Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 1037 - файл
.pdf
186 M. Papi and E. Fiscarelli
obtained with a fungal culture. In immunocompromised patients, the inhalation of
conidia may lead to pulmonary infection and multi-organ involvement.
Mycetoma
The disease is characterised by numerous deformations and disabilities, high
morbidity, and in its late stage it is potentially fatal (Sehgal 1990). Mycetoma is
endemic in the so-called “mycetoma belt” that includes various countries across the
world, but it is reported extensively in Sudan, Mexico, and India.
Mycetoma can be caused by bacteria (actinomycete mycetoma) or by soil and
plant saprophytic fungi (eufungal mycetoma). Firstly and most frequent in Central
and South America, secondly in Africa. Mycetomas have in common some characteristics: (a) the penetration of etiological agents through continuous skin
swounds caused by thorns, shrubs, wood chips, that is why mycetoma is considered
an occupational disease among farmers, (b) the long latency time (months or years),
(c) the characteristic, although not exclusive, location to the ankles and feet
(Madura’s foot) (Sehgal 1990; Verma and Jha 2019) (Fig. 26), (d) the formation of
nodular and plaque lesions, poorly inflammatory followed by the development of
abscesses, fistulas and ulcerations: the latter drain a purulent serum exudate containing granules, that are, the colonies of etiological agents and may help the
histological diagnosis, (e) the not uncommon involvement of muscles tendons
ligaments joints and bones, with consequent deformities and functional impotence
such as alterations in walking, (f) the chronic clinical course and the frequent
Fig. 26 Madura’s foot (with kind permission of Prof. Stefano Veraldi)
Atypical Wounds and Wounds Resulting from Infection 187
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
absence of local symptoms and systemic clinical manifestations, (g) the
histopathological picture characterized by granulomas and the frequent resistance to
systemic antifungal s drugs. Diagnosis in suspected lesions is made with the help of
grain examination, microscopy, imaging (radiography, ultrasonography, magnetic
resonance imaging) and culture, and more recently by molecular methods such as
PCR and molecular sequencing (Ahmed et al. 2017).
Ecthyma Gangrenosum
Ecthyma gangrenosum is usually seen in immunocompromised patients with leukaemia, lymphoma, other malignant diseases, severe burns or organ transplant, or in
people receiving immunosuppressive therapy (Singh et al. 2005). It is one of the
major dermatologic manifestations of severe, systemic pseudomonas aeruginosa
infection (Burnett et al. 2022).
It has ben also reported as the consequence of staphylococcus aureus (Santhaseelan and Muralidhar 2017), group A streptococcus, serratia marcescens,
escherichia coli and other bacterial species.
It is characterized by unique or multiple necrotic lesions which tend to enlarge,
ulcerate and to be covered by sloughy-purulent material (Fig. 27). If a bacteriemia
Fig. 27 Ecthyma gangrenosum (multiple ulcers of the lower limb) in a patient with leukemia
188 M. Papi and E. Fiscarelli
is excluded antibiotic therapy should be started in accordance with ba cteriological
exams. The patient should be investigated for the immunological condition and
potential viral infections.
Microbiological Investigations: Methods and Drawing
Techniques
Mainly Qualitative Methods
Swab: it is performed by moving the swab in a rotary manner inside the deepest
ulcer area or margins and, afterwards, inside the culture medium. It can also be
quantitative if performed on a specific lesion area and subsequently shaken in a
certain quantity of growth medium for a specific period of time.
Curettage: aspiration with needle: to remove the material from the ulcer surface
a disposable curette or a syringe to aspirate material of a purulent sac can be used.
It is advisable that the described techniques are preceded by the ulcer lavage with
physiologic salt solution to reduce the risk of developing occasional contaminants.
Qualitative and Quantitative Methods
Biopsy: it is performed after ulcer lavage with physiologic salt solution, local
anaesthesia (lidocaine injection, xylocaine), rotary movement and light pressure
performed with a disposable 4 mm diam eter punch. The tissue fragment obtained
can be homogenized and then weighed before being placed in the culture medium.
It allows to evaluate the presence of microbes in depth and to monitor the extent of
microbic proliferation. Sometimes, it requires a light compressive haemostasis.
Deep-tissue biopsy is a qualitative and quantitative culture of wound tissue.
Irrigation—aspiration: it is mainly used in presence of deep ulcers or ulcers
caused by pressure. It allows taking material from anfractuous areas or in sites
where a biopsy cannot easily be performed. It consists in irrigation, through 1 ml
sterile syringe of 0.9% sterile saline solution, followed by a light massage of the
ulcer margins. Immediately after, 1 ml of saline solution is again injected through a
new syringe and, after a light massage, 0.25 ml of fluid is inspired.
It is advisable that the microbiological laboratory carries out culture tests for
aerobic and anaerobic germs, especially in the presence of a real infection.
The most often isolated microbial species in the cutaneous ulcers are reported on
Table 4.
Particular a
diabetic patients where anaerobic germs are frequently present (Clostridium perfrigens, Bac
occasionally, gangrene.
tion should be given to the ulcers caused by pressure and in
tten
teroides fragilis, Peptostreptococcus spp). They often cause sepsis and,
Atypical Wounds and Wounds Resulting from Infection 189
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Table 4 Pathogenic
microbial species more
commonly found in the
cutaneous ulcers
Gram+
• Staphylococcus aureus
• Staphylococcus coagulase neg.
• Streptococcus group A, D
• Pepto-streptococcus spp
Mycetes
• Candida albicans
Gram–
• Pseudomonas aeruginosa
• Acinetobacter
• Escherichia coli
• Proteus spp
• Bacteroides
spp
As an adjunct to wound cultures, culture-independent investigation of the
microbial DNA applying pyrosequencing, polymerase chain reaction (PCR)-denaturing gradient gel electrophoresis, and quantitative real-time PCR have identified a
greater range of bacteria than traditional
culture techniques (Renick and Tang 2021;
Rerkasem and Mani 2015).
Laboratory Markers
In addition to the wound culture techniques, laboratory markers can also be measured to aid the diagnosis of wound infection. These markers include C-reactive
protein (CRP), procalcitonin, presepsin, microbial DNA, and bacterial protease
activity.
In response to inflammation and infection, CRP, a peptide produced in the liver,
is stimulated by cytokines, primarily interleukin-6, and employed in complement
binding and phagocytosis by macrophages.
The Future
Many new technologies have been created in recent years to diagnose infected
wounds. Traditional imaging modalities such as radiography and magnetic resonance imaging have still a role in the diagnostics, and new hybrid imaging techniques, including single-photon emission computed tomography, computed
tomography (CT) and positron emission tomography (PET)/MRI, are being utilized
as wound infection diagnostic tools, mainly in research at present.
190 M. Papi and E. Fiscarelli
References
Ahmed AA, van de Sande W, Fahal AH. Mycetoma laboratory diagnosis: review article. PLoS
Negl Trop Dis. 2017;11(8): e0005638.
Alavi A, Kirsner R. Hemoglobinopathies and leg ulcers. Int J Low Extrem Wounds. 2015;14
(3):213–6.
Alavi A, Mayer D, Hafner
entity. Adv Ski Wound Care. 2012;25(12): 563–72.
Alavi A, Hafner J, Dutz JP, et al. Livedoid vasculopathy: an in-depth analysis using a modified
Delphi approach. J Am Acad Dermatol. 2013;69(6):1033–1042.
Bilgic A, Ozcobanoglu S, Bozca BC, et al. Livedoid vasculopathy: a multidisciplinary clinical
approach to diagnosis and management. Int J Womens Dermatol. 2021;7(5Part A):588–599.
Bulte CA, Hoegler KM, Kutlu O, et al. Hydroxyurea: a reappraisal of its cutaneous side effects and
their management. Int J Dermatol. 2021;60(7):810–7.
Burnett JR, DeSalvo J, Halvorson S. Ecthyma gangrenosum, a cutaneous manifestation of
systemic infection. CMAJ. 2022;194(12):E461. https://doi.org/10.1503/cmaj.211430.
Clancey JK. Mycobacterial skin ulcers in Uganda: description of a new mycobacterium
(Mycobacterium buruli). J Pathol Bacteriol. 1964;88:175–87.
Cohen H, Cuadrado MJ, Erkan D, et al. 16th international congress on antiphospholipid antibodies
task force report on antiphospholipid syndrome treatment trends. Lupus. 2020;29(12):1571–93.
Conde Montero E, Guisado Muñoz S, Pérez Jerónimo L, et al. Martorell hypertensive ischemic
ulcer successfully treated with punch skin grafting. Wounds. 2018;30:E9–12.
Connor J Jr, Minniti CP, Tisdale JF. Sickle cell anemia and comorbid leg ulcer treated with
curative peripheral blood stem cell transplantation. Int J Low Extrem Wounds. 2017;16
(1):56–9.
Croitoru D, Naderi-Azad S, Sachdeva M, et al. A wound care specialist’s approach to pyoderma
gangrenosum. Adv Wound Care. 2020;9(12):686–94.
Flores MG, Herrera-Argaez G, Vazquez-Martinez O, et al. Cutaneous manifestations of
antiphospholipid syndrome. Lupus. 2021;30(4):541–8.
Gaisne R, Péré M, Menoyo V, et al. Calciphylaxis epidemiology, risk factors, treatment and
survival among French chronic kidney disease patients: a case-control study. BMC Nephrol.
2020;21(63). https://doi.org/10.1186/s12882-020-01722-y.
Gardette E, Moguelet P, Bouaziz JD, et al. Livedoid vasculopathy: a french observational study
including therapeutic options. Acta Derm Venereol. 2018;98(9):842.
Gil T, Pistunovich Y, Kulikovsky M, et al. A prospective case-control study of non-healing
wounds of the lower limbs-the value of biopsies for ulcerating carcinoma. J Eur Acad Derm
Venereol. 2015;29:337–45.
Guarner J. Buruli ulcer: review of a neglected skin mycobacterial disease. J Clin Microbiol.
2018;56(4):e01507–17.
Hafner J, Keusch G, Wahl C, et al. Uremic small-artery disease with medial calcification and
intimal hyperplasia (so-called calciphylaxis): a complication of chronic renal failure and benefit
of parathyroidectomy. J Am Acad Dermatol. 1995;33:954–62.
Handler MZ, Patel PA, Kapila R, et al. Cutaneous and mucocutaneous leishmaniasis: clinical
perspectives. J Am Acad Dermatol. 2015;73(6):897–908.
Hoffman MD. Atypical ulcers. Dermatol Ther. 2013;26(3):222–
Janowska
Aging. 2019;14:2137–43.
Janowska A, Romanelli M, Teresa Oranges T, et al. Prognostic
atypical wounds: a case series. Int J Low Extrem Wounds. 2020. https://doi.org/10.1177/
1534734620970292,(153473462097029).
Johnson P
Mycobacterium ulcerans disease. New York: Springer;2019. p. 61–76.
Jorizzo JL. Livedoid vasculopathy: what is it? Arch Dermatol. 1998;134:491.
V, Oranges
A, Dini
D. B
uruli ulcer in Australia. In: Pluschke G, Roltgen K, editors. Buruli ulcer.
J, et al. Martorell hypertensive ischemic ulcer. An underdiagnosed
35.
T, et al. Atypical ulcers: diagnosis and management. Clin Interv
indicators of wound healing in
Atypical Wounds and Wounds Resulting from Infection 191
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Kaul S, Kaur I, Mehta S, et al. Cutaneous tuberculosis. Part I: pathogenesis, classification, and
clinical features. J Am Acad Dermatol. 2022a;S0190-9622(22)00202-X. https://doi.org/10.
1016/j.jaad.2021.12.063.
Kaul S, Jakhar D, Mehta S, et al. Cutaneous tuberculosis. Part II: Complications, diagnostic
workup, histopathological
features, and treatment. J Am Acad Dermatol. 2022b;S0190-9622
(22);00203-1. https://doi.org/10.1016/j.jaad.2021.12.064.
Khan K, Giannone AL, Mehrabi E, et al. Marjolin’s ulcer complicating a pressure sore: the clock is
ticking. Am J Case Rep. 2016;17:111 – 4.
Knight JS, Kanthi Y. Mechanisms of immunothrombosis and vasculopathy in antiphospholipid
syndrome. Semin Immunopathol. 2022;44(3):347–362.
Kodumudi V, Jeha GM, Mydlo N, et al. Management of cutaneous calciphylaxis. Adv Ther.
2020;37(12):4797–807.
Kumar S, Basu S, Bhartiya SK, et al. The Buruli ulcer. Int J Low Extrem Wounds. 2015;14
(3):217–23.
Lanzkron S, Strouse JJ, Wilson R. Systematic review: hydroxyurea for the treatment of adults with
sickle cell disease. Ann Intern Med. 2008;148:939–55.
Lee JM, Kim IH. Case series of recalcitrant livedoid vasculopathy treated with rivaroxaban. Clin
Exp Dermatol. 2016;41:559–61.
Lima Pinto AP, Silva NA Jr, Osorio CT, et al. Martorell’s ulcer: diagnostic and therapeutic
challenge. Case Rep Dermatol. 2015;7(2):199–206.
Mani R, Margolis D, Shukla V, et al. Optimizing technology use for chronic lower-extremity
wound healing: a consensus document. Int J Low Extrem Wounds. 2016;15(2):102– 19.
Manry J. Human genetics of Buruli ulcer. Hum Genet. 2020;139(6–7):847–53.
Martí-Carvajal AJ, Knight-Madden JM, Martinez-Zapata MJ. Interventions for treating leg ulcers
in people with sickle cell disease. Cochrane Database Syst Rev. 2021;1(1):CD008394. https://
doi.org/10.1002/14651858.CD008394.pub.
Marzano AV, Borghi A, Meroni PL, et al. Pyoderma gangrenosum and its syndromic forms:
evidence for a link with autoinflammation. Br J Dermatol. 2016;175:882–91.
Maverakis E, Marzano AV, Le ST, et al. Pyoderma gangrenosum. Nat Rev Dis Primers.
2020;6:81. https://doi.org/10.1038/s41572-020-0213-x.
Meireles CB, Maia LC, Soares GC, Teodoro IPP, et al. Atypical presentations of cutaneous
leishmaniasis: a systematic review. Acta Trop. 2017;172:240– 54.
Miteva M, Romanelli P. Histopathology of wounds. In: Mani R, Romanelli M, Shukla VK,
editors. Measurements in wound healing: science and practice. Springer; 2012.
Monfort JB, Senet P. Leg ulcers in sickle-cell disease: treatment update. Adv Wound Care. 2019;9
(6):348–435.
Murad AA, Daly T, Mulligan N, et al. Extensive warfarin-induced skin necrosis successfully
treated with negative pressure wound therapy. BMJ Case Rep. 2014:bcr2013203510
Onesti MG, Fioramonti P, Fino P, et al. Skin ulcer caused by venous extravasation of heroin. Int
Wound J. 2014;11(4):409–411.
Panuncialman J, Hammerman S, Carson P, et al. Wound edge biopsy sites in chronic wounds heals
rapidly and do not result in delayed overall healing of the wounds. Wound Repair Regen.
2010;18:21–5.
Papi M. Macroangiopathic ulcers of the lower extremities: a daily challenge. Int J Low Extrem
Wounds. 2006;5(2):76–7.
Papi M, Didona B. Unusual clinical presentation of vasculitis: what some clinical aspects tell us
about the pathogenesis. Clin Dermatol. 1999;17(5):559–64.
Papi M, Papi C. Vasculitic ulcers. Int J Low Extrem Wounds. 2016;15(1):6–16.
Papi M, Didona B, Chinni LM, et al. Koebner phenomenon in an ANCA-positive patient with
pyoderma
gangrenosum. J Dermatol. 1997;24(9):583–6.
Papi M, Didona B, De Pità O, et al. Livedo vasculopathy versus small vessel cutaneous vasculitis:
citokyne and platelet P-selectin studies. Arch Dermatol. 1998;134(4):447–52.
192 M. Papi and E. Fiscarelli
Papi M. Le ulcere microangiopatiche. Vasculiti, infiammazione e microangiopatie occlusive dei
piccoli vasi cutanei. Marrapese; 2008.
Papi M, Papi C. Biologics in Microangiopathic wounds. Int J Low Extrem Wounds.
(4):205–13.
Papi M, Didona B, De Pità O et al. Multiple skin tumors on light-exposed areas during long-term
treatment with hydroxyurea. J Am Acad Dermatol. 1993;28(3):485–486.
Pranteda G, Grimaldi M, Lombardi M, et al. Basal cell carcinoma: differences according to
anatomic location and clinical-pathological subtypes. G Ital Dermatol Venereol.
2014;149:423–6.
Renick P, Tang L. Diagnostics for wound infections. 2021;10(6):317–27.
Rerkasem K, Mani R. Infection, immune disorders, hemoglobinopathies, and lower extremity
wounds: are we doing enough? Int J Low Extrem Wounds. 2015;14(3):211–2.
Roldan-Mari R, Contreras-RuizJ, Arenas R, et al. Fixed sporotrichosis as a cause of a chronic ulcer
on the knee. Int Wound J. 2009;6(1):63–6.
Sacchelli L, Baraldi C, Misciali C, et al. Neoplastic leg ulcers. Dermatopathology 2018;5
(3–4):113–6.
Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by
methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient. BMJ
Case Rep. 2017:bcr2017220983. Published 2017 Aug 3. https://doi.org/10.1136/bcr-2017-
220983.
Sarifakioglu E. Nicolau syndrome after diclofenac injection. J Eur Acad Dermatol Venereol.
2007;21(2):266–7.
Sehgal VN. Leg ulcers caused by deep mycotic infection. Clin Dermatol. 1990;8(3–4):157–65.
Senet P, Combemale P, Debure C. Malignancy and chronic leg ulcers. The value of systematic
wound biopsies: a prospective, multicenter, cross-sectional study Arch Dermatol. 2012;148
(6):704–8
Shanmugam VK, McNish S, Shara N, et al. Chronic leg ulceration associated to polycythemia vera
responding to Ruxolitinib (Jakafi). J Foot Ankle Surg. 2013;52(6):781–5.
Shavit E, Alavi A, Sibbald RG. Vasculitis-what do we have to know? A review of literature. Int J
Low Extrem Wounds. 2018;17(4):218–226.
Singh N, Devi M, Devi S. Ecthyma gangrenosum: a rare cutaneous manifestation caused by
Pseudomonas aeruginosa without bacteremia in a leukemic patient. Indian J Dermatol Venereol
Leprol. 2005;71:128–9.
Sirieix ME, Debure C, Baudot N. Leg ulcers and hydroxyurea. Arch Dermatol. 1999;135
(7):818–20.
Sönmez Ergün S, Yildiz K, Baygöl EG, et al. Heroin-induced chronic symmetrical skin ulcers of
the forearms in a young adult. Eur J Dermatol. 2012;22(3):414.
Tang J, Kirsner RS. Atypical ulcers. In: Mani R, Romanelli M, Shukla VK, editors. Measurements
in wound healing: science and practice. Springer; 2012.
Terrier DR, Durel C-A, et al. French recommendations for the management of systemic
necrotizing vasculitides (polyarteritis nodosa and ANCA-associated vasculitides. Orphanet J
Rare Dis. 2020;15(Suppl 2):351. https://doi.org/10.1186/s13023-020-01621-3.
Tottoli EM, Dorati R, Genta I, et al. Skin wound healing process and new emerging technologies
for skin wound care and regeneration. Pharmaceutics. 2020;12(8):735. https://doi.org/10.3390/
pharmaceutics12080735.
Tremblay D, Kosiorek HE, Dueck AC, et al. Evaluation of therapeutic strategies to reduce the
number of thrombotic events in patients with polycythemia vera and essential thrombo-
cythemia. Front Oncol. 2021;10:636675. Published 2021 Feb 16. https://doi.org/10.3389/fonc.
2020.636675.
Velasco M
Verma
L, Alegria V, Briz AS, et al. Occlusive nonvasculitic vasculopathy. Am J
Dermatopathol. 2017;39(9):637–62.
A. Mycetoma: reviewing a neglected disease. Clin Exp Dermatol. 2019;44(2):123– 9.
P, Jha
2018;17
Atypical Wounds and Wounds Resulting from Infection 193
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Weishaupt C,
Strolin A, Kahle B, et al. Anticoagulation with rivaroxaban for livedoid
vasculopathy (RILIVA): a multicentre, single-arm, open-label, phase 2a, proof-of-concept
trial. Lancet Haematol. 2016;3:e72–79.
Wirth K, Schoepf E, Mertelsmann R, et al. Leg ulceration with associated thrombocytosis: healing
of ulceration associated with treatment of the raised platelet count. Br J Dermatol.
1998;138:533–5.
Yotsu RR, Richardson M, Ishii N. Drugs for treating Buruli ulcer (Mycobacterium ulcerans
disease). Cochrane Database Syst Rev. 2018;8(8):CD012118. Published 2018 Aug 23. https://
doi.org/10.1002/14651858.CD012118.pub2.
Biofilms and Impaired Wound Healing:
How Do We Detect the Presence
of Biofilms in Chronic Wounds
Non-invasively
Ida C. Thaarup and Thomas Bjarnsholt
Abstract
The pervasive presence of biofilms in chronic wounds is a well-acknowledged
phenomenon. A recent meta-review estimat ed that 80% of all chronic wounds
contain biofilms and this number is thought to be an underestimation, as the
presence of a biofilm can be difficult to establish. The presence of a biofilm is
believed to prevent a wound from progressing through the normal phases of
healing, which are haemostasis, inflammation, proliferation, and remodelling.
Biofilms are thought to arrest the wound in the inflammatory state, causing an
exaggerated immune response with continuous tissue damage and harmful
change to the wound microenvironment. Therefore, a key to successful wound
healing is to focus on biofilm detection and subsequent biofilm eradication.
Non-invasive biofilm detection methods present a new and challenging field of
study. One of the main chall enges lies within the random spatial dist ribution of
wound biofilms. Despite the limit ed number of studies in this particular area,
biofilms are currently thought to exist in an unstructured, heterogeneous fashion
within the wound, occupyi ng different spatial regions and both shallow and
deeper layers of the wound. Several distinct species are thought to be present
within a single wound creating many different microenvironments. Regardless of
these challenges, a handful of non-invasive techniques have been developed that
I. C. Thaarup T. Bjarnsholt (&)
Costerton Biofilm Centre, Department of Immunology and Microbiology,
University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark
e-mail: tbjarnsholt@sund.ku.dk
I. C. Thaarup
e-mail: icthaarup@sund.ku.dk
T. Bjarnsholt
Department of Clinical Microbiology, Copenhagen University Hospital,
Juliane Maries Vej 22, 2100 Copenhagen, Denmark
© The Author(s), under
R. Mani (ed.), Chronic Wound Management,
https://doi.org/10.1007/978-3-031-26110-7_10
exclusive license to Springer Nature Switzerland AG 2023
195
196 I. C. Thaarup and T. Bjarnsholt
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
attempt to survey and locate biofilms in wounds using both direct and indirect
methods. In this chapter, we begin by introducing the reader to the devastating
effect biofilms have in a wound environment. This will incl ude some of the
complex interactions between the microbes, their host, and the surrounding
microenvironment. We then cover the conventional methods used today to detect
wound microbes and subsequently we introduce a number of new, non-invasive
methods to de
their infancy and have yet to be tested in human subjects, while others are further
along in their development. Finally, we discuss the importance of biofilm
detection in wounds and other concerns which might be just as important to
consider.
Keywords
tect the presence of wound biofilms. Some methods are still in
Biofilms Detection methods Biological markers Imaging techniques
How Biofilms Impair Wound Healing
Disruption of Immune and Skin Cells
Normal wound healing is often described to progress through four overlapping
phases of healing: haemostasis, inflammation, prolifera tion including tissue
regeneration and finally, remodelling (Zhao et al. 2016). In wounds that are progressing normally, the inflammatory phase usually only lasts a few days. However,
in the case of an infection, the presence of bacteria is thought to cause a deviant and
exaggerated immune response, stalling the wound in the inflammatory phase of
healing (Grice and Segre 2012). A meta-review has estimated that up to 80% of all
chronic wounds contain bacterial biofilms (Malone et al. 2017a); however, these
numbers are often thought to be underestimated since the presence of a biofilm can
be difficult to prove due to the heterogeneous distribution in the wounds. While
biofilms have already been shown to slow the healing of trauma-induced wounds
(Schierle et al. 2009; Zhao et a l. 2010; Seth et al. 2012), the specific methods by
which biofilms slow the healing of chronic wounds, and the conclusive proof that
they do so, is still being investigated. However, many in vivo and in vitro investigations have been performed, and in combination with clinical observations, they
have uncovered several mechanisms by microbial biofilms that might lead to
delayed healing.
Excessive neutrophil numbers have been observed in many chronic biofilm
infections, furthering the belief that the presence of a biofilm exaggerates the
immune response (Bjarnsholt et al. 2008). When present in excessive numbers, the
neutrophils produce compounds such as reactive oxygen species and proteolytic
enzymes in such amounts that they cause damage to neighbouring tissue. The
Соседние файлы в папке @xirurgi_2025