess)

Local immune respond


Resident macrophage ,low level of complement protein,immunoglobulin Macrophage secrete wide array of substance ,some of which appear to regulate the cellular component of the host defense response. TNF-alpha,IL-1beta,6,8, INF-gamma Concurrently ,a counterregulatory respond:TNFBP,IL-1 receptor antagonist,IL-4,10

Local immune respond


Local immune respond lead to
Microbial opsonization Phagocytosis Extracellular microbial destruction(C5b6-9membran attack complex) Intracellular microbial destruction(phagocytic vacuoles) The classic and alternate complement pathway Complement protein fragment(C3a,C4a,C5a),bacterial cell wall compartment,enzyme that are expelled form leucocyte enhance vascular permeability

Systemic immune respond


C5a,microbial cell wall peptides(N-formylmethionine),secreting cytokine(IL-8) attract PMNs Further reflux of inflammatory fluid and large number of PMNs This process begin within several minute and peak within hours or days

Systemic immune respond


Magnitude of response are related to
Initial number of microbes Rate of microbial proliferation in relation to containment and killing by host defenses Microbial virulence Potency of host defenses

definitions
Possible out come ,can occur after microbial invasion
Eradication Containment: presence of purulence(hallmark of chronic infection) Locoregional infection with or without distant spread of infection Systemic infection:failure of resident and recruited host defense at local level

definitions
Identification of microorganisms in host tissue or the bloodstream,plus an inflammatory response. Classic finding(local manifestations): rubor,calor,dolor Systemic manifestations:elevated temperature,elevated WBC,tacycardia,tachypnea

Systemic inflammatory response syndrome(SIRS)


Temperature<36, >38 c HR >90 beats/min RR> 20 or PaCO2 <32 WBC >12000, or <4000 or band form >10%

photo

Systemic inflammatory response syndrome(SIRS


SIRS mediated by the production of a cascade of proinflammatory mediator
lipopolysaccharide-endotoxin from gram negative bacterias peptidoglycans and teichoic acids from gram positive bacteria mannam from yeast and fungi)

Severe sepsis
Severe sepsis:sepsis + new onset organ failure Severe sepsis has mortality rate 51/100000 population per year Clinical criteria
Need for ventilatory support Oliguria unresponsive to aggressive fluid resuscitation Hypotension requiring vasopressor

Septic shock
State of acute circulatory failure Persistent arterial hypotension(SBP<90) despite adequate fluid resuscitation without other identifiable cause 40% of patients with severe sepsis Mortality rate 45-60%

definitions
New classification scheme for sepsis PIRO staging Further investigation is ongoing to evaluate the clinical utility .

microbiology
Bacteria
Responsible for majority of surgical infections Grams stain ,morphology ,pattern of division ,presence and location of spores Aerobic skin commensals(SSIs) and enteric bacteria(UTIs and bacteremia as nasocomial infection in immunocompromise host or chroically ill) are frequent cause surgical infection

Gram negative bacteria


Gram negative: bacilli in family enterobacteriaceae(E. coli, Klepsiella pneumoniae,Serratia marcescens,enterobacter,Citrobacter,Acinetocacter spp.) Other include: Pseudomonas spp. ,Xanphomonas spp.

anaerobe
Anaerobic bacteria do not possess the enzyme catalase(allow for metabolism of reactive oxygen species) Propionibacterium acne are skin flora cause acne Microflora of oropharynx and colorectum

Acid fast bacilli


Mycobacterium tuberculosis,Nocardia spp. Slowgrowing ,need culture for week to month DNA base analysis

fungi
Special stain(potassium hydroxide,india ink,methenamine silver,Giemsa) Form of branching and septation ,growth characteristic in special media Nasocomial infection as a part of polymicrobial infections or fungemia- Candida spp. Rare cause of aggressive soft tissue infections(Mucor, Rhozopus,Absidia spp)

fungi
Oppotunistic pathogens(Aspergillus spp.,Blastomyces dermatitisis,Coccidioides immitis,Cryptococcus neoformans)

virus
Small size Necessity for growth within cell Indentified by indirect means(host antibody response) Viral DNA or RNA using PCR Occur in immunocompromised patients particularly receiving immunosuppression to prevent rejection of a solid organ allograft

virus
Adenovirus,Cytomegalovirus,Ebstein-Barr virus,herpes simples virus,varicellar-zoster virus Hepatitis B and C virus ,HIV is blood borne Pathogens

Prevention and treatment of surgical infection


Prophylaxis: maneuver to diminish the presence of exogenous(surgeon and OR environment) and endogenous microbe .
Mechanical Chemical Anitimicrobial modality

Prevention
Antisepsis and sterile technique reduced infection rate But this modalities are not capable to sterilizing the hands or skin ,although the inoculum can be reduced . Some degree of microbial contamination

Prevention
Indication for give antimicrobial agent
Procedure which associated with significant number of microbes Procedure in whom the consequences of any type of infection are severe

Source control
Drainage of all purulent material Debridement of all infected, devitalized, debris Remove of foreign bodies Remediation of the underlying cause Ongoing source of contamination and aggressive, rapidly spreading infection required operative intervention

treatment of surgical infection


Antimicrobial agent are secondary important to effective surgery Rarely that surgical infection can be cured only by antibiotic alone and never in face of an ongoing source of contamination Delay in operative intervention lead to increase morbidity and mortality

Appropriate use of antimicrobial agent

Antimicrobial prophylaxis
Prophylaxis : administration of an antimicrobial agent before initiation of surgical procedures. To reduce the number of microbes that enter the tissue or body cavity Agent are selected according to their activity against microbe likely to present at the surgical site.

Antimicrobial prophylaxis
Start 30-60 min before operation If duration of operation exceed the serum drug half life, patient should be received an additional dose. No benefit of post operative dose.

Empirical therapy
The use of an antimicrobial agent or agent when the risk of infection is high, base on underlying disease process or when significant contamination are occurred. Prophylaxis merge in to empirical therapy in which the risk of infection increase because of intraoperative finding. In critical ill patients ,severe sepsis ,septic shock.

Empirical therapy
Limited to short course of drug 3-5 days Curtail as soon as possible Can merge into therapy

Antimicrobial therapy
Therapy are related to microbiological data(culture, antibiotic sensitivity pattern) Monomicrobial infection
Nasocromial infection(UTI, pneumonia, bacteremia) Initial treatment are empirical treatment ,related to institutional and unit specific drug sensitivity pattern. Tailor antibiotic after culture and sensitivity report

Antimicrobial therapy
Polymicrobial infection
Source control Culture result are less important because demonstrate limit of mirobes predominant. Antibiotic regimen should not be modified only from culture information. Treatment of intra-abdominal infection should cover aerobic and anaerobic activity(10-30% failure rate)

duration
Prophylaxis limited to single dose administration. Empirical therapy should be limited to 3-5 day and should stop if no local or systemic infection are discovered Patients who have SIRS,less than half of them got infected.

duration
Monoicrobial infection
3-5 day for UTIs 7-10 days for pneumonia 7-14 days for bacteremia 6-12 wk for osteomyelitis, endocarditis, prosthetic infection

duration
Polymicrobial infection(peritonitis)
12-24 h penetrating GI trauma(no extensive contamination) 3-5 days for therapy for perforated or gangrenous appendicitis 5-7 day for peritoneal soilage with moderate degree contamination 7-14 day for extensive peritoneal soilage or in immunosuppressed host

duration
In post operative antibiotic treatment for serious intra-abdominal infection
No elevated WBC Lack of band form Lack of fever

assurance that infection has been eradicated.30 Under these circumstances, antibiotics can be discontinued .

Antibiotic selection
MIC of a standard pure inoculum of 10 5 CFU/ml Sensitivities are report in relation to achievable blood level of each antibiotic. Least toxic and least expensive and agent which bacterium are most sensitive(most importance). Serious infection may required two or more agent especially drug resistant pathogen.

Shifting from iv to oral form


Commonly , agent are given in iv form for 1-2 wk then continue treatment course with oral form .
Patient must have clinical improvement Oral agent should be capable of achieving high serum level

allergy
Urticaria, bronchospasm , anaphylaxis Not indigestion or vomitting Penicillin allergy is common (0.7-10%) Penicillin allergy cross react with carbapenems, cephalosporins(5-7%),and extremely small in monobactams. Incase of certain drug is life saving and have history of allergy to drug in same class
Intradermal testing using a dilute solution desensitization

misuse
Financial impact ADR New infection(C. dificile colitis) MDR pathogen