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Wound infection is the invasion of a wound by
proliferating microorganisms to a level that
invokes a local, spreading and/or systemic
response in the host. Microorganisms multiply
within the wound, developing a range of virulence factors to overcome the host defenses leading to local tissue damage and impeding wound
healing [65, 66].
In 2016, the International Wound Infection
Institute (IWII) stated that the concept of critical
colonization, which suggests a specic moment
when microbial burden reaches a critical level
(above 105cfu/mL of exudate or per gram of tissue), was not representative of the science.
Consensus was reached that the term local wound
infection more accurately represented the phase
of infection in which covert (subtle) local clinical
indicators of infection (e.g., pocketing, epithelial
bridging, and hypergranulation) can be identied
by expert wound clinicians. These clinical indicators are primarily observed in the hard-to-heal
wound or before the wound exhibits overt (classic) signs and symptoms of erythema, warmth,
swelling, purulent discharge, delayed wound
healing beyond expectations, new or increasing
pain, and increasing malodour. The term local
wound infection is now well accepted as describing a phase within the IWII-WIC [49, 56].
The International Wound Infection Institute
(IWII) has developed a tool to conceptualize the
impact that microorganisms have on the host, the
wound and on wound healing. The IWII-WIC,
based on expert consensus, is a way to conceptualize the microbiological process, informed by
clinical presentation of wounds [49].
It is composed by ve stages: contamination,
colonization, local infection (covert and overt
stages), spreading infection, and systemic
infection.
Contamination is used to refer to a stage in
which there is presence within the wound of
microorganisms that are presumed not to be proliferating. No signicant host reaction is evoked
and no delay in wound healing is clinically
observed [67]. In a contaminated wound, the host
defenses destroy microorganisms through a process called phagocytosis [68, 69].
Colonization is used to refer to a stage in
which the presence of microorganisms within the
wound that are presumed to be undergoing limited proliferation. In a colonized wound, no signicant host reaction is evoked, and no delay in
wound healing is clinically observed [67]. Due to
the protective function of the skin microbiome,
all open wounds are colonized with microorganisms at the time of skin breakdown [70], but at
this stage the virulence appears to be low.
Microorganisms that colonize a wound may also
arise from exogenous sources or as a result of
environmental exposure.
Local infection is used to refer to a stage of
infection in which there is presence and proliferation of microorganisms within the wound that
evoke a response from the host, often including a
delay in wound healing. Local infection is contained within the wound and the immediate periwound region (less than 2cm). Local infection
often presents with subtle signs and symptoms
[56, 57] that may not be immediately recognized
but are important to research.
Subtle signs and symptoms of wound infection include [71, 72]:
• Hypergranulation.
• Bleeding, friable granulation.
• Epithelial bridging and pocketing in granula-
tion tissue.
• Increasing exudate.
• Delayed wound healing beyond expectations.
As local wound infection progresses, classic
cardinal (overt) signs and symptoms that are traditionally associated with local infections generally become evident and are more recognizable
as an indicator of wound infection. However,
these symptoms may be masked in people with
compromised immune systems and/or poor vascular perfusion.
Overt (classic) signs and symptoms of wound
infection may include [71, 72]:
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• Erythema (which may present differently
depending on the individual’s skin tone).
• Local warmth.
• Swelling.
• Purulent discharge.
• Wound breakdown and enlargement.
• New or increasing pain.
• Increasing malodour.
Spreading infection (also referred to as cellu-
litis) describes the stage of infection in which
there is invasion of the surrounding tissue by
infective microorganisms that have spread from a
wound. Microorganisms proliferate and spread to
a degree that signs and symptoms extend beyond
the wound border [73, 74]. Spreading infection
may involve deep tissue, muscle, fascia, organs,
or body cavities. Spreading infection signs and
symptoms may include [71, 75]:
• Extending induration.
• Lymphangitis (swelling of lymph glands).
• Crepitus.
• Wound breakdown/dehiscence with or without satellite lesions.
• Spreading inammation or erythema greater
than 2cm from the wound edge.
Systemic infection refers to the stage of infec-
tion in which microorganisms spread throughout
the body via the vascular or lymphatic systems,
evoking a host response that affects the body as a
whole. In the context of wound infection, microorganisms spread from a locally infected wound.
Systemic inammatory response can also be triggered by a local wound infection through other
pathways, for example release of toxins or a dysregulated immune system. Systemic signs and
symptoms of infection may include [75, 76]:
• Malaise.
• Lethargy or nonspecic general deterioration.
• Loss of appetite.
• Fever/pyrexia.
• Severe sepsis.
• Septic shock.
• Organ failure.
• Death.
33.6 How toDiagnose Wound
Infection
Diagnosis of wound infection is a clinical
decision based on the presence of signs and
symptoms of infection including the classic
cardinal signs of heat, pain, swelling, suppuration, erythema, and fever [77]. Microbiological
results are used to provide information on the
presence or absence of microorganisms and to
identify the organisms and their sensitivities.
Antimicrobial treatment can be selected based
on susceptibilities of the specific pathogen(s).
Elevated inflammatory markers and positive
blood cultures also quantify the presence of
infection. Because all wounds are contaminated with microorganisms (i.e., not all microorganism contamination is associated with
adverse effects), a wound should only be cultured to guide the selection of treatment after
making a clinical diagnosis of wound infection based on signs and symptoms, or when
there remains a high clinical suspicion of
wound infection [56].
Clinical diagnosis of wound infection can be
conrmed with haematological, radiological, and
microbiological investigations. The purposes are
to identify systemic effects, to assess for presence of osteomyelitis, to identify complications,
to identify causative microorganisms and to
select antibiotic therapy [56].
Diagnostic investigations
Haematological markers
White blood cell (WBC)
counts (e.g., granulocytes,
lymphocytes, monocytes)
WBCs indicate an
immune response
C-reactive protein (CRP)
Erythrocyte
sedimentation rate (ESR)
Blood cultures Performed to detect an
Microbiology Diagnostic investigations
purpose
Detect presence of
infection in the body;
Detect inammation
related to infection
Detect inammation
related to infection
infection in the blood and
identify the causative
organism(s). A positive
blood culture indicates
bacteraemia
purpose
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Haematological markers
Wound culture Identify causative
Radiological
investigations
Plain X-rays Identify presence of
White cell/bone scan
Magnetic resonance
imaging (MRI)
Computerised
tomography (CT)
Fluorodeoxyglucose
positron emission
tomography (PET)
Leukocyte scintigraphy
(with or without CT)
Ultrasound Identify extent of abscess,
Diagnostic investigations
purpose
organism(s) of infection
Construct antibiogram
based on sensitivity
testing
Diagnostic investigations
purpose
osteomyelitis or abscess
uid collection or
haematoma
The following methods can be used to collect
a sample from the wound for microbiological
analysis:
• Tissue biopsy or curettage.
• Wound uid aspirate (i.e., pus collection).
• Debrided viable tissue from the ulcer base via
sharp debridement.
• Wound swab.
Where pus is present, it can be aspirated
using a sterile syringe and needle and transferred to an appropriate specimen collection jar
[78]. Tissue biopsy is the preferred sampling
method. It provides both quantitative and qualitative information. A tissue biopsy enables both
the identication of the organism(s) present in
the wound and the virulence [63].
When performing a swab, the Levine technique should be performed: After cleansing the
wound using an inert (chemically inactive)
wound cleanser, two wound swabs should be collected. In the laboratory, the rst sample is used
for a Gram stain to determine if the bacteria are
Gram-positive (e.g., Staphylococcus aureus and
Streptococcus epidermidis) or Gram-negative
(e.g., Escherichia coli and Pseudomonas aeruginosa). These results are usually available from
the laboratory within hours. A second wound
swab should be placed in transport medium and
is used to identify the species of bacteria [56].
Despite being the most widely used wound specimen collection method, microbiological analysis
of a wound swab can only identify microorganisms on the surface of a wound and not the
organism(s) beneath the surface of the wound
[79]. Additionally, not all microorganisms collected on a wound swab will survive during transportation to the laboratory, inuencing the
accuracy of wound swab results [56].
Recent advances in DNA-sequencing technology and the development of molecular techniques
to identify and quantify microorganisms have
revolutionized our view of the microbial world.
Characterization of the bacterial microbiome
takes advantage of the 16S rRNA gene, present in
all prokaryotes, but not eukaryotes. The 16S
rRNA gene encodes a structurally and functionally essential component of the ribosome, and
contains species-specic hypervariable regions
that are markers to identify bacteria, and highly
conserved regions that allow broad-range amplication by polymerase chain reaction (PCR) [80,
81].
16S rRNA gene sequencing allows characterization of the microbiome based on all three
dimensions: microbial load, microbial diversity,
and presence of pathogens [32]. The most utilized regions in current published research
involving skin and wounds are the V4 region and
V1–V3 region.
Although these techniques are much more
sensitive than culturing, the quality of DNA
extraction varies according to species and so may
still carry some inherent bias. They also do not
distinguish between live and dead bacteria and
are much more time-intensive and require costly
equipment [82].
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Classication ofWound Infections
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MatteoBassetti, AntonioVena,
andNadiaCastaldo
34
34.1 Introduction
Management of infected wounds is complex
mainly because distinguishing a chronic uninfected wound from an infected wound may be
challenging. In addition, chronic wound infections, which can delay the healing process, have
been associated with a high rate of recurrence
and complications (e.g., osteomyelitis, need for
amputation), with a signicant impact on quality
of life (e.g., increased pain), disability, hospitalization, mortality, and healthcare costs [1, 2].
It has been estimated that different type of
wounds, with or without infection, affect almost
eight million people worldwide [3]. A recent retrospective analysis conducted in the U.S. found
that the prevalence for all chronic wounds is
1–2% among the whole population, with total
healthcare costs estimated from $28.1 to $96.8
billion [4]. Similar ndings have been reported in
European studies [5].
M. Bassetti (*) · A. Vena
Infectious Diseases Unit, Policlinico San Martino
Hospital-IRCCS, Genoa, Italy
Department of Health Sciences (DISSAL), University
of Genoa, Genoa, Italy
e-mail: matteo.bassetti@hsanmartino.it
N. Castaldo
Department of Pulmonology, University of Udine and
Azienda Sanitaria Universitaria Integrata di Udine,
Udine, Italy
The prevalence of chronic and infected
wounds is currently increasing, mainly due to the
aging of global population. It has been estimated
that almost 3% of people aged more than 60years
will develop lower limbs ulcers during their lifetime, and almost 33% of these wounds will last
more than 6months. The risk of infection in such
population is extremely high, with an overall
prevalence of wound infections of 22–27% [6, 7].
Amongst people living with diabetes, the risk is
even higher. The lifetime risk of developing
lower limb ulcers amongst diabetic patients is
15–25% [8, 9], the risk of developing diabetic
foot infections (DFI) is 60%, and 20% of these
will require amputation [10].
34.2 Classication According
totheType ofWound (the
Wound Healing Society
System)
The pathogenesis of infection is common to
almost all skin and soft tissue infections,
including wounds. The majority of infected
wounds results from a traumatic injury (e.g.,
mechanic friction, prolonged pressure, burns,
animal or human bites, surgery). The rupture of
skin integrity allows the bacteria commonly
colonizing the skin to infect the host and to
translocate to deeper structures. The likelihood
of the microbiological population to infect the
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
https://doi.org/10.1007/978-3-031-45453-0_34
369
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wound strongly relates to the microbiological
load, the virulence of the pathogens, and the
host defense [11]. This explains the microbiology of infected ulcers. Most of them arise from
endogenous microorganisms, which colonize
the skin and the mucosa. In some cases, the
causative organisms penetrate from the external environment.
Wound infections are often polymicrobial,
with Gram-positive (Staphylococcus aureus, and
streptococci) being the most common isolated
pathogens, followed by Gram-negative bacilli
(Proteus spp., Escherichia coli, Klebsiella spp.,
and Pseudomonas aeruginosa), and anaerobes
(Peptostreptococcus, Clostridium spp) [12].
Origin of the wound, size and duration of the
wound, body location, and patient’s comorbidity
may inuence the wound colonization and the
subsequent infection [13].
Traditionally, wounds are classified as
acute or chronic according to how long the
wound will heal. Acute wounds (e.g., abrasions, thermal wounds, cuts, and surgical
wounds) usually result from an external injury.
Generally, these wounds tend to heal within
3 weeks from the occurrence [14]. However,
many intrinsic and extrinsic factors contribute
to slowing the healing process and to chronicize the wounds. These include local conditions (recurrent trauma, poor vascular
perfusion, and venous hypertension), immune
status, and chronic diseases (diabetes, autoimmune disease, neurological defect, nutritional
deficiency, and aging) [15, 16]. Despite the
lack of a universally approved definition of
“chronic wound”, the majority of authors consider as chronic, those wound that do not heal
after a period ranging from 4 weeks to
3 months [17]. According to the Wound
Healing Society, chronic wounds are classified
into four major groups, based on the causative
etiologies: diabetic foot ulcers, venous ulcers,
arterial insufficiency ulcers, and pressure
ulcers [16]. The epidemiology of infections
associated with acute wound and the four
major groups of chronic wounds will be discussed below.
34.2.1 Acute Wounds: Burns,
Traumatic Ulcers, andBite
Wounds
Among acute wounds, burns, surgical site, and
traumatic ones are the most prone to infection
[18]. Burn injuries are responsible for 180,000
deaths per year in the U.S [19, 20]. It has been
estimated that 75% of all burn injury-related
deaths are attributed to wound infections and
other infection complications beyond respiratory
injuries [21]. The FDA categorizes thermal injuries as either burns or ulcers, with ulcers meaning
wounds that have failed to heal [22]. Most of the
available classications of the burns are based on
their depth, surface area, and location. However,
others coexisting conditions such as patient’s age
and comorbidity should be also considered as
well [23, 24]. Wound infections after thermal
injuries frequently involve polymicrobial population (primarily Gram-positive bacteria including
methicillin-resistant S. aureus, but also Gram-
negative bacteria such as P. aeruginosa,
Acinetobacter spp., and Klebsiella spp., and
fungi) [25–28].
Animal bites affect 200 per 100,000 persons
per year in the U.S [29]. Human bites occur with
a highly variable frequency and may be either
directly or indirect caused (e.g., a traumatic
impact between the limb of a person with another
person’s teeth).
Most of the bite wounds derive from animals
(especially dogs) and mostly affect children [30].
Infectious complications are frequent. It has been
estimated that 10–20% of bite wounds become
infected, with highly variable rates based on the
nature of the bite (ranging from 30–50% in case
of cat bites, to 20–25% for human bites), the
depth, the level of contamination, and the site
[30–32].
As for etiology, up to 60% of infections in
bite wounds are polymicrobial [33, 34]. They
are generally caused by pathogens from the normal oral ora of the biting animal/human, and
from victim’s skin microbiota [35, 36].
Infections of human bites generally include S.
aureus, Streptococcus spp., Peptostreptococcus
34 Classication ofWound Infections
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371
spp., Fusobacterium spp., and Eikenella spp.
Cat bites generally become infected with
Pasteurella spp., Capnocytophaga spp., S.
aureus, Bartonella henselae, Bacteroides spp.,
and Fusobacterium spp.; dog bites more frequently involve Pasteurella spp., Bacteroides
spp., Fusobacterium spp., Capnocytophaga
canimorsus, and S. aureus [37].
Traumatic wounds (e.g., abrasions, laceration,
and cuts) are caused by local injuries with extensive tissue loss, which might also interest bone
and internal organs. These ulcers generally occur
in elderly patients with chronic use off corticosteroids [38]. Causative pathogens of traumatic
wound infections are more frequently those of
skin microbiota. Gram negatives and microbiological ora from external environment (including fungi) can also be the culprit. Lethal septic
complications, including necrotizing infections,
abdominal infections, and necrotizing fasciitis
have been described after traumatic wounds [39].
Invasive fungal infections are known complications of traumatic wounds, especially in those
caused by work accidents, war bombing, and
natural disasters [40].
34.2.2 Diabetic Foot Ulcers
Diabetic foot ulcers (DFUs) are frequent complications of diabetes. They occur in consequence to
a skin ulceration resulting from peripheral neuropathy or vasculopathy. Neuropathic and vascular changes cause foot deformities and loss of
sensation, as to facilitate the skin injury and subsequent wound. Specically, the high-pressure
areas are those at highest risks of damage from
repetitive trauma and stress [41]. Poor vascularization and altered immune status compromise
wound healing and predispose to infection.
Diabetic foot infections (DFIs) are generally
caused by colonizing bacteria (one or more),
which proliferate and cause tissue damage, leading to clinical infection. Infection in DFU is clinically dened by the presence of signs of
inammation or purulence, although other non-
classical signs may appear (e.g., non-purulent
secretions, abnormal granulation tissue, and
odor) [42]. According to the European Study
Group on Diabetes and the Lower Extremity
(EURODIALE), 58% of DFUs develop an infection [43]. The risk for DFIs is higher in presence
on some predisposing factors: deeper DFUs,
wounds present for >30days, recurrent wounds,
traumatic wounds, severe neuropathy or vascular
insufciency, a history of previous lower extremity amputation, coexistence with renal insufciency. Most available classication systems
have been specically developed for infected
DFIs (see below).
34.2.3 Venous Ulcers
Leg venous ulcers (LVUs) result from venous
valve incompetency, with subsequent venous
hypertension and venostasis. LVUs are the most
frequent type of lower limb vascular ulcer,
accounting for 80% of all leg wounds of vascular
origin [44]. Main contributing risk factors to
LVUs include concomitant artery disease, immobility, trauma, cancer, oedema, obesity, previous
limb wounds, phlebitis, deep venous thrombosis,
diabetes, advanced age, obesity, and smoking
habits [45].
Microbial colonization of LVUs is a frequent
nding. Risk of microbial invasion and progression to infection are augmented by the same factors predisposing to venous disease. Signs of
cellulitis, delayed healing, increase in skin temperature, increase in ulcer pain, changes in granulation tissue, bleeding, foul odor, necrotic
spots, and ulcer size enlargement are some of
the signs of LVU infection [46]. The most common microorganisms isolated in venous ulcer
infections are Gram positives from cutaneous
microbiota (primarily S. aureus) followed by P.
aeruginosa and E. coli. Less frequently, other
Enterobacterales, Streptococci, Acinetobacter
baumannii, coagulase- negative staphylococci,
and Stenotrophomonas maltophilia are also iso-
lated [47].
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M. Bassetti et al.
34.2.4 Arterial Insuciency Ulcers
Arterial disease-related wounds cause up to 30%
of leg ulcers [48]. Atherosclerotic peripheral arterial disease is the major cause of arterial ulcers,
and it generally occur in patients with specic
risk factors (e.g., smoking, diabetes, dyslipidemia, hypertension, and advanced age) [49].
Other causes of arterial ulcers are diabetes, rheumatic diseases, vasculitis, pyoderma gangrenosum, and haemoglobinopathies [50].
Similar to venous ulcers, microbiological colonization of arterial wounds is quite frequent.
Poor arterial blood supply signicantly reduces
tissue’s resistance to infection, especially in
elderly and diabetic patients [51, 52].
Furthermore, inappropriate local oxygenation
can mask the traditional signs and symptoms of
infection, thus interfering with diagnosis [51,
52]. Accordingly, a high index of suspicion is
required when evaluating arterial ulcers to successfully achieve a positive diagnosis, even in the
absence of clear signs of inammation [53]. The
diagnosis of infected arterial wounds always
requires comprehensive physical exam, microbiological, and clinical assessment of the wound
site by a multi-specialist team. Most frequent
microbiological isolates in infected arterial ulcers
are the same of DFIs (e.g., S. aureus and
β-hemolytic streptococci). Interestingly, longterm lesions and those with more severe are more
prone to Gram-negative bacteria and anaerobes
infections [54, 55].
34.2.5 Pressure Ulcers
Pressure (or decubitus) ulcers (PUs) are skin
tears caused by continuous compression on bony
prominences. PUs frequently occur in hospitalized, bedridden, and frail patients. It has been
estimated a prevalence of pressure ulcers of
11–40% in nursing homes, 3–26% in hospitals,
and 39% among patients with spinal cord injuries
[56–59]. In recent years, incidence rates of PUs
have signicantly increased [60], probably
reecting the rapid changing in medical practices
as well as the increasing aging population that
confront us with more complex underlying
diseases.
Notably, PUs occur relatively early after
admission. Nonetheless, 15% of elderly patients
will develop PUs within the rst week hospital
stay [61]. Several risk factors for the development of PUs have been described including
advanced age, male sex, poor mobility, malnutrition, low body mass index, incontinence, neurological impairment, chronic health conditions
(e.g., diabetes mellitus, renal failure, and heart
failure), external pressure or friction, shear stress,
immobility, and local moisture [62, 63].
Tissue necrosis and exposure of deep tissues
predispose pressure wounds to colonization and
subsequent local infections, necrotizing skin and
soft tissue infections, osteomyelitis, and sepsis.
Non-healing of ulcers signicantly increases the
risk of infection. The microbiological colonization of PUs is dependent on host immunity and
environmental factors, including the wound care,
the previous antibiotic treatments, the site of the
ulcer, the presence of neurogenic bladder dysfunction, external condom catheter use, and bacteriuria [64]. PUs infections are generally
polymicrobial (Staphylococcus spp.,
Enterococcus spp., Proteus mirabilis, Escherichia
coli., Pseudomonas spp., and anaerobes) [35].
As for clinical assessment, pressure ulcers
require a rapid identication of patients at risk
and early recognition of signs of decubitus ulcers
formation. In addition, an appropriate clinical
evaluation of decubitus sores is of paramount
importance when assessing the focus of the infection in a critical ill patient with sepsis or septic
shock. Several assessment tools have been proposed to identify the patients at risk, and consequently prevent PUs. Currently, each institution
uses different tools, and none of them has been
universally accepted [64–66]. The severity of
pressure ulcers is generally graded according to
The National Pressure Ulcer Advisory Panel into
four stages, from non-blanchable erythema of
intact skin (stage I) to full-thickness skin loss
involving deeper structures, such as muscle,
bone, or joint structures (stage IV) [67].
Approximately, half of PUs of stage II and 95%
of stage III and IV do not heal within 8weeks
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