MOPH Guideline - Skin and Soft Tissue Infections v0.3 - Quality Check

THE DIAGNOSIS & MANAGEMENT OF
SKIN & SOFT TISSUE INFECTION
7th December 2020

7th December 2022
Version History
Version Status Date Editor Description
1.0 Final 7th December 2020 Guidelines Team Version for Publication.
Citation
Suggested citation style:
Ministry of Public Health Qatar. National Clinical Guideline: The Diagnosis and Management of Skin and
Soft Tissue Infection (2020).
Abbreviations
The abbreviations used in this guideline are as follows:
ART Antiretroviral Therapy

BIT Burrow Ink Test
CA-MRSA Community-Associated Methicillin-Resistant Staphylococcus aureus
CT Computed Tomography
EPSD Epidermal Parasitic Skin Diseases
FGSI Fournier’s Gangrene Severity Index
HIV Human Immunodeficiency Virus
HrCLM Hookworm-Related Cutaneous Larva Migrans
LRINEC Laboratory Risk Indicator for Necrotising Fasciitis
MMR Measles-Mumps-Rubella
MCV Molluscum Contagiosum Virus
MMRV Measles-Mumps-Rubella-Varicella
MRI Magnetic Resonance Imaging
MRSA Methicillin-Resistant Staphylococcus aureus
MSSA Methicillin-Sensitive Staphylococcus aureus
NSAID Non-Steroidal Anti-Inflammatory Drug
S. aureus Staphylococcus aureus
S. pyogenes Streptococcus pyogenes
SSTIs Skin and Soft-Tissue Infections
VZV Varicella Zoster Virus
The Diagnosis and Management of Skin and Soft Tissue Infection

(Date of next revision: 7th December 2022) 2
Table of Contents
1 Information about this Guideline ...........................................................................................................6
1.1 Objective and Purpose of the Guideline ........................................................................................6
1.2 Scope of the Guideline ...................................................................................................................6
1.3 Editorial Approach..........................................................................................................................6
1.4 Sources of Evidence .......................................................................................................................6
1.5 Evidence Grading and Recommendations .....................................................................................7
1.6 Guideline Development Group Members ......................................................................................8
1.7 National Clinical Guidelines & Pathways Committee members ....................................................9
1.8 Responsibilities of Healthcare Professionals................................................................................10
2 Skin & Soft Tissue Infection - Pathway .................................................................................................11
3 Key Recommendations of the Guideline ..............................................................................................12
4 Background Information.......................................................................................................................14
4.1 Definition......................................................................................................................................14
4.2 Classification ................................................................................................................................14
4.3 Prevalence ....................................................................................................................................14
4.4 Risk Factors ..................................................................................................................................14
4.5 Prognosis ......................................................................................................................................15
5 Clinical Assessment...............................................................................................................................16
5.1 Clinical Presentation.....................................................................................................................16
5.2 History ..........................................................................................................................................16
5.3 Examination .................................................................................................................................16
6 Investigation .........................................................................................................................................18
7 General Principles of Management ......................................................................................................19
7.1 Principles of Care .........................................................................................................................19
7.2 Principles of Antimicrobial Treatment .........................................................................................19
7.3 Emergency Referral ......................................................................................................................20
7.4 Referral to Specialist Care ............................................................................................................20
7.5 Follow-Up .....................................................................................................................................21
8 Abscesses ..............................................................................................................................................22
8.1 Classification and Aetiology .........................................................................................................22
8.2 Clinical Presentation and Assessment..........................................................................................22
8.3 Management ................................................................................................................................22
9 Folliculitis, Furunculosis, and Carbunculosis ........................................................................................24
9.1 Aetiology ......................................................................................................................................24
9.3 Investigation .................................................................................................................................25
9.4 Management ................................................................................................................................25

9.4.1 Folliculitis .................................................................................................................................25
9.4.2 Furunculosis and Carbunculosis ...............................................................................................26
10 Impetigo ...............................................................................................................................................28
10.1 Aetiology ......................................................................................................................................28
10.3 Management ................................................................................................................................28
11 Cellulitis and Erysipelas ........................................................................................................................30
11.1 Aetiology ......................................................................................................................................30
11.3 Management ................................................................................................................................31
12 Bites ......................................................................................................................................................33
12.1 Aetiology ......................................................................................................................................33
12.3 Management ................................................................................................................................34
13 Diabetic Foot Infections........................................................................................................................37
13.1 Aetiology ......................................................................................................................................37
13.3 Management ................................................................................................................................37
14 Infected Burns ......................................................................................................................................39
14.1 Aetiology ......................................................................................................................................39
14.3 Management ................................................................................................................................40
15 Necrotising Skin and Soft Tissue Infections ..........................................................................................41
15.1 Aetiology ......................................................................................................................................41
15.3 Investigation and Diagnosis .........................................................................................................42
15.3.1 Fournier’s Gangrene ............................................................................................................43
15.3.2 Clostridial Myonecrosis........................................................................................................43
15.4 Management ................................................................................................................................43
16 Viral Skin and Soft Tissue Infections .....................................................................................................45
16.1 Aetiology ......................................................................................................................................45
16.3 Investigation and Management of Specific Viral SSTIs ................................................................46
16.3.1 Measles ................................................................................................................................46
16.3.2 Rubella .................................................................................................................................48
16.3.3 Infectious Mononucleosis ....................................................................................................49
16.3.4 Herpes Zoster .......................................................................................................................50
16.3.5 Molluscum Contagiosum .....................................................................................................50
17 Parasitic Skin Infections ........................................................................................................................52

17.1 Aetiology ......................................................................................................................................52
17.3 Diagnosis and Management.........................................................................................................53
17.3.1 Scabies .................................................................................................................................53
17.3.2 Pediculosis ...........................................................................................................................54
17.3.3 Tungiasis ..............................................................................................................................56
17.3.4 Hookworm-Related Cutaneous Larva Migrans ....................................................................56
17.3.5 Leishmaniasis .......................................................................................................................57
17.3.6 Loiasis...................................................................................................................................59
18 Key Considerations for Patient Preferences .........................................................................................61
19 Performance Measures ........................................................................................................................62
20 References ............................................................................................................................................63
Appendix: Detailed Description of the Literature Search .........................................................................66
Acknowledgements ......................................................................................................................................68

1 Information about this Guideline
1.1 Objective and Purpose of the Guideline
The purpose of this guideline is to define the appropriate diagnosis and management of skin and soft tissue
infections in adults and children. The objective is to guide the appropriate investigation, treatment and
referral of patients presenting to provider organisations in Qatar. It is intended that the guideline will be
used primarily by healthcare professionals in both primary care and specialist settings.
1.2 Scope of the Guideline
This guideline covers the following aspects of care:

• General recommendations on clinical presentation, assessment, and investigation of skin and soft
tissue infections (SSTIs).
• General principles of care and antimicrobial prescribing for SSTIs.
• Criteria for emergency and non-emergency referral to specialist care.
• Specific features and management of abscesses, folliculitis, furunculosis, carbunculosis, impetigo,
cellulitis and erysipelas, animal and human bites, diabetic foot infections, infected burns,
necrotising SSTIs, and viral SSTIs.
1.3 Editorial Approach
This guideline document has been developed and issued by the Ministry of Public Health of Qatar (MOPH),
through a process which aligns with international best practice in guideline development and localisation.
The guideline will be reviewed on a regular basis and updated to incorporate comments and feedback from
stakeholders across Qatar.
The editorial methodology, used to develop this guideline, has involved the following critical steps:
• Extensive literature search for well-reputed, published evidence relating to the topic.
• Critical appraisal of the literature.
• Development of a draft summary guideline.
• Review of the summary guideline with a Guideline Development Group, comprised of practising
healthcare professionals, subject matter experts and patient representatives, from across Qatar.
• Independent review of the guideline by the National Clinical Guidelines & Pathways Committee,
appointed by the MOPH, from amongst stakeholder organisations across Qatar.
Whilst the MOPH has sponsored the development of the guideline, the MOPH has not influenced the
specific recommendations made within it.
1.4 Sources of Evidence
The professional literature published in the English language has been systematically queried using
specially developed, customised, and tested search strings. Search strategies are developed to allow
efficient yet comprehensive analysis of relevant publications for a given topic and to maximise retrieval of
articles with certain desired characteristics pertinent to a guideline.
For each guideline, all retrieved publications have been individually reviewed by a clinical editor and
assessed in terms of quality, utility, and relevance. Preference is given to publications that:

1. Are designed with rigorous scientific methodology.
2. Are published in higher-quality journals (i.e. journals that are read and cited most often within
their field).
3. Address an aspect of specific importance to the guideline in question.
Further information about the literature search and appraisal process is included in the appendix.
1.5 Evidence Grading and Recommendations
Recommendations made within this guideline are supported by evidence from the medical literature and
where possible the most authoritative sources have been used in the development of this guideline. In
order to provide insight into the evidence basis for each recommendation, the following evidence hierarchy
has been used to grade the level of authoritativeness of the evidence used, where recommendations have
been made within this guideline.
Where the recommendations of international guidelines have been adopted, the evidence grading is
assigned to the underlying evidence used by the international guideline. Where more than one source has
been cited, the evidence grading relates to the highest level of evidence cited:
• Level 1 (L1):
o Meta-analyses.
o Randomised controlled trials with meta-analysis.
o Randomised controlled trials.
o Systematic reviews.
• Level 2 (L2):
o Observational studies, examples include:
▪ Cohort studies with statistical adjustment for potential confounders.
▪ Cohort studies without adjustment.
▪ Case series with historical or literature controls.
▪ Uncontrolled case series.
o Statements in published articles or textbooks.
• Level 3 (L3):
o Expert opinion.
o Unpublished data, examples include:
▪ Large database analyses.
▪ Written protocols or outcomes reports from large practices.
In order to give additional insight into the reasoning underlying certain recommendations and the strength
of recommendation, the following recommendation grading has been used, where recommendations are
made:
▪ Recommendation Grade A (RGA): Evidence demonstrates at least moderate certainty of at least

moderate net benefit.
▪ Recommendation Grade B (RGB): Evidence is insufficient, conflicting, or poor and demonstrates
an incomplete assessment of net benefit vs harm; additional research is recommended.
▪ Recommendation Grade C (RGC): Evidence demonstrates potential harm that outweighs benefit;
additional research is recommended.
▪ Recommendation of the GDG (R-GDG): Recommended best practice based on the clinical
experience of the Guideline Development Group members.

1.6 Guideline Development Group Members
The following table lists members of the Guideline Development Group (GDG) nominated by their
respective organisations and the Clinical Governance Group. The GDG members have reviewed and
provided feedback on the draft guideline relating to the topic. Each member has completed a declaration
of conflicts of interest, which has been reviewed and retained by the MOPH.
Guideline Development Group Members
Name Title Organisation

Senior Consultant Infectious Diseases, Al
Dr Yasser Mahmoud Eldeeb Khor Hospital, Clinical Associate Hamad Medical Corporation
Professor, Qatar University
Consultant Dermatologist, Head of
Dermatology and Venereology Section,
Al Khor Hospital
Dr Mohamed Ibrahim Khalil Assistant Professor of Clinical
Hamad Medical Corporation
Allam Dermatology, Weill-Cornell Medicine
Qatar
Clinical Assistant Professor of
Dermatology, Qatar University
Director of Nursing, Outpatient, Hamad
Ms Shaikha Ali Al Qahtani General Hospital & Wound Care Service, Hamad Medical Corporation
Corporate Nursing & Midwifery
Consultant Dermatologist, Head of
Dr Ra’ed Mahmoud Alsmadi Al Ahli Hospital
Dermatology Department
Dr Ahmed Atef Ammar Quality & Patient Safety Manager Doha Clinic Hospital
Medical Director, Infection Prevention
Dr Simon Dobson and Control, Antimicrobial Stewardship Sidra Medicine
Consultant
Senior Consultant, Head Microbiology &
Dr Emad Basir Ibrahim
Virology Division, Chair of Infection Hamad Medical Corporation
Elmagboul
Control, HGH
Dr Waad Ibrahim Majeed Consultant of Dermatology &
Primary Health Care Corp
Kadori Venereology
Senior Consultant Dermatology,
Dr Adel M. Kamal Al Emadi Hospital
Chairman Dermatology Department
Senior Consultant Paediatric Infectious
Disease, Paediatric Infectious Disease
Dr Eman Al Maslamani Fellowship Programme Director, Sidra Medicine
Assistant Professor of Clinical Pediatric
Weill-Cornell Medicine-Qatar
Dr Kamalanathan Nallu Specialist Dermatologist Qatar Red Crescent Society
Assistant Professor of Clinical Medicine, Weill Cornell Medicine -
Dr Amine Rakab
Assistant Dean for Clinical Learning Qatar
Dr Devaraju Lakshman Rao Specialist Dermatologist Aster DM Healthcare
Ministry of Interior Medical
Dr Afzal Hussain Sahib Senior Specialist Dermatologist
Services
Dr Nahla Hassan Sharaf Infection Control Specialist Ministry of Public Health

Guideline Development Group Members

Dr Mohanad Osman Ahmed
Specialist Family Physician Primary Health Care Corp
Suliman
Dr Maliha Babar Thapur Consultant Infectious Diseases Hamad Medical Corporation
Dr Binny Thomas Clinical Pharmacy Specialist Hamad Medical Corporation

General Surgeon, Head of Sports Groin
Dr Zarko Vuckovic Aspetar
Pain Center
1.7 National Clinical Guidelines & Pathways Committee members
The following table lists members of the National Clinical Guidelines & Pathways Committee (NCGPC),
appointed by the MOPH. The NCGPC members have reviewed and provided their feedback and approval
of the guideline document. Each member has completed a declaration of conflicts of interest, which has
been reviewed and retained by the MOPH.
National Clinical Guidelines & Pathways Committee (NCGPC) Members

Chair of the NCGPC,
Ms Huda Amer Al-Katheeri Director- Strategic Planning & Ministry of Public Health
Performance Department
Shk Dr Mohammed Hamad J. Al Co-Chair of NCGPC,
Ministry of Public Health
Thani Director of Public Health
Chair Clinical Practice Guidelines
Prof Anthony Akobeng Sidra Medicine
Committee
Dr Alshaymaa Mohammed A.
Consultant Family Medicine Qatar Petroleum
M. Al-Motawa
Accreditation Coordinator, Dept of
Dr Basil Bashqawi Ministry of Public Health
Health Professions
Associate Professor of Medicine Weill Cornell Medicine -
Dr Abi Khalil Charbel
Consultant Cardiology Qatar
Dr Paul Dijkstra Director of Medical Education Aspetar
Consultant Endocrinology and Internal
Dr Mohamed Elrishi Al Ahli Hospital
Medicine
Dr Dahlia Mustafa Hassan Consultant Family Medicine Primary Health Care Corp
Dr Ghassan Youseph Hommos Consultant Endocrinology Al Emadi Hospital

Senior Consultant,
Dr Hani Benhassen Kilani Executive Director for Corporate Clinical Hamad Medical Corporation
Policy and Guidelines
College of Medicine, Qatar
Dr Egon Toft VP and Dean
University

1.8 Responsibilities of Healthcare Professionals
This guideline has been issued by the MOPH to define how care should be provided in Qatar. It is based
upon a comprehensive assessment of the evidence as well as its applicability to the national context of
Qatar. Healthcare professionals are expected to take this guidance into account when exercising their
clinical judgement in the care of patients presenting to them.
The guidance does not override individual professional responsibility to take decisions which are
appropriate to the circumstances of the patient concerned. Such decisions should be made in consultation
with the patient, their guardians, or carers and should consider the individual risks and benefits of any
intervention that is contemplated in the patient’s care.

2 Skin & Soft Tissue Infection - Pathway
Click on a box below to see the relevant page of the Pathway.
Key
Information about Background Abbreviations used Performance
Recommendations
this Guideline Information in the Guideline Measures
of the Guideline
Clinical
Presentation
Necrotising Skin &

Soft Tissue History Examination
Infections
Emergency Referral Investigation
General Principles of
Management
Folliculitis,
Cellulitis & Viral Skin & Soft Parasitic Skin & Soft
Abscesses Furunculosis and Impetigo
Erysipelas Tissue Infections Tissue Infections
Carbunculosis
Referral Criteria to
Specialist Care
Diabetic Foot
Infected Burns Bites
Infections
Key:
Follow-Up
Information
Red Flags
Self Care
Primary Care
Secondary Care

3 Key Recommendations of the Guideline
The key recommendations of this guideline are:
Examination (Section 5.3):

• All patients suspected for SSTI should be examined for1:
o Sepsis syndrome.
o Systemic signs of infection (e.g. fever, raised white blood cell count).
o Systemic toxaemia.
o Life-threatening conditions.
o Other medical emergency conditions (see Section 7.3).
Investigation (Section 5.4):

• Laboratory investigations are not always required for the diagnosis but they may be ordered in
case of1,5,10 [L1, RGA]:
o Unclear symptoms.
o Atypical presentations.
o Damage estimation.
o Possibility of an alternative diagnosis.
o Differentiation between similar infections that require different management.
• Consider the following options:
o Blood tests for2,4,13–16:
▪ Complete blood count.
▪ Inflammatory markers.
▪ Glucose levels.
▪ HBA1C levels.
o Microbiological examination3,4,9,10,12–15.
o Urine sample12,13,17.
o Histological tests (e.g. if osteomyelitis is suspected)3.
o Diagnostic imaging studies1,3,4,10,13,14,16.
o Biopsy (e.g. if leishmaniasis, mycobacterial infection, eosinophilic folliculitis or non-
infective dermatosis is suspected)10,11.
o Tests for the presence of a specific virus3,12,17:
o Surgical exploration of the wound (for selected cases)5,10.
General Principles of Management (Section 7):

• Prompt recognition and selection of appropriate treatment regimen are key factors limiting the
morbidity and mortality associated with SSTIs5.
• Mild purulent SSTIs usually don’t require any specific treatment as they often drain
naturally3,10,13,15,18 [L1, RGA].
• Moderate purulent infections should be treated with incision and drainage3,10,13,18 [L1, RGA].
• Postoperative wound management and adequate nutritional support are vital for the good
outcome [R-GDG].
• Antibiotic therapy should be initiated as soon as their necessity is recognised19,20 [L1]:
o Empiric broad-spectrum therapy to cover the most likely pathogens is recommended as
the initial step2,19,21 [L1, RGA].
o Empiric antimicrobial therapy should be narrowed when culture tests and susceptibility
results become available2,3,10,19,21 [L1, RGA].
• The duration of antibiotic therapy will depend upon the microorganism identified on culture and
the clinical course of the patient1,3,10,24 [L1, RGA].

Emergency Referral (Section 7.3):
• The following conditions should be considered a medical emergency2,3,5,9,14,16,25,26:
o Rapidly progressing infection despite treatment.
o SSTI with systemic signs of infection.
o Signs of systemic sepsis.
o Diagnosis of necrotising SSTIs or identification of a necrotic area.
o Infected burn wounds with the high concentrations of bacteria (>105 colony-forming
units).
o Other life-threatening or limb-threatening conditions (e.g. ulceration with limb
ischaemia).
• Prompt surgical consultation is recommended for patients with aggressive SSTIs (e.g. necrotising
fasciitis or gas gangrene)10 [L1, RGA].
Treatment of Specific Skin and Soft Tissue Infections:

• Refer to the sections below for further information on the diagnosis and management of specific
SSTIs:
o Abscesses (Section 8).
o Folliculitis, Furunculosis and Carbunculosis (Section 9).
o Impetigo (Section 10).
o Cellulitis and Erysipelas (Section 11).
o Bites (Section 12).
o Diabetic Foot Infections (Section 13).
▪ See also MOPH National Clinical Guideline on the Chronic Complications of
Diabetes Mellitus.
o Infected Burns (Section 14).
o Necrotising Skin and Soft Tissue Infections (Section 15).
o Viral Skin and Soft Tissue Infections, including (Section 16):
▪ Measles.
▪ Rubella.
▪ Infectious Mononucleosis.
▪ Herpes Zoster.
▪ Molluscum Contagiosum.
o Parasitic Skin Infections, including (Section 17):
▪ Scabies.
▪ Pediculosis.
▪ Tungiasis.
▪ Hookworm-Related Cutaneous Larva Migration.
▪ Leishmaniasis.
▪ Loiasis.

4 Background Information
4.1 Definition
Skin and soft-tissue infections (SSTIs) include a variety of pathological conditions that result from microbial
invasion of the skin and its supporting structures and involve the skin, underlying subcutaneous tissue,
fascia, or muscles1,2.
4.2 Classification
SSTIs are categorised by:

• Origin3:
o Primary:
▪ Microorganisms invade otherwise healthy skin.
o Secondary:
▪ Microorganisms infect skin damaged due to underlying disease or trauma.
• Presence of purulent inflammation3:
o Purulent infections (e.g. furuncles, carbuncles, abscesses).
o Non-purulent infections (e.g. erysipelas, cellulitis, necrotising fasciitis).
• Severity of clinical presentation3:
o Mild.
o Moderate.
o Severe.
• Anatomical extent4:
o Focal.
o Diffuse.
• Prognosis1:
o Uncomplicated:
▪ Superficial infections (e.g. cellulitis, simple abscesses, impetigo, and furuncles).
▪ Low risk for life- or limb-threatening SSTIs unless they are improperly treated.
o Complicated:
▪ Deep soft-tissue infections (e.g. necrotising infections, infected ulcers, infected
burns, and major abscesses)
▪ High risk for life-threatening conditions.
▪ Further classified as non-necrotising and necrotising.
4.3 Prevalence
The true prevalence of SSTIs remains largely unknown as mild infections are typically self-limiting and
usually do not require medical attention3.
4.4 Risk Factors
Risk factors for SSTIs include2,3:

• Age (children or older adults).
• Asplenia.
• Presence of other diseases:
o Cardiopulmonary disease.
o Diabetes mellitus.
o Hepatorenal disease.

o Obesity.
o Peripheral neuropathy.
o Lymphoedema or lymphatic insufficiency.
o Pre-existing skin diseases.
o Peripheral arteriovenous insufficiency.
• Trauma, including:
o Cuts.
o Animal or human bites.
o Surgery.
• Immunosuppression:
o Human immunodeficiency virus (HIV) infection.
o Chemotherapy.
o Antiretroviral therapy.
o Disease-modifying antirheumatic drugs.
• Debility.
• Prolonged hospitalisation and long-term care.
• Long-term intravascular access.
• Dialysis (peritoneal, haemodialysis).
• Crowded living conditions.
• Poor hygiene (including sharing of personal items).
• Poor nutrition.
• Alcohol and substance abuse.
• Physical contact (e.g. sports activities).
• Occupation:
o Health care professionals.
o Military personnel.
4.5 Prognosis
Necrotising SSTIs are associated with poor clinical prognosis1. Any delay in diagnosis or treatment of these
conditions correlates with a poor outcome and possible death1,5. Fournier’s Gangrene Severity Index (FGSI)
may be used as a standard score to predict the prognosis of the patients1,6.
In Qatar, the highest mortality among patients with necrotising fasciitis was reported among those with
the infection in the chest, axilla and gluteal regions7. Patients with necrotising fasciitis of the perineum and
genitalia had the lowest mortality.
Assessment of the complicating factors (e.g. underlying diseases) and appropriate use of antibiotics are
essential to optimise outcomes of patients presenting with SSTIs3,4. Among the signs that predict a poor
outcome are5,8,9:
• Diabetes mellitus.
• Obesity.
• Heart failure.
• Leukopenia.
• Thrombocytopenia.
• Haemolysis.
• Severe renal failure.
• Myoglobinuria.
• Immunosuppression.
• Systemic illness.
• Sepsis.
• Other.

5 Clinical Assessment
5.1 Clinical Presentation
SSTIs are diverse in their clinical presentations3. Clinical features of common SSTIs are listed in each of the
sections that relate to them.
In general:
• Mild infections present with local symptoms only, such as2,3,5:
o Warmth.
o Erythema.
o Oedema.
o Tenderness.
o Pain.
• Moderate to severe infections are associated with systemic signs of infection3,5:
o Fever >38ºC.
o Tachycardia (heart rate >100 beats/min).
o Tachypnoea (respiratory rate >20 breaths/min).
o Hypotension.
o White blood cells >12*103 cells/mm3.
o Fatigue.
o Nausea or vomiting.
5.2 History
Important points to elicit include the following3,5,10–14:

• Age of the patient.
• Presence of long term conditions (e.g. diabetes mellitus).
• History of pre-existing skin diseases.
• Recent trauma (e.g. wounds and bites).
• Recent surgery.
• Previous antimicrobial therapy.
• Immunisation status.
• Allergies if known.
• Recurrent hospital admissions.
• Lifestyle and hobbies.
Additional points in the history to elicit relating to specific infections are provided in the sections relating
to those infections.
5.3 Examination
All patients suspected for SSTI should be examined for1:

• Sepsis syndrome.
• Systemic signs of infection (e.g. fever, raised white blood cell count).
• Systemic toxaemia.
• Life-threatening conditions.
• Other medical emergency conditions (see Section 7.3).
If none of the above are detected, a physical examination should be performed, including1,3,10 [L1]:
• Examination of the wound.

• Screening for the local signs of infection such as:
o Heat.
o Pain.
o Swelling.
o Erythema.
o Tenderness.
o Delayed healing.
o Discharge from the wound site.
o Presence of an abnormal smell (e.g. foul smell in Fournier’s gangrene).
• Presence of damage to surrounding or underlying structures.
• Testing for pain or loss of sensation.
• Presence of discoloration.
• Presence of crepitus.
• Examination of lymph nodes.
• Screening for Nikolsky sign (i.e., epithelial desquamation resulting from slight pressure or rubbing
the skin or oral mucosa).
• Screening for insect bites, abrasions, surgical wounds.
• Screening for obesity or malnutrition.
Particular points in the examination of specific infections, are provided in the sections relating to those
infections.

6 Investigation
Laboratory investigations are not always required for the diagnosis but they may be ordered in case of1,5,10
[L1, RGA]:
• Unclear symptoms.
• Atypical presentations.
• Damage estimation.
• Possibility of an alternative diagnosis.
• Differentiation between similar infections that require different management.
Consider the following options:

• Blood tests for2,4,13–16:
o Complete blood count.
o Inflammatory markers.
o Glucose levels.
o HBA1C levels.
• Microbiological examination3,4,9,10,12–15:
o Open wound – tissue specimens.
o Purulent wounds – pus culture.
o Ulcerated skin – tissue biopsy or curettage.
o Non-open wounds – needle aspiration.
o Sepsis syndrome or severe infection – blood culture.
o Gram stain.
o Throat swabs.
o Tzanck smear (if herpes infection is suspected).
• Urine sample12,13,17.
• Histological tests (e.g. if osteomyelitis is suspected)3.
• Diagnostic imaging studies1,3,4,10,13,14,16:
o Ultrasound (e.g. to differentiate simple cellulitis from necrotising fasciitis).
o Doppler vascular examination.
o X-ray (e.g. in septic arthritis or osteomyelitis).
o Magnetic resonance imaging (MRI) (e.g. in necrotising infections).
o Computed tomography (CT) (e.g. in necrotising infections).
• Biopsy (e.g. if leishmaniasis, mycobacterial infection, eosinophilic folliculitis or non-infective
dermatosis is suspected)10,11.
• Tests for the presence of a virus3,12,17:
o Virus specific antibodies in serum (e.g. in measles).
o Polymerase chain reaction (e.g. in varicella zoster virus, VZV).
o Real-time polymerase chain reaction (e.g. in measles).
o Fluorescent antibody staining of infected cells.
o Molecular genotyping of virus.
o Serologic tests.
• Surgical exploration of the wound (for selected cases)5,10.

7 General Principles of Management
7.1 Principles of Care
Prompt recognition and selection of appropriate treatment regimen are key factors limiting the morbidity
and mortality associated with SSTIs5.
Mild purulent SSTIs usually don’t require any specific treatment as they often drain naturally3,10,13,15,18 [L1,
RGA]. Moderate purulent infections should be treated with incision and drainage3,10,13,18 [L1, RGA]. In
children, minimally invasive techniques (e.g. stab incision, haemostatic rupture of septations, in-dwelling
drain placement) are preferred2 [L1, RGA].
Topical and/or oral antibiotic administration is usually required in purulent cases that don’t resolve
naturally within several days and in mild to moderate non-purulent infections1,3,10 [L1, RGA]. If patients do
not improve (or worsen) after 48h of treatment, they should receive antibiotics against methicillin-resistant
Staphylococcus aureus (MRSA)2 [L1, RGA].
Postoperative wound management and adequate nutritional support are vital for the good outcome [R-
GDG].
7.2 Principles of Antimicrobial Treatment
Should antibiotic treatment be or is likely to become an issue, an early microbiology culture and sensitivity
of relevant specimens is essential (see Section 6) [R-GDG].
Antibiotic therapy should be initiated as soon as their necessity is recognised19,20 [L1]:

• Empiric broad-spectrum therapy to cover the most likely pathogens is recommended as the initial
step2,19,21 [L1, RGA].
• Patients unresponsive to antimicrobial therapy should be re-evaluated clinically and
microbiologically whenever possible 1,21 [L2, RGA].
• Empiric antimicrobial therapy should be narrowed when culture tests and susceptibility results
become available2,3,10,19,21 [L1, RGA].
When selecting antibiotics for empirical antibiotic therapy, consider the following3,19,21,22 [L1, RGA]:
• Most likely microorganism(s) and known susceptibility patterns in Qatar.
• Localisation of infection.
• Clinical severity.
• Relevant drug interactions.
• Recent antibiotic use (past 90 days).
• Individual health conditions of the patient (e.g. allergy).
• Characteristics of the medication:
o Antimicrobial infusion time.
o Pharmacokinetics of the antimicrobial.
o Potential adverse effects.
If there is uncertainty on the appropriate patient-specific antimicrobial therapy, consult an infectious

disease specialist and/or clinical pharmacist for advice and guidance23 [L1].
The duration of antibiotic therapy will depend upon the microorganism identified on culture and the clinical
course of the patient1,3,10,24 [L1, RGA]. A typical duration of treatment ranges from 5 to 10 days8.

Therapy with intravenous antibiotics is usually required for 7-14 days for hospitalised patients2 but may be
extended depending on the patient’s condition2,10 [L1, RGA]. Intravenous antimicrobials may also be
continued at home under close supervision after initiation in the hospital or emergency department 2 [L1,
RGA].
Intravenous antibiotics should be discontinued when2,14 [L1]:

• Drainage or debridement is completed.
• The clinical picture improves.
• The patient can tolerate oral intake.
21
Blood levels of aminoglycosides and vancomycin should be monitored, particularly in elderly patients
[L2, RGA].
7.3 Emergency Referral
The following conditions should be considered a medical emergency2,3,5,9,14,16,25,26:

• Rapidly progressing infection despite treatment.
• SSTI with systemic signs of infection.
• Signs of systemic sepsis.
• Diagnosis of necrotising SSTIs or identification of a necrotic area.
• Infected burn wounds with the high concentrations of bacteria (>105 colony-forming units).
• Other life-threatening or limb-threatening conditions (e.g. ulceration with limb ischaemia).
Prompt surgical consultation is recommended for patients with aggressive SSTIs (e.g. necrotising fasciitis
or gas gangrene)10 [L1, RGA].
7.4 Referral to Specialist Care
Hospitalisation and specialist care are required if at least one of the following is present1,2,16,27–29:
• Severe or complicated SSTIs.
• Bullous impetigo, particularly in infants ≤1 year of age.
• Infection near the eyes or nose (including periorbital cellulitis).
• Failed outpatient treatment.
• Patient is immunocompromised or has unstable comorbid illnesses.
• High risk of complications.
• Inability to tolerate oral medications.
• Problems with feeding.
• Infection overlying or near an indwelling medical device.
• Recurrent SSTI.
• Uncontrolled infection despite adequate outpatient antimicrobial therapy.
• MRSA colonisation.
• Uncommon pathogens are suspected.
• Need for surgical intervention under anaesthesia (including surgical debridement).
Consider a consultation with an infectious disease specialist, surgeon, dermatologist or microbiologist

when required1,10 [L1, RGA].
Consider referral to a diabetologist if a patient is suspected for diabetes that has not been previously
diagnosed30 [L1, RGA].

7.5 Follow-Up
Close follow-up is necessary during and after treatment. Before discharge, patients should receive a plan
for follow-up care in the outpatient setting31,32 [L1, RGA].
Following discharge from inpatient care, primary healthcare professionals should focus on9:
• Reviewing and adjusting long-term medication.
• Identifying new physical, mental, and cognitive problems.
• Educating patients and caregivers about:
o Good personal hygiene.
o Self-isolation (if required).
o Vaccination.

8 Abscesses
8.1 Classification and Aetiology
There are two main types of abscesses13 [L1]:

• Cutaneous abscess:
o Develops within the epidermis and dermis (e.g. boils).
o Cutaneous abscess is diagnosed if1 [L1]:
▪ Induration and erythema are limited only to a defined area of the abscess and do
not extend beyond its borders; and
▪ The abscess does not extend into deeper tissues; and
▪ The abscess does not have a multiloculated extension.
• Deep abscess:
o Develops inside an organ or in the spaces between organs. Examples include13:
▪ Anorectal abscess.
▪ Bartholin's cyst.
▪ Dental abscess.
▪ Peritonsillar abscess.
• The diagnosis of a deep abscess requires more complex analysis. Laboratory investigations should
be performed in addition to symptom assessment13 [L1, RGA].
Abscesses are usually caused by gram-positive cocci, e.g. Staphylococcus aureus (S. aureus)3,14. They may
also be polymicrobial, including anaerobes.
8.2 Clinical Presentation and Assessment
The features of an abscess include1–3,5,13:

• Signs and symptoms of inflammation (pain, redness, heat and swelling).
• Collection of pus with surrounding granulation.
• Openings that drain pus.
• Swollen lymph nodes.
• Possible overlying skin necrosis.
• Features attenuated in cold abscess.
• Axilla, groin, and/or perineal abscess can occur in hidradenitis suppurativa.
• Fever.
In addition to general history taking and examination, described in Sections 5.2 and 5.3, enquire about
the following3,10,13:
• Presence of underlying inflammatory condition (e.g., hidradenitis suppurativa).
• History of staphylococcal infections.
• Recent injury in the area of abscess.
8.3 Management
Small skin abscesses don’t require any specific treatment13,18 [L1, RGA]. Incision, surgical drainage, and
local wound care are sufficient treatment for large cutaneous abscesses1,3,10 [L1, RGA]. Consider applying
warm moist compresses to facilitate pus elimination and reduce swelling3,13 [L1, RGA].
Systemic antibiotic therapy is not required in the absence of systemic inflammatory response syndrome 1–
3,10 [L1, RGA].

For complicated abscesses, antimicrobial therapy should be based on results of wound cultures1,5 [L1, RGA]
and administered when clinically indicated2,3,5,33 [L1, RGA]. Clinical indications for antimicrobial therapy
include2,3,5,33:
• Patient is of an extreme age (children and older adults).
• Patient has associated comorbidities or immunosuppression.
• The disease is severe or extensive.
• If the abscess is deep (e.g. intra-abdominal).
• There is associated septic phlebitis.
• There are signs and symptoms of systemic illness.
• Recurrent abscesses formation.
• Abscess is difficult to drain completely.
• Incision and drainage alone do not improve the condition.
Empirical antimicrobial regimens are provided in Table 8.3 below. See also the notes in Section 7.2 on
general principles of antimicrobial treatment of SSTIs.
Type of
Empirical Antimicrobials Additional Notes
Abscess
Oral flucloxacillin or cephalexin. If methicillin-sensitive S. aureus (MSSA) is
isolated.
Moderately
Typical duration is 5-10 days for outpatients
Severe
and 7-14 days for inpatients.
Abscess
Trimethoprim/sulfamethoxazole or If community-associated MRSA (CA-MRSA) is
doxycycline, or clindamycin. confirmed.
Intravenous cloxacillin or cefazolin, or If MSSA is suspected or cultured.
Severe clindamycin.
Abscess Intravenous vancomycin or daptomycin, or If MRSA is suspected or cultured.
linezolid.
Table 8.3: Empirical Antimicrobials for the Treatment of Complicated Abscesses 10,14.
Antimicrobials are usually ineffective without drainage13,14. Consider the following options to drain deep
abscesses13 [L1, RGA]:
• Percutaneous abscess drainage:
o If the internal abscess is small.
• Surgical drainage:
o If the abscess is too large to be drained with a needle.
o If a needle is not possible to use safely in the area of the abscess.
o The needle drainage has not been effective in removing all of the pus.
Other treatment approaches to decolonise bacteria from the body may also be considered3,10,13 [L1, RGA]:
• Nasal decolonisation with mupirocin (twice daily for 5 days).
• Daily washes with chlorhexidine or antiseptic soap.
• Decontamination of personal items.
If recurrent abscess occurs at a site of previous infection, the site should be inspected for local causes (e.g.
pilonidal cyst, hidradenitis suppurativa, or foreign material)10 [L1, RGA]. Adult patients with recurrent
abscesses that began in early childhood should be evaluated for neutrophil disorders10 [L1, RGA].

9 Folliculitis, Furunculosis, and Carbunculosis
9.1 Aetiology
Causes of folliculitis, furunculosis and carbunculosis, include3,5,11,15:

• Immunocompetent patients:
o S. aureus.
o Candida.
o Dermatophytes.
o Pseudomonas aeruginosa.
o Malassezia furfur.
• Immunosuppressed patients:
o S. aureus.
o Klebsiella.
o Enterobacter spp.
o Proteus spp.
Table 9.2(1) outlines the differentiating features of folliculitis, furunculosis, and carbunculosis.
Type of Infection Specific Features

• Usually occur in areas with increased sweating but may affect any area of
the body except the palms and soles.
• Presents as follicular-based papules or pustules.
Folliculitis
• May be associated with pruritic skin conditions, acne, or steroid use.
• Pruritus, painful or painless papules or pustule.
• Swelling.
• Furuncles are deeper than folliculitis.
Furuncle • Painful swollen boils.
• Systemic features of infection.
• Carbuncles are larger that furuncles.
• Carbuncles involve skin and subcutaneous tissue.
Carbuncle • Usually occur over thicker skin of neck, back, and lateral thighs.
• Drain through multiple pores.
• Systemic features of infection.
Table 9.2(1): Differentiating Features of Folliculitis, Furunculosis and Carbunculosis 1–3,5,15,18.
the following11:
• Prolonged use of oral antibiotics.
• Use of topical corticosteroids.
• Frequent shaving.
• Increased sweating.
• Hot tub and/or swimming pool exposure.
• Medications that increase risk of folliculitis (e.g. lithium and cyclosporine).
Consider alternative diagnoses as listed in Table 9.2(2).

Folliculitis Furunculosis and Carbunculosis
• Acne vulgaris. • Cystic acne.
• Papulopustular rosacea. • Hidradenitis suppurativa.
• Drug-induced folliculitis. • Cellulitis.
• Hidradenitis suppurativa. • Osteomyelitis.
• Scabies. • Orf.
• Pseudofolliculitis barbae. • Anthrax.
• Keratosis pilaris. • Arthropod bite.
• Acne keloidalis nuchae.
Table 9.2(2): Differential Diagnoses for Patients with Suspected Folliculitis, Furunculosis or Carbunculosis 11,15.
9.3 Investigation
Histopathology is usually not required for the diagnosis11 [L2]. Potassium hydroxide preparation may be
used to diagnose demodex folliculitis or pityrosporum folliculitis11 [L2].
If folliculitis is suspected, specify the type of infection11 [L2] i.e.:

• Superficial bacterial folliculitis.
• Pityrosporum folliculitis.
• Viral folliculitis.
• Demodex folliculitis.
• Eosinophilic folliculitis.
9.4 Management
9.4.1 Folliculitis
Simple cases of folliculitis resolve spontaneously within a few days3,11. In more extensive cases, incision and
drainage may be considered along with administration of antibiotics3,11 [L1, RGA].
Demodex folliculitis should be treated with anti-parasitic agents11 [L2, RGA]:

• First-choice medication is topical permethrin 5% cream.
• Second-choice treatment is antibiotic therapy (see Table 9.4.1).
Viral folliculitis secondary to molluscum contagiosum infection may be treated with11 [L2, RGA]:
• Curettage.
• Cryotherapy.
• Topical cantharidin.

Type of SSTI Empirical Antimicrobials Additional Notes
Staphylococcal Topical mupirocin or Not recommended for children younger than 2

folliculitis clindamycin. months.
Ampicillin, trimethoprim-
Gram-negative Oral antibiotic treatment that cover
sulfamethoxazole, or
folliculitis pseudomonas are recommended.
ciprofloxacin.
Pityrosporum Systemic therapy with oral antifungal agents is
Itraconazole or fluconazole.
folliculitis recommended.
Oral acyclovir, valacyclovir, or If caused by infection with VZV or herpesvirus
Viral folliculitis
famciclovir. infections.
Oral ivermectin or Consider dual therapy ivermectin and
Demodex folliculitis
metronidazole. metronidazole.
Table 9.4.1: Empirical Antimicrobial Regimens for Treatment of Folliculitis 2,11.
Consider the following treatment options in patients with eosinophilic folliculitis11 [L2, RGA]:
• First-choice is the antiretroviral therapy (ART) to treat the patient’s underlying HIV.
• Complimentary treatment after ART initiation may include:
o Topical corticosteroids.
o Antihistamines.
o Phototherapy.
o Itraconazole or isotretinoin.
9.4.2 Furunculosis and Carbunculosis
Small furuncles don’t require any specific treatment3,10,15,18 [L1, RGA]. If they do not improve after 2-3 days
of moist heat, a topical antimicrobial and drainage are required3 [L1, RGA]. Large furuncles and all
carbuncles should be treated with incision and drainage3,10,15,18 [L1, RGA].
Systemic antimicrobials are not recommended for routine use3,10,15,18 [L1, RGB] but may be considered in
patients with carbuncles18 [L1, RGA] or with evidence of systemic infection10 [L1, RGA].
Type of SSTI Empirical Antimicrobials Additional Notes

Oral cephalosporins (e.g.
cephalexin) or flucloxacillin.
Moderate to Clindamycin, tetracyclines,

Severe cases of trimethoprim-sulphamethoxazole, If MRSA is suspected or cultured.
Furunculosis or linezolid, or glycopeptide.
Carbunculosis Topical antibiotics may be used as adjunctive
therapy.
Topical clindamycin or mupirocin.
Mupirocin should be applied twice daily to the
inner nares for 12 to 30 days.
Table 9.4.2: Empirical Antimicrobial Regimens for Treatment of Furunculosis and Carbunculosis 11,15.
If patients have recurrent carbuncles, the following treatments may also be considered15 [L2, RGA]:
• Bathing with a benzoyl peroxide wash or antibacterial soap.
• Decolonisation of the patient’s nares with mupirocin.

To prevent spread of infection, the patient should be advised on prophylactic measures18 [L1, RGA],
including:
• Washing hands after touching affected areas.
• Using a separate face cloth and towel.
• Washing underwear, bed linen, and towels at a high temperature.
• Appropriate wound dressing until the wound healed completely.

10 Impetigo
10.1 Aetiology
Impetigo is typically caused by gram-positive cocci (e.g. S. aureus), group A Streptococcus, or a mix of
staphylococci and streptococci2,3,5,10.
The presenting features of impetigo are1–3,5:

• Erythematous, vesicular, and pruritic lesions.
• Affects skin of the face and limbs.
• Can occur at any age but most commonly affects children.
• Associated with mild soreness and redness.
• May cause glomerulonephritis.
• Vesicles may enlarge (bullae).
• May spread to lymph nodes, bones, joints, or lungs.
It is important to differentiate between the two main types of impetigo3,5 [L1, RGA]:
• Non-bullous:
o Small fluid-filled vesicles that develop into pustules, that then rupture to leave golden-
yellow crusts.
• Bullous:
o Vesicles that develop into yellow fluid-filled bullae, that then rupture to leave brown
crusts.
10.3 Management
Treatment options for patients with impetigo are1,3,5,10,29 [L1, RGA]:

• Localised non-bullous impetigo:
o First-choice: Hydrogen peroxide 1% cream applied 2-3 times/day for 5 days29.
o Second-choice: A short course of a topical fusidic acid 2%, mupirocin 2% or retapamulin
applied 2-3 times/day for 5 days2,3,29.
• Widespread non-bullous impetigo:
o First-choice: A short course of a topical fusidic acid 2%, mupirocin 2% or retapamulin
applied 2-3 times/day for 5 days2,3,29. Along with topical, systemic regimen is necessary:
consider cephalexin, or flucloxacillin [R-GDG].
o Second-choice: Empirical antimicrobial therapy directed against MSSA (oral cloxacillin or
cephalexin)3,5,10,29.
o Antimicrobial therapy using oral penicillin if the cultures reveal only streptococci10.
• Bullous impetigo:
o Empirical antimicrobial therapy based on oral antibiotics against Gram-positive
bacteria1,29.
o Consider using mesh gauze sponges or brushes and antibacterial soap5.
o Soaking in soapy warm water may be used to facilitates crust removal3.
• If MRSA is suspected or cultured from swabs:
o Use oral trimethoprim-sulfamethoxazole, doxycycline, or clindamycin5,10. Check for
history of sulphonamides drug allergy and contraindications (e.g., pregnancy and age
restrictions) before prescribing [R-GDG].
Combination treatment with topical and oral antibiotics is not recommended29 [L1, RGB].

Patients with impetigo, and their parents or carers if appropriate, should be advised about:
• Good hygiene measures to reduce the spread of impetigo to other areas of the body and to other
people29 [L1, RGA].
• Disinfection of towels and bedding5 [L2].
• Seeking medical help if29 [L1, RGA]:
o Symptoms worsen rapidly or significantly.
o Infection has not improved after completing a course of treatment.
If the infection is worsening, has not improved, or has recurred after completing a course of appropriate
treatment, consider the following5,29 [L1, RGA]:
• Sending a skin swab for microbiological testing.
• Adjusting antibiotics appropriately after receiving culture results.
• Taking a nasal swab and starting treatment for decolonisation.

11 Cellulitis and Erysipelas
11.1 Aetiology
Cellulitis is an infection of the dermis and the subcutaneous tissue1. Erysipelas is usually referred to as a
type of superficial cellulitis involving the face10.
Typical microorganisms in cellulitis infection are group A b-hemolytic Streptococcus species and S.
aureus1,5,14. Cellulitis and erysipelas in patients without penetrating trauma and no evidence of MRSA are
typically caused by gram-positive Streptococcus pyogenes (S. pyogenes)1,3.
The diagnosis must be supported by the clinical presentation and at least two of the four criteria should be
present diagnose cellulitis16 [L2]:
• Warmth.
• Erythema.
• Oedema.
• Tenderness.
Differentiate between the two types of cellulitis3,16 [L1, RGA]:

• Non-purulent:
o Without purulent drainage or exudate or associated abscess.
• Purulent:
o Associated with purulent drainage or exudate in the absence of a drainable abscess.
Consider alternative diagnoses16,28:

• Chronic venous stasis dermatitis.
• Chronic venous insufficiency.
• Necrotising fasciitis (see Section 15).
• Septic arthritis.
• Deep vein thrombosis.
• Inflammatory reaction to an immunisation or an insect bite.
The differentiating features of cellulitis and erysipelas are provided in the table below:
Type of
Specific Features
Infection
• Usually present in the lower extremities.
• Localised over areas of skin breakdown (e.g. insect bites, abrasions, surgical
wounds).
• Begins as a hot, red, oedematous, sharply defined eruption.
Cellulitis • Non-elevated and poorly defined margins.
(purulent, non- • Signs and symptoms of infection.
purulent) • Regional lymphadenopathy is common.
• Leucocytosis may develop.
• Can be purulent or non-purulent.
• Can progress to adjacent tissue leading to an abscess, septic arthritis, or
osteomyelitis.

Type of
Specific Features
Infection
• Bright red, tender plaque with well-demarcated margin.
• Distinctly raised inflamed skin.
• Usually occur over face, ears, or lower legs.
Erysipelas • Often preceded by flu-like symptoms.
• Lymphangitis or lymphadenitis.
• Leucocytosis.
• Burning pain.
Table 11.2: Differentiating Features of Cellulitis and Erysipelas1–3,5.
11.3 Management
Cellulitis and erysipelas should be managed with antimicrobial therapy as per the table below 1,3,28 [L1,
RGA]. Consider antibiotic prophylaxis in patients with recurrent cellulitis or erysipelas28 [L1, RGA].
Type of
infection or Empirical Antimicrobials Additional Notes
Prophylaxis
First-choice antibiotics should be directed primarily
against Gram-positive streptococci.
Oral penicillin V.
Antibiotic therapy for 5 days is usually sufficient
but may be extended if no improvement observed.
Cellulitis or
If MSSA is suspected or cultured.
Erysipelas Cloxacillin, cephalexin, or
Antibiotic therapy for 5 days is usually sufficient
clindamycin.
but may be extended if no improvement observed.
First-choice antibiotics for paediatric population.
Cefazolin or cloxacillin.
If fasciitis suspected add clindamycin.
Oral penicillin V or erythromycin. Prophylactic administration may be considered in

Prophylaxis Intramuscular benzathine patients with 3-4 episodes of cellulitis per year
penicillin. despite attempts to treat predisposing factors.
Table 11.3: Recommended Antimicrobials for Treatment and Prophylaxis of Cellulitis and Erysipelas 3,10,16,21.
Intravenous systemic antibiotics are recommended in patients with3,10 [L1, RGA]:

• Moderate cases of cellulitis with systemic signs of infection if:
o Cellulitis associated with penetrating trauma.
o Systemic inflammatory-response syndrome is present.
o Infection is due to the injection drug use.
o MRSA is cultured.
• Severe cases of cellulitis if:
o Cellulitis is not responding to oral antibiotic therapy.
o Patient is immunocompromised.
o There are clinical signs of deeper infection.
o Systemic inflammatory-response syndrome is present.
If required, consider adjuvant therapy when necessary, including:

• Non-steroidal anti-inflammatory drugs (NSAIDs) may be used to reduce inflammatory signs [R-
GDG].

• Systemic corticosteroids are applicable only for patients who do not have diabetes 3,10 [L1, RGB]:
o Consider prednisone 40 mg daily for 7 days.
• Wound management for cellulitis with open wound.
• Compression stockings, decongestive therapy.
• Emollients may be used to keep skin hydrated.
• Immobilisation and elevation of the affected extremity may also be helpful in facilitating drainage3
[L1, RGA].
Additional investigations for underlying diseases that worsen the prognosis (e.g. diabetes mellitus or
peripheral arterial occlusive disease) may be required4 [L2].
Treatment of predisposing factors should be provided to all patients3,10,28 [L1, RGA]. These include3,10,28:
• Obesity.
• Oedema.
• Venous insufficiency.
• Eczema.
• Underlying cutaneous disorders.
• Fissuring, scaling, and maceration in the interdigital toe spaces.
Possible complications of cellulitis should be reviewed and evaluated3 [L1, RGA]. These include3,16:
• Abscess.
• Septic arthritis.
• Osteomyelitis.
• Endocarditis.
• Bacteraemia.
• Sepsis.

12 Bites
12.1 Aetiology
Note that only 10–20% of bite wounds become infected, including1:

• 30-50% of cat bites.
• 5-25% of dog bites.
• 20-25% of human bites.
Consider different types of bites34:

• Large wild animal bites (e.g. wild dogs).
• Small wild animal bites (e.g. mice, rats).
• Large pet animal bites (e.g. dogs, cats, horses).
• Small indoor pet animal bites (e.g. hamsters, guinea pigs).
• Human bites (including a clenched fist injury).
The common pathogens associated with bite wound infections are SSTIs2–4,10,35:
• Dog bites:
o Aerobic organisms:
▪ Pasteurella spp.
▪ Streptococcus spp.
▪ Staphylococcus spp.
▪ Capnocytophaga canimorsus.
o Anaerobic organisms:
▪ Fusobacterium spp.
▪ Porphyromonas spp.
▪ Prevotella spp.
▪ Bacteroides spp.
▪ Propionobacterium spp.
▪ Peptostreptococcus spp.
• Cat bites:
▪ Pasteurella spp.
▪ Streptococcus spp.
▪ Staphylococcus spp.
▪ Moraxella spp.
▪ Porphyromonas spp.
▪ Prevotella spp.
▪ Bacteroides spp.
▪ Propionobacterium spp.
• Human bites:
▪ Veillonella spp.
▪ Prevotella spp.
▪ Veillonella spp.

Features of an infection in a bite wound, include2,3,10,35:

• Infection sets in 8-72 hours after animal bites.
• May involve tendons, tendon sheaths, bone, and joints.
• Lymphadenitis or lymphangitis.
• Fever.
• Leucocytosis.
• Animal contacts.
• How and when the bite occurred.
• Tetanus immunisation status.
• Immunisation history of the animal if available.
• Medical history of the human biter, if known (e.g. viral hepatitis, HIV, other transmissible diseases).
12.3 Management
Gentle but deep irrigation of the wound with sterile normal saline is recommended to remove foreign
materials and pathogens1,3,34,35 [L1, RGA]. Irrigation under pressure should be avoided1 [L1, RGC].
NB: Primary closure of wounds should be avoided unless the wound is on the face or neck3,10,35 [L1, RGC].
Universal antimicrobial prophylaxis is not recommended1 [L1, RGB] but may be considered in some
patients, e.g. in case of face or neck wounds with primary closure [R-GDG]. It is also not recommended if
the patient presents ≥24h after the bite with no clinical signs of infection1 [L1, RGB].
Patients who are at increased risk of infection, or have immunocompromising conditions (e.g. asplenia,
advanced liver disease), or implants (e.g. artificial heart valves), should receive antibiotic therapy for 3-5
days for1,3,10 [L1, RGB]:
• Fresh deep wounds.
• Joint, bone or tendon injuries.
• Wounds in critical bodily areas: hands, feet, areas near joints, face, genitals.
All children with bite wounds receiving antibiotic therapy should be re-evaluated within 24-48 hours to
monitor for signs and symptoms of infection35 [L2, RGA].

First choice pre-emptive antibiotics.
• Amoxicillin/clavulanate.
Antibiotic therapy for 7-10 days is usually sufficient.
• Second-generation cephalosporins (cefuroxime,
cefoxitin).
• Third-generation cephalosporins (ceftriaxone,
cefotaxime).
• Fluoroquinolones (ciprofloxacin, levofloxacin, Alternative options of pre-emptive antibiotics.
moxifloxacin). Antibiotic therapy for 7-10 days is usually sufficient.
• Carbapenems.
• Doxycycline.
• Trimethoprim/sulfamethoxazole plus
clindamycin or metronidazole.
Table 12.3(1): Recommended Antimicrobials for use in Infected Bites2–4,10,35.

All patients should be considered for post-exposure prophylaxis to infectious organisms1–3 [L1, RGA]:
• With dog bites3,35:
o Rabies (rabies virus).
o Tetanus (Clostridium tetani).
o Leptospirosis (Leptospira spp.).
o Tularaemia (Francisella tularensis).
• With cat bites3,35:
o Cat-scratch disease (Bartonella spp.).
o Sporotrichosis (Sporothrix spp.).
o Rabies (rabies virus).
• With rodent bites35:
o Rat-bite fever (Streptobacillus moniliformis or Spirillium minus).
o Leptospirosis (Leptospira spp.)
• With human bites1,2,35:
o Hepatitis B and C.
o Herpes (herpes simplex virus).
o Cytomegalovirus infection.
o Syphilis (Treponema pallidum).
o HIV.
Tetanus toxoid should be administered to patients without a toxoid vaccination in the last 10 years (see
Table 12.3(2))10 [L1, RGA].
Possible complications should be reviewed and evaluated35 [L2, RGA]. These include35:
• Cellulitis (see Section 11).
• Osteomyelitis.
• Tenosynovitis.
• Tendinitis.
• Orbital cellulitis.
• Brain abscesses.

Age Vaccination History Clean, Minor Wounds All Other Wounds
0-6 years Unknown or not up-to-date on DTaP (If DTaP is not DTaP
DTaP series based on age available, OK to give Tdap) TIG
Up-to-date on DTaP series based No indication No indication

on age
7-10 years Unknown or incomplete DTaP Tdap and recommend Tdap and recommend catch-
series catch-up vaccination up vaccination
TIG
Completed DTaP series AND <5 No indication No indication
years since last dose
Completed DTaP series AND ≥5 No indication Td, but Tdap preferred if child
years since last dose is 10 years of age
11 years Unknown or <3 doses of tetanus Tdap and recommend Tdap and recommend catch-
and older toxoid containing vaccine catch-up vaccination up vaccination
TIG
3 or more doses of tetanus toxoid No indication No indication
containing vaccine AND <5 years
since last dose
3 or more doses of tetanus toxoid No indication Tdap preferred (if not yet
containing vaccine AND 5-10 years received) or Td
since last dose
3 or more doses of tetanus toxoid Tdap preferred (if not yet Tdap preferred (if not yet
containing vaccine AND >10 years received) or Td received) or Td
since last dose
Table 12.3(2): Tetanus Vaccination and TIG for Wound Management 36.
DTaP – Diphtheria and Tetanus toxoids and acellular pertussis vaccine.
Tdap – tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis.
TIG – Tetanus immune globulin.
Td – tetanus and diphtheria toxoids.

13 Diabetic Foot Infections
13.1 Aetiology
The pathogens commonly encountered in diabetic foot infections include3,14,30:
Type of Infection Most Common Pathogens
Mild to moderate cases • Staphylococcus spp.

• S. aureus.
Moderate to severe cases and wounds, • Streptococcus agalactiae.
longstanding ulcers, or those previously • Gram-negative bacilli.
treated with antibiotics. • Gram-negative rods.
• Anaerobic bacteria.
Infections of the ischemic foot • Anaerobic pathogens
Table 13.1: Common Pathogens Causing Bacterial SSTIs in the Feet of Diabetic Patients 3,14,30.
Diabetic foot infection (DFI) is typically a deep abscess, cellulitis of the dorsum, or a mal perforans ulcer 3.
Localised signs of infection may be present but pain and systemic signs of infection are usually absent3 [L1].
Laboratory studies may be required to determine the appropriate management3 [L1, RGA]:
• Imaging.
• Cultures obtained from deep tissue samples post-debridement.
If a DFI is suspected, enquire about30:

• History of diabetes.
• History of penetrating trauma.
• Possibility of extension of local infection.
13.3 Management
All patients with DFI should be offered the multidisciplinary foot care service14,26 [L1, RGA] that has access
to 26 [L1]:
• Rehabilitation services.
• Plastic surgery.
• Psychological services.
• Nutritional services.
• General and vascular surgery.
• Podiatry.
• Endocrinology.
• Occupational therapy.
• Tissue viability team.
• Other services listed in NCG on Chronic Complications of Diabetes Mellitus by MOPH 37.

Treatment of a DFI is based on the extent and severity of the infection26,30 [L1, RGA]:
• Mild infections:
o Should be treated with oral antibiotics.
o Treatment in the outpatient setting is sufficient. Hospitalisation is not required.
• Selected patients with moderate infections and all patients with severe infections:
o Should be treated with parenteral antibiotics.
o Require hospitalisation, surgical consultation, and additional evaluation.
o Surgical debridement and drainage of deep tissue abscesses and infections may be
required30.
o For more details, refer to the MOPH National Clinical Guideline on Chronic Complications
of Diabetes Mellitus37.
As most DFIs are polymicrobial, no single antibiotic regimen is clearly superior to another30 [L1, RGB].
Consider regimens listed in Table 13.3.
DFIs are frequently complicated with osteomyelitis3,30.
Type of Infection Empirical Antimicrobials Additional Notes
Ulcer with Superficial

Cefuroxime axetil or Cloxacillin. Duration of treatment is two weeks.
Inflammation <2 cm
Ulcer with Co-amoxiclav or ampicillin/sulbactam. First-choice medications.

Inflammation (>2 cm)
and Extension into
Fascia Moxifloxacin or ertapenem. Second-choice medications.
All Other Cases Linezolid or clindamycin. If MRSA is suspected or cultured.
Table 13.3: Selection of Empirical Antibiotics for Treatment of DFI21.

14 Infected Burns
14.1 Aetiology
Infections of burn injuries can be caused by1,25:

• Gram-positive bacteria:
o S. aureus.
o S. pyogenes.
o Streptococcus agalactiae.
o Enterococcus spp.
• Gram-negative bacteria:
o Pseudomonas aeruginosa.
o Acinetobacter spp.
o Escherichia coli.
o Klebsiella.
o Enterobacter.
o Serratia.
o Proteus.
• Anaerobic organisms:
o Bacteroides.
o Fusobacterium spp.
• Fungi/yeasts:
o Candida tropicalis.
o Candida krusei.
o Candida albicans.
o Non-albicans Candida spp.
o Aspergillus.
o Fusarium.
o Rhizopus.
o Mucor.
Burn wound colonisation should be diagnosed when25 [L2]:

• Bacteria are present at low concentrations (<105 colony-forming units) on the wound's surface.
• Surrounding erythema or cellulitis is not evident; but
• Deterioration of the wound surface can be observed.
Burn infection should be diagnosed when25 [L2]:

• Bacteria are present at high concentrations (>105 colony-forming units) in the burn wound and
scab.
• Cellulitis is evident.
• Warmth within the area, pain or tenderness, advancing swelling, or induration are present.

14.3 Management
Irrigation of the wound and debridement of necrotic tissue and the eschar, should be performed to
decrease the incidence of invasive burn wound infection1,25 [L1, RGB].
Broad-spectrum antimicrobial agents effective against both aerobic and anaerobic organisms and
antifungals may be considered in the patients with1,25 [L1, RGA]:
• Systemic signs of infection.
• Compromised immune status.
• Severe comorbidities.
• Associated severe cellulitis.
• Severe and deep wounds.
Antibiotic prophylaxis in burn injuries is not generally recommended1 [L1, RGB].

15 Necrotising Skin and Soft Tissue Infections
15.1 Aetiology
The causative organisms responsible for necrotising skin and soft tissue infections, include3,5,10,14:
• S. pyogenes.
• S. aureus.
• Clostridium perfringens.
• Clostridium septicum.
• Vibrio vulnificus.
• Aeromonas hydrophilia.
• Enterobacteriaceae.
• Bacteroides spp.
• Clostridium spp.
• Peptostreptococcus spp.
The differentiating features of the different types of necrotising SSTIs are provided in the table below.

Necrotising Fasciitis • Usually affects the genitalia, perineum, or lower extremities.
• Starts with erythema, tenderness, warmth, swelling, and pain.
• Spread of infection involves any or all layers of the soft tissue.
• Signs and symptoms of infection are present.
• Overlying redness and cutaneous anaesthesia.
• Tense overlying oedema, bullae, and induration of apparently uninvolved
tissues.
• Skin discoloration and crepitus are present.
• Pain is disproportionate to the physical findings.
• Rapid progression despite antibiotics.
Clostridial • Usually occur after abdominal surgery on the gastrointestinal tract.

Myonecrosis • Starts as sudden onset of pain at the site of trauma or surgical wound.
(Gas Gangrene) • Severe pain at site followed by skin changes (e.g. pale, bronze, purplish red).
• Tenderness, induration, blistering, and tissue crepitus.
• Haemorrhagic bullae are common.
• Gas production.
• Muscle necrosis.
• Diaphoresis.
• Systemic signs of infection and toxaemia are present.
Fournier’s Gangrene • Develops in genital area and/or perineum but may extend up to the
abdominal wall, or down into the thigh areas, or into the perirectal and
gluteal spaces, and into the retroperitoneum. Testicular involvement is rare.
• Cellulitis, patches of gangrene, foul smell.
• Signs and symptoms of infection.
• Suppuration and necrosis of overlying skin.
Table 15.2: Clinical Presentations of Necrotising SSTIs1–3,5.

the following1–3,5:
• Recent history of penetrating or blunt trauma.
• Presence of perianal abscesses or decubitus ulcers or recent surgery.
• Abdominal operations on the gastrointestinal tract that were complicated by superficial wound
infections.
• Spread from a genital site such as Bartholin abscess, episiotomy wound, or a minor vulvovaginal
infection.
• Urological manipulation.
• History of obesity or malnutrition.
• Intravenous drug abuse.
15.3 Investigation and Diagnosis
Necrotising fasciitis is an aggressive SSTI involving the superficial fascia, which comprises all the tissue
between the skin and underlying muscles5,10:
• Polymicrobial necrotising fasciitis spreads in 3-5 days3.
• Streptococcal necrotising fasciitis can progress within 1-2 days3.
• “Idiopathic” or “spontaneous” necrotising fasciitis should be considered in the absence of trauma
or another cause for the infection5 [L2, RGA].
Imaging studies may provide useful information when the diagnosis is uncertain1 [L1, RGB], but they should
not delay surgical consultation and further interventions1 [L1, RGC].
Laboratory investigations and surgical exploration may be required to make the definitive diagnosis3,5,10
[L1, RGA]:
• The LRINEC Scoring systems for indicating a necrotising SSTI are provided in Table 15.3 below.
o Scores >6 are indicative, scores >8 are strongly predictive.
• Surgical findings include:
o Swollen and dull-grey fascia.
o Wooden-hard induration of the subcutaneous tissues.
o Absence of true pus even after deep dissection.
o Tissue planes can be readily dissected with a gloved finger or a blunt instrument.
Test Laboratory Values Score

>13.5 g/dL (>135 g/L) 0
Haemoglobin 11 - 13.5 g/dL (110-135 g/L) 1
<11 g/dL (<110 g/L) 2
<15 000 cells/mm3 (<15.0*109 cells/L) 0
White Cell Count 15 000 - 25 000 cells/mm3 (15.0-25.0 x 109 cells/L) 1
>25 000 cells/mm3 (>25.0 x 109 cells/L)) 2
<150 mg/L (<1 430 nmol/L) 0
CRP
≥150 mg/L (≥1 430 nmol/L) 4
≥135 mEq/L (≥135 mmol/L) 0
Sodium
<135 mEq/L (<135 mmol/L) 2
≤1.6 mg/dL (≤141 µmol/L) 0
Creatinine
>1.6 mg/dL (>141 µmol/L) 2
≤180 mg/dL (≤10 mmol/L) 0
Blood Glucose
>180 mg/dL (>10 mmol/L) 1
Table 15.3: The LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) Scoring System2,38.

15.3.1 Fournier’s Gangrene
Fournier’s gangrene is a necrotising fasciitis of the perineal, genital (the scrotum and penis or vulva) and
perianal region10,39 [L1, RGA].
15.3.2 Clostridial Myonecrosis
Clostridial myonecrosis (gas gangrene) is an acute infection by clostridium or bacillus of healthy living tissue
characterised by gas production and muscle necrosis1,3. Spontaneous gangrene may develop in the absence
of trauma. It usually occurs in patients with neutropenia or gastrointestinal malignancy10 [L1].
Recurrent gas gangrene may occur several decades after the primary infection5 [L2].
Laboratory investigations and surgical exploration may be required to make the definitive diagnosis 1,3,5,10
[L1, RGA]:
• Laboratory abnormalities include:
o Common blood test abnormalities (see Table 15.3).
o Positive blood culture results.
• Surgical findings include:
o At early stages, muscles are pale, oedematous and unresponsive to stimulation.
o At later stages, muscles become frankly gangrenous, black, and extremely friable.
15.4 Management
Surgical exploration with aggressive, total debridement of all devitalised and necrotic tissue is essential in
all cases of necrotising SSTIs2–5,14 [L1, RGA]:
• Patients may require repeated surgeries to debride all affected tissue2,10 [L1, RGA].
• When extremities are involved, amputation may be required5 [L2, RGA].
• Diverting colostomy should be avoided when other methods available to avoid wound
contamination1 [L1, RGA]. In cases with faecal contamination, faecal diversion should be
considered1,5 [L1, RGA]. The following options are available1:
o Colostomy.
o Faecal tube system.
• Frequent operations and dressing changes should be provided when necessary5 [L2, RGA].
Negative pressure wound therapy for wound care after complete removal of necrosis in necrotizing
infections may be considered1 [L1, RGB].
Antibiotic treatment of necrotising infections should also be prompt and aggressive1 [L1, RGA]:
• The infection must be immediately treated with high-dose parenteral broad-spectrum antibiotics
directed against the polymicrobial aerobic and anaerobic microorganisms (see Table 15.4)1–3,5 [L1,
RGA].
• The antibiotic spectrum can be narrowed once culture tests become available1,2,5 [L1, RGA].
• Cultures of the superficial wound may not reflect organisms in the deep tissue infection10 [L1,
RGC].

• Ampicillin/sulbactam plus
clindamycin. First-choice antibiotics for patients with polymicrobial infections.
• Pipracillin/tazobactam plus Antibiotic therapy is usually required for 2-3 weeks.
clindamycin
If MRSA is suspected or cultured.
Add vancomycin Vancomycin treatment should be avoided in patients with renal
impairment.
Parenteral aqueous penicillin G Group A streptococcal and clostridial infections.

plus clindamycin. Antibiotic therapy is usually required for 2-3 weeks.
Doxycycline plus ciprofloxacin or

If Aeromonas hydrophila or Vibrio vulnificus is suspected or cultured.
ceftriaxone.
Table 15.4: Selection of Antimicrobials for Treatment of Necrotising SSTIs 2,3,10,21.
All patients should receive supportive care to maintain oxygenation and tissue perfusion, including fluid
resuscitation, organ support and nutritional support14 [L2, RGA]. Hyperbaric oxygen therapy is not
recommended in necrotising fasciitis3,10 [L1, RGB].

16 Viral Skin and Soft Tissue Infections
16.1 Aetiology
Viral SSTIs are commonly caused by3,10,12,17,40:

• Herpes virus.
• VZV.
• Measles morbillivirus.
• Rubella virus.
• Molluscum contagiosum virus (MCV).
• Epstein-Barr virus.
Differentiating features of different viral skin and soft tissue infections are provided in the table below.

Herpes Zoster • Unilateral rash, not crossing the body’s midline.
• Starts as an erythematous, maculopapular rash.
• Disseminated rash (in immunocompromised patients).
• Vesicles transform into pustules that crust over and heal in 2-4 weeks.
• Episodic or continuous symptoms of pain.
• Itching and/or tingling.
• Postherpetic neuralgia as a complication.
Measles • Fever ≥38°C.

(Rubeola) • Malaise.
• Cough, coryza, and conjunctivitis.
• Pathognomonic enanthem.
• Maculopapular rash spreading from the head to the trunk and to the lower
extremities.
• Photophobia.
• Stomatitis.
Rubella • Slight fever.

(German measles) • Mild, maculopapular rash starting on the face and spreading all over the
body.
• Lymphadenopathy of posterior auricular or suboccipital lymph nodes.
• Nausea and mild conjunctivitis.
Infectious • Malaise.
Mononucleosis • Extreme fatigue.
• Fever.
• Pharyngitis.
• Head and body aches.
• Adenopathy of lymph nodes in the neck and armpits.
• swollen liver or spleen or both.
• Rash.

Molluscum • In children: lesions on the face, neck, trunk and arms.
Contagiosum • In adults: lesions on the genitals, pubic region, lower abdomen, upper
thighs, and/or buttocks.
• Dome-shaped, smooth-surfaced, pearly, firm, skin-coloured, pink, yellow or
white papules, 2-5 mm in diameter with central umbilication.
• Mechanical evacuation of content reveals a cheesy material containing
degenerated keratinocytes and viral particles.
• Local pruritus or discomfort may be present.
• Eczema in surrounding skin.
• Infection on eyelid margins can cause chronic conjunctivitis.
Table 16.2: Clinical Presentations of Viral SSTIs3,10,12,17,40–42.
• Travel history.
• Expose to a person with febrile rash illness.
• Chemotherapy treatment in the past year.
• Hematopoietic stem cell transplantation.
• Solid organ transplant.
16.3 Investigation and Management of Specific Viral SSTIs
The investigation and management of each of the common viral SSTIs is provided in the following
subsections.
16.3.1 Measles
16.3.1.1 Measles Diagnosis
Sometimes immunocompromised patients do not develop the rash12. Laboratory investigations should be
used to objectively confirm the suspected diagnosis12 [L1, RGA]:
• Measles-specific IgM antibody in serum.
• Measles RNA in the throat swab.
• Urine samples.
Severity should be assessed to define proper management and treatment27 [L1, RGA]:
• Uncomplicated measles:
o No manifestation other than skin rash.
• Complicated measles:
o Increased breath rate without chest indrawing:
▪ ≥40 breaths/minute if aged >1 year.
▪ ≥50 breaths/minute if aged <1 year.
o Some dehydration.
o Stridor only when the child is upset or crying.
o Mouth ulcers not affecting intake of food or fluids.
o Pus draining from the eyes.
o Acute otitis media, duration <14 days.
• Severe complicated measles:

o Not able to drink or breastfeed.
o Convulsions.
o Lethargic or unconscious.
o Deep or extensive mouth ulcers.
o Chest indrawing and rapid breathing.
o Stridor in a calm child.
o Corneal clouding or ulcers, or vision affected.
o Mastoiditis.
o Severe malnutrition and dehydration.
All suspected measles cases should be reported local health departments within 24 hours12 [L1].
16.3.1.2 Measles Prevention
Measles infection can be prevented with measles-containing vaccine12 [L1, RGA]:

o It is usually administered as either the combination measles-mumps-rubella (MMR) vaccine or
measles-mumps-rubella-varicella (MMRV) vaccine12.
o Routine childhood immunisation is recommended12 [L1, RGA]:
o MMR vaccine:
▪ The first dose should be applied at 12-15 months of age.
▪ The second dose should be applied at 4-6 years of age or at least 28 days after
the first dose.
o MMRV vaccine:
▪ The minimum interval between doses is three months.
o Infants 6-11 months old traveling abroad should receive one dose of MMR vaccine12 [L1, RGA].
They should also receive 2 more doses according to the routinely recommended schedule (see
above)12 [L1, RGA].
16.3.1.3 Measles Management
There is no specific treatment for measles12,27 [L1]. The condition usually improves within 7-10 days.
General principles of management directed at12,27 [L1, RGA]:

• Relieving common symptoms27.
• Providing nutritional support and promoting breastfeeding.
• Providing vitamin A.
• Assessment and treatment of common complications if they arise12,27. Multiple complications
should be treated at the same time27 [L1, RGA].
o Otitis media.
o Bronchopneumonia.
o Laryngotracheobronchitis.
o Diarrhoea.
o Pneumonia.
o Croup.
o Malnutrition.
o Mouth ulcers.
o Eye complications.
If measles is diagnosed, prompt measures should be taken to stop the spread of infection12 [L1, RGA].
• Patients are considered to be contagious from 4 days before to 4 days after the rash appears.
• Up to 9 out of 10 susceptible persons with close contact to a measles patient will develop measles.

• The virus is transmitted by:
o Direct contact with infectious droplets.
o Airborne spread when an infected person breathes, coughs, or sneezes.
• The virus remains infectious in the air for up to 2h after an infected person leaves an area.
16.3.2 Rubella
16.3.2.1 Rubella Diagnosis
Some cases may be difficult to recognise as the rash resembles other rash illnesses17. Other cases may be
subclinical or unapparent. Laboratory testing is required to confirm the diagnosis17,43 [L1, RGA]:
• Blood samples for serologic testing.
• Throat and nasal swab.
• Urine samples.
16.3.2.2 Rubella Prevention
Rubella can be prevented with rubella-containing vaccines (MMR or MMRV)12,17,43 [L1, RGA]:
• Refer to Section 16.3.1.1 for types of vaccine and immunisation schedule for children.
16.3.2.3 Rubella Management
There is no specific antiviral therapy for rubella17 [L1]. Symptoms are usually mild and do not require any
specific treatment. Children with rubella usually recover within 1 week, for adults it may take longer.
If rubella is diagnosed, control measures should be taken to prevent spreading of infection17 [L1, RGA]:
• Patients are contagious from 7 days before to 7 days after the rash appears. They are most
contagious on days 1-5 after the appearance of the rash, when it is erupting.
• All patients with rubella should be isolated for at least 7 days after they develop rash.
• The virus is transmitted by:
o Direct contact with an infected person.
o Contact with droplets of nasopharyngeal secretions.
Possible complications of rubella include17,43:

• Arthralgia.
• Arthritis.
• Thrombocytopenic purpura.
• Encephalitis.
• Congenital rubella syndrome.
• Miscarriage, foetal death, stillbirth.

16.3.3 Infectious Mononucleosis
16.3.3.1 Infectious Mononucleosis Diagnosis
Laboratory investigations are required to make the definitive diagnosis40 [L1]. Typical abnormalities
include:
• Specific antibodies in serum.
• Atypical lymphocytosis.
• Neutropenia.
• Abnormal liver function.
Consider alternative diagnoses40:

• Streptococcal pharyngitis.
• Viral pharyngitis.
• Acute cytomegalovirus.
• Toxoplasmosis.
16.3.3.2 Infectious Mononucleosis Management
Vaccination for infectious mononucleosis is not available44 [L1]. There is also no specific antiviral therapy
for infectious mononucleosis 17 [L1]. Most people recover within 2-4 weeks44. Some patients may feel
fatigued for longer. Rarely, symptoms of infectious mononucleosis can last >6months44.
Advise patients to:

• Drink fluids and hydrated40,44 [L1, RGA].
• Get rest44 [L1, RGA].
• Take over-the-counter medications for pain relief and fever40,44[L1, RGA]:
o Nonsteroidal anti-inflammatory drugs.
o Acetaminophen.
o Throat lozenges, sprays or gargling with a 2 percent lidocaine.
• Avoid the following medications40,44 [L1, RGB]:
o Penicillin antibiotics (e.g. ampicillin or amoxicillin).
o Corticosteroids (e.g. prednisone).
o Acyclovir.
o Ranitidine.
o Antihistamines.
• Self-isolate to stop transmitting virus via44:
o Bodily fluids, especially saliva.
o Blood (including blood transfusions and organ transplantations).
o Semen during sexual contact.
Possible complications of infectious mononucleosis should be reviewed and evaluated40:

• Splenomegaly.
• Hepatomegaly.
• Splenic rupture.
• Acute interstitial nephritis.
• Haemolytic anaemia.
• Myocarditis and cardiac conduction abnormalities
• Neurologic abnormalities.
• Cranial nerve palsies
• Encephalitis.
• Meningitis.

• Mononeuropathies.
• Retrobulbar neuritis.
• Thrombocytopenia.
• Upper airway obstruction.
16.3.4 Herpes Zoster
Diagnostic testing is not usually required3 [L1, RGB], but may be considered in patients with atypical
presentations or with suspected herpes simplex virus3 [L1, RGA].
Consider alternative diagnoses10:

• Atypical varicella.
• Herpes simplex virus.
Antiviral therapy is the main treatment option for patents with VZV10 [L1, RGA]. Consider the following
medications10 [L1, RGA]:
• Acyclovir.
• Famciclovir.
• Valacyclovir.
Oral administration is recommended in otherwise healthy patients or in immunocompromised patients

with mild cases of VZV10 [L1, RGA]. Immunocompromised patients with more extensive cases should
receive intravenous administration10 [L1, RGA].
16.3.5 Molluscum Contagiosum
16.3.5.1 Molluscum Contagiosum Diagnosis
Molluscum contagiosum (MCV) has two main subtypes mainly transmitted by direct physical contact,
including auto-inoculation 41,42.
The diagnosis is usually done on clinical and dermoscopic grounds 41 [L1]. Consider in vivo confocal
microscopy to distinguish the condition from other skin infections 41 [L1].
Laboratory investigations are not usually required. The following tests may be considered in unclear cases:
• Histological examination.
• Polymerase chain reaction.
• Electron microscopy.
Differential diagnoses include 41:

• Genital warts (condyloma acuminata).
• Flat warts.
• Lichen planus or nitidus.
• Secondary syphilis condylomata lata.
• Pyogenic granuloma.
• Ectopic sebaceous glands.
• Dermal cyst.
• Vulvar lymphangioma circumscriptum.
• Keratoacanthoma.

• Basal cell carcinoma.
• Amelanotic melanoma.
16.3.5.2 Molluscum Contagiosum Management
Molluscum contagiosum is a benign and usually and self-limiting viral infection of the skin 41. In most
immunocompetent patients, the signs and symptoms resolve in 3 months to 3 years when an immune
response develops 42:
• Most children do not require treatment 42 [L2, RGA].
• Adults patients with sexually transmitted MCV usually request treatment. Active therapy is also
indicated in patients with 41 [L1, RGA]:
o Extensive involvement.
o Disease persistence.
o Cosmetic reasons.
o Fear of disease spread and scarring.
o Complications (e.g. pruritus, inflammation, and secondary infection).
Treatment Additional Notes
Cautery Immediate results. Local anaesthetics may be required.
Curettage Less suitable for genital skin because of pain.
Liquid nitrogen cryotherapy Should be applied with caution.
Podophyllotoxin* May be patient-applied.
Imiquimod*
Not generally recommended but may be considered if other
treatments are not suitable. Should be applied with caution.
Squeezing/piercing lesions
Topical Medications:
• Salicylic, lactic, glycolic and
trichloroacetic acids.
• Benzoyl peroxide 5%.
• Aluminium acetate solution Not generally recommended but may be considered if other
(Burrow's solution 1:30). treatments are not suitable. Varying evidence for efficacy has
• Hydrogen peroxide. been reported for non-genital molluscum.
• Iodine.
• Potassium hydroxide. No recommendation can be given regarding the use for genital
• Silver nitrate. infections.
• Nitric oxide.
• Cantharidin. Topical treatments should be avoided in pregnancy and
• Lemon myrtle oil. breastfeeding.
• Tea tree oil.
• Tretinoin.
• Adapalene.
Table 16.3.5.2: Selection of Medication for Treatment of Molluscum Contagiosum 41,42.
Sharing towels, sponges or bathing together should be discouraged to reduce the spread of infection to
healthy individuals 41,42 [L2, RGA].

17 Parasitic Skin Infections
17.1 Aetiology
Most common parasites causing skin infections include 45,46:

• Epidermal parasitic skin diseases (EPSD):
o Scabies:
▪ Sarcoptes scabiei.
o Pediculosis:
▪ Pediculus humanus var. capitis.
▪ Pediculus humanus var. corporis.
▪ Phthirus pubis.
o Tungiasis – consider in immigrants and travellers from the Caribbean, sub-Saharan Africa
and South America:
▪ Female sand flea Tunga penetrans.
o Hookworm-related cutaneous larva migrans (HrCLM) – consider in immigrants and
travellers from developing countries:
▪ Ancylostoma caninum.
▪ Ancylostoma braziliense.
▪ Uncinaria stenocephala.
• Cutaneous leishmaniasis – Leishmania parasites (>20 different species).
• Loiasis – tissue nematode Loa loa.
Differentiating features of different parasitic skin infections are provided in the table below.

Scabies 45–48 • Symptoms may not appear for up to 2 months after being infested.
• In re-infested individuals, symptoms appear 1-4 days after exposure.
• Itching and a skin rash (pruritus). Severe itching at night.
• Itching and rash may affect much of the body or be limited to common sites
(e.g., between the fingers, armpits, waist). The head, face, neck, palms, and
soles often are involved in infants and very young children.
• Tiny intra-epidermal burrows sometimes can be seen on the skin.
• Skin sores contaminated with secondary bacterial infection (e.g. group A
Streptococci) may be present.
• Cellulitis, boils, and pyomyositis may develop if untreated.
• Lymphangitis and generalised lymphadenopathy.
• Crusted scabies may develop in the elderly, immunocompromised or
physically incapacitated individuals. It is characterised by vesicles and thick
crusts over the skin that can contain many mites.
Pediculosis 46,49 • On the first infestation, sensitisation commonly takes 4 to 6 weeks.
• Pruritus.
• Intense itching can lead to scratching and subsequent excoriations and
secondary cellulitis.
• If untreated, the skin may become lichenified and hyperpigmented.

Tungiasis 45,50,51
• Itching and local irritation.
• Pain and sensation of a foreign body.
• Lesions, 99% of which occur at the feet. Most lesions occur on the nail rim.
• Desquamation of the surrounding skin.
• Heavy inflammation often surrounds the lesions.
• Secondary bacterial infection is often present.
• Suppuration, ulceration and lymphangitis can develop.
• Gangrene or necrosis of surrounding tissue may occur.
Hookworm-Related • Serpiginous rash with pruritus.
Cutaneous Larva • Raised red lines on the feet or lower part of the legs.
Migration52,53 • Scratching lines can lead to bacterial infections.
Leishmaniasis 54,55 Cutaneous leishmaniasis:
• Painless and chronic skin lesions occurring at sites of infected sand fly bites.
• Slow spontaneous healing.
• May be associated with mucosal leishmaniasis.
Mucocutaneous leishmaniasis:
• Chronic unexplained congestion/secretions.
• Partial or total destruction of mucous membranes of the nose, mouth and
throat.
Visceral leishmaniasis:
• Irregular bouts of fever.
• Weight loss.
• Enlargement of the spleen and liver
• Anaemia.
Loiasis 56
• Presence of an eye worm.
• Calabar swellings.
• Unexplained peripheral eosinophilia.
Table 17.2: Clinical Presentations of Parasitic SSTIs.
17.3 Diagnosis and Management
17.3.1 Scabies
17.3.1.1 Scabies Diagnosis
A suspected diagnosis of a scabies infestation can be made on the basis of clinical distribution and
appearance of the skin lesions. A definite diagnosis of scabies should be made on microscopic identification
of the mites, eggs or faecal pellets (scybala) from the scrapings of the skin burrows.
Consider applying other tests when required 48 [L1, RGB]:

o Burrow ink test (BIT) to identify the burrows.
o Dermoscopy.
o Detecting parasitic DNA from cutaneous scales.
o Optical coherence tomography.
The differential diagnosis for scabies includes48 [L1]:

o Impetigo.
o Folliculitis.

o Papular urticarial.
o Atopic, contact or seborrhoeic dermatitis.
o Dermatitis herpetiformis.
o Psoriasis.
o Pytiriasis rosea.
o Secondary syphilis.
o Lymphoma and pseudolymphoma (if scabies presents with nodules).
17.3.1.2 Scabies Management
Treatment should be applied simultaneously for household members and sexual contacts to prevent
reinfestation 47 [L1, RGA].
Several scabicides are available only by prescription to treat human scabies (see Table 17.3.1.2)47,48.
Medications Additional Notes

Two (or more) applications, each about a week apart, may be required
Permethrin cream 5% to eliminate all mites.
Applicable in children ≥2 months.
May be used in children.
Crotamiton lotion (or cream) 10%
Frequent treatment failure has been reported.
Malathion aqueous 0.5% liquid May be used if permethrin cream is inappropriate.
Sulphur ointment 5%-10% Applicable in children <2 month of age.
Benzyl benzoate 25% emulsion

Second-line treatment option. The use should be restricted to patients
Lindane lotion 1%
who have failed treatment with or cannot tolerate other medications.
Oral ivermectin
Table 17.3.1.2: Selection of Medications for Treatment of Scabies 47,48.
Bedding, clothing, and towels used by infested persons and their household, sexual, and close contacts
anytime during the 4 days before treatment should be decontaminated by 47 [L1, RGA]:
o Washing at high temperature (60°C) and drying in a hot dryer; or
o Dry-cleaning; or
o Sealing in a plastic bag for at least 72 hours.
Oral antihistamines to control pruritus should be avoided during pregnancy when possible, especially
during the first trimester 48 [L1, RGC]. If required, consider chlorpheniramine 48 [L1].
17.3.2 Pediculosis
17.3.2.1 Pediculosis Diagnosis
Lice infestation is diagnosed definitively by visual inspection 46,49 [L1]:

o At least one live louse must be observed on the hair (head or pubic lice) or in the seams of clothing
(body lice).
o The presence of nits (louse eggs that may or may not be viable) on examination is not enough to
diagnose pediculosis as they may remain on the hair for months after successful treatment.

Consider using bright light, magnifying lenses, and/or combing the hair with a “lice comb” for the hair
inspection 46,57 [L1]. Search behind the ears and on the back of the neck. Patients with pubic lice should be
evaluated for sexually transmitted infections 46 [L1].
17.3.2.2 Pediculosis Management
All family members of the patient with pediculosis should be examined and treated 46 [L1, RGA].
Treatment options include topical insecticides and oral agents (see Table 17.3.2.2) 46,49 [L1, RGA]. Repeat
treatment (two applications 7 to 10 days apart) is usually required for complete eradication 46 [L1].
Medications Additional Notes
Permethrin 1% First-line treatment option.

Pyrethrins 1% Applicable in children ≥2 months.
Benzyl alcohol lotion 5% Applicable in children ≥6 months.

Pyrethrins 0.3%/piperonyl butoxide 4%
Should be avoided in patients with chrysanthemum allergy.
shampoo or mousse
Crotamiton lotion (or cream) 10% May be used in children.
Malathion lotion 0.5%
Spinosad* 0.9% May be considered if first-line treatment is inappropriate.
Oral ivermectin
May be considered if first-line treatment is inappropriate.
Isopropyl myristate 50% and ST-
Not recommended for use on infants or children <4 years
cyclomethicone 50%
of age.
Not generally recommended and should be avoided when
Lindane lotion possible. It should not be used in children, older persons, or
adults weighing less than 50 kg.
Carbaryl Prohibited due to carcinogenic effects.
Table 17.3.2.2: Selection of medications for treatment of pediculosis 46,49,58.
* - Spinosad has not been evaluated for the treatment of pediculosis pubis.
Bedding, clothing, and towels used by infested persons and their household should be decontaminated by
washing at high temperature (≥50°C) 46 [L1, RGA].
Wet combing is not recommended as a primary treatment, but may considered as adjuvant treatment 46,49
[L1, RGB].
The following treatment measures are not recommended 46,49 [L1, RGB]:
o Sprays, carpet treatments, and other chemical environmental decontamination measures.
o Household products (such as mayonnaise, petroleum jelly, olive oil, tub margarine, etc.).
o Natural products (e.g., tea tree oil).
o Aromatherapy.
o Using flammable, toxic and dangerous substances (e.g., gasoline or kerosene) or using products
intended for treating lice in animals is strictly prohibited 49 [L1, RGC].

17.3.3 Tungiasis
17.3.3.1 Tungiasis Diagnosis
The diagnosis of tungiasis is made by clinical inspection and is based on the morphological characteristics
of the different developmental stages c [L1].
A biopsy of lesions is not generally recommended 51 [L2, RGB] but may be considered in cases with atypical
presentation (e.g. is lesions have a pseudoepitheliomatous appearance at the ectopic site) 51.
17.3.3.2 Tungiasis Management
Limited treatment options are available for patients with tungiasis, see table below.

Topical application of a two-component
First-line treatment.
dimeticone of low viscosity.
Surgical extraction* The use is discouraged unless first-line treatment is applicable.
Table 17.3.3.2: Selection of medications for treatment of tungiasis 50,51,59.
* Surgical extraction of burrowed sand fleas should be performed by sterile instruments in an appropriately equipped health
facility 50 [L1, RGA]. The wound should be dressed appropriately. The tetanus vaccination status needs to be verified and a
booster vaccination given, if indicated.
The following medications are not recommended due to proven inefficiency or insufficient evidence of
efficiency 50,51 [L1, RGB]:
• Topical metrifonate.
• Oral or topical thiabendazole.
• Oral or topical ivermectin.
17.3.4 Hookworm-Related Cutaneous Larva Migrans
17.3.4.1 Hookworm-Related Cutaneous Larva Migrans Diagnosis
Hookworm-Related Cutaneous Larva Migrans (HrCLM) is a clinical diagnosis based on the presence of the
typical signs and symptoms, and exposure history to zoonotic hookworm 53 [L1]. Blood tests and biopsy are
usually not necessary for diagnosis 52 [L2, RGB].
Differential diagnoses include 52,53:

• Hookworm.
• Gnathostomiasis.
• Strongyloidiasis.
• Cutaneous pili migrans.
• Myiasis.
• Loiasis.
• Scabies.
• Schistosomiasis.
• Tinea corporis.
• Contact dermatitis.

17.3.4.2 Hookworm-Related Cutaneous Larva Migrans Management
Hookworm-Related Cutaneous Larva Migrans (HrCLM) is usually a self-limiting infection. In most patients,
the signs and symptoms resolve after 5-6 weeks without medical treatment. The larva will die in the skin
and the itchiness and red lines will go away 53.
For multiple lesions or severe infestation consider treatment with anti-worm medications see table below.
Medication Additional Notes
Oral albendazole This drug is contraindicated in children younger than 2 years age.
Oral ivermectin One-time dose is usually required.
Topical thiabendazole 10% solution

If infection is local.
Topical thiabendazole 15% ointment
Table 17.3.4.2: Selection of Medications for Treatment of HrCLM 52,53.
Adjuvant treatment to help control symptoms and to resolve secondary bacterial infections may be
considered 53.
The following treatment options are not recommended:

• Cryotherapy 52,53 [L1, RGB].
• Topical or oral steroids 52 [L2, RGB].
• Antibiotics 52 [L2, RGB].
17.3.5 Leishmaniasis
17.3.5.1 Leishmaniasis Diagnosis
There are three main forms of the disease 54,55,60:

• Cutaneous leishmaniasis.
• Mucocutaneous leishmaniasis.
• Visceral leishmaniasis.
Cutaneous Leishmaniasis:
• Diagnosed by clinical manifestation with parasitological tests 55 [L1].
• Tissue specimens should be collected from a lesion(s) 54 [L1].
• Full-thickness skin biopsy may be considered 54 [L1].
• Differential diagnoses include 60:
o Staphylococcal or streptococcal infection.
o Mycobacterial ulcer.
o Leprosy.
o Fungal infection.
o Cancer.
o Sarcoidosis.
o Tropical ulcer.

Mucocutaneous Leishmaniasis:
• Diagnosed by clinical manifestation with parasitological tests 55 [L1].
• Tissue specimens should be collected from a lesion(s) 54 [L1].
• Biopsy specimens may be considered 54 [L1].
o Allergic rhinitis.
o Paracoccidioidomycosis and other deep mycoses.
o Cancrum oris.
o Lymphoma and other neoplasia.
o Leprosy.
o Sarcoidosis.
Visceral Leishmaniasis:
• Diagnosed by combining clinical signs with parasitological, or serological tests 55 [L1].
• Collection of tissue aspirates (bone marrow is preferred) or biopsy specimens is recommended 54
[L1].
• Serum should be collected for antibody testing 54 [L1].
• Blood sample should be obtained in immunocompromised patients 54 [L1].
o Chronic malaria.
o Schistosomiasis.
o Other systemic infections.
Multiple diagnostic approaches are available to detect leishmaniasis 54 [L1]:

• Visualisation of the characteristic amastigote in smears.
• Histopathology.
• Parasite isolation by in vitro culture.
• Molecular detection of parasite DNA.
17.3.5.2 Leishmaniasis Management
Treatment should be given after confirmation of disease 60 [L1]. Empiric treatment may be indicated on the
basis of an individualised risk-benefit assessment 54 [L1].
Immunocompetent patients with cutaneous leishmaniasis and low risk for mucocutaneous leishmaniasis
may be observed without treatment until the lesion is healing spontaneously 54 [L1, RGA].
All patients diagnosed as with visceral leishmaniasis require prompt and complete treatment 55 [L1, RGA].
Available antileishmanial medicines are listed in Table 17.3.5.2.

Old World Cutaneous Leishmaniasis

Paromomycin ointments
Intralesional pentavalent antimonials
Applications of localised heat (50°C for 30 sec).
Thermotherapy
Local anaesthesia is required.
Cryotherapy Application of liquid nitrogen (–195°C) to the lesion.
New World Cutaneous Leishmaniasis
Pentavalent antimonials Less effective in children under 5 years of age.
Pentamidine
Paromomycin sulfate
Miltefosine
Ketoconazole
New World Mucocutaneous Leishmaniasis
Pentavalent antimonials Consider a combination with oral pentoxifylline.
Amphotericin B deoxycholate
Liposomal amphotericin B
Pentamidine
Miltefosine
Visceral Leishmaniasis
Pentavalent antimonials:
• Sodium stibogluconate First-line treatment.
• Meglumine antimoniate
Amphotericin B deoxycholate
Second-line treatment.
Lipid formulations of amphotericin B
Combination treatment is preferred.
Miltefosine
Monotherapy should be limited to liposomal amphotericin B.
Paromomycin (aminosidine)
Table 17.3.5.2: Selection of Medication for Treatment of Leishmaniasis 60.
17.3.6 Loiasis
17.3.6.1 Loiasis Diagnosis
The standard diagnostic test for the diagnosis of loiasis is demonstration of microfilariae on a daytime
(10AM to 2PM) Giemsa-stained thin or thick blood smear 56 [L1]. The timing of the blood smear should be
adjusted to reflect local time of the infection.
Consider concentration techniques in patients with low numbers of circulating microfilariae 56 [L1]:
• Nuclepore™ filtration.
• Knott’s concentration.
• Saponin lysis.

17.3.6.2 Loiasis Management
All patients with loiasis must be assessed by a specialist as treatment is very complex and comprises high
risks for encephalopathy and blindness 56 [L1, RGA].
Surgical excision of migrating adult worms may be performed 56 [L1, RGA]. Antiparasitic medications are
still required after surgery 56 [L1, RGA]. Available medicines are listed in the table below.
Medication Indication*
For patients with symptomatic loiasis and MF/mL <8,000.

Diethylcarbamazine Contraindicated in patients with with onchocerciasis because of the risk of
blindness and/or severe exacerbation of skin disease.
For patients with symptomatic loiasis and MF/mL <8,000 who have failed 2
rounds of diethylcarbamazine.
Albendazole
For patients with symptomatic loiasis and MF/ml ≥8,000 to reduce level to
<8,000 prior to treatment with diethylcarbamazine.
Apheresis followed by
For patients with symptomatic loiasis, with MF/mL ≥8,000.
diethylcarbamazine
Table 17.3.6.2: Selection of Medication for Treatment of Loiasis 56.

* - The selection of treatment should be based on the number of microfilariae of Loa Loa per mL.

18 Key Considerations for Patient Preferences
Patient preferences refer to patient perspectives, beliefs, expectations, and goals for health and life, and
to the steps employed by individuals in assessing the potential benefits, harms, costs, and limitations of
the management options in relation to one another. Patients may have preferences when it comes to
defining their problems, identifying the range of management options and selecting or ranking the
outcomes used to compare these options.
It is important for healthcare professionals to develop an understanding of the patient as an individual and
the unique way in which each person experiences a condition and its impact on their life.
The following recommendations are therefore made for physicians and other healthcare professionals
regarding general principles of patient care in Qatar:
• Respect Patients: Treat patients with respect, kindness, dignity, courtesy and honesty. Ensure that
the environment is conducive to discussion and that the patient's privacy is respected, particularly
when discussing sensitive, personal issues. Ask the patient how they wish to be addressed and
ensure that their choice is respected and used.
• Maintain Confidentiality: Respect the patient's right to confidentiality and avoid disclosing or
sharing patients’ information without their informed consent. In this context, students and anyone
not directly involved in the delivery of care should first be introduced to the patient before starting
consultations or meetings, and let the patient decide if they want them to stay.
• Clarify Third-Party Involvement: Clarify with the patient at the first point of contact whether and
how they like their partner, family members or carers to be involved in key decisions about their
care or management and review this regularly. If the patient agrees, share information with their
partner, family members or carers.
• Obtain Informed Consent: Obtain and document informed consent from patients, in accordance
with MOPH policy and guidance.
• Encourage Shared Decision Making: Ensure that patients are involved in decision making about
their own care, or their dependent’s care, and that factors that could impact the patient’s
participation in their own consultation and care including physical or learning disabilities, sight,
speech or hearing impairments and problems with understanding, reading or speaking English are
addressed.
• Disclose Medical Errors: Disclose errors when they occur and show empathy to patients.
• Ensure Effective Communication: Explore ways to improve communication including using

pictures, symbols or involving an interpreter or family members. Avoid using medical jargon. Use
words the patient will understand and confirm understanding by asking questions.
• Ensure Continuity of Care: Provide clear and timely sharing of patient information between
healthcare professionals especially at the point of any transitions in care.

19 Performance Measures
A list of potential performance measures is given below in Table 19.1.
Number Numerator Denominator

SSTI01 The number in the denominator who received The number of patients who were
antibiotics as per guideline recommendations. diagnosed with an SSTI in the last 12
months and were prescribed antibiotic
treatment.
SSTI02 The number in the denominator in whom The number of patients diagnosed with an
antibiotics were de-escalated following the culture SSTI requiring antibiotic therapy in the last
result. 12 months with positive culture results.
Table 19.1: Performance Measures.

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Appendix: Detailed Description of the Literature Search
A systematic search for existing literature on the low back pain was performed in the period June 7th – July
1st, 2019.
The search for clinical practice guidelines on the diagnosis and/or management of skin and soft tissue
infections was performed in the PubMed database and websites of relevant organisations and societies
including the World Health Organization, American Academy of Family Physicians, American Academy of
Dermatology Association, and other. The present guideline is primarily based on practice guidelines by
Infectious Diseases Society of America and World Society of Emergency Surgery and the Surgical Infection
Society Europe and is supplemented with other relevant studies.
Peer-reviewed scientific publications were found in PubMed and via Google Scholar Internet search engine.
Non-peer reviewed studies were identified in bioRxiv. Books were checked on PubMed. Information
published on medical websites and drug prescribing information sheets were found via Google search
engine.
The included publications were identified using the term “skin or soft tissue infection” and specified with
the following terms in combinations:
Management, risk factors, aetiology, pathogens, prognosis, prevalence, presentation, symptoms,

examination, imaging, differential/alternative diagnosis, screening, primary/secondary care,
(non)complicated, abscess, folliculitis, furuncle, furunculosis, carbuncle, impetigo, human/animal bites,
erysipelas, cellulitis, necrotizing, gangrene, herpes, measles, rubella, mononucleosis, diabetic foot, referral
criteria, emergency, management, treatment, antibiotics, antimicrobials, antiseptic, debridement, wound,
paediatric, children, recovery, outcome, follow-up, performance, quality measures/standards.
Figure A.1 on the next page demonstrates graphically the results of the search and application of exclusion
criteria.

Fig A.1: Literature search results and application of exclusion criteria.

Acknowledgements
The following individuals are recognised for their contribution to the successful development of the
National Clinical Guideline.
MOPH National Clinical Guidelines Team:
• Ms Huda Amer Al-Katheeri, Director of Strategic Planning & Performance Dept, MOPH .
• Dr Nawal Al Tamimi, Head of Healthcare Quality & Patient Safety Section, MOPH.
• Dr Rasha Bushra Nusr, Quality Improvement Senior Specialist, MOPH.
• Dr Rasmeh Ali Salameh Al Huneiti, Guideline & Standardisation Specialist, MOPH.
• Dr Bushra Saeed, Quality Improvement Coordinator, MOPH.
• Dr Mehmood Syed, Project Clinical Lead.
• Dr Samuel Abegunde, Physician Executive.
• Dr Natalia Siomava, Senior Medical Writer.
• Ms Rouba Hoteit, Medical Writer.
Special Recognition:
• Ms Dhouha Hamdani, Infection Control Specialist, Ministry of Public Health.

• Dr Eman Radwan, Risk Management Analyst, Ministry of Public Health.
• Dr Jameela Al Ajmi, Senior Consultant Infectious Diseases and Infection Control, Executive Director
Corporate Infection Prevention and Control, Hamad Medical Corporation.


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THE DIAGNOSIS & MANAGEMENT OF

SKIN & SOFT TISSUE INFECTION

7th December 2020

Version Status Date Editor Description

ART Antiretroviral Therapy

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

1.2 Scope of the Guideline

This guideline covers the following aspects of care:

1.3 Editorial Approach

1.4 Sources of Evidence

The Diagnosis and Management of Skin and Soft Tissue Infection

1.5 Evidence Grading and Recommendations

▪ Recommendation Grade A (RGA): Evidence demonstrates at least moderate certainty of at least

The Diagnosis and Management of Skin and Soft Tissue Infection

Guideline Development Group Members

Name Title Organisation

The Diagnosis and Management of Skin and Soft Tissue Infection

Name Title Organisation

Dr Binny Thomas Clinical Pharmacy Specialist Hamad Medical Corporation

1.7 National Clinical Guidelines & Pathways Committee members

National Clinical Guidelines & Pathways Committee (NCGPC) Members

Name Title Organisation

Dr Ghassan Youseph Hommos Consultant Endocrinology Al Emadi Hospital

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

Necrotising Skin &

Emergency Referral Investigation

The Diagnosis and Management of Skin and Soft Tissue Infection

Examination (Section 5.3):

Investigation (Section 5.4):

General Principles of Management (Section 7):

The Diagnosis and Management of Skin and Soft Tissue Infection

Treatment of Specific Skin and Soft Tissue Infections:

The Diagnosis and Management of Skin and Soft Tissue Infection

SSTIs are categorised by:

4.4 Risk Factors

Risk factors for SSTIs include2,3:

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

Important points to elicit include the following3,5,10–14:

All patients suspected for SSTI should be examined for1:

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

Consider the following options:

The Diagnosis and Management of Skin and Soft Tissue Infection

7.2 Principles of Antimicrobial Treatment

Antibiotic therapy should be initiated as soon as their necessity is recognised19,20 [L1]:

If there is uncertainty on the appropriate patient-specific antimicrobial therapy, consult an infectious

The Diagnosis and Management of Skin and Soft Tissue Infection

Intravenous antibiotics should be discontinued when2,14 [L1]:

7.3 Emergency Referral

The following conditions should be considered a medical emergency2,3,5,9,14,16,25,26:

7.4 Referral to Specialist Care

Consider a consultation with an infectious disease specialist, surgeon, dermatologist or microbiologist

The Diagnosis and Management of Skin and Soft Tissue Infection

The Diagnosis and Management of Skin and Soft Tissue Infection

There are two main types of abscesses13 [L1]: