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CHAPTER 21 Basic Microbiology
361
• bedside curtains
• urine bottles
• toilets
• dust
• air
• air-conditioning systems.
Methods of Spread of Infection
• Contact, e.g. hands, clothing.
• Airborne:
• droplets and respiratory tract infection
• dust
• scales shed from skin
• aerosols
• nebulizers
• air conditioning.
• Ingestion:
• food poisoning
• overcrowded wards (especially psychiatric and
geriatric)
• faecal–oral spread
• poor kitchen hygiene
• carriers.
Sources of Wound Contamination
• Direct inoculation:
• Patient’s residual ora
• Patient’s skin contamination
• Surgeon’s hands
• contaminated instruments
• contaminated dressings
• contaminated procedure
• drains, catheters, i.v. lines.
• Airborne contamination:
• skin of sta and patient
• air ow in operating theatre.
• Haematogenous spread:
• i.v. lines
• sepsis at other sites.
Prevention and Control of Hospital-Acquired
Infection
e following are important factors in the prevention and
control of hospital-acquired infection:
• Education of sta; hand washing; correct disposal of
waste, e.g. soiled dressings; good nursing care; safe
environment, e.g. appropriate space between beds,
clean toilets, etc.; good theatre technique; good aseptic
surgical technique.
• Skin infection and antisepsis.
• Sterilization and disinfection.
• Prophylactic antibiotics.
• Protective clothing.
• Isolation of patients with established infection or colonized with pathogens.
• Appropriate design of hospital buildings.
• Sta health:
• exclude sta suering from infection from contact
with patient
• protect sta, e.g. hepatitis B immunization
• surveillance, e.g. infection control
• monitoring of infection rates
• careful tracking of potentially dangerous bacteria
• appropriate policy-making.
Control of Staphylococcal Outbreaks
• Exclude personnel with skin sepsis or skin lesions from
the surgical team.
• Exclude and treat carriers of Staphylococcus aureus.
• Personnel should wear:
• protective theatre clothing
• caps to cover hair
• clean theatre clothes
• gowns
• masks.
• Alcohol hand rubs before and aer patient contact.
• Wear gloves.
• eatre environment:
• correct direction of air ow
• keep oors clean
• horizontal surfaces, e.g. trolleys, should be reduced
to a minimum as they act as dust traps
• clean walls and ceilings on regular basis
• operating lights should be kept clean and dust-free.
• Patient:
• bed linen and clothes must not be allowed in theatre
area
• shaving must be carried out immediately prior to
surgery and not some time before, which allows
staphylococci to colonize small lacerations in skin
• skin at and around the operation should be
disinfected
• wounds should be isolated from surroundings by
sterile drapes.
Fig. 21.1 shows how staphylococcal infection may spread.
Meticillin (Methicillin)-Resistant Staphylococcus
aureus (MRSA)
• MRSA is a major nosocomial pathogen.
• Causes severe morbidity and mortality.
• Infection/colonization rates vary with time and place.
• 10–40% of nosocomial S. aureus infections may be
meticillin-resistant.
Other patient
Infected patient
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362
Fig. 21.1 The spread of staphylococcal infection.
SECTION III Pathology
Infected wound
air/dust/bedclothes
Hand of nurse
or doctor
Cross infection
Staphylococci
Wound (initially clean)
Staphylococci
Staphylococci
Staphylococci
Carrier
(skin/nose)
• Many inpatients are colonized or infected.
• Hospital personnel may be carriers.
• Located in inguinal, perineal, axillary or anterior nares
areas.
• Spread by hands, usually of nursing or medical sta.
Risk Factors for Colonization
• Advanced age.
• Previous hospitalization.
• Length of hospitalization.
• Stay in intensive treatment unit (ITU).
• Chronic illness.
• Prior and prolonged antibiotic therapy.
• Presence of wound.
• Exposure to colonized or infected patient.
• Presence of invasive indwelling devices.
Clinical Presentation
• Pneumonia.
• Line sepsis.
• Surgical site infection.
• Intra-abdominal sepsis.
• Osteomyelitis.
• Toxic shock syndrome.
Infection Control
• Screening of patients and sometimes sta.
• If MRSA suspected, take swabs from:
• hairline
• nose
• axilla
• groin
• perineum.
• Alcohol hand rubs.
• Use of gowns and gloves when appropriate.
• Isolation of infected or colonized patient (barrier
nursing).
• Environmental cleaning.
Management
Carriers
• Application of antiseptics, e.g. mupirocin, to nose and
skin.
• Use antiseptic soaps and shampoos.
• May need 3 weeks’ treatment.
• Check swabs at 3 days and 3 weeks aer use of antiseptics.
Patients with MRSA
• Nurse in isolation.
• Vancomycin or teicoplanin are most oen used.
• Co-trimoxazole or tetracycline are useful if no resistance.
• Linezolid, quinupristin and dalfopristin are newer
alternatives.
SURGICALLY IMPORTANT
MICROORGANISMS
Surgically important microbes may be divided into:
• conventional pathogens: those that may cause infection
in the previously healthy person
• conditional pathogens: those that cause infection in
those who have a predisposition to infection
• opportunistic pathogens: those that are usually of low
virulence but will cause infection in the immunocompromised patient.
Examples of the above are shown in Box 21.1.
Microorganisms that are of the greatest signicance in surgery are usually bacteria. ey may be classied as follows:
• Shape:
• bacilli: rod-shaped
• cocci: spherical.
• Gram staining:
• Gram-positive: blue
• Gram-negative: pink.
• Growth requirements:
• aerobic
• anaerobic
• facultatively anaerobic.
CHAPTER 21 Basic Microbiology
363
BOX 21.1 Microbial Infections
Conventional
Staphylococcus aureus: wound infection
Haemophilus influenzae: chest infection
Neisseria gonorrhoeae: gonorrhoea
Conditional
Pseudomonas aeruginosa: wound infection
Klebsiella: urinary tract infection
Opportunistic
Pneumocystis carinii: chest infection
Candida albicans: oesophagitis
Aspergillus fumigatus: aspergillosis
Gram-Positive Cocci
Staphylococci
• Arranged in grape-like clusters.
• Divided into coagulase-positive and coagulase-negative.
• Coagulas e-positive staphylococci are called Staphylococ-
cus aureus.
• S. aureus are responsible for the following:
• supercial infections, e.g. boils, abscesses, styes,
conjunctivitis, wound infections
• deep infection, e.g. septicaemia, endocarditis, osteo-
myelitis, pneumonia
• food poisoning
• toxic shock syndrome.
• Coagulase-negative staphylococci, e.g. Staphylococcus
epidermidis, are of lower pathogenicity, and rarely cause
infection in healthy people.
• S. epidermidis forms part of the normal skin ora.
• S. epidermidis and other coagulase-negative staphylococci may be responsible for infection in association
with foreign bodies, e.g.
• prosthetic cardiac valves
• implanted pacemakers and debrillators
• prosthetic joints
• intravenous lines
• continuous ambulatory peritoneal dialysis
• vascular gras.
• ese infections may lead to septicaemia and endocarditis, and become life-threatening.
• Treatment with antibiotic is usually inadequate and the
prosthesis nearly always requires removal.
• S. saprophyticus, a commensal, may cause UTIs in sexually active women.
PVL-producing Staphylococcus aureus (Panton–Valentine
leukocidin)
• PVL is a toxin produced by some strains of S. aureus.
• It is a virulence factor and usually causes cellulitis and
abscesses.
• It is associated with community-acquired infections
and spread by close contact (sports, gyms) and shared
items (towels, razors).
• Infections are managed as per normal S. aureus and
decolonized as per MRSA.
Antibiotic sensitivity
• S. aureus appears in multiple resistant forms in hospital
practice.
• Recently there has been an increase in MRSA, posing a
major threat to surgical patients.
• Antibiotics that may be active against S. aureus include:
• penicillin (90% of hospital strains are resistant)
• ucloxacillin (active against β-lactamase-producing
organisms but not MRSA)
• erythromycin
• clindamycin
• fusidic acid
• cephalosporins
• vancomycin.
Streptococci and Enterococci
• Spherical or oval cocci occurring in chains or pairs.
• Classied by their ability to lyse red blood cells present
in blood-containing culture medium.
• Further divided by serology into Lanceeld groups on
the basis of polysaccharide antigens on their surface.
• Species responsible for sepsis are β-haemolytic strains
where colonies completely lyse the blood cells on a cultured plate.
• ese β-haemolytic types include Lanceeld groups A,
B, C and G.
Lancefield group A
Streptococcus pyogenes causes:
• tonsillitis and pharyngitis
• peritonsillar abscess (quinsy)
• otitis media
• mastoiditis
• wound infection with cellulitis and lymphangitis
• erysipelas
• necrotizing fasciitis.
Antibiotic sensitivity
• All strains are sensitive to penicillin.
• Patients sensitive to penicillin should be treated with
erythromycin, but some strains are resistant.
• At present clindamycin is a good second-line or additional anti-streptococcal agent.
Lancefield group D
• Includes enterococci.
• Enterococcus faecalis is the most important, surgically,
in this group.
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SECTION III Pathology
• E. faecalis may cause UTIs and abdominal wound
infections, and may be isolated from the bile in acute
cholecystitis.
Antibiotic sensitivity
• Enterococci are sensitive to ampicillin.
• Moderately resistant to penicillin.
• Resistant to cephalosporins.
Viridans streptococci
• Alpha-haemolysis on blood-containing culture plates
with a green discoloration (hence, viridans).
• Most human strains are commensals of the upper respiratory tract and of low pathogenicity.
• May be responsible for endocarditis.
• Streptococcus milleri may be classied with this group
but is more oen now classied with pyogenic streptococci; it may cause liver, lung, or brain abscesses.
Streptococcus pneumoniae (pneumococcus)
• S. pneumoniae consists of encapsulated diplococci.
• Virulence correlates with presence of capsule, probably
because this prevents or inhibits phagocytosis.
• S. pneumoniae is responsible for the following:
• lobar pneumonia
• chronic bronchitis
• meningitis
• sinusitis
• conjunctivitis
• septicaemia (especially in splenectomized patients).
Antibiotic sensitivity
• Most streptococci are sensitive to penicillin but some
strains of S. pneumoniae show resistance.
Gram-Positive Rods
Anaerobic Gram-positive rods are mainly soil saprophytes,
but a few are pathogens.
• Clostridium perfringens (gas gangrene).
• C. tetani (tetanus).
• C. botulinum (botulism).
• C. difficile (pseudomembranous colitis).
Clostridium difficile
• Anaerobic Gram-positive bacillus that occasionally
presents in normal adult bowel.
• It has become a major problem in hospital-acquired
infections and its prevention is a major aim of all NHS
trusts.
• It produces a cytotoxin.
• Carriage is oen asymptomatic.
• Spectrum of illness from mild diarrhoea to fulminant
pseudomembranous colitis.
• Diagnosis is by detection of toxin in stool.
• Main susceptibilities are advanced age, chronic illness,
cancer and surgery.
• Illness precipitated, and spread promoted by antibiotics.
• Parenteral cephalosporins, quinolones and clindamycin known to be especially risky.
• Recent high rates of morbidity and mortality in
European and North American hospitals.
• Spread is faecal–oral and hands are very important in
spread.
• As alcohol-resistant spores – washing with soap is the
appropriate mode of hand hygiene.
• Control requires tight restriction of antibiotic use,
improvement in infection control and detection, isolation and treatment of cases.
• Treatment is by metronidazole in mild cases and oral
vancomycin in the sick or high risk.
Gram-Negative Cocci
• Neisseria (pairs).
• N. meningitidis (meningococcus): meningitis and
septicaemia.
• N. gonorrhoeae (gonococcus): gonorrhoea.
• N. gonorrhoeae may cause fever and severe lower
abdominal pain (salpingitis in females), or be the cause
of a urethral discharge in males.
• Gram stain from a smear of a high vaginal swab in the
female or urethral discharge in the male may conrm
diagnosis by demonstrating the presence of Gramnegative intracellular diplococci. It is imperative to perform culture or molecular detection.
Gram-Negative Bacilli
is is a large group of microorganisms of surgical
importance.
Facultative Anaerobes (Enterobacteria, Coliforms)
Escherichia coli
• Normal inhabitant of human intestine.
• Some strains produce powerful toxins.
• An important cause of sepsis and diarrhoea.
• Examples of sepsis include:
• UTIs
• wound infection, along with anaerobes, especially
aer surgery on the lower GI tract
• peritonitis – along with anaerobes
• biliary tract infections
• septicaemia.
• Examples of diarrhoeal illnesses include:
• infantile gastroenteritis
• traveller’s diarrhoea
• haemorrhagic diarrhoea can present as rec-
tal bleeding and can cause haemolytic-uraemic
syndrome.
CHAPTER 21 Basic Microbiology
365
Klebsiella
• Klebsiella spp. inhabit the human intestine.
• Some strains are saprophytic in soil, water and vegetation.
• Klebsiella causes:
• UTIs
• septicaemia
• pneumonia (rare).
Proteus
• Proteus spp. cause:
• UTIs
• wound infections, e.g. burns, pressure sores
• septicaemia.
Salmonella
• Inhabit animal GI tract.
• Predominantly animal pathogens which can produce
disease in humans.
• Salmonella typhi diers from other species in that man
is the only natural host.
• Foodstus from animal sources are the usual source of
transmission of infection.
• ey cause:
• enteric fever, typhoid or paratyphoid; these are due
to S. typhi and S. paratyphi A, B, C
• gastroenteritis (food poisoning), usually due to S.
enteritidis or S. typhimurium
• osteomyelitis (rare)
• septic arthritis (rare).
• Salmonella typhi may survive in symptomless carriers
and persist in the gall bladder.
• Faecal carriage may occur via biliary tract colonization.
• Epidemics may occur, especially if the carrier is a
food-handler.
Shigella
• Intestinal parasite in man.
• Causes dysentery.
• Shigella dysenteriae produces exotoxin, which causes
most severe illness.
• Shigella sonnei is most common cause of dysentery in
the UK.
Yersinia
• Animal parasite which occasionally causes disease in
humans.
• Yersinia pseudotuberculosis and Y. enterocolitica are the
most common, causing food poisoning and possibly
mesenteric adenitis.
Other enterobacteria
• ese include Enterobacter, Citrobacter, Providencia,
Morganella and Serratia.
• Human and animal intestinal parasites, but some
strains are saprophytes.
• Moist hospital environments may act as reservoirs.
• Oen multi-resistant to antibiotics.
• ey may cause the following:
• UTIs
• wound infection aer abdominal surgery
• respiratory infections in hospitalized patients
• septicaemia.
Antibiotic sensitivity
• Sensitivity should be determined, as some strains may
be resistant to the more commonly used antibiotics.
• Antibiotics used against enterobacteria include ampicillin, amoxicillin, trimethoprim, aminoglycosides,
ciprooxacin, cephalosporins (second- and third-generation) and chloramphenicol.
• For UTIs the antimicrobial drugs trimethoprim and
nitrofurantoin may be appropriate.
Aerobic Gram-Negative Bacilli
Pseudomonas aeruginosa
• Inhabits water and soil.
• Organism survives in moist environments in hospitals,
and may also survive in aqueous antiseptics and other
uids.
• Important cause of hospital-acquired infections.
• It has a characteristic green appearance of exudate on
dressings and an unpleasant odour.
• Particularly aects patients with serious underlying
conditions, e.g. burns, malignancies.
• Aects patients with urinary catheters, endotracheal
tubes.
• Frequent cause of sepsis in the immunocompromised
patient.
• Is a pathogen in the following conditions:
• UTIs, especially with indwelling catheters
• burns
• wound infections
• septicaemia
• pressure sores
• venous stasis ulcers
• chest infections, especially patients on mechanical
ventilation and those with cystic brosis
• eye infections (it may contaminate certain types of
eye drops).
Antibiotic sensitivity
• Presence of P. aeruginosa is not necessarily an indica-
tion for antibiotic therapy, especially if isolated from a
supercial site.
• Clinical and bacteriological assessment in the individual patient is appropriate before prescribing
antibiotics.
• P. aeruginosa is resistant to most common antibiotics.
• e most suitable antibiotics are aminoglycosides, certain β-lactams, e.g. penicillins (ticarcillin, piperacillin),
ciprooxacin, cephalosporins (ceazidime).
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SECTION III Pathology
Anaerobic Gram-Negative Bacilli
Bacteroides
• Found in lower GI tract, female genital tract, and mouth.
• Important in abdominal and gynaecological sepsis.
• Oen found along with other organisms, notably
coliforms.
• Also important in dental and oropharyngeal disease.
Antibiotic sensitivity
• Bacteroides fragilis (most important in surgery). It is
penicillin-resistant due to β-lactamase production.
• Bacteroides are sensitive to metronidazole.
Other Gram-Negative Bacilli
Campylobacter
• Curved or spiral rods which are microaerophilic.
• Found in various animal species, including chickens,
domestic animals and seagulls.
• Campylobacter is the most common cause of bacterial
food poisoning in the UK.
Haemophilus influenzae
• Found mainly in the respiratory tract.
• Oen part of the normal ora.
• May cause respiratory disease, especially communityacquired respiratory disease.
• Exists in non-capsulated and capsulated strains.
• Non-capsulated strains are responsible for exacerbations of chronic bronchitis and bronchiectasis.
• Capsulated strains cause severe infections in young
children, e.g. meningitis, acute epiglottis, osteomyelitis,
arthritis and orbital cellulitis.
• Septicaemia with H. influenzae may occur as part of
post-splenectomy sepsis.
• A vaccine is available against H. influenzae type b (Hib).
Antibiotic sensitivity
H. influenzae is sometimes sensitive to ampicillin, tetracycline, ciprooxacin, cephalosporins (second- and thirdgeneration and co-trimoxazole). Chloramphenicol should
be reserved for severe infections, e.g. meningitis and acute
epiglottitis.
Pasteurella multocida
• Small, ovoid, Gram-negative bacillus.
• Inhabits respiratory tract of many animals, notably
dogs and cats.
• In man it may cause septic wounds aer animal bites.
• Sensitive to penicillin, tetracycline, erythromycin and
aminoglycosides.
Helicobacter pylori
• Gram-negative spiral, motile, microaerophilic bacterium.
• Transmission by faecal–oral, oral–oral or iatrogenic
(endoscopes and endoscopists).
• Associated with gastritis, peptic ulceration, gastric lymphoma, gastric cancer.
• Diagnostic tests include:
• urea breath test
• mucosal biopsy (Campylobacter-like organism
[CLO] test)
• histopathological examination
• serology.
• Eradication therapy involves triple therapy with a
1-week course of a proton pump inhibitor plus amoxicillin plus clarithromycin (in penicillin-sensitive
patients, metronidazole is substituted for amoxicillin).
PATHOPHYSIOLOGY OF SEPSIS
e incidence of sepsis has been increasing over the last
25 years; it is the commonest cause of death in ITU.
Systemic Inflammatory Response
Syndrome (SIRS)
Development of SIRS is manifest by two or more of:
• temperature >38°C or <36°C
• tachycardia >90 beats/min
• tachypnoea >20 breaths/min or PaCO2 < 4.25 kPa
• WBC >12 × 109/L or <4 × 109/L.
Note: immunocompromised patients can be septic without eliciting an inammatory response.
Systemic Inflammatory Response Syndrome and
Multi-Organ Dysfunction Syndrome (MODS)
Primary precipitating event → inammatory response →
SIRS → MODS → multi-organ failure (MOF)
Primary Precipitating Event
e main causes are:
• localized or generalized sepsis
• peritonitis (especially associated with pancreatitis)
• burns
• trauma
• haemorrhage.
Inflammatory Response
e immune system responds to tissue damage by instituting an inammatory response. Initially this is protective,
but later may become destructive, resulting in the detrimental eects observed in SIRS.
ree stages in the development of SIRS have been
described.
Stage I
As a result of local insult, the local environment produces
cytokines which:
• provoke an inammatory response
• promote wound repair
• recruit reticuloendothelial cells.
CHAPTER 21 Basic Microbiology
367
Stage II
• Cytokines are released into the circulation to enhance
local response.
• Macrophages and platelets are recruited.
• Growth factor production is stimulated.
• Acute phase response, which is controlled by a simultaneous decrease of pro-inammatory mediators and
release of endogenous antagonists.
• ese mediators hold the initial inammatory response
in check until the wound is healed, infection resolves
and homeostasis is restored.
Stage III
• is occurs if homeostasis is not restored.
• Massive systemic reaction with cytokines becomes
destructive.
• Loss of integrity of microcirculation.
• Dysfunction of various distant organs.
Mediators of SIRS include:
• endotoxin
• tumour necrosis factor (TNF)
• interleukins, chiey IL-1, IL-6
• cells, e.g. endothelial cells, neutrophils
• secondary inammatory mediators
• arachidonic acid metabolites, e.g. prostaglandins,
thromboxane
• nitric oxide
• platelet activating factor (PAF)
• stress hormones, catecholamines, steroids, insulin
• other mediators, e.g. histamine, bradykinin, serotonin.
Clinical Definition of Sepsis Syndrome
is involves the progression from:
SIRS → sepsis → severe sepsis → septic shock (refrac-
tory shock) → death
• Sepsis: SIRS resulting from documented infection.
• Severe sepsis: sepsis associated with evidence of endorgan dysfunction, hypoperfusion, hypotension.
• Septic shock: severe sepsis with refractory hypotension
(in spite of adequate volume resuscitation).
Clinical Effects of Sepsis Syndrome
ese depend upon the precipitating cause, degree of
organ involvement and severity. ey include:
• overt or occult infection
• ushed, warm periphery
• hypotension
• tachycardia
• tachypnoea
• hypoxia
• metabolic acidosis
• deranged clotting function (abnormality of clotting
cascade in inammatory response).
Septic shock (refractory shock)
• Peripheral vascular failure.
• Persistent hypotension resistant to vasoconstrictors.
• Usually high output due to low systemic vascular resistance (SVR) and increased heart rate.
• Usually myocardial depressant factor.
• Cardiac dysfunction also due to:
• metabolic acidosis
• hypoxaemia.
• Microcirculatory changes due to:
• vasodilatation
• A–V shunting (maldistribution of ow)
• increased capillary permeability
• interstitial oedema
• decreased O2 extraction.
• Defect of O2 utilization at cellular level.
Multi-Organ Dysfunction Syndrome
• Progression from SIRS.
• Results in end-organ dysfunction.
• Diagnosed dysfunction of two or more organ systems.
• Results from hypoperfusion and ischaemia of tissues.
• e clinical picture depends on organ systems aected.
Factors Leading to Multi-Organ Failure
• Excessive release of endogenous mediators, including
TNF-α, IL-1, IL-6.
• Impaired local microvascular perfusion interfering
with O2 delivery to tissues, with disruption of cellular
metabolic functions.
• Impaired intestinal barrier function, with bacterial translocation releasing endotoxins into the portal circulation.
• Damage to reticuloendothelial function.
• Immune depression with T- and B-cell depression.
• T-suppressor cell stimulation resulting in increased
vulnerability to infection.
Clinical Picture of Multi-Organ Dysfunction
e clinical picture depends on the organ systems involved.
Respiratory
• Acute respiratory distress syndrome (ARDS) may follow SIRS.
• Hypoxia.
• Signs and symptoms of respiratory failure.
• Nosocomial pneumonia in 70% of patients.
Cardiovascular
• Endothelial damage, leading to interstitial oedema.
• Vasodilatation, leading to hypotension.
• Tissue hypoxia.
• Lactic acidosis.
• Myocardial dysfunction due to eects of inammation,
circulating myocardial depressant factor, endotoxin.
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SECTION III Pathology
Renal
• Oliguria (<0.5 mL/kg/h urine production).
• Elevated urea and creatinine.
Hepatic
• Reduced drug metabolism.
• Reduced hormone metabolism.
• Poor control of glucose homeostasis.
• Failure of synthesis, e.g. clotting factors.
• Failure to conjugate bilirubin (hyperbilirubinaemia).
Gastrointestinal tract
• Atrophy of mucosa due to hypoperfusion and ischaemia.
• Increased risk of bacterial translocation into portal
system, stimulating liver macrophages to produce cytokines with amplication of SIRS.
Cerebral
• Confusion.
• Agitation.
• Stupor.
• Coma.
• Above due to hypoperfusion, septic encephalopathy,
metabolic encephalopathy.
Haematological
• Anaemia.
• Leucopenia.
• rombocytopenia.
• Leucocytosis.
• Abnormal coagulation; APPT ↑, PT ↑, frank disseminated intravascular coagulation (DIC).
Metabolic
• Hyperglycaemia due to sepsis and catecholamines
(both cause insulin resistance).
• Lactic acidosis, generalized catabolic state.
If MODS continues unchecked, then organ dysfunction
will become irreversible (MOF). is is potentially preventable with appropriate treatment.
Failure of individual organs in MOF oen follows a
predictable pattern: rst respiratory failure; then hepatic,
intestinal and renal; and nally cardiac failure.
• previous compromise of organ function.
SURGICAL SEPSIS
e term ‘sepsis’ covers several purulent infections, which
the surgeon may encounter in surgical practice.
Skin Infections
Boils, Styes and Carbuncles
• Denitions:
• boil (furuncle): an infection of a hair follicle
• stye (hordoleum): an infection in a hair follicle on an
eyelid
• carbuncle: a group of boils interconnected in the
subcutaneous tissue by tracts.
• ese infections are painful but not serious.
• Antibiotics are rarely indicated for boils and styes, but
may be appropriate for carbuncles.
• Infection is usually due to S. aureus, which is usually an
endogenous strain carried in the nose or skin.
• Boils may be recurrent, appearing in crops over several
weeks or months.
• May be a presenting sign of diabetes.
• Antibiotic therapy is indicated only for certain cases, e.g.
boils on the ‘dangerous area’ of the face where venous
drainage is to the cavernous sinus and where cavernous
sinus thrombosis may result; also in immunocompromised patients.
Erysipelas
• Spreading infection of the skin due to S. pyogenes.
• Presents as a raised, red, indurated area of skin which is
sharply demarcated.
• Patient may present with high fever and may appear toxic.
• Rare condition at present; responds well to penicillin.
Cellulitis
is is the spread of infection of the subcutaneous tissue.
Principles of Treatment of Sepsis Syndrome
ese include:
• eradication of source of infection
• treatment of sepsis-associated metabolic, cardiovascular and multi-organ disturbances
• inhibition of toxic mediators, e.g. activated protein C is
used.
Mortality is related to the number of organs that are failing:
• 1 organ: 70% survival
• 2 organs: 50% survival
• 4 organs: mortality approaches 100%.
Prognosis is aected by:
• older age
Acute Pyogenic Cellulitis
• Usually due to S. pyogenes.
• Presents as a red, painful swelling, usually of a limb,
being commonly associated with lymphangitis and
lymphadenitis.
• Likely to appear in a lymphoedematous limb.
• Treatment is with penicillin and/or clindamycin.
Anaerobic Cellulitis
• Rare.
• Usually due to anaerobes or clostridia, but more oen
is due to synergistic infection with both aerobes and
anaerobes.
CHAPTER 21 Basic Microbiology
369
• Causative organisms are usually a combination of
anaerobes (Bacteroides, clostridia, anaerobic cocci) and
aerobes (coliform, P. aeruginosa and S. pyogenes).
• Clinically, redness and oedema present around a wound
(surgical or traumatic).
Anaerobic cellulitis may progress in two ways:
• Bacterial gangrene:
• skin becomes purple and ischaemic, and eventually
undergoes necrosis
• Fournier’s gangrene of the scrotum and Meleney’s
gangrene are examples (see below).
• Necrotizing fasciitis:
• in this condition the skin remains normal in the
early stages while the infection spreads along fascial
plains, causing extensive necrosis
• later, the overlying skin becomes deprived of its
blood supply, losing its sensation, eventually becoming purple-black and undergoing necrosis
• necrotizing fasciitis is a life-threatening condition in
which the patient is seriously ill with fever, toxaemia
and occasionally septic shock
• wide excision of the area of necrosis and infection is
required, together with appropriate antibiotics
• the mortality rate is high.
Fournier’s Gangrene
• Rapidly progressive gangrene of scrotum of spontaneous onset.
• Elderly diabetics particularly prone, but may occur in
otherwise healthy young men.
• Caused by synergy between faecal bacteria and anaerobes.
Meleney’s Gangrene
• Occurs at site of abdominal surgery or at site of accidental abrasion of the skin.
• Originally attributed to synergy between a microaerophilic, non-haemolytic streptococcus and S. aureus;
however, other bacteria may be involved.
• Best considered as infection caused by a combination of
anaerobic and aerobic bacteria which forms a cellulitis
followed by gangrene.
Fournier’s gangrene and Meleney’s gangrene probably
have similar aetiological factors, and only the site of infection distinguishes the two.
Lymphangitis and Lymphadenitis
• Denitions:
• lymphangitis: a non-suppurative infection of lym-
phatic vessels that drain an area of cellulitis
• lymphadenitis: infection of the regional lymph
nodes as a result of infection in an area which they
drain.
• Lymphadenitis usually, but not always, results from cellulitis and lymphangitis.
• Occasionally the lymph nodes suppurate and form an
abscess.
• Lymphangitis produces red, tender streaks along the
lines of lymphatics extending from the area of cellulitis
towards regional lymph nodes.
• Lymphadenitis is represented by enlarged, tender
regional lymph nodes.
• Occasionally the overlying skin is red and the glands
are uctuant.
• Treatment of both lymphadenitis and lymphangitis depends on isolation of the appropriate infecting
organism.
Gas Gangrene
• Rare disease in peacetime, but closely associated with
grossly contaminated wounds due to war injuries.
• Clostridial spores are widely distributed in the
environment.
• May enter traumatic or surgical wounds.
• Contamination may also occur from the patient’s own
faecal ora (C. perfringens is a normal bowel inhabitant).
• May occur after elective surgery, e.g. GI tract, lower
limb amputation, vascular surgery on ischaemic
limb.
• In case of trauma it is due to contamination of wounds
by dirt and soil containing clostridia derived from animal faeces.
• Infection favoured by extensive wounds with presence
of necrotic tissue, which provide an anaerobic environment for clostridia to proliferate.
• Anaerobic environment initiates conversion of spores
to vegetative, toxin-producing pathogens.
• Clostridia proliferate and produce toxins that diuse
into surrounding tissue.
• Toxins destroy local microcirculation.
• is allows further invasion, which can advance
extremely rapidly.
• Alpha toxin of C. perfringens kills muscle cells and
destroys fat.
• Gas formation occurs.
• As disease advances, toxins are released into systemic
circulation.
Clinical features
• Patients are generally toxic and unwell.
• Exhibit pallor, restlessness, delirium, tachycardia, jaundice, and ultimately septic shock and death.
• Local signs of gas gangrene include:
• myositis or myonecrosis
• gas formation with palpable crepitus
• mottled discoloration of overlying skin.
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SECTION III Pathology
• Plain X-ray shows gas in subcutaneous tissue and fascial plains.
Diagnosis
• Clinical features.
• Specimens of exudate and tissue for Gram staining
when typical Gram-positive bacilli are seen.
Treatment
• Adequate resuscitation.
• Debridement or amputation should be considered to
remove all aected tissue or limb.
• Organisms are usually sensitive to penicillin.
• Hyperbaric oxygen may be helpful.
Prevention
• Benzylpenicillin antibiotic prophylaxis in those with:
• contaminated wounds
• amputations
• diabetics undergoing elective peripheral vascular
surgery.
Tetanus
• Rare condition in UK: <100 cases reported each year.
• Caused by C. tetani, an anaerobic Gram-positive bacil-
lus, which produces a neurotoxin.
• Found in soil and faeces.
• Neurotoxin enters peripheral nerves and travels to spinal cord, where it blocks inhibitory activity of spinal
reexes.
• Disease follows the implantation of spores into deep,
devitalized tissues.
Clinical features
• Neurotoxic blockade of inhibitory activity of spinal
reexes results in characteristic features of disease.
• Facial muscle spasm produces trismus.
• Typical facial appearance, i.e. risus sardonicus
(lockjaw).
• Spasm in back muscles produces opisthotonos (arching
of the neck and back due to spasm).
• Stiness in the neck, back and abdomen follows,
together with generalized spasm, which may cause
asphyxia.
• Muscles remain in spasm between convulsions.
• Death may also occur from inhalation of vomit with
aspiration pneumonia.
Diagnosis
• Diagnosis is usually clinical.
• Attempts at bacteriological conrmation oen fail.
Prevention
• Tetanus is rare because of active immunization programmes in childhood with tetanus toxoid.
• All children should be immunized; this is carried out
at 2, 3 and 4 months; preschool; and between 13 and 18
years of age.
• Aer the 5th dose, immunity remains for life and further boosters are not required.
Treatment
Preventative.
• Patients attending A&E with new trauma, however
mild, should have a booster dose of tetanus toxoid if
they have not had a full course.
• Contaminated and penetrated wounds should be
debrided.
• Prophylactic penicillin should be administered.
• ose with contaminated wounds should be given
human antitetanus immunoglobulin.
Treatment in suspected case
• Passive immunization with antitetanus immunoglobulin.
• Adequate wound debridement.
• Intravenous benzylpenicillin.
• Intensive care support.
• Despite the supportive measures, mortality is about 50%.
Abscesses
• A localized collection of pus.
• Walled o by a barrier inammatory reaction (pyogenic membrane). Fibrosis occurs, ‘encapsulating’ the
abscess.
• erefore, impossible to treat abscesses satisfactorily
with antibiotics alone.
• Surgical drainage is necessary.
• Without treatment abscesses tend to ‘point’ spontaneously to the nearest epithelial surface, e.g.:
• skin (boil)
• gut (pelvic abscess to rectum)
• bronchus (lung abscess).
• Spontaneous drainage oen leads to healing, provided
the initiating stimulus has been eliminated.
• If spontaneous drainage does not eliminate the initiating
stimulus, a chronic abscess forms, oen resulting in a continuously discharging sinus which intermittently develops, discharges and heals, e.g. stitch abscess and stitch
sinus which does not settle until the stitch is removed.
• Treatment of abscesses inappropriately with antibiotics
alone may halt expansion of the abscess and sterilize the
pus, giving rise to a sterile abscess or ‘antibioma’.
• Pyogenic abscesses are caused by a wide variety of bacteria and occur at many dierent sites (Table 21.1).
• Abscesses do not necessarily form at the site of primary
infection, but may form at a distant site, e.g. pelvic or
subphrenic abscesses aer perforated appendicitis.
• ‘Metastatic’ abscesses may form as a result of haematogenous spread or ‘pyaemic’ spread of infected thrombi,
e.g. portal pyaemia following appendicitis may result
in liver abscesses; infective endocarditis may result in
cerebral abscesses.
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