This document summarizes various skin and soft tissue infections, including their causes, symptoms, and treatments. Erysipelas is a streptococcal infection of the skin that causes a painful, erythematous rash. Impetigo is a contagious superficial infection commonly caused by streptococci or staphylococci in children. Folliculitis is a bacterial infection of hair follicles that causes papules and pustules. Boils are deeper hair follicle infections forming tender, red swellings. Carbuncles are clusters of interconnected boils. Cellulitis is a spreading bacterial skin infection beneath the skin. Necrotizing fasciitis is a severe infection of the fascia requiring aggressive
Skin, Soft Tissue, & Bone Infections Symposia - The CRUDEM FoundationThe CRUDEM Foundation
This is the Skin, Soft Tissue, & Bone Infections Symposia presented in Milot, Haiti at Hôpital Sacré Coeur in 2011. CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
Include infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis.
Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection
Skin, Soft Tissue, & Bone Infections Symposia - The CRUDEM FoundationThe CRUDEM Foundation
This is the Skin, Soft Tissue, & Bone Infections Symposia presented in Milot, Haiti at Hôpital Sacré Coeur in 2011. CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
Include infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis.
Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection
Molluscum contagiosum Made Extremely SimpleDrYusraShabbir
A brief description of a very common viral infection affecting children and adults. Molluscum Contagious is an infectious contagious disease. Useful information regarding the symptoms and treatment of the rash are available for medical students, doctors, dermatologists, ophthalmologists, gynaecologist, pediatricians and nurses. Helpful for studying for exams. Reference: Rooks, Textbook of Dermatology
DETAILED DISCUSSION OF NECROTIZING FASCIITIS.
A SOFT TISSUE INFECTION. USUALLY CALLED AS FLESH EATING BACTERIAL INFECTION. CAUSED BY BACTERIA. AFFECTS THE SOFT SKIN TISSUES
Skin warts are benign tumours caused by infection of keratinocytes with HPV, visible as well‐defined hyperkeratotic protrusions. We will explore the detailed types, presentation, and treatment modalities of most common warts.
Erysipelas is a bacterial skin infection that usually affects the top most layer of the skin. Erysipelas is very rare, but requires immediate treatment. Erysipelas is often associated with other skin infection known as cellulitis, which affects the lower layers of the skin.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Definition:
Madura foot or mycetoma (tumour-like)
Chronic granulomatous disease characterised by localised infection of subcutaneous tissues and sometimes bone characterised by discharging sinuses filled with organisms like actinomycetes or fungi.
History:
Gill first described the disease in the Madura district of India in 1842.
Hence the term Madura foot.
Pathophysiology:Typically present in agricultural workers(hands shoulders and back – from carrying contaminated vegetation and other burdens).
Causes:Due to fungi – eumycetoma (40%) or
Actinomycetes – (actinomycetoma) 60%
Actinomycetoma may be due to Actinomadura madurae Actinomadura pelletieri Streptomyces somaliensis Nocardia species
Clinical Features:Slow spreading skin infection
Local swelling
Small hard painless nodules
Ulceration
Pus discharge
Scarred skin & discoloration
Itching
Pain and burning sensation
Lab studies:Direct microscopy
Blood – leukocytosis & neutrophilia
Culture of exudates
Skin biopsy
Serology
DNA sequencing has been used for identification in difficult cases.
Microscopy:Serosanguinous fluid containing the granules examined using – 10% KOH and Parker ink or calcofluor white mounts
Tissue sections stained using H&E(Hematoxylin and Eosin stain) , PAS(Periodic Acid Shiffs Stain) and Grocott’s methenamine silver(GMS).
Actinomycotic grains contains very fine filaments.
Fungal grains contain short hyphae (branched filaments) that are often swollen
Culture:Sabouraud’s dextrose agar or mycobiotic agar to isolate fungi
Blood agar to isolate bacteria
Agar plates are cultured at 25-30 degree celcius and 37 degree celcius for up to six weeks . Fungi grow more quickly than actinomycetes.
Treatment;Due to the slow ,relatively pain –free progression of the disease, mycetoma is often at an advanced stage when diagnosed.
Antifungals
Antibiotics
Treatment of any secondary infections
Amputation-in severe cases
Molluscum contagiosum Made Extremely SimpleDrYusraShabbir
A brief description of a very common viral infection affecting children and adults. Molluscum Contagious is an infectious contagious disease. Useful information regarding the symptoms and treatment of the rash are available for medical students, doctors, dermatologists, ophthalmologists, gynaecologist, pediatricians and nurses. Helpful for studying for exams. Reference: Rooks, Textbook of Dermatology
DETAILED DISCUSSION OF NECROTIZING FASCIITIS.
A SOFT TISSUE INFECTION. USUALLY CALLED AS FLESH EATING BACTERIAL INFECTION. CAUSED BY BACTERIA. AFFECTS THE SOFT SKIN TISSUES
Skin warts are benign tumours caused by infection of keratinocytes with HPV, visible as well‐defined hyperkeratotic protrusions. We will explore the detailed types, presentation, and treatment modalities of most common warts.
Erysipelas is a bacterial skin infection that usually affects the top most layer of the skin. Erysipelas is very rare, but requires immediate treatment. Erysipelas is often associated with other skin infection known as cellulitis, which affects the lower layers of the skin.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Definition:
Madura foot or mycetoma (tumour-like)
Chronic granulomatous disease characterised by localised infection of subcutaneous tissues and sometimes bone characterised by discharging sinuses filled with organisms like actinomycetes or fungi.
History:
Gill first described the disease in the Madura district of India in 1842.
Hence the term Madura foot.
Pathophysiology:Typically present in agricultural workers(hands shoulders and back – from carrying contaminated vegetation and other burdens).
Causes:Due to fungi – eumycetoma (40%) or
Actinomycetes – (actinomycetoma) 60%
Actinomycetoma may be due to Actinomadura madurae Actinomadura pelletieri Streptomyces somaliensis Nocardia species
Clinical Features:Slow spreading skin infection
Local swelling
Small hard painless nodules
Ulceration
Pus discharge
Scarred skin & discoloration
Itching
Pain and burning sensation
Lab studies:Direct microscopy
Blood – leukocytosis & neutrophilia
Culture of exudates
Skin biopsy
Serology
DNA sequencing has been used for identification in difficult cases.
Microscopy:Serosanguinous fluid containing the granules examined using – 10% KOH and Parker ink or calcofluor white mounts
Tissue sections stained using H&E(Hematoxylin and Eosin stain) , PAS(Periodic Acid Shiffs Stain) and Grocott’s methenamine silver(GMS).
Actinomycotic grains contains very fine filaments.
Fungal grains contain short hyphae (branched filaments) that are often swollen
Culture:Sabouraud’s dextrose agar or mycobiotic agar to isolate fungi
Blood agar to isolate bacteria
Agar plates are cultured at 25-30 degree celcius and 37 degree celcius for up to six weeks . Fungi grow more quickly than actinomycetes.
Treatment;Due to the slow ,relatively pain –free progression of the disease, mycetoma is often at an advanced stage when diagnosed.
Antifungals
Antibiotics
Treatment of any secondary infections
Amputation-in severe cases
history of TB,epidemiology, clinical features, lab diagnosis, treatment, MDR TB, XDR TB, TDR TB, and mechanism of drug resistant, methods of identification of resistant drugs
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
4. Erysipelas
• Strep. Infections of dermis
• Well demarcated, painful,
erythematous
• indurated plaques, Blisters &
ulceration
• Abrupt fever with chills
• Face, legs
• common in very young, old,
debilitated patients
• lymphoedematous
• erysipelas and Cellulitis overlap
often
• Treatment: Penicillin IV/IM
5. Impetigo
• A contagious superficial infection of the skin
• Staphylococci or β-haemolytic streptococci
• common in children
• usually involves the skin of the face, often around the
mouth and nose.
• spread by direct contact
• Minor abrasions and other skin lesions predispose to
infections
• Prevention is by good personal hygiene , particularly
hand washing with soap.
6. • It has two forms:
1. Non-bullous
Streptococcus pyogenes
"honey-crust" lesions
2. Bullous
Staphylococcus aureus
rupture of the bullae
"varnish-like" crust
9. • Other close contacts should be examined
• children should avoid school for 1week after
starting therapy.
• resistant to treatment or recurrent
– take nasal swabs and check other family
members.
• Eradication of nasal carriage
– Nasal mupirocin
10. Folliculitis
• Infections of the
superficial part of the
hair follicle
• itchy or tender papules
and pustules.
• Staphylococcus aureus
11. • Small pustules often
pierced by a hair
• Legs, face – (sycosis
barbae)
• commoner in humid
climates and when
occlusive clothes are worn.
• Extensive, itchy folliculitis
in HIV infection.
12. Treatment
• topical antiseptics
• topical sodium fusidate
• mupirocin containing ointment
• oral antibiotics
– flucloxacillin or erythromycin
• If chronic – Detect and treat carrier state
13. Boils (furuncles)
• Staph. Infections of the deeper part of hair follicle
• most common on the face, neck, armpit, buttocks, and
thighs
• On central face
– danger of cavernous sinus thrombosis
• Tender, red, cone shaped swelling
• heal with scarring
• Recurrences may occur
• Exclude carrier state
• Treatment: Antibiotics
• If large – need incision
14. CARBUNCLE
• Deep staph. Infection of
several adjacent hair
follicle
• cluster of boils that form a
connected area of infection
• neck, back, thighs
• In diabetics & debilitated
• Treatment
– Antibiotics,
– Surgical incision
15. Ecthyma
• By both streptococci and
staphylococci
• Ulcer forms under a
crusted surface of the
infection
• Heals with scarring
16. • Poor hygiene and malnutrition are predisposing
factors
• Minor injuries and other skin conditions
determine the site
• Treatment-
– Improved hygiene and nutrition
– Antibiotics
(phenoxymethylpenicillin and flucloxacillin)
17. Cellulitis
• Infection of normal skin flora or exogenous
bacteria
(S. aureus and ß-haemolytic streptococci)
• Deep skin or subcutaneous layer
• Hx of Trauma and Ulceration
• Organisms enter through breach in skin
• Infection can spread to blood stream
Bacteremia /septicemia.
• lower leg , hand ,nose ,periorbital
18. Clinical features
• Acute localised pain
• Oedema
• lymphangitis
&lymphadenitis
– Hot painful erythema
streaking, progressing
proximally from the
affected area, tracking
along lymphatics
• +/- blister
• Fever, Malaise,
Leucocytosis
22. Investigations
• Swabs taken from relevant sites (from leading
edge or aspirating blisters)
• Gram stain and Blood cultures
• Serological-
– antistreptolysin O titre (ASOT)
– antiDNAse B titre (ADB)
26. Skin abscess
• Subcutaneous
• localized collection
of pus
• surrounded by
granulation tissue
• Hx of
– penetrating injury
– infection of haematoma
27. Features:
Cellulitis present
Swollen
Soft center
feels like fluid
underneath
Painful
Tender
Cellulitis
Abscess
• S. aureus is the common infecting organism
• Poor hygiene is predisposing
• Rx- incision and drainage
28. Necrotizing fasciitis
• Surgical emergency
• Polymicrobial Infection of the fascia
Type 1- E.coli, Pseudomonas, Proteus, Bacteroides,
Clostridium
Type 2- Streptococcus
• May proceed rapidly to underlying muscle.
• Diagnosis is often delayed
• Primarily a clinical diagnosis
• Rapid progression to septic shock
• Mortality 30-50%
29.
30. Clinical Features
• Severe pain at the site
of initial infection
• Tissue necrosis.
• spreading erythema
• pain
• soft tissue crepitus
– (infection tracks rapidly
along the tissue planes)
• Fever ,Tachycardia
31. Diagnose on
signs and
symptoms.
Imaging- air in
the tissues.
32. Clinical findings in necrotising fasciitis
Early findings
1. Pain
2. Cellulitis
3. Pyrexia
4. Tachycardia
5. Swelling
6. Skin anesthesia
Late findings
1. Severe pain
2. Skin discoloration (purple or
black)
3. Blistering
4. Hemorrhagic bullae
5. Crepitus
6. Discharge of “dishwater” fluid
7. Severe sepsis or systemic
inflammatory response syndrome
8. Multi-organ failure
34. • urgent surgical exploration
– Extensive debridement or
– amputation (if necessary)
Necrotizing fasciitis after debridement
35. •
Staphylococcal scalded skin syndrome
• exfoliate or epidermolytic
toxin.
• rapidly spreading tender
erythema
• Dermonecrosis
• Outer layer of the epidermis
peel off
• Blistering
• Ritter's Disease of the
Newborn - most severe form
of SSSS
36. • Affects
– infants, immunosuppressed , renal disease,
Malignancy
• Mortality – higher in adult
• Diagnosis
– Clinical
– Culture
– Frozen section examination of skin – shows split
• Treatment: IV antibiotics & nursing care
or Self limiting.
37. Hidradenitis suppurativa
• Infection in Apocrine sweat glands
• Common in Axillae and groin and in females
• Multiple tender swellings
• Enlarging and discharging pus
• Recurrence
• worse in obese individuals
• Rx-
– weight loss
– oral retinoids (Vitamin A)
– Zinc gluconate
38. Erythrasma
• Chronic skin infection of
Corynebacterium
• Macular wrinkled, slightly scaly pink
,brown or macerated white areas
• armpits ,groin or between toe webs
• Coral pink under Wood’s light
• prevalent among diabetics, the
obese, and in warm climates
• Rx – Topical fusidic acid ,Miconazole
39. Pyomyositis
• S. aureus & Streptococcus
infection of the skeletal
muscles
• pus-filled abscess
• most common
in tropical areas- “ myositis
tropicans”
• can affect any skeletal muscle
• most often infects the large
muscle groups
e.g.-quadriceps or gluteal
muscles
41. Gangrene
• Clinical situation where extensive tissue
necrosis is complicated by bacterial infection
Dry gangrene
Wet gangrene
Gas gangrene
• Predisposing factors
– Serious injuries
– Ischemia due to atherosclerosis and PVD
– Diabetes
42. Dry Gangrene
• The result of
ischaemic coagulative
necrosis.
• Black, dry, sharply
demarcated
• Secondary bacterial
infection is insignificant
E.g. Gangrene of
extremities in
thrombo-embolic
occlusion of vessels
43. Wet Gangrene
• Tissue necrosis is complicated by severe infection.
• Swollen, reddish-black foul smelling tissue.
• Extensive liquefaction of dead tissue occurs due to
invasion of organisms & acute inflammation.
• No clear demarcation between dead and viable
tissue.
• Occurs in extremities and internal organs
E.g. Diabetic gangrene of foot
Gangrene of bowel
44.
45. Gas Gangrene
(Clostridial myonecrosis)
• Clostridium perfringens
• Extensive tissue
destruction
• gas production by
fermentative action of
bacteria.
• Swollen reddish-black
foul smelling tissue
with crepitus.
46. Treatment
• usually surgical debridement
• amputation (if necessary)
• Antibiotics alone are not effective