Dr. Ali El-ethawi provides an overview of common bacterial skin infections. He discusses the normal skin flora and how changes can allow infections to occur. The most common bacteria that cause skin infections are Staphylococcus aureus and Streptococcus pyogenes, which can result in issues like impetigo, cellulitis, and ecthyma. Rarer causes include Pseudomonas aeruginosa. Treatment involves topical or oral antibiotics based on the specific infection as well as treating any predisposing conditions.
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.
Lichenoid Dermatoses, Characteristics of Lichenoid Dermatoses, What are the Major Lichenoid Dermatoses, Lichen planus (LP), Introduction of LP, Epidemiology of LP, Etiology of LP, Pathogenesis of LP, Clinical Features & Clinical variants of LP, Histopathology of LP, Immunohistochemistry of LP, Differential Diagnosis of LP, Treatment of LP
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.
Lichenoid Dermatoses, Characteristics of Lichenoid Dermatoses, What are the Major Lichenoid Dermatoses, Lichen planus (LP), Introduction of LP, Epidemiology of LP, Etiology of LP, Pathogenesis of LP, Clinical Features & Clinical variants of LP, Histopathology of LP, Immunohistochemistry of LP, Differential Diagnosis of LP, Treatment of LP
INTRODUCTION OF PSORIASIS, EPIDEMIOLOGY OF PSORIASIS, CLINICAL FEATURES OF PSORIASIS, PROGNOSIS OF PSORIASIS, HISTOPATHOLOGY OF PSORIASIS, TRIGGERING FACTORS OF PSORIASIS, PATHOGENESIS OF PSORIASIS
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
Subspecialty of dermatology and pathology focused on performing and interpreting tests on human tissue samples to provide scientific data and consultative opinions to referring clinicians
Melanoma
Cutaneous Melanoma
also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.
Classification Of Melanoma
I : De novo melanoma
A. Melanoma in situ (MIS)
B. Lentigo maligna melanoma (LMM)
C. Superficial spreading melanoma (SSM)
D. Nodular melanoma (NM)
E. Acral-lentiginous melanoma (ALM)
F. Melanoma of the mucous membranes
G. Desmoplastic melanoma
II Melanoma arising from precursors
Melanoma arising in dysplastic nevomelanocytic nevi
B. Melanoma arising in congenital nevomelanocytic nevi
C. Melanoma arising in common NMN
Etiology And Pathogenesis
The etiology and pathogenesis of cutaneous melanoma are unknown.
Epidemiologic studies demonstrate a role for genetic predisposition and sun exposure in melanoma development.
The major genes involved in melanoma development reside on chromosome 9p21.
Etiology
UVR, mostly of the UVB spectrum (290–320 nm) that induces mutations in suppressor genes. The propensity for multiple BCC may be inherited. Associated with mutations in the PTCH gene in many cases.
Predisposing Factors
Genetic markers (CDKN2a mutation)
Skin type I/II
Family history of dysplastic nevi or melanoma
Personal history of melanoma
Ultraviolet irradiation, particularly sunburns during childhood and intermittent burning exposures
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Six Signs of Malignant Melanoma (ABCDE Rule):
A- Asymmetry in shape—one-half unlike the other half.
B- Border is irregular—edges irregularly scalloped, notched, sharply defined.
C- Color is not uniform; mottled—haphazard display of colors; all shades of brown, black, gray, red, and white.
D- Diameter is usually large.
E- Elevation is almost always present and is irregular—surface distortion is assessed by side-lighting. others use E for Enlargement— a history of an increase in the size of lesion is one of the most important signs of malignant melanoma.
Lentigo Maligna Melanoma (LMM)
INTRODUCTION OF PSORIASIS, EPIDEMIOLOGY OF PSORIASIS, CLINICAL FEATURES OF PSORIASIS, PROGNOSIS OF PSORIASIS, HISTOPATHOLOGY OF PSORIASIS, TRIGGERING FACTORS OF PSORIASIS, PATHOGENESIS OF PSORIASIS
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
Subspecialty of dermatology and pathology focused on performing and interpreting tests on human tissue samples to provide scientific data and consultative opinions to referring clinicians
Melanoma
Cutaneous Melanoma
also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.
Classification Of Melanoma
I : De novo melanoma
A. Melanoma in situ (MIS)
B. Lentigo maligna melanoma (LMM)
C. Superficial spreading melanoma (SSM)
D. Nodular melanoma (NM)
E. Acral-lentiginous melanoma (ALM)
F. Melanoma of the mucous membranes
G. Desmoplastic melanoma
II Melanoma arising from precursors
Melanoma arising in dysplastic nevomelanocytic nevi
B. Melanoma arising in congenital nevomelanocytic nevi
C. Melanoma arising in common NMN
Etiology And Pathogenesis
The etiology and pathogenesis of cutaneous melanoma are unknown.
Epidemiologic studies demonstrate a role for genetic predisposition and sun exposure in melanoma development.
The major genes involved in melanoma development reside on chromosome 9p21.
Etiology
UVR, mostly of the UVB spectrum (290–320 nm) that induces mutations in suppressor genes. The propensity for multiple BCC may be inherited. Associated with mutations in the PTCH gene in many cases.
Predisposing Factors
Genetic markers (CDKN2a mutation)
Skin type I/II
Family history of dysplastic nevi or melanoma
Personal history of melanoma
Ultraviolet irradiation, particularly sunburns during childhood and intermittent burning exposures
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Six Signs of Malignant Melanoma (ABCDE Rule):
A- Asymmetry in shape—one-half unlike the other half.
B- Border is irregular—edges irregularly scalloped, notched, sharply defined.
C- Color is not uniform; mottled—haphazard display of colors; all shades of brown, black, gray, red, and white.
D- Diameter is usually large.
E- Elevation is almost always present and is irregular—surface distortion is assessed by side-lighting. others use E for Enlargement— a history of an increase in the size of lesion is one of the most important signs of malignant melanoma.
Lentigo Maligna Melanoma (LMM)
The skin is not only the largest organ of the body, but it also forms a living biological barrier with several functions.
Pyodermas are any pyogenic skin disease (has pus). Skin infections can be caused by bacteria (often Staphylococcal or Streptococcal) either invading normal skin, or affecting a compromised skin barrier
Some bacterial skin infections resolve without serious morbidity. However, skin infections can be severe and result in sepsis or death, particularly in vulnerable patient groups.
This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
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.
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
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
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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.
2. The normal skin flora
• Normal skin is heavily colonized by bacterial flora (harmless
commensals) such as;
• coagulase negative staphylococci (e.g; S. epidermidis) .
• Micrococcus species.
• Aerobic coryneforms.
• Anaerobic propionibacterium species, e.g. P. acnes, P.
granulosum, commonly inhabit the sebaceous hair follicles.
• Yeasts, pityrosporum
• Protects the skin from bacterial infections through bacterial
interference.
• Colonization is more dense in ;intertriginous and occluded sites.
3. Predisposition to skin infection
• Chronic S. aureus carrier state (nares, axillae,perineum,
vagina)
• Warm weather/climate, high humidity
• Skin disease, especially atopic dermatitis, familial
pemphigus
• Social situation: poor hygiene, crowded living conditions,
neglected minor trauma
• Chronic disease:, diabetes mellitus, HIV/AIDS, solid
organ transplant recipient & obesity
• Immunodeficiency, bactericidal defects (e.g., chronic
granulomatous disease)& cancer chemotherapy
4. Bacteria cause disease by
• direct invasion of tissues,
• by secreting toxins,
• by causing immunologic consequences
that result in disease.
Bacteria, like viruses, may also sometimes result in exanthems (rashes).
5. The most common bacteria to cause skin
infections are
• Staphylococcus aureus ;
– Impetigo (school sores)
– Folliculitis
– Furunculosis (boils)
– Staphylococcal scalded skin syndrome
– Toxic shock syndrome
– Botryomycosis (pyoderma vegetans)
Streptococcus pyogenes
– Cellulitis
– Erysipelas
– Impetigo
– Necrotising fasciitis
– Scarlet fever
• Overgrowth of cornebacterium spp
Erythrasma
Pitted Keratolysis
Trichomycosis
6. Less commonly, other bacteria may cause skin
infections;
• Pseudomonas aeruginosa;
wound infections, athlete's foot, gram negative folliculitis, chronic paronychia, spa pool follic
• Erysipelothrix insidosa, cause of erysipeloid (usually an animal infection)
• treponema species cause syphilis (STD) , yaws and pinta
• Hemophilus species ;, cause of chancroid (STD) and cellulitis in young children
• Neisseria species, cause of gonorrhoea (STD) and meningococcal disease .
• Calymmatobacterium granulomatis ; granuloma inguinale (STD)
• Klebsiella rhinosclermatis; cause of rhinoscleroma
• Bacillus anthracis ; anthrax
• Clostridium perfringens and other species cause gas gangrene
Calymmatobacterium granulomatis, cause of granuloma inguinale
7. IMPETIGO AND ECTHYMA
Etiology: S. aureus; also, group-A streptococci (GAS)
Infections of the epidermis (impetigo),
Infections which may extend into the dermis (ecthyma)
Clinical findings:
▪ Impetigo: crusted erosions
▪ Ecthyma: crusted deep erosions or ulcers.
Impetigo is a common, contagious, superficial skin infection that is produced by streptococci,
staphylococci, or a combination of both bacteria
There are two different clinical presentations:
bullous impetigo (primarily a staphylococcal disease)
nonbullous impetigo. a streptococcal disease,
but staphylococci are isolated from the majority of lesions in both bullous and nonbullous impetigo
C/F : Both begin as vesicles with a very thin, fragile roof consisting only of stratum corneum. And may
become pustular before rupturing to leave extending area of exudation & yellow crusting
Symptoms of itching and soreness are mild; systemic symptoms are infrequent.
.
8.
9. impetigo
Impetigo may occur as 1ry inf. after a minor skin injury such as an insect bite or as 2ry inf. of
pre-existing dermatoses, e.g. pediculosis, scabies & eczemas.
course ;The disease is self-limiting, but when untreated it may last for weeks or months.
complication; Post -streptococcal glomerulonephritis may follow impetigo.
MANAGEMENT
Treatment of predisposing causes, e.g. pediculosis & scabies.
Remove the crusts: by olive oil or hydrogen peroxide.
Topical antibiotic ointment;
e.g. bacitracin, mupiracin or Fusidic acid
Systemic antibiotics; e.g. penicillin, erythromycin & cloxacillin.
are indicated especially in the presence of
• fever
• lymphadenopathy,
• in extensive infections involving scalp, ears, eyelids
• if a nephritogenic strain is suspected.
10.
11.
12.
13. Ecthyma
• is characterized by ulcerations that are covered by adherent crusts.
• Poor hygiene is a predisposing factor.
• Ecthyma has many features similar to those of impetigo But it heal with scarring
• Distribution : more common on distal extremities.
14. Furuncle and Carbuncles
Furuncle (abscess or boil) ;is a walled-off collection of pus
that is a painful, firm, or fluctuant mass.
Carbuncles ;are aggregates of infected hair follicles.
The infection originates deep in the dermis and the subcutaneous tissue, forming a
broad, red, swollen, slowly evolving, deep, painful mass that points and drains
through multiple openings.
Malaise, chills, and fever precede or occur during the active phase.
Deep extension into the subcutaneous tissue may be followed by sloughing and
extensive scarring.
Sites ; Areas with thick dermis (i.e., the back of the neck, the back of the
trunk, and the lateral aspects of the thighs) are the preferred sites.
Treatment ;of an abscess, furuncle, or carbuncle is incision and drainage plus
systemic antimicrobial therapy
15.
16. ERYSIPELAS AND CELLULITIS
• Acute, spreading infections of dermal and subcutaneous tissues
• Characterized by a red, hot, tender area of skin
• In most instances there is fever and leukocytosis .
• Both may be accompanied by lymphangitis and lymphadenitis.
• Often originating at the site of bacterial entry
• Erysipelas involves the superficial layers of the skin and cutaneous
lymphatics; cellulitis extends into the subcutaneous tissues.
• Caused most frequently by group A streptococcus (erysipelas) or S.
aureus .
• Cellulitis is differentiated clinically from erysipelas by two physical findings:
cellulitis lesions are primarily not raised, and demarcation from uninvolved
skin is indistinct.
• Erysipelas ;if untreated ,the condition can even be fatal ,but it responds
rapidly to systemic pencillin ,some times given intravenously
• Treatment of cellulites; is elevation , rest -sometime in hospital – and
systemic antibiotics, sometimes given intravenously .
17.
18.
19.
20. Staphylococcal scalded skin syndrome
(SSSS)
Etiology: S. aureus.
Age: occurs mainly in newborns and infants < 2years.
Also, older immunocompromised persons
Pathogenesis: toxin-mediated epidermolytic disease.
Clinical syndromes: Erythema and widespread
detachment of the superficial layers of the epidermis,
resembling scalding
D. Dx; TSS, Kawasaki syndrome, drug-induced
toxic epidermal necrolysis (TEN).
21. painful, tender, diffuse erythema was followed by generalized epidermal
sloughing and erosions.
S. aureus had colonized the nares with perioral impetigo, the site of exotoxin
production.
22.
23.
24. Management:
Prophylaxis ; Prevent spread of toxigenic S.aureus in neonatal care
units.
General Care Hospitalization is recommended for neonates and young
children.
Topical Therapy Baths or compresses for debridement of necrotic
superficial epidermis.
Topical antimicrobial agents; like for impetigo lesions: mupirocin,
bacitracin, or silver sulfadiazine ointment.
Systemic Antimicrobial Therapy.
Adjunctive Therapy Replace significant water and electrolyte loss
intravenously in severe cases.
25. TOXIC SHOCK SYNDROME (TSS)
Etiology: Toxin-producing S. aureus and GAS
Clinical setting
▪ Staphylococcal TSS
• Menstrual (MTSS) (rare after 1984)
• Non menstrual (NMTSS)
▪ Streptococcal TSS
Clinical manifestations
▪ Rapid onset of fever and hypotension
▪ Skin findings
• Early: generalized skin and mucosal erythema
• Late: desquamation in early convalescence
▪ Organ hypoperfusion and multisystem failure
Management: systemic antibiotic to treat infection and stop toxin production.
Irrigation of the infected site are needed .
Supportive RX.
26. ERYTHRASMA
From the Greek: “red spot”
Age of Onset ; Adults
Etiology: Corynebacterium minutissimum
Distribution: intertriginous areas of webspaces of feet, groins, axillae,
submammary areas
Clinical findings: well-demarcated red or tan patches, ± scale
D.DX; from dermatophytosis and noninfectious intertrigo
Diagnosis: Clinical findings, absence of fungi on direct microscopy, positive
Wood lamp examination( shows coral red fluorescence )
Prevention/Prophylaxis,
Topical antiseptic alcohol gels: isopropyl, ethanol.
Topical Therapy Preferable.
Topical erythromycin or clindamycin solution twice daily for 7 days.
Sodium fusidate ointment, mupirocin ointment or cream.
Topical antifungal agents; clotrimazole,.
Systemic Antibiotic Therapy ; A macrolide or a tetracycline for 7 days.
27.
28. PITTED KERATOLYSIS
• Etiology: Kytococcus sedentarius
• Age of onset: young adults.
• Sex: males > females.
Distribution: plantar feet, web spaces of feet
Predisposition: hyperhidrosis and Occlusive footwear
• Clinical findings: eroded pits of variable depth occur as defects in thickly
keratinized skin
• Usually asymptomatic , but with Foot odor.
29. TRICHOMYCOSIS
Etiology: Corynebacterium ;gram-positive diphtheroid.
age &sex ; adults, males > females.
Distribution: axillae (trichomycosis axillaris),
pubic hair (trichomycosis pubis)
Predisposition: hyperhidrosis
Clinical findings:
granular concretions (yellow, black, or red) on hair shaft.
Hair appears thickened, beaded, firmly adherent.
Insoluble adhesive may erode cuticular and cortical keratin.
Management:
shave off affected hair.
Benzoyl peroxide wash.
Alcohol gel.
Topical erythromycin or clindamycin.
30.
31. Scarlet fever (scarlatina)
Age of Onset :Children.
Incidence : Much less than in the past.
Etiology :Usually group A β-hemolytic S. pyogenes . Uncommonly,
ET-producing S. aureus.
• Incubation Period : Rash appears 1–3 days after onset of
infection.
• PRODROMAL AND ERUPTIVE PHASE .
The sudden onset of fever and pharyngitis is followed shortly by
nausea, vomiting, headache, and abdominal pain.
• enlarged cervical lymph nodes .
32. Scarlet fever.
Evolution of signs and symptoms.
Temp
> 38°C
33. Exanthem (skin rash)
Face: flushed with perioral pallor.
• Initial punctate lesions become confluently erythematous, i.e., scarlatiniform (Numerous
papules giving a sandpaper-like texture to the skin.)
• Palms/soles usually spared.
• Linear petechiae (Pastia sign) occur in body folds.
• Tongue
• White tongue: Initially is white with scattered red, swollen papillae (white strawberry
tongue).
• Red strawberry tongue: By the fourth or fifth day, the hyperkeratotic membrane is
sloughed, and the lingular mucosa appears bright red.
Desquamation: Exanthem fades within 4–5 days and is followed by desquamation
on the body and extremities and by sheet-like exfoliation on the palms/fingers and
soles/toes.
In subclinical or mild infections, exanthem and pharyngitis may pass unnoticed.
In this case patient may seek medical advice only when exfoliation on the hand and soles
is noted.
34.
35.
36. • MANAGEMENT
• Symptomatic Therapy Aspirin or acetaminophen for fever and/or
pain.
• Systemic Antimicrobial Therapy Penicillin is the drug of choice
because of its efficacy in prevention of rheumatic fever. Goal is to
eradicate GAS throat carriage.
• Others: cephalosporins, erythromycin , or the newer macrolides.
• Follow-Up Re-culture of throat recommended for individuals with
history of rheumatic fever or if a family member has history of
rheumatic fever.
37. CUTANEOUS ANTHRAX
Synonym : Malignant pustule
Etiology: Bacillus anthracis
Zoonosis
Pathogenesis: toxin-mediated
Portal of entry:
▪ Skin: cutaneous abrasions
▪ Inhalations (woolsorters’ disease)
▪ Ingestion
Cutaneous anthrax accounts for 95% of anthrax cases in United States
Clinical findings of cutaneous anthrax:
▪ Black eschar surrounded by edema and purple vesicles
• Management: Cutaneous anthrax can be self-limited, but antibiotic therapy is
recommended.
• Drug of choice :
• Ciprofloxacin, 400 mg IV q12h, or doxycycline,100 mg IV q12h, is optimal.
Alternatives : None.
• Surgery for excision of eschar is contraindicated.