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SEARCH RESULTS FOR: Cellulitis

Orbital Cellulitis: Pathogenesis and clinical findings

Orbital Cellulitis: Pathogenesis and clinical findings Authors: Amanda Marchak Reviewers: Jaimie Bird Dr. Rupesh Chawla* * MD at time of publication Staphylococcus aureus, Streptococcus pyogenes Note: Orbital cellulitis is an extremely serious infection. If not caught and treated early, it can lead to death. CT should be performed if suspected. Involves the orbit Panopthalmitisb Endopthalmitisc Blindness Streptococcus pneumoniae, Moraxella catarrhalis, Haemophilus influenza Local infection or break in skin Eye surgery or trauma Direct inoculation Sinusitis (more common) Periorbital cellulitis1,2 Hematogenous spread Contiguous spread of infection Pathogens reach orbital tissue (posterior to the orbital septum) Spreads to periorbital tissue (anterior to the orbital septum) Localized inflammation Conjunctival chemosisa Eyelid and periorbital edema Pain on palpation Induration Warmth Orbital Cellulitis Inflammation of orbital tissue Proptosis Spreads to surrounding structures Subperiosteal abscess Brain abscess Cavernous sinus thrombosis Meningitis Subdural empyema Orbital abscess Notes: Impinges on ocular muscles Impaired extra- ocular movements Pain with eye movement or opthalmoplegia Definitions: Impinges on nerves Afferent pupillary defect Decreased visual acuity Exposes cornea Corneal drying and scarring a. Chemosis: Edema of the bulbar conjunctiva b. Panopthalmitis: inflammation of all coats of the eye including intraocular structures. c. Endopthalmitis: inflammation of the interior of the eye. 1. See slide on Periorbital Cellulitis for how sinusitis can lead to the development of periorbital cellulitis 2. The micro-organism responsible for periorbital cellulitis varies depending on how the pathogen was introduced to the system. Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 5, 2018 on www.thecalgaryguide.com

Periorbital Cellulitis: Pathogenesis and Clinical Findings

Periorbital Cellulitis: Pathogenesis and Clinical Findings Authors: Amanda Marchak Reviewers: Jaimie Bird Dr. Rupesh Chawla* * MD at time of publication Staphylococcus aureus, Streptococcus pyogenes (most common organisms) Note: Also referred to as preseptal cellulitis Dacryoadenitisa Conjunctivitisb Acute chalazionc Dacryocystitisd Hordeolume Streptococcus pneumoniae, Moraxella catarrhalis, non-typable Haemophilus influenza (most common organisms) Abrasion Insect bite Burns Trauma Local infection Contiguous spread of infection Sinusitis Otitis media Hematogenous spread Local break in skin Micro-organisms enter Definitions: Note: Eye exam should reveal normal: - extra-ocular movements and globe position - pupillary reflex and visual acuity If any are abnormal, the presentation is no longer considered periorbital cellulitis, as the infection has likely spread beyond the preseptal compartment/orbital septum. If the eye cannot be assessed, the patient NEEDS a CT scan. Pathogens reach dermis and subcutaneous periorbital tissue Periorbital Cellulitis a. Dacryoadenitis: infection of the lacrimal glands b. Conjunctivitis: inflammation of the conjunctiva c. Chalazion: a benign, painless bump or nodule inside the upper or lower eyelid which results from healed internal hordeolums that are no longer infectious. d. Dacryocystitis: an infection of the lacrimal sac, secondary to obstruction of the nasolacrimal duct at the junction of lacrimal sac. e. Hordeolum: localized infection or inflammation of the eyelid margin involving hair follicles of the eyelashes or meibomian glands. Spreads beyond preseptal compartment/orbital septum Involves the orbit Orbital cellulitis See slide on Orbital Cellulitis: Pathogenesis and clinical findings Localized inflammation Pain on palpation Induration Warmth Eyelid and periorbital edema Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 5, 2018 on www.thecalgaryguide.com

Sinusitis: Pathogenesis and clinical findings

Sinusitis: Pathogenesis and clinical findings Authors: Amanda Marchak Reviewers: Nicola Adderley Jim Rogers Danielle Nelson* * MD at time of publication Abbreviations URTI – Upper respiratory tract infection Nasal obstruction/ congestion Hyposmia Headache Facial pain/pressure Maxillary tooth pain Ear pain/ fullness Osteomyelitis of frontal bone Chemical irritants Cystic Fibrosis Direct toxic effect on cilia Viral URTI Allergies Inflammation of paranasal sinuses Edematous passageways Septal deviation Adenoid hypertrophy Polyps Turbinate hypertrophy Tumors Foreign body Dysfunctional cilia Congenital and/or craniofacial abnormality Obstruct sinus ostia Cilia unable to clear mucus from sinuses Mucus unable to drain through ostia Post-nasal drip Mucus overflows from the sinuses Cough Mucus accumulates in sinuses Occupies a larger volume Applies ↑ pressure to sinus walls Mucopurulent discharge Bacterial1 overgrowth in sinuses Bacterial infection spreads to adjacent structures Halitosis Pharyngitis Throat clearing Dental root infection Immunodeficiency Note: Irritates the back of the throat Perforation of the Schneiderian membrane2 Passage of bacteria into the sinuses Fever Fatigue Subperiosteal orbital abscess Orbital abscess Orbital edema ↑ susceptibility to bacteria 1. The most common bacteria are Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis. Staphylococcus aureus and Group A Streptococcus may be seen, but are less common. However, in cases of dental root infection, oral anaerobes become more common, while Pseudomonas species are associated with foreign bodies. 2. The Schneiderian membrane is the membranous lining of the maxillary cavity. Cavernous sinus thrombosis Meningitis Cerebral abscess Subdural abscess Epidural abscess Periorbital or orbital cellulitis Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 5, 2018 on www.thecalgaryguide.com

Cellulitis

Cellulitis: Pathogenesis, clinical findings and complications Authors: Tegan Evans, Spencer Yakaback Reviewers: Brian Rankin, Timothy Fu, Laurie Parsons*, Yan Yu* * MD at time of publication Cracked skin Surgery Normal Skin Epidermal layer Dermal-Epidermal Junction Dermal layer Subcutaneous fat Resident skin flora: Coagulase-negative Staphylococci* Transient skin flora: Staphylococcus aureus* Streptococcus pyogenes Gram negative bacteria Fungi Pathogen in deep dermis and subcutaneous fat *most common pathogens Break in skin barrier (may not be obvious) and entry of pathogen Risk Factors: Immunocompromised Host: -Diabetes mellitus+ -Lymphedema -Malnourishment -Older patient+ -Obesity+ -Peripheral vascular disease General Infection Risk: -History of cellulitis+ +highest risk factors Risk Factors for MRSA Cellulitis: Increased exposure to MRSA: -Contact sports -Crowded living conditions -Health care workers -Indigenous descent -Sharing towels, equipment Increased susceptibility: -Immunodeficiency -Young age Direct inoculation (e.g. trauma) Organism virulence overwhelms host defense mechanisms (related to risk factors) Cellulitis: A bacterial infection in which pathogens penetrate deep dermis and/or subcutaneous fat Cytokines activate immune response Accumulation of pus (bacteria, white blood cells, dead skin) Abscess formation Infection spreads to nearby lymph nodes Lymphadenitis Infection spreads through lymph vessels Ascending lymphangitis Local inflammatory response in skin Pain Warmth Edema Erythema (redness) with indistinct margins Vesicles and bullae Organisms penetrate blood vessels Bacteremia (presence of bacteria in blood) Systemic inflammation Distant spread to bone Osteomyelitis Distant spread to endocardium (inner lining of heart chambers and valves) Endocarditis Fever Malaise Chills Sepsis (rarely) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published September 27, 2020 on www.thecalgaryguide.com

Celulitis

Celulitis: Patogénesis, hallazgos clínicos y complicaciones Autores: Tegan Evans, Spencer Yakaback Revisores: Brian Rankin, Timothy Fu, Laurie Parsons*, Yan Yu* * MD en el momento de la publicación Traducción: Anagabriela Duarte María Rosario Talavera* Piel agrietada Cirugía Inoculación directa (e.j., trauma) Organismos penetran los vasos sanguíneos Bacteremia (presencia de bacterias en sangre) Piel normal Capa epidérmica Unión dérmica- epidérmica Capa dérmica Grasa subcutánea Flora cutánea residente: Staphylococcus coagulasa negativos* Flora cutánea transitoria: Staphylococcus aureus* Streptococcus pyogenes Bacterias gram negativas Hongos Patógeno en dermis profunda y grasa subcutánea *patógenos más comunes Rotura de la barrera cutánea (puede que no sea evidente) y entrada de patógenos Virulencia del organismo supera los mecanismos de defensa del huésped (asociado a los factores de riesgo) Celulitis: Una infección bacteriana en la que los patógenos penetran la dermis profunda y/o la grasa subcutánea Citocinas activan la respuesta inmune Acumulación de pus (bacterias, glóbulos blancos, piel muerta) Formación de abscesos Factores de riesgo: Huésped inmunodeprimido: -Diabetes mellitus+ -Linfedema -Desnutrición -Paciente adulto mayor+ -Obesidad+ -Enfermedad vascular periférica Riesgo de infección general: -Historia de celulitis+ +factores de riesgo mayores Factores de riesgo para celulitis por SARM: Mayor exposición a SARM: -Deportes de contacto -Hacinamiento -Trabajadores de la salud -Ascendencia indígena -Compartir toallas, equipos Mayor susceptibilidad: -Inmunodeficiencia -Edad temprana Infección se propaga a los ganglios linfáticos cercanos Linfadenitis infección se propaga a través de los vasos linfáticos Linfangitis ascendente Respuesta inflamatoria local en la piel Diseminación a distancia en endocardio (revestimiento interno de las cámaras y válvulas del corazón) Endocarditis SARM: Staphylococcus aureus resistente a meticilina Dolor Calor Fiebre Malestar Diseminación a distancia en el hueso Osteomielitis Escalofríos Inflamación sistémica Edema Eritema (enrojecimiento) con márgenes indefinidos Vesículas y ampollas (poco frecuente) Sepsis Abreviaturas: Leyenda: Patofisiología Mecanismo Signos/Síntomas/Hallazgos de Laboratorio Complicaciones Publicado el 27 Septiembre, 2020 en www.thecalgaryguide.com

postpartum-puerperal-fever-pathogenesis-and-complications

Postpartum (Puerperal) Fever: Pathogenesis and complications Author: Lindey Felske Reviewers: Brianna Ghali Ran (Marissa) Zhang Ingrid Kristensen* * MD at time of publication Breast Feeding Delayed gastric emptying in pregnancy ↑ Risk of aspiration during delivery Inhalation of gastric contents Chemical burn of the airways from gastric acid Tissue injury Chemokines released by alveolar cells recruit neutrophils Accumulation of neutrophils and plasma exudate in alveoli Aspiration Pneumonia Delivery (Vaginal or Cesarean Section) Tissue damage: Urinary tract catheterization Foreign body can: Introduce bacteria into bladder Provide a biofilm surface for bacterial adhesion Cause mucosal irritation Invasion of bacteria into urinary tract mucosa • • • • Perineal tear/episiotomy (perineal incision) Abdominal incision site Uterine damage Retained products of conception (RPOC) Bacteria enter open tissue Production of antimicrobial peptides and proinflammatory mediators in epidermis Cellulitis Necrosis of RPOC (good medium for bacterial growth) Post-operative pain Hypoventilation from shallow breathing Low volume in alveoli Alveolar collapse Endogenous cervicovaginal flora migrate into the uterine cavity Infiltration of bacteria into endometrium Endometrial TLR4 receptors recognize the endotoxin of Gram-negative bacteria Secretion of proinflammatory cytokines (IL-6, IL-8) and prostaglandin E(2) Activation of coagulation cascade Coagulation in areas of hemostasis (e.g., deep veins) Deep vein thrombosis Dislodged DVT travels to pulmonary arteries Pulmonary embolism • • • Skin openings in breasts (milk ducts +/- cracks) Bacteria from skin and/or saliva enter body Milk backup from blocked duct or poor breastfeeding technique Milk stasis provides environment for bacterial growth Upregulation of IFN- γ, and IL-12A cytokines in milk ducts Mastitis Collection of inflammatory exudate Breast abscess Cytokine expression and inflammatory cell infiltration Sloughing of urinary tract lining to reduce bacterial load Atelectasis Maternal fever (> 38.0°C) within 6 weeks of delivery Urinary tract infection Endometritis Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 4, 2022 on www.thecalgaryguide.com The image part with relationship ID rId4 was not found in the file.

Acute Otitis Externa Complications

Acute Otitis Externa (Swimmer’s Ear): Complications Acute Otitis Externa (AOE) Authors: Charmaine Szalay-Anderson Vaneeza Moosa Reviewers: Shayan Hemmati Shahab Marzoughi Ben Campbell Justin Lui* * MD at time of publication Spread to subcutaneous tissue Chronic otitis externa (>6 weeks) Chronic inflammation of the outer ear Fibroblast activation for collagen and extracellular matrix components production for tissue repair Excess accumulation of tissue Ear canal fibrosis (thickening) Ear canal stenosis (narrowing) Damage/obstruction to ear canal structures with impaired fluid drainage & pressure buildup Inflammation of the outer ear Recurrent or non-resolving acute otitis externa Dissemination of infection Spread to connective tissue and cartilage Perichondritis (inflammation of ear cartilage) Spread of Pseudomonas aeruginosa in an immunocompromised host or due to antibiotic resistance Rapid infectious spread through soft tissue to mastoid and/or temporal bone Malignant (necrotizing) otitis externa *can be life threatening Inflammation of connective tissue and bony structures Spread to tympanic membrane Myringitis (inflammation of tympanic membrane) Swelling and thinning of tissue Tympanic membrane perforation (tear) Immune reaction with inflammation Dead white blood cell, bacteria & tissue debris accumulation in the ear canal Pus formation with purulent otorrhea (discharge from ear) Localized pus accumulation Abscess Ear canal blockage Periauricular/ pinna (outer ear) cellulitis Facial cellulitis Erosion of temporal bone decreasing bony sound conduction Permanent conductive hearing loss Direct toxicity of pathogens to surrounding nerves Cranial nerve (CN) VII (facial) palsy (+/- CN X, XI, XII) Out-of- proportion primary otalgia (ear pain) Sensation of fullness in the ear Temporary hearing loss Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Dec 4, 2022; updated Feb 7, 2024 on www.thecalgaryguide.com

Onychomycosis

Dermatophyte Onychomycosis: Pathogenesis and clinical findings Authors: Holly Zahary Loreman Reviewers: Mina Youakim Elise Hansen Shahab Marzoughi Jodi Hardin* * MD at time of publication Host Risk Factors Environmental Risk Factors Immuno- compromised ↓ Immune response to infection Older age Peripheral vascular disease Reduced blood circulation Diabetes Pre-existing nail dystrophy Previous nail trauma Integrity of nail unit is compromised Micro- traumatic pressure on nail Dark, warm shoe environment Optimal conditions for fugal growth Exposure to tinea pedis or onychomycosis Direct spread of infection to nail unit High blood sugar favoring infection Dermatophytes invade corneocytes on stratum corneum, the uppermost non- living layer of keratinized skin Compromise/breaking of hyponychial seal or cuticle (connection between hyponychium and nail plate) Proximal Subungual White Superficial Tinea infection (e.g. Tinea Pedis, Corporis, Capitis) Infection spreads to distal hyponychial space Dermatophytes colonize local tissue in nail plate and nail bed Dermatophytes feed on keratinized tissue General Symptoms (All Subtypes) Spongiosis (Intercellular edema) Acanthosis (Thickening of stratum spinosum layer of epidermis) Hyperkeratosis (Thickening of stratum corneum In effort to rid infection) Papillomatosis (Projections of dermal papillae) Secondary damage to nail matrix Loss of nail Keratinocytes produce an acute, low-grade inflammatory cytokine response Onychomycosis Dermatophytic infection of the nail bed Inflammation promotes ↑ fluid to tissues for ↑ immune cell delivery Widespread inflammation thickens parts of the epidermis in efforts to shed the infection Inflammation and epidermal hyperplasia (↑ growth of cells) influence local dermal papillae (group of cells just beneath the hair follicle) to proliferate and project above the skin Distal Subungual Superinfecting bacteria or other fungi proliferate beneath the compromised nail imparting a yellowish appearance Distal Subungual Subtype (Thick yellow nails, keratin and debris accumulate distally underneath nail plate) Dermatophytes invade the proximal end of the nail plate Dermatophytes penetrate through the cuticle to the newly forming nail plate moving distally Proximal Subungual Subtype (Whitish discolouration of nail plate that begins proximally and moves distally, indicative of immunosuppression) Fungi predominantly invade various areas of the superficial nail plate layers eventually joining together White Superficial Subtype (Chalky white scale that spreads slowly beneath nail plate, well-defined “white islands” that coalesce as disease progresses) The entirety of the nail plate is infected by the dermatophytes Widespread inflammation thickens the nail plate as well as beneath the nail (subungual hyperkeratosis) in efforts to shed the infection Total Dystrophic Subtype (End-stage nail disease, entire nail becomes thick and dystrophic) Local spread of infection Dermatophytes spread causing cracks in the skin deeper into toe Abnormal keratinization in hyponychium Keratin accumulates between nail plate and hyponychium Fissure (splits in the skin) Bacteria enters lymphatics and bloodstream Cellulitis Sepsis Onycholysis (nail plate separates from nail bed) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Mar 13, 2024 on www.thecalgaryguide.com Dermatophyte Onychomycosis: Pathogenesis and clinical findings Authors: Holly Zahary Loreman Reviewers: Mina Youakim Elise Hansen Shahab Marzoughi Jodi Hardin* * MD at time of publication Host Risk Factors Environmental Risk Factors Immuno- compromised ↓ Immune response to infection Older age Peripheral vascular disease Reduced blood circulation Diabetes Pre-existing nail dystrophy Previous nail trauma Integrity of nail unit is compromised Micro- traumatic pressure on nail Dark, warm shoe environment Optimal conditions for fugal growth Exposure to tinea pedis or onychomycosis Direct spread of infection to nail unit High blood sugar favoring infection Dermatophytes invade corneocytes on stratum corneum, the uppermost non-living layer of keratinized skin Compromise/breaking of hyponychial seal or cuticle (connection between hyponychium and nail plate) Proximal Subungual White Superficial Distal Subungual Superinfecting bacteria or other fungi proliferate beneath the compromised nail imparting a yellowish appearance Distal Subungual Subtype (Thick yellow nails, keratin and debris accumulate distally underneath nail plate) Infection spreads to distal hyponychial space Dermatophytes colonize local tissue in nail plate and nail bed Dermatophytes feed on keratinized tissue Keratinocytes produce an acute, low-grade inflammatory cytokine response Onychomycosis Dermatophytic infection of the nail bed Inflammation promotes ↑ fluid to tissues for ↑ immune cell delivery Widespread inflammation thickens parts of the epidermis in efforts to shed the infection Inflammation and epidermal hyperplasia (↑ growth of cells) influence local dermal papillae (group of cells just beneath the hair follicle) to proliferate and project above the skin General Symptoms (All Subtypes) Spongiosis (Intercellular edema) Acanthosis (Thickening of stratum spinosum layer of epidermis) Hyperkeratosis (Thickening of stratum corneum In effort to rid infection) Papillomatosis (Projections of dermal papillae) Secondary damage to nail matrix Loss of nail Tinea infection (e.g. Tinea Pedis, Corporis, Capitis) Dermatophytes invade the proximal end of the nail plate Dermatophytes penetrate through the cuticle to the newly forming nail plate moving distally Proximal Subungual Subtype (Whitish discolouration of nail plate that begins proximally and moves distally, indicative of immunosuppression) Fungi predominantly invade various areas of the superficial nail plate layers eventually joining together White Superficial Subtype (Chalky white scale that spreads slowly beneath nail plate, well-defined “white islands” that coalesce as disease progresses) The entirety of the nail plate is infected by the dermatophytes Widespread inflammation thickens the nail plate as well as beneath the nail (subungual hyperkeratosis) in efforts to shed the infection Total Dystrophic Subtype (End-stage nail disease, entire nail becomes thick and dystrophic) Dermatophytes spread deeper into toe Bacteria enters lymphatics and bloodstream Abnormal keratinization in hyponychium Keratin accumulates between nail plate and hyponychium Local spread of infection causing cracks in the skin Fissure (splits in the skin) Cellulitis Sepsis Onycholysis (nail plate separates from nail bed) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published MONTH, DAY, YEAR on www.thecalgaryguide.com Dermatophyte Onychomycosis: Pathogenesis and clinical findings Authors: Holly Zahary Loreman Reviewers: Mina Youakim Elise Hansen Shahab Marzoughi Jodi Hardin* * MD at time of publication Host Risk Factors Environmental Risk Factors Immuno- Older compromised age ↓ Immune response to infection Peripheral vascular disease Reduced blood circulation Diabetes Pre-existing nail dystrophy Previous nail trauma Integrity of nail unit is compromised Micro- traumatic pressure on nail Dark, warm shoe environment Optimal conditions for fugal growth Exposure to tinea pedis or onychomycosis Direct spread of infection to nail unit High blood sugar favoring infection Dermatophytes invade corneocytes on stratum corneum, the uppermost non-living layer of keratinized skin Compromise/breaking of hyponychial seal or cuticle (connection between hyponychium and nail plate) Tinea infection (e.g. Tinea Pedis, Corporis, Capitis) Infection spreads to distal hyponychial space Dermatophytes colonize local tissue in nail plate and nail bed Dermatophytes feed on keratinized tissue Keratinocytes produce an acute, low-grade inflammatory cytokine response Onychomycosis Dermatophytic infection of the nail bed General Symptoms (All Subtypes) Spongiosis (Intercellular edema) Acanthosis (Thickening of stratum spinosum layer of epidermis) Papillomatosis (Projections of dermal papillae) Hyperkeratosis (Thickening of stratum corneum In effort to rid infection) Secondary damage to nail matrix Loss of nail Proximal Subungual White Superficial Distal Subungual Distal Subungual Subtype (Thick yellow nails, keratin and debris accumulate distally underneath nail plate) Proximal Subungual Subtype (Whitish discolouration of nail plate that begins proximally and moves distally, indicative of immunosuppression) White Superficial Subtype (Chalky white scale that spreads slowly beneath nail plate, well-defined “white islands” that coalesce as disease progresses) Total Dystrophic Subtype (End-stage nail disease, entire nail becomes thick and dystrophic) Local spread of infection causing cracks in the skin Dermatophytes spread deeper into toe Abnormal keratinization in hyponychium Keratin accumulates between nail plate and hyponychium Onycholysis (nail plate separates from nail bed) Fissure (splits in the skin) Bacteria enters lymphatics and bloodstream Cellulitis Sepsis Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Legend: Published MONTH, DAY, YEAR on www.thecalgaryguide.com Dermatophyte Onychomycosis: Pathogenesis and clinical findings Authors: Holly Zahary Loreman Reviewers: Mina Youakim Elise Hansen Shahab Marzoughi Jodi Hardin* * MD at time of publication Host Risk Factors Environmental Risk Factors Immuno- Older compromised age ↓ Immune response to infection Peripheral vascular disease Reduced blood circulation Diabetes Pre-existing nail dystrophy Previous nail trauma Integrity of nail unit is compromised Micro- traumatic pressure on nail Dark, warm shoe environment Optimal conditions for fugal growth Exposure to tinea pedis or onychomycosis Direct spread of infection to nail unit High blood sugar favoring infection Dermatophytes invade corneocytes on stratum corneum, the uppermost non-living layer of keratinized skin Compromise/breaking of hyponychial seal or cuticle (connection between hyponychium and nail plate) Tinea infection (e.g. Tinea Pedis, Corporis, Capitis) Infection spreads to distal hyponychial space Dermatophytes colonize local tissue in nail plate and nail bed Dermatophytes feed on keratinized tissue Keratinocytes produce an acute, low-grade inflammatory cytokine response Onychomycosis Dermatophytic infection of the nail bed Proximal Subungual White Superficial General Symptoms (All Subtypes) Spongiosis (Intercellular edema) Acanthosis (Thickening of stratum spinosum layer of epidermis) Papillomatosis (Projections of dermal papillae) Hyperkeratosis (Thickening of stratum corneum In effort to rid infection) Secondary damage to nail matrix Loss of nail Distal Subungual Distal Subungual Subtype (Thick yellow nails, keratin and debris accumulate distally underneath nail plate) Proximal Subungual Subtype (Whitish discolouration of nail plate that begins proximally and moves distally, indicative of immunosuppression) White Superficial Subtype (Chalky white scale that spreads slowly beneath nail plate, well- defined “white islands” that coalesce as disease progresses) Total Dystrophic Subtype (End-stage nail disease, entire nail becomes thick and dystrophic) Local spread of infection causing cracks in the skin Dermatophytes spread deeper into toe Abnormal keratinization in hyponychium Keratin accumulates between nail plate and hyponychium Onycholysis (nail plate separates from nail bed) Bacteria enters lymphatics and bloodstream Fissure (splits in the skin) Cellulitis Sepsis Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Legend: Published MONTH, DAY, YEAR on www.thecalgaryguide.com Dermatophyte Onychomycosis (Tinea Unguium): Pathogenesis, clinical findings, Authors: Holly Zahary Loreman Reviewers: Elise Hansen Name Name* * MD at time of publication and complications Host Risk Factors Environmental Risk Factors Immuno- compromised ↓ immune response to infection Older age Peripheral vascular disease Diabetes Pre-existing nail dystrophy Previous Nail Trauma Integrity of nail unit is compromised Micro-traumatic pressure on nail Dark, warm shoe environment Optimal conditions for fugal growth Exposure to tinea pedis or onychomycosis Direct spread of infection to nail unit Reduced blood circulation High blood sugar, favoring infection Tinea pedis infection (see ‘Tinea Capitis, Tinea Corporis, and Tinea Pedis’) Infection spreads to distal hyponychial space Dermatophytes colonize local tissue in nail plate and nail bed Dermatophytes feed on keratinized tissue Proximal Subungual White Superficial Dermatophytes invade corneocytes on stratum corneum, the uppermost non-living layer of keratinized skin Compromise/breaking of hyponychial seal or cuticle (connection between hyponychium and nail plate) Keratinocytes produce an acute, low-grade inflammatory cytokine response Onychomycosis (Tinea Unguium) (dermatophytic infection of the nail bed) Distal Subungual General Symptoms (All Subtypes) Spongiosis Intercellular edema Acanthosis Thickening of stratum spinosum layer of epidermis Papillomatosis Projections of dermal papillae Hyperkeratosis Thickening of stratum corneum In effort to rid infection Secondary damage to nail matrix Loss of nail Distal Subungual Subtype Thick yellow nails, keratin and debris accumulate distally underneath nail plate Proximal Subungual Subtype Whitish discolouration of nail plate that begins proximally and moves distally, indicative of immunosuppression White Superficial Subtype Chalky white scale that spreads slowly beneath nail plate, well-defined “white islands” that coalesce as disease progresses Total Dystrophic Subtype End-stage nail disease, entire nail becomes thick and dystrophic Local spread of infection causing cracks in the skin Dermatophytes spread deeper into toe Abnormal keratinization in hyponychium Keratin accumulates between nail plate and hyponychium Onycholysis (nail plate separates from nail bed) Tissue Damage Cellulitis Sepsis Bacteria enters lymphatics and bloodstream Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Legend: Published MONTH, DAY, YEAR on www.thecalgaryguide.com