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SKIN,SOFT TISSUE AND
JOINTS INFECTIONS.
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT:
hermyc@live.com
OBJECTIVES
1) Introduction
2) Anatomy of the skin.
3) Defence mechanism of the skin.
4) Pathogenesis of skin infection.
5) Common skin, soft tissue and joints infection.
6) Treatment modality (paper review)
7) References
INTRODUCTION
• According to Ramakrishnan et al; skin and soft
tissue infection result from microbial invasion
of the skin and its supporting structures.
• Skin and soft tissue infection are classified as
simple (uncomplicated) or complicated
(necrotizing or non necrotizing) and involves
skin,subcutaneous fat, fasciae layer and
musculotendinous structures.
INTRODUCTION....
• Common simple skin and soft tissue infections
include cellulitis, erysipelas, impetigo, ecthyma,
folliculitis, furuncles,curbuncles,absecces and
trauma related infections.
• Complicated infection extends into and involving
the underlying deep tissues including deep
abscess, decubitus ulcers, necrotizing fasciitis,
Fournier's gangrene and infections from human or
animal bites.
• Skin and soft tissue infections
• Classification
 Anatomical
 Nosocomial versus
community acquired
 Sources (endogenous
versus. exogenous)
Introduction
Mangram et al., 1999. Infect Control Hosp Epidemiol 1999 Apr;20(4):250-78
Henriksen et al., J Hosp Infect.2010 Jul;75(3):173-7.
• Linkage with epidemiological predispositions, aetiologies,
prognosis and local relevance
EPIDEMIOLOGY
Global perspective:
 Globally, surgical site infection rate have been reported to
range from 2.5% to 41.9% in 2007.
Tanzania
 According to Mawalla et al, surgical site infection rates
among patients undergoing major surgeries at Bugando
Medical Centre were 26%, of whom 86.2% had superficial
surgical site infection and 13.8% had deep surgical site
infection in 2011.
 According to Mpogoro et al,cummulative incidence of
surgical site infection among women undergoing cesarean
section at Bugando Medical Centre was 10.9% in 2014.
ANATOMY OF THE SKIN
Source: TeachMe Anatomy 2020
DEFENCE MECHANISM OF THE
SKIN
Source: ResearchGate 2020
PATHOGENESIS OF SKIN
INFECTION
• According to Mangram et al; for most surgical
site infection, the source of pathogen is the
endogenous flora of the patients skin, mucous
membrane or hollow viscera.
• When the mucous membrane or skin is incised
the exposed tissues are at risk of contamination
with endogenous flora.
PATHOGENESIS OF SKIN
INFECTION..
• These organisms are usually aerobic gram
positive cocci eg staphylococci, but may also
include fecal flora eg anaerobic bacteria and
gram negative aerobes when incision are made
near the perineum.
• When gastrointestinal organ is opened during
an operation and is the source of pathogens,
gram negative bacilli eg E.coli, gram positive
organisms eg enterococci and sometimes
anaerobes eg bacillus fragilis are typical
surgical site infection isolates.
PATHOGENESIS OF SKIN
INFECTION..
• Seeding of the operative site from a distant focus of
infection can be another source of surgical site
infection pathogens, particularly in patients who have
prosthesis or other implant placed during the
operation.
• Furthermore, according to Mangram et al; exogenous
sources of surgical site infection pathogens include
surgical personel, the operating room environment,
all tools, instruments and materials brought to the
sterile field during an operation.
PATHOGENESIS OF SKIN
INFECTION...
• Exogenous flora are primarily aerobes,
especially gram positive organisms eg
staphylococci and streptococci.
• Fungi from endogenous and exogenous
sources rarely cause surgical site infection and
their pathogenesis is not well understood.
PATHOGENESIS OF SKIN
INFECTION...
• According to Kazimoto et al, the commonest
causative agents of skin and soft tissue infections
are; staph.aureus (71.4%), enterobacter cloacae
complex (14.6%), klebsiella pneumoniae (12.4%)
and Pseudomonas aeroginosa (11.8%)
• According to Silago et al, commonest isolates
from patients with osteomyelitis who underwent
surgical treatment at Bugando Medical Centre
from Dec 2017 to July 2018 were staph. areus by
85.1%.
PATHOGENESIS OF SKIN
INFECTION
Environ
mental
factors
• Physical (abrasion,
trauma, burn)
• Chemicals(corrosives
Agent
factors
E.g. Staph.
Aureus,
Strept.
Pneumoniae
• Release of Toxins
• Release antigen like
proteins
• Produce surface
proteins
• Release membrane
vesicles
Host
• Microbiome
barrier
• Physical Barrier
• Signal transducer
• Immune response
Skin and Soft
Tissue Infection
RISK FACTORS
According to Mangram
et al in 1999;
CLINICAL FEATURES
According to Ramakrishnan et al, patients with
simple skin and soft tissue infections presents
with;
Erythema
Edema
Warmth
Pain on the affected site
Induration (erysipelas & cellulitis).
CLINICAL FEATURES..
• For complicated infections like Necrotizing
fasciitis,patients present with the following
features;
Severe pain
Rapid progresion of infection
Cutaneous anaesthesia
Hemorrhage or bullous changes
Crepitus (indicating gas in soft tissue)
COMMON SKIN AND SOFT
TISSUE INFECTION
Cellulitis anterior to abdominal wall.
Source:
Ramakri
shnan et
al 2015.
COMMON SKIN AND SOFT
TISSUE INFECTION..
Furuncle.
Source:Ra
makrishna
n et al
2015.
SEVERE FORM OF SKIN AND
SOFT TISSUE INFECTION
Necrotizing fasciitis
Source:
Medscape
• There are two types;
Type I –consists of anaerobic species (eg
Bacteroides) in combination with one or more
of facultative anaerobes
(E.colli,enterobacter,klebsiela).
Type II-consists of Group A strept alone or in
combination with s.aureus
• Common sites are abdominal wall, perianal,
groin areas (for type II) and post-operative
wound (for type I).
• Investigations;
Culture (blood/exudates)
CT/MRI (r/o bone involvement)
• Treatment;
Surgical debridement
Antibiotics (depend on culture result)
FOURNIERS’ GANGRENE
Source:
American
Urological
Associatio
n.
• A form of necrotizing fasciitis occurring
mainly in male genitalia and perineum of both
sexes.
• It may be confined to the scrotum or it may
extend to involve the perineum, penis and
abdominal wall.
• Pathogens: mixed pathogens; facultative
anaerobes (E.colli,Klebsiela,Enterococci) and
anaerobes (bacteroids,clostridium)
Clinical features;
• Foul odor – anaerobics
• Dark purple areas develop and progress to
scrotal gangrene
• Investigation;
C&S (blood/exudates)
MRI & CT scan (demonstrate tissue gas and
distinguish from cellulitis).
Treatment;
Surgical debridement
Antibiotics (depend on culture result)
Diabetic Ulcer
Classification of
Diabetic Ulcers
• Classified according
to extent of infection
Mild
Moderate
Severe
Source: Research Gate
2012
Diabetic Ulcer.......
Mild:
• If the infection is <2cm beyond ulcer margin.
Moderate:
• More extensive/invasive infection associated
with necrosis,gangrene,abscess,deep soft tissue
or skeletal involvement or both.
Severe:
• Presence of systemic complication
eg,Fever,hypotension,acidosis.
• Specific Investigation
Blood sugar level (RBG/HBA1c)
Culture (blood/exudates)
CT/MRI
Treatment;
Surgical debridement
Insulin therapy
Antibiotics
JOINT INFECTION
• Common joint infection are;
Septic bursitis
Septic Arthritis
Specific features;
Joint pain
Joint swelling
Reduced range of movement.
SEPTIC BURSITIS
Source:
The Sports
Medicine
Review Oct
2019
• More than 80% of septic bursitis are caused
by staphylococcus aureus and the remaining
due to strept,mycobacteria and fungi.
• The commonest sites are the olecranon and
prepatellar and infrapatella bursae.
• Risk factors;
Excessive kneeling: People who work on their
knees for long periods.
Sports :Eg. wrestling, football and volleyball
• Investigation:
 Gram stain (Microscopy)
Culture and sensitivity (aspirates)
• Treatment:
Incision & drainage
Antibiotics
SEPTIC ARTHRITIS
Source:Stee
mkr.com
• Bacteria arthritis is considered a medical
emergency because of its potential for rapid
joint destruction with irreversible loss of
function.
• S. aureus is the most common cause of septic
arthritis and in sexually active young adults, N.
Gonorrhea is a frequent pathogen.
RISK FACTORS FOR
NONGONOCOCCAL ARTHRITIS
• Major risk factors
 Rheumatoid arthritis
 Advanced age
 DM
 Chronic renal failure
 Endocarditis
 Penetrating joint injury
• Minor risk factors
Osteoarthritis
Chronic liver disease
Gout
Malignancy
RISK FACTORS FOR
GONOCCOCAL ATHRITIS
Low social economic status
MSM
Illicit drug abusers
Multiple sexual partners
• Clinical manifestation;
Nongonoccocal arthritis is monoarticular in
80-90% of cases with the knee being the site of
infection in approx.50% of patients.
Gonoccocal arthritis is
monoarticular/oligoarticular in 42-85% of
patients with disseminated gonoccocal
infection(DIG).
• Specific Investigation are;
Synovial fluid culture (non gonococcal
bacteria)
NAATs (for N.gonorrhea,obtained from first
voided urine)
• Treatment;
For nongonoccocal; I&D,Antimicrobial
therapy (Vancomycin for
MRSA,Cephalosporin for gram (-) rods eg
E.coli,pseudomonas) for 4 weeks.
For gonococcal; IV ceftriaxone 1g for 1 week.
PAPERS REVIEW
• Aim of papers review is;
To identify common microbial isolates from
surgical site infections.
To identify treatment modality of skin and soft
tissue infections based on local and regional
antimicrobial susceptibility results
• HAIs in African countries ranges from 2.5% to 14.8%, (twice as high
as the average European prevalence)
• HAI due to MDR bacteria have emerged as a public health problem
worldwide causing increased morbidity, mortality and cost
• The highest prevalence occur in ICUs, in acute surgical &
orthopaedic wards, and in patients with underlying diseases
• The overall cumulative incidence of surgical site infection was
10.9% with predominance of S. aureus and K. pneumoniae
• Some of the risk factors: multiple vaginal examinations, prolonged
duration of operation and operation performed junior doctors
• Patients with a SSI had a longer average hospital stay than those
without a SSI (12.7 ± 6.9 vs. 4 ± 1.7 days; p < 0.0001) and the case
fatality rate was 2.9%.
• No significant difference in the occurrence of SSI between
the two groups
• Pre-operative single dose is recommended so as to reduce:
 Staff work load
 Medical related cost and
 Antimicrobial resistance ??
Common bacterial isolates from SSI
Source: Seni et al 2013
Empirical treatment regimens
Source: Lipsky et al 2020
Drug susceptibility to common
causative of SSI
Source: Seni et al 2013
Source: Seni J. Lecture series., 2019
Conclusion
• Patients with complicated infections, including
suspected necrotizing fasciitis and gangrene,
require empiric polymicrobial antibiotic
coverage, inpatient treatment, and surgical
consultation for debridement.’
References
1. Kalyanakrishnan Ramakrishnan; Robert c. Salinas, and Nelson
Ivan, Agudelo Higuita: skin and soft tissue infections 2015
American Academy of family physicians
2. Jeremiah Seni, Christine F Najjuka , David P Kateete , Patson
Makobore , Moses L Joloba , Henry Kajumbula , Antony Kapesa
and Freddie Bwanga; Antimicrobial resistance in hospitalized
surgical patients: a silently emerging public health concern in
Uganda. BMC Research Notes 2013, 6:298.
3. Silago V, Mushi MF, Remi BA, Mwayi A, Swetala S, Mtemisika
CI, Mshana SE.Methicillin resistant Staphylococcus aureus
causing osteomyelitis in a tertiary hospital, Mwanza,
Tanzania. J Orthop Surg Res. 2020 Mar 5;15(1):95.doi:
10.1186/s13018-020-01618-5.PMID: 32138758
4. Kazimoto T, Abdulla S, Bategereza L, Juma O, Mhimbira F, Weisser M,
Utzinger J, von Müller L, Becker SL. Causative agents and antimicrobial
resistance patterns of human skin and soft tissue infections in
Bagamoyo, Tanzania. Acta Trop. 2018 Oct;186:102-106. doi:
10.1016/j.actatropica.2018.07.007. Epub 2018 Jul 10.PMID: 30006029
5. Lipsky BA, Senneville É, Abbas ZG, Aragón-Sánchez J, Diggle M, Embil
JM, Kono S, Lavery LA, Malone M, van Asten SA, Urbančič-Rovan V,
Peters EJG; International Working Group on the Diabetic Foot
(IWGDF). Guidelines on the diagnosis and treatment of foot infection
in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res
Rev. 2020 Mar;36 Suppl 1:e3280. doi:
10.1002/dmrr.3280.PMID: 32176444
6. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis
WR. Guideline for Prevention of Surgical Site Infection, 1999. Centers
for Disease Control and Prevention (CDC) Hospital Infection Control
Practices Advisory Committee. Am J Infect Control. 1999 Apr;27(2):97-
132; quiz 133-4; discussion 96.PMID: 10196487
7. Brian Mawalla,Stephen E Mshana, Phillipo L Chalya,Can Imirzalioglu
and William Mahalu.Predictors of surgical site infections among
patients undergoing major surgery at Bugando Medical Centre in
Northwestern Tanzania.BMC Surgery 2011, 11:21
http://www.biomedcentral.com/1471-2482/11/21
8. Filbert J Mpogoro, Stephen E Mshana, Mariam M Mirambo, Benson R
Kidenya, Balthazar Gumodoka and Can Imirzalioglu.Incidence and
predictors of surgical site infections following caesarean sections at
Bugando Medical Centre, Mwanza, Tanzania. Antimicrobial Resistance
and Infection Control 2014, 3:25
http://www.aricjournal.com/content/3/1/25

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SKIN,SOFT TISSUE AND JOINTS INFECTIONS_07Dec2021.pptx

  • 1. SKIN,SOFT TISSUE AND JOINTS INFECTIONS. DR.HAMISI MKINDI,MD. TO DOWNLOAD CONTACT: hermyc@live.com
  • 2. OBJECTIVES 1) Introduction 2) Anatomy of the skin. 3) Defence mechanism of the skin. 4) Pathogenesis of skin infection. 5) Common skin, soft tissue and joints infection. 6) Treatment modality (paper review) 7) References
  • 3. INTRODUCTION • According to Ramakrishnan et al; skin and soft tissue infection result from microbial invasion of the skin and its supporting structures. • Skin and soft tissue infection are classified as simple (uncomplicated) or complicated (necrotizing or non necrotizing) and involves skin,subcutaneous fat, fasciae layer and musculotendinous structures.
  • 4. INTRODUCTION.... • Common simple skin and soft tissue infections include cellulitis, erysipelas, impetigo, ecthyma, folliculitis, furuncles,curbuncles,absecces and trauma related infections. • Complicated infection extends into and involving the underlying deep tissues including deep abscess, decubitus ulcers, necrotizing fasciitis, Fournier's gangrene and infections from human or animal bites.
  • 5. • Skin and soft tissue infections • Classification  Anatomical  Nosocomial versus community acquired  Sources (endogenous versus. exogenous) Introduction Mangram et al., 1999. Infect Control Hosp Epidemiol 1999 Apr;20(4):250-78 Henriksen et al., J Hosp Infect.2010 Jul;75(3):173-7. • Linkage with epidemiological predispositions, aetiologies, prognosis and local relevance
  • 6. EPIDEMIOLOGY Global perspective:  Globally, surgical site infection rate have been reported to range from 2.5% to 41.9% in 2007. Tanzania  According to Mawalla et al, surgical site infection rates among patients undergoing major surgeries at Bugando Medical Centre were 26%, of whom 86.2% had superficial surgical site infection and 13.8% had deep surgical site infection in 2011.  According to Mpogoro et al,cummulative incidence of surgical site infection among women undergoing cesarean section at Bugando Medical Centre was 10.9% in 2014.
  • 7. ANATOMY OF THE SKIN Source: TeachMe Anatomy 2020
  • 8. DEFENCE MECHANISM OF THE SKIN Source: ResearchGate 2020
  • 9. PATHOGENESIS OF SKIN INFECTION • According to Mangram et al; for most surgical site infection, the source of pathogen is the endogenous flora of the patients skin, mucous membrane or hollow viscera. • When the mucous membrane or skin is incised the exposed tissues are at risk of contamination with endogenous flora.
  • 10. PATHOGENESIS OF SKIN INFECTION.. • These organisms are usually aerobic gram positive cocci eg staphylococci, but may also include fecal flora eg anaerobic bacteria and gram negative aerobes when incision are made near the perineum. • When gastrointestinal organ is opened during an operation and is the source of pathogens, gram negative bacilli eg E.coli, gram positive organisms eg enterococci and sometimes anaerobes eg bacillus fragilis are typical surgical site infection isolates.
  • 11. PATHOGENESIS OF SKIN INFECTION.. • Seeding of the operative site from a distant focus of infection can be another source of surgical site infection pathogens, particularly in patients who have prosthesis or other implant placed during the operation. • Furthermore, according to Mangram et al; exogenous sources of surgical site infection pathogens include surgical personel, the operating room environment, all tools, instruments and materials brought to the sterile field during an operation.
  • 12. PATHOGENESIS OF SKIN INFECTION... • Exogenous flora are primarily aerobes, especially gram positive organisms eg staphylococci and streptococci. • Fungi from endogenous and exogenous sources rarely cause surgical site infection and their pathogenesis is not well understood.
  • 13. PATHOGENESIS OF SKIN INFECTION... • According to Kazimoto et al, the commonest causative agents of skin and soft tissue infections are; staph.aureus (71.4%), enterobacter cloacae complex (14.6%), klebsiella pneumoniae (12.4%) and Pseudomonas aeroginosa (11.8%) • According to Silago et al, commonest isolates from patients with osteomyelitis who underwent surgical treatment at Bugando Medical Centre from Dec 2017 to July 2018 were staph. areus by 85.1%.
  • 14. PATHOGENESIS OF SKIN INFECTION Environ mental factors • Physical (abrasion, trauma, burn) • Chemicals(corrosives Agent factors E.g. Staph. Aureus, Strept. Pneumoniae • Release of Toxins • Release antigen like proteins • Produce surface proteins • Release membrane vesicles Host • Microbiome barrier • Physical Barrier • Signal transducer • Immune response Skin and Soft Tissue Infection
  • 15. RISK FACTORS According to Mangram et al in 1999;
  • 16. CLINICAL FEATURES According to Ramakrishnan et al, patients with simple skin and soft tissue infections presents with; Erythema Edema Warmth Pain on the affected site Induration (erysipelas & cellulitis).
  • 17. CLINICAL FEATURES.. • For complicated infections like Necrotizing fasciitis,patients present with the following features; Severe pain Rapid progresion of infection Cutaneous anaesthesia Hemorrhage or bullous changes Crepitus (indicating gas in soft tissue)
  • 18. COMMON SKIN AND SOFT TISSUE INFECTION Cellulitis anterior to abdominal wall. Source: Ramakri shnan et al 2015.
  • 19. COMMON SKIN AND SOFT TISSUE INFECTION.. Furuncle. Source:Ra makrishna n et al 2015.
  • 20. SEVERE FORM OF SKIN AND SOFT TISSUE INFECTION Necrotizing fasciitis Source: Medscape
  • 21. • There are two types; Type I –consists of anaerobic species (eg Bacteroides) in combination with one or more of facultative anaerobes (E.colli,enterobacter,klebsiela). Type II-consists of Group A strept alone or in combination with s.aureus
  • 22. • Common sites are abdominal wall, perianal, groin areas (for type II) and post-operative wound (for type I). • Investigations; Culture (blood/exudates) CT/MRI (r/o bone involvement)
  • 25. • A form of necrotizing fasciitis occurring mainly in male genitalia and perineum of both sexes. • It may be confined to the scrotum or it may extend to involve the perineum, penis and abdominal wall. • Pathogens: mixed pathogens; facultative anaerobes (E.colli,Klebsiela,Enterococci) and anaerobes (bacteroids,clostridium)
  • 26. Clinical features; • Foul odor – anaerobics • Dark purple areas develop and progress to scrotal gangrene
  • 27. • Investigation; C&S (blood/exudates) MRI & CT scan (demonstrate tissue gas and distinguish from cellulitis). Treatment; Surgical debridement Antibiotics (depend on culture result)
  • 28. Diabetic Ulcer Classification of Diabetic Ulcers • Classified according to extent of infection Mild Moderate Severe Source: Research Gate 2012
  • 29. Diabetic Ulcer....... Mild: • If the infection is <2cm beyond ulcer margin. Moderate: • More extensive/invasive infection associated with necrosis,gangrene,abscess,deep soft tissue or skeletal involvement or both. Severe: • Presence of systemic complication eg,Fever,hypotension,acidosis.
  • 30. • Specific Investigation Blood sugar level (RBG/HBA1c) Culture (blood/exudates) CT/MRI Treatment; Surgical debridement Insulin therapy Antibiotics
  • 31. JOINT INFECTION • Common joint infection are; Septic bursitis Septic Arthritis Specific features; Joint pain Joint swelling Reduced range of movement.
  • 33. • More than 80% of septic bursitis are caused by staphylococcus aureus and the remaining due to strept,mycobacteria and fungi. • The commonest sites are the olecranon and prepatellar and infrapatella bursae.
  • 34. • Risk factors; Excessive kneeling: People who work on their knees for long periods. Sports :Eg. wrestling, football and volleyball • Investigation:  Gram stain (Microscopy) Culture and sensitivity (aspirates)
  • 35. • Treatment: Incision & drainage Antibiotics
  • 37. • Bacteria arthritis is considered a medical emergency because of its potential for rapid joint destruction with irreversible loss of function. • S. aureus is the most common cause of septic arthritis and in sexually active young adults, N. Gonorrhea is a frequent pathogen.
  • 38. RISK FACTORS FOR NONGONOCOCCAL ARTHRITIS • Major risk factors  Rheumatoid arthritis  Advanced age  DM  Chronic renal failure  Endocarditis  Penetrating joint injury • Minor risk factors Osteoarthritis Chronic liver disease Gout Malignancy
  • 39. RISK FACTORS FOR GONOCCOCAL ATHRITIS Low social economic status MSM Illicit drug abusers Multiple sexual partners
  • 40. • Clinical manifestation; Nongonoccocal arthritis is monoarticular in 80-90% of cases with the knee being the site of infection in approx.50% of patients. Gonoccocal arthritis is monoarticular/oligoarticular in 42-85% of patients with disseminated gonoccocal infection(DIG).
  • 41. • Specific Investigation are; Synovial fluid culture (non gonococcal bacteria) NAATs (for N.gonorrhea,obtained from first voided urine)
  • 42. • Treatment; For nongonoccocal; I&D,Antimicrobial therapy (Vancomycin for MRSA,Cephalosporin for gram (-) rods eg E.coli,pseudomonas) for 4 weeks. For gonococcal; IV ceftriaxone 1g for 1 week.
  • 43. PAPERS REVIEW • Aim of papers review is; To identify common microbial isolates from surgical site infections. To identify treatment modality of skin and soft tissue infections based on local and regional antimicrobial susceptibility results
  • 44. • HAIs in African countries ranges from 2.5% to 14.8%, (twice as high as the average European prevalence) • HAI due to MDR bacteria have emerged as a public health problem worldwide causing increased morbidity, mortality and cost • The highest prevalence occur in ICUs, in acute surgical & orthopaedic wards, and in patients with underlying diseases
  • 45. • The overall cumulative incidence of surgical site infection was 10.9% with predominance of S. aureus and K. pneumoniae • Some of the risk factors: multiple vaginal examinations, prolonged duration of operation and operation performed junior doctors • Patients with a SSI had a longer average hospital stay than those without a SSI (12.7 ± 6.9 vs. 4 ± 1.7 days; p < 0.0001) and the case fatality rate was 2.9%.
  • 46. • No significant difference in the occurrence of SSI between the two groups • Pre-operative single dose is recommended so as to reduce:  Staff work load  Medical related cost and  Antimicrobial resistance ??
  • 47. Common bacterial isolates from SSI Source: Seni et al 2013
  • 49. Drug susceptibility to common causative of SSI Source: Seni et al 2013
  • 50. Source: Seni J. Lecture series., 2019
  • 51.
  • 52. Conclusion • Patients with complicated infections, including suspected necrotizing fasciitis and gangrene, require empiric polymicrobial antibiotic coverage, inpatient treatment, and surgical consultation for debridement.’
  • 53. References 1. Kalyanakrishnan Ramakrishnan; Robert c. Salinas, and Nelson Ivan, Agudelo Higuita: skin and soft tissue infections 2015 American Academy of family physicians 2. Jeremiah Seni, Christine F Najjuka , David P Kateete , Patson Makobore , Moses L Joloba , Henry Kajumbula , Antony Kapesa and Freddie Bwanga; Antimicrobial resistance in hospitalized surgical patients: a silently emerging public health concern in Uganda. BMC Research Notes 2013, 6:298. 3. Silago V, Mushi MF, Remi BA, Mwayi A, Swetala S, Mtemisika CI, Mshana SE.Methicillin resistant Staphylococcus aureus causing osteomyelitis in a tertiary hospital, Mwanza, Tanzania. J Orthop Surg Res. 2020 Mar 5;15(1):95.doi: 10.1186/s13018-020-01618-5.PMID: 32138758
  • 54. 4. Kazimoto T, Abdulla S, Bategereza L, Juma O, Mhimbira F, Weisser M, Utzinger J, von Müller L, Becker SL. Causative agents and antimicrobial resistance patterns of human skin and soft tissue infections in Bagamoyo, Tanzania. Acta Trop. 2018 Oct;186:102-106. doi: 10.1016/j.actatropica.2018.07.007. Epub 2018 Jul 10.PMID: 30006029 5. Lipsky BA, Senneville É, Abbas ZG, Aragón-Sánchez J, Diggle M, Embil JM, Kono S, Lavery LA, Malone M, van Asten SA, Urbančič-Rovan V, Peters EJG; International Working Group on the Diabetic Foot (IWGDF). Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev. 2020 Mar;36 Suppl 1:e3280. doi: 10.1002/dmrr.3280.PMID: 32176444
  • 55. 6. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR. Guideline for Prevention of Surgical Site Infection, 1999. Centers for Disease Control and Prevention (CDC) Hospital Infection Control Practices Advisory Committee. Am J Infect Control. 1999 Apr;27(2):97- 132; quiz 133-4; discussion 96.PMID: 10196487 7. Brian Mawalla,Stephen E Mshana, Phillipo L Chalya,Can Imirzalioglu and William Mahalu.Predictors of surgical site infections among patients undergoing major surgery at Bugando Medical Centre in Northwestern Tanzania.BMC Surgery 2011, 11:21 http://www.biomedcentral.com/1471-2482/11/21 8. Filbert J Mpogoro, Stephen E Mshana, Mariam M Mirambo, Benson R Kidenya, Balthazar Gumodoka and Can Imirzalioglu.Incidence and predictors of surgical site infections following caesarean sections at Bugando Medical Centre, Mwanza, Tanzania. Antimicrobial Resistance and Infection Control 2014, 3:25 http://www.aricjournal.com/content/3/1/25

Editor's Notes

  1. Skin is divided into 3 layers; Epidermis-Avascular layer and contains multiple epithelial cells eg melanocytes,keratinocytes,corneocytes. This layer constitute the first line of defence against invading micro-organisms, protection against mechanical impact and prevent excessive loss of water from the body (thermoregulation). Dermis-This is vascular layer that contains blood vessels, hair follicles, sweat glands, sebacious gland, nerve endings and arrector pilli muscles. Hypodermis/subcutaneous tissue-The lower layer of the skin that contains adipose tissues, cutaneous vascular plexus and sensory nerve fibres.
  2. Defence mechanism of the skin involves two layers; 1/: Epidermal layer- consist of microbiome layer and physical barrier. Microbiome layer contains beneficial bacteria eg staph. Epidermis,staph.aureus,corynebacterium spps,propionbacterium spps and micococcus spps. Physical barrier contains tight junction, melanocytes, coryneocytes, keratinocytes ,langerhans cells and T cells 2/: Dermal layer-consists of engulfing cells (eg macrophages,T cells), fibroblasts and immune response cells eg cytokines and AMP-antimicrobial peptide
  3. The clinical presentation of most skin, soft tissue infections (SSTIs) is the culmination of two steps process; Invasion of pathogens Clinical effects due to interaction of bacteria and host defence. Several means by which bacteria penetrate the skin barrier are; ulceration/trauma/surgery/burns. Recognition of pathogens by the host defence system through; presence of microbiome and physical barrier and signal transducer (keratinocytes,langerhans cells) on epidermal layer and stimulation of host inflammatory response (eg release macrophages,T cells,Cytokines,Antimicrobial peptide ). Cascade of inflammatory reaction takes place where by the pathogen Evade the host defence by releasing surface protein that alter its hydrophobicity. Release toxins (exotoxins), membrane vesicles and antigen like protein that inactivate compliment system of the host. If the host immune system suppress the pathogens, healing process take place through cell regeneration. If the immune system failed to suppress the pathogens, skin and soft tissue infection develops.
  4. Systemic features of infection may follow, their intensity reflecting the magnitude of infection. Tense overlying edema and bullae when present may help to distinguish necrotizing fasciitis from non necrotizing infections.
  5. Superficial and small abscesses respond well to drainage and seldom require antibiotics. Immunocompromised patients require early treatment and antimicrobial coverage for possible atypical organisms.