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societies are trying to pursue studies and
consensus on telemedicine, for example, cardiologists, who are very advanced for the pathology that well combines with telemonitoring,
others, for example, gastroenterologists, do not
have much evidence on telehealth, telemonitoring and teleconsultation. On telehealth, then (a
telehealth delivered by non-medical health professions, to put it simply) the evidence is virtually
absent. And so why should physicians prescribe a
telehealth service (unquestionable judgment) or
telemonitoring, or teleconsultation without evidence to support them?
Worse are the other aspects of the standard of
care that transcend clinical assessment: suitability of technological equipment, hygienic conditions. One would need a team of engineers and
environmental hygiene experts, and then, who
will verify and certify digital literacy?
32.1 The Provider Center
andtheService Center
task of distribution of medical devices to the
patient’s home, their installation, maintenance as
well as pick-up and sanitization at the end of the
service. The Provider Center, managed mainly by
healthcare providers, provides telemedicine services for patient monitoring; clinical parameters
are monitored and health alerts are handled.”
It is not very clear whether it is meant to talk
ONLY about telemonitoring, since in the previous schemes published by AGENAS and
approved at the state-regions conference, the service center is also indispensable in telehealth and
tele-assistance. We understand this paragraph in
the original concept, expressed in the initial sentence: the provider center is the health center, the
ASL itself, the service center is the technology
and related services partner. So, the service center does not have alarm nurses or doctors, the service center is a technical partner, the provider
center is a clinical partner. In some cases, these
two souls may physically coexist in the same
place but with quite different professionals.
We have seen the “bad,” but we also see the good:
some of the denitions found in the 2014 telemedicine guidelines and then apparently completely forgotten in the 2020 guidance reappear
in the guidelines: the presence of two types of
competency centers, which are indispensable: the
service center and the provider center. The
Ofcial Gazette (OG) denes them as follows:
“For each regional telemedicine infrastructure
there must be the presence of one or more Service
Centers, with purely technical tasks, and one or
more Provider Centers, with purely healthcare
tasks. The two entities, depending on the different territorial contexts, may also coexist in a single organization. The Service Center, managed
mainly by technical staff, takes charge of all technological aspects such as platform maintenance,
account management, help desk for all users
taken over by the regional telemedicine infrastructure, monitoring the proper functioning
(including the management of technical alert
messages) of medical devices, training on the use
of medical devices to patients/caregivers, etc.
The Service Center can also be entrusted with the
32.2 Do Televisit Platforms Have
toBeMedical Devices?
Another interesting point is well understood:
must televisit platforms be certied medical
devices? Here, the guidelines seem very clear:
“Where medical devices are used in the Televisit
service, again, as indicated above for
Teleconsultation, the software and ‘hardware for
the delivery of the service shall be certied as a
medical device with appropriate risk class within
the regional telemedicine infrastructure” Only if
medical devices are used in the service must the
televisit platforms or teleconsultation/ telehealth
APPs also be certied as DM; however, if you
ask a patient or caregiver or RSA nurse to measure blood pressure and verbally communicate
the data, you don’t need certication as a medical
device for the platform.
And this claries the confusion generated by
what was stated in the 2020 national guidance on
telemedicine that stated as follows:
Remote healthcare delivery: necessary elements and standards. Listed below are the set of
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minimum and sufcient elements to implement a
service with the functionality to deliver a service
at a distance. Basic features: (...) g. certication
of the hardware and/or software, as a medical
device, suitable for the type of service to be provided in telemedicine.
Many distinguished speakers talk about “mandatory certication for telehealth, teleconsultation, Telehealth platforms.” Now it is clear: the
obligation exists only if one uses medical devices
integrated into the platform.
Are we there? Almost, and as any good manager knows almost is never the right answer.
Nicolo Carosio,“ the “father“ of all soccer radio/
television announcers, in 1954, the year RAI
broadcasting ofcially began, became famous for
his “almost goal!” exclamation emphasizing an
action nished just wide of the goal.
32.3 Electronic Prescription
inPractice
Regions did their homework, even in the preCOVID era, some electronic prescriptions had to
be printed on the “red” prescription sheet, the old
one, especially for more expensive drugs. This
rule has been abolished everywhere and today all
prescriptions can be printed on white paper, still
missing the “white prescription,” for class C
drugs as an electronic prescription. The Minister
of Innovation has claried that even with only the
Electronic Recipe Number (NRE) the pharmacist
can supply the drug. Unfortunately, despite the
numerous clarications sent, many pharmacies,
while accepting the NRE code, do not provide the
drug until after printing the prescription directly
at the pharmacy, resulting in longer “queues”
outside pharmacies. Some do not accept the NRE
code and refuse to provide the medication.
32.3.1 Televisit
Recognized, reimbursed, recommended--but
practically not easy to do. General practitioners
in most regions of Italy do telephone-medicine,
certainly not televisit, there is a lack of wide-
spread platforms that can be used by GPs, most
of the centers of high specialization are within
hospital companies which in most cases are
very slow to start off path of specialist televisits.
According to CIRM, the International Radio
Medical Center, even experienced professionals
have to undergo specic training before being
put on shift and starts by doing only short and
“simple” shifts, only when a technician is present, who can help him in the technical problems
of using the platform. He does not do overnights, so that he can ask more experienced colleagues for clarications on complex cases. A
2018 [2] article published in “Pediatric
research,” one of the world’s most prestigious
journals on the subject, part of the Nature
group, titled “Physicians’ experiences, attitudes
and challenges in a Pediatric Telemedicine
Service” explored the experiences, attitudes,
and challenges of physicians in a pediatric telemedicine service in Israel. Fifteen physicians
who had been working in Clalit’s “Online
Pediatrician” service for the past 5years were
interviewed. The main difculties highlighted
were the problem of remote diagnosis, treating
patients who are not well known, working without assistants, emergencies and the sometimes
excessive call load, in addition to technologyrelated difculties and a “moral conict”
between the desire to meet parents’ expectations and maintaining standards of care.
Physicians do assert that at times these nonmedical factors also inuenced their decisions.
The article’s conclusions stated: “In the eld of
telemedicine, physicians face various difculties and challenges, requiring expertise, quality,
and skill. Special measures are needed to obtain
appropriate diagnoses and decisions” It must
also be premised that in Clalit, telemedicine can
only be done by those with at least ve years of
experience in the branch. We have heard about
physicians “thrown” into televisits without any
specic training and even of residents placed in
televisits. Learning how to swim takes more
than just the pool; it takes competent instructors, suitable tools, time, and commitment. The
same applies to telehealth, teleconsultation, and
telecooperation.
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32.4 Return toNormality
inSpecialist Outpatient
Clinics intheNHS
Despite the proclamations, great efforts are being
made by all professionals to recover what has
been lost in recent months, but in a system with
waiting lists, for example, in my eld, Angiology,
of several months, which was already working as
hard as possible with the doctors and available
equipment, increasing services is not easy;
indeed, it is impossible and ends up at the expense
of denied services to poor people that cannot
always be ltered. Associations of cancer
patients, patients with rheumatic and rare diseases, active citizens are becoming the interpreters of the “cry of pain” of those who have no
voice, the most fragile, who are paying for it on
their skin, literally. A patient of mine waited three
months to have a skin graft done on a lesion
(ulcer) on her Achilles tendon, and when it was
possible to do so, after three months of pain
fought even with opioids, the lesion had tripled in
size.
32.5 Articial Intelligence
Telemedicine and artificial intelligence find
their meeting point in the home setting, where
the healthcare provider, caregiver, or the user
himself can obtain evidence of wound
improvement through integrated systems that
can evaluate and transmit images and information of different formats that may use artificial
intelligence; the latter, in addition to offering
algorithms for treatment choice, should prevent biased evaluation by operators. Depending
on the modality of image capture (light conditions, different equipment), they may determine over or under estimation of wound
progress.
A further example of such systems is Negative
Pressure Therapy equipment provided with teleassistance, in this case, an automated virtual
assistant that provides answers to specic questions, e.g., guidance for remote resolution of
alarms or decision support in whether or not the
clinician responsible for that therapy should be
consulted.
Systems that rely on neural networks and rely
on algorithms to determine the presence or
absence, for example, of surgical site infection
are currently being developed; subsequently via
telemedicine, the transmission of images to the
specialist can take place [3].
The role of articial intelligence, understood as a
system capable of replicating human behavior is
to support the specialist’s decision, primarily in
assessing the progress of the injury, usually
anchored in aspects such as variation in size, or
signs of inammation and the color and quality
of the exudate.
In fact, it is more correct to speak about
machine learning, the ability of the system to
learn and improve based on the data provided to
it; given a stream of data, e.g., photographic
images of similar lesions, the system recognizes
a pattern and can make a prediction on this data,
e.g., of healing or infection; it is intuitive how
this represents an ‘opportunity for the healthcare
community: in fact, numerous clinical entities are
approaching this branch.
References
1. Barakat-Johnson M, Jones A, Burger M, Leong T,
Frotjold A, Randall S, Kim B, Fethney J, Coyer
F. Reshaping wound care: Evaluation of an articial intelligence app to improve wound assessment
and management amid the COVID-19 pandemic.
Int Wound J. 2022;19(6):1561–77. https://doi.
org/10.1111/iwj.13755. Epub 2022 Feb 25. PMID:
35212459; PMCID: PMC9111327.
2. 2-11-2022 Gazzetta Ufciale Della Repubblica
Italiana Serie generale—n. 256.
3. Fletcher RR, Schneider G, Hedt-Gauthier B,
Nkurunziza T, Alayande B, Riviello R, Kateera
F.Use of convolutional neural nets and transfer learning for prediction of surgical site infection from
color images. Annu Int Conf IEEE Eng Med Biol
Soc. 2021;2021:5047–50. https://doi.org/10.1109/
EMBC46164.2021.9630430.
Part VI
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Infection in Wound Care
Infection Diagnosis
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GiovanniPapa, PaolaPini, StefanoDi Bella,
andGiuliaBenedettaSidoti
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33.1 Flora ontheSkin:
TheMicrobiome
Normal skin is rich of commensal bacterial ora,
viruses, and fungi, collectively called microbiota.
It is rich of Gram-positive, Gram-negative, and
anaerobic bacteria, viruses, protozoa, and fungal
species differently distributed on the skin,
depending on the characteristics of the different
areas in terms of sebaceous moist/dry composition and different pH.
33.1.1 Bacteria
An individual’s skin microbiota is established
intra-partum, with maternal delivery playing a
vital role in microbial composition [1] and by the
rst contacts with people that handle newborns.
The main phyla detected are Actinobacteria
(corrig. Phyl. Actinomycetota), followed by
G. Papa · G. B. Sidoti (*)
Plastic Surgery Unit, University of Trieste, Cattinara
Hospital, Trieste, Italy
e-mail: giovanni.papa@asugi.sanita.fvg.it
P. Pini
Ospedale di Gazzaniga, ASST Bergamo Est,
Bergamo, Italy
S. Di Bella
Infectious Diseases Department, Clinical Department
of Medical, Surgical and Health Sciences, University
of Trieste, Trieste, Italy
Firmicutes (corrig. Phyl. Bacillota),
Proteobacteria (corrig. Phyl. Pseudomonadota),
and Bacteroidetes (corrig. Phyl. Bacteroidota).
Foot-skin microbiota has the least temporal stability and has been classied as a moist niche
enriched in Actinobacteria (Corynebacteriaceae)
and Firmicutes (Staphylococcaceae) [2–4].
Dry sites (e.g., volar forearm, hypothenar palm,
and buttock), despite demonstrating the greatest
microbial diversity and variability overall, contain
a greater abundance of β-proteobacteria,
Flavobacteriales, and other Gram-negative organisms [5].
Recent literature has revealed that the healthy
skin microbiome extends into the sub-epidermal
compartments with higher proportions of
Proteobacteria (Burkholderiales and
Pseudomonadales species) and Actinobacteria
and a lower abundance of Firmicutes [6].
33.1.2 Fungi
Fungal species often differ by anatomical location (head, torso, arm, leg, and feet) independently of moisture or sebaceous content [7].
While cultivation methods in earlier studies have
shown that the Malassezia genus is the major
component of the skin fungal community,
sequencing of 18S rDNA in healthy patients has
conrmed that Malassezia organisms (which
© 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_33
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includes some known pathogens) dominate the
mycobiome on most skin sites [8, 9].
A survey by Dowd etal. [10] of chronic wound
infections using molecular diagnostic reports
showed that 23% of the wounds in the study tested
positive for fungal species. The most abundant
were in the genus Candida, but others included
Malassezia, Curvularia, Phoma, Cladosporium,
and Trichophyton. Interestingly, there was a negative correlation between Staphylococcus and
Candida. Candida was also negatively correlated
with other fungi, such as Alternaria, Cochliobolus,
and Engyodontium. There were some qualitative
differences between species observed between
various etiologies of chronic wounds, but statistical signicance was not reported.
33.1.3 Viruses
The virome of normal skin has been demonstrated
to have high interpersonal diversity, with some of
the most commonly observed strains including
Papillomaviridae, Polyomaviridae, and
Herpesviridae, with differences between different
parts of the body [11, 12]. There are also lots of
phages, bacterial viruses [13]. The virome is still a
challenge, that is why scientists talk about “Viral
Dark Matter” dened as metagenomic sequences
originating from viral genomes that have not been
aligned with their host microbes [14].
33.2 Bacteria inAcute
andChronic Wounds
33.2.1 Acute Wounds
The bacterial composition and diversity of
wounds became increasingly similar to the
microbiota of adjacent healthy skin, with the relative abundance of Staphylococcus increasing
and Pseudomonas decreasing in the wound compared with adjacent skin. Interestingly, at any
time point, Gram-positive organisms were more
abundant than Gram-negative [32].
Burn wounds in these patients revealed an
increased abundance of thermophile microbes
such as Aeribacillus, Caldalkalibacilus, and
Nesterenkonia and decreased abundance of
Corynebacterium, both in the wound center and
the skin margin. Indeed, topical antibiotics have
largely aided burn wound outcomes by effectively
treating Pseudomonas colonization. However,
changes in the cutaneous microbiome were also
associated with post-burn complications, with
Corynebacterium demonstrating a positive correlation with burn wound infection, and
Staphylococcus and Propionibacterium demonstrating a negative correlation with post-burn
infection [33].
wounds is even associated with the mechanism of
injury. The most dominant microbes in open fracture wounds and adjacent skin include
Staphylococcus, Corynebacterium, Streptococcus,
Acinetobacter, Anaerococcus, Finegoldia, and
Pseudomonas [34].
infection occurring within 30days after a surgical
operation or within 1year if an implant is left in
place after procedure, and affects either incision or
deep tissues at the operation site. In most postoperative SSIs, the causative pathogens originate
from endogenous ora of the patient’s skin,
mucous membranes or hollow viscera. The most
isolated bacterial pathogens are Staphylococcus
aureus, Enterobacteriaceae, Coagulase Negative
Staphylococci, Enterococci, and Pseudomonas
aeruginosa.
the surgical procedure involved, recent reports
have documented an increasing proportion of
Gram-positive organisms and a decreasing
number of Gram-negative organisms associated with SSIs. Furthermore, there has been an
increase in incidence of SSIs attributed to
antimicrobial- resistant pathogenic bacteria
like methicillin- resistant S. aureus (MRSA)
and vancomycin-resistant S. aureus [35, 36].
33.2.2 Chronic Wounds: Bacteria
Compared with published sequence analyses of
bacteria from normal skin, chronic wounds have
more anaerobes, Gram-negative rods, and Gram-
The microbial composition of open fracture
Surgical site infection (SSI) is dened as an
Although the isolated pathogens depend on
andCharacteristics
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positive cocci, with less commensals such as
Propionibacterium [15, 18, 19].
Polymicrobial biolms, which foster pathogenic microbial growth and disrupt the coordinated events of wound healing, are highly
abundant in chronic wounds and play a vital role
in the pathogenesis of impaired cutaneous healing
[21]. Biolms provide continuous stimulation to
the innate immune system, which ultimately
delays progression to the proliferative phase of
wound healing [17, 22].
In a large clinical observation study of 2963
patients with wound samples from 910 DFUs,
916 VLUs, 767 DUs, and 370 non-healing surgical wounds, Wolcott etal. [23] demonstrated that
Staphylococcus was the most frequently encountered genera. S. aureus and S. epidermidis were
identied as the most abundant species in chronic
wounds. Moreover, although bacterial diversity
was independent of chronic wound type,
Pseudomonas aeruginosa exhibited a higher relative abundance overall in chronic wounds demonstrating biolm formation [16].
Facultative anaerobes are overrepresented
in the microbiome of non-healing wounds. In
contrast, healed wounds appeared to be
enriched with anaerobes. The presence of
pathogenic facultative anaerobes may render
the wound refractory to oxygen therapies, suggesting that oxygen therapies should be targeted against wounds with low levels of
facultative anaerobes [24].
The presence of anaerobes was related to
ulcer depth [25] and to poor prognosis [26]
Bacteria settle and are inuenced by nutrient
availability compounds such as dioxygen
(anoxic at the wound center or within the biolm and hypoxic at the edge [27–31]). In addition, glycemic control and the duration of
diabetes affected the dominance and diversity of
the microbiota. Lower levels of HbA1c and
recent diabetes were associated with higher
diversity of this microbiota, whereas the high
HbA1c level and a long lifetime with diabetes
increased the predominance of some genera in
the wound’s microbiota [20]. Interaction
between aerobic and anaerobic bacteria worsen
tissue infections.
33.3 Molecular Aspects:
Interactions Between
Bacteria andTheir Inuence
onWound Healing
Mechanistic insight into the relationship of the
altered microbiome and cutaneous inammation
has been aided by preclinical studies, including
animal models and invitro systems. Although the
ideal cutaneous wound model has not yet been
established, all these model systems may provide
valuable mechanistic insight and act as screening
tools for modulation of the human skin microbiome [22].
Skin commensals inuence a variety of cell signaling and homeostatic processes including keratinocyte proliferation, epithelial differentiation, and
epidermal blood vessel growth. While elevations
of microbial bioburden often result in infection,
high diversity of skin commensals, as seen in
healthy microbial colonization, are also involved
in both the benign induction of the immune system
and the attenuation of the immune response. For
example, skin CD8+ T cells specically elicited
by S. epidermidis promote rapid keratinocyte progression via upregulation of toll-like receptors
(TLR) and downstream modulation of TNF-α [39,
40]. In addition, S. epidermidis’ production of
lipoteichoic acid decreases cutaneous inammation via TLR2 signaling [41]. The ability of S. epidermidis to modulate the innate immune response
in non-infectious skin wounds coincides with its
ability to accelerate wound healing in various skin
model and highlights the ability for bacterial products to reduce cutaneous inammation.
S. aureus biolm increased the release of
tumor necrosis factor α (TNF-α) and decreased
the release of interleukin (IL)-6, matrix metalloproteinase (MMP-3) and VEGF from human dermal broblasts. Biolms have a detrimental
effect on human dermal broblasts migration and
ultimately result in cellular apoptosis [37].
Murine wound models have reinforced our
understanding that S. aureus and S. epidermidis
biolms delay wound re-epithelization in uninfected wounds, and this process has been shown
to be inuenced by quorum sensing. For example, Schierle et al. demonstrated that when
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exposed to quorum sensing inhibitors (RNAIII
inhibiting peptide), the cutaneous integrity of
these murine wounds was restored, abolishing
biolm formation and obliterating bacterial bioburden. Quorum sensing inhibitors represent a
broad range of enzymes and compounds that are
produced both naturally and synthetically [38].
Both S. epidermidis and the typically lowabundant S. aureus [42] induce expression of
AMPs (antimicrobial peptides) in human keratinocytes, ultimately beneting skin by providing
host protection from invasion of other pathogenic
microorganisms [43, 44].
Although S. aureus is a (normal) commensal of
human skin ora in 20–40% of population (albeit
rare), overabundance of this microbe is associated
with high rates of skin infection especially with
production of superantigens (SAg) that have varying effects at the local and systemic levels. While
exceptionally deleterious in high systemic concentrations, in small amounts, SAg production by S.
aureus decreases local downstream production of
interleukins like IL-17 and subsequent neutro-
philic chemotactic factors in cutaneous tissue,
resulting in decreased purulence of skin wounds
and decreased skin inammation compared to
non-SAg producing strains [45, 46].
In addition, Secor etal. demonstrated that S.
aureus biolms resulted in signicantly elevated
keratinocyte cytokines, such as IL-1B, IL-6, chemokine ligand (CXCL)-8, CXCL-1, and TNF-α,
demonstrating the potentially destructive effect
these microbial products have on cutaneous
inammation [47].
The impact of Pseudomonas colonization on
host epithelial tissue, once again highlights the
diverse responses in integumentary cell signaling
initiated by differing microbe levels. The various
effects of skin microbiota on cell signaling pathways suggest that small amounts of these potentially pathogenic microbes may in some cases aid
rather than harm host cutaneous tissue regeneration [22].
Table 33.1 is a summary of the positive and
negative effects of the principal bacteria on
wound healing [22]
Table 33.1 Effects of bacteria on wound healing
Bacteria Positive effects Negative effects
Staphylococcus
epidermidis
Staphylococcus
aureus
Streptococcus
group A
Pseudomonas
aeruginosa
Stimulates keratinocyte production of
host AMPs
Induces CD8+ T and IL-17A+ T cells
Enhances innate barrier immunity and
limits pathogen invasion in absence of
inammation
At a local level, supoer antigen
production results in less skin
inammation and purulence due to
decreased production of exotoxins and
neutrophilic chemotactic factors
Amplies innate immune response of
skin via production of AMPs (hBD-3,
bHD2, LL-37, RNAse7)
Stimulates production of AMPs,
promote epithelial differentiation
Activates plasminogen which promotes
ketatinocytes chemotaxis and potential
re-epithelization
Accelerates epithelialization and
neovascularization in acute wounds
Suppresses staphylococcal pathogens in
polymicrobial wounds
Occasionally
pathogenic
Implicated in
production of biolm
Usually pathogenic
Implicated in
production of biolms
and delayed wound
healing in chronic
wounds
Superantigen
production elicits
robust activation of
immune system
Usually pathogenic
Express proteases
which prevent
neutrophil recruitment
Produces hyaluronidase
Usually pathogenic
Implicated in
production of biolms
and delayed wound
healing
Associated signaling
pathways
NF-kB, TRAF1, TLR2/
CD36/CD14-p38, MAPK,
EGFR, TRAP
TRAP, ERK, NF/kB,
TLR-2,
phosphatidylinositol
3-kinase/AKT
NF/kB
Nod2
TAK1/MKK/p38
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33.4 Biolm: Denition,
Diagnosis, andImplications
onTherapy
A prevalence study conrmed almost 80% of
chronic wounds contained biolms, leading the
authors to conclude that biolms are ubiquitous
in a chronic wound [48].
Theoretical constructs of wound biolm to
date have primarily focused on extrapolating
that is known from invitro studies of biolms to
the chronic wound clinical environment. It is
also extremely important to acknowledge the
differences between a laboratory microenvironment in which an invitro biolm is grown and
studied, and the environment of an acute or
chronic wound (in vivo) that experiences biolm [49].
Research has established that, in the in vivo
setting, an infectious microenvironment develops, with low oxygen (hypoxic conditions), pH
changes, and slow-growing microbial cells [50].
As described in the literature, in vitro biolms
are initiated by planktonic microorganisms and
follow a dened developmental cycle. The
invitro hallmark of biolms is the presence of a
self-produced matrix of extracellular material
composed of polysaccharides, proteins, extracellular DNA and supporting cross-linking metal
ions such as calcium, magnesium, and iron.
However, this knowledge may not directly translate to biolm behaviour within a wound. How
biolms develop in chronic and acute wounds is
still unknown. Wound biolms can be embedded
in slough, debris, necrotic, and other tissues, and
the wound dressing itself [49].
Apart from being present both in aggregates
and as single cells, microorganisms are present
on both the wound surface and embedded beneath
the surface of the wound bed within the extracellular matrix [51].
Bjarnsholt etal. [52] conducted a systematic
review of the size of the biolm aggregates in
clinical biolm infections. The dimension of the
biolm in chronic wounds ranged from 5 to
200μm.
The article by Bjarnsholt etal. [53] found similarities between the etiology of the chronic lung
infection of cystic brosis patients and chronic
wounds with respect to biolm formation and
accumulation of polymorphonuclear leukocytes
(PMN) around the bacterial biolms. There were
also indications that the PMNs exhibited impaired
antimicrobial function in the vicinity of the biolms. It was proposed that this lack of efcacy
was due to PMN killing by secreted virulence
factors, such as rhamnolipid produced by
Pseudomonas aeruginosa [54].
Current science has demonstrated that biolms cannot be observed by the naked eye in biological systems such as a chronic wound without
the assistance of diagnostic techniques [55].
Currently, there is no gold standard for wound
sampling to identify biolm or the presence of
microorganisms. If a wound is hard-to-heal and is
not responding to standard protocols of care (e.g.,
antimicrobial intervention), it should be assumed
that tolerant microorganisms, within a biolm,
are present. In the absence of laboratoryconrmed diagnosis, the best practice suggests
that presence of biolm be presumed in wounds
displaying signs and symptoms of chronic
inammation [49].
Criteria that are indicative of possible wound
biolm that have been established through expert
consensus are [56, 57]:
• Failure of appropriate antibiotic treatment.
• Recalcitrance to appropriate antimicrobial
treatment.
• Recurrence of delayed healing on cessation of
antibiotic treatment.
• Delayed healing despite optimal wound man-
agement and health support.
• Increased exudate/moisture.
• Low-level chronic inammation.
• Low-level erythema.
• Poor granulation/friable hypergranulation.
• Secondary signs of infection.
Biolms have increased tolerance to antimicrobial treatments. There is a growing body of
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evidence and agreement amongst wound
33.5 Wound Infection
clinicians and scientists that debridement represents a necessary process in reducing the presence of a biolm within a wound [49].
Most bacterial cells present in outer layers of
the biolm frequently meet antibiotics and are
more susceptible to various antibiotics. These
exposed cells in the biolm quickly die on exposure to antibiotics. However, it is believed that the
persistent cells in the biolm are found to be resistant to the entire removal of biolm- producing
bacteria. These wild-type persistent cells remain in
a dormant state in the presence of antibiotics and
usually tolerate them [58]. Roberts and Steward
found about 0.1–10% persistent cells in a biolm
[59]. Furthermore, Lewis described that when
antibiotic treatment is stopped, the persistent cells
become metabolically active to restart the formation of biolm [60].
Wound risk factors
Acute wounds
• Contaminated or dirty wounds
• Traumatic injuries
• Operation is classied as contaminated or
dirty
• Inappropriate hair removal
• Operative factors (e.g., prolonged surgery,
blood transfusion or hypothermia)
Environmental risk factors
• Unhygienic environment (e.g., dust, unclean surfaces, or presence of mould/mildew)
• Hospitalisation (due to increased risk of exposure to antibiotic resistant microorganisms)
• Inadequate hand hygiene and aseptic technique
• Inadequate management of moisture (e.g., due to exudate, incontinence or perspiration)
Individual (host) risk factors
• Poorly controlled diabetes (i.e., hyperglycaemia)
• Peripheral neuropathy (sensory, motor and autonomic)
• Neuroarthropathy
• Radiation therapy or chemotherapy
• Conditions associated with hypoxia and/or poor tissue perfusion (e.g., anaemia, cardiac disease, respiratory
disease, peripheral arterial disease, renal impairment or rheumatoid arthritis)
• Immune system disorders (e.g., acquired immune deciency syndrome)
• Connective tissue disorders (e.g., Ehlers-Danlos syndrome)
• Corticosteroid use
• Malnutrition or obesity
• Alcohol, smoking or illicit drug use
• Poor compliance with treatment plan
Chronic wounds
• Duration of wound
• Large wounds
• Anatomically located near a site of potential contamination
• Foreign body presence (e.g., drains, sutures or wound dressing
• Haematoma
• Necrotic or sloughy wound tissue
• Impaired tissue perfusion
• Increased exudate and oedema that is not adequately managed
• Wounds over bony prominences or probing to bone
• Involvement of tissue deeper than skin and subcutaneous tissues
The primary determinants of the pathological
process through which presence of bacteria and
other microorganisms results in wound infection
are the immune system, the number and the species of microorganism, the combination of the
ora [49]. Some microorganisms appear to synergistically overwhelm the individual’s immune
system more rapidly, through either collaborative
or competitive processes [61, 62].
The symbiotic relationship between the host
and the colonizing microorganism becomes
pathogenic when the host’s immune system
becomes compromised by the virulence of organisms present within a wound, [63] and wound
infection occurs [64].
The following chart explain the risk factors for
wound infection.
(e.g., perineum or sacrum) acute and chronic wounds
fragments)
(e.g., tendon, muscle, joint or bone)
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