Skin and Soft Tissue Flashcards
how to do pathogens get into the skin
hair follicles
-skin breaks
how does skin defend against infection
- acts as physical barrier
-chemical barrier with low pH and fatty acids to inhibit pathogen growth
-NF on superficial skin only not soft tissue/deep layer
What is NF on skin or pathogenic
Staph aureus
*Staph lugdunensis
*Enterobacterales
*Enterococcus spp.
*Candida spp.,
*Malassezia furfur
MANIFESTATIONS OF SKIN INFECTIONS
lesions and what types
lesion- area of skin that is responding to injury or infection
Rash -large bumpy itchy
1-Exanthem - rash on skin surface (contact dermatitis)
2-Enanthem - rash on mucus membrane - tongue
Abscess- pus, bacteria and dead tissue
1. superficial - in skin
2.Deep/internal - inside body tissue, organ or between organs
INFECTIOUS DERMATITIS
-Inflammation & rash on skin surface.
-genetic, immune related or allergy
-leads to infection by bacteria/fungus is called Infectious dermatitis
2 Types of dermatitis that can lead to skin infection
Intertrigo & Erythrasma
-inflammation due to moisture in skin folds like armpit, toe web causing friction = skin breakdown
-usually by candida Dermatophytes, Malassezia, S. aureus Enterobacterales
*Erythrasma due to Corynebacterium minutissimum
PYODERMA
inflammatory skin disorders characterized by production of pus.
Types of Pyodermas
:Impetigo
Folliculitis
Furuncle (boil)
Carbuncle
Erysipelas
Cellulitis
Impetigo
-caused MOSTLY by staph then GAS
-children 2-5
-GBS in newborns
-Affects skin- around nose & mouth or arms & legs
-vesicles that become rupturing pustules
-yellow discharge with gold crust
-contagious
-Bullous form (blisters on skin) due to S. aureus that makes exfoliative toxin
PYODERMA DUE TO FOLICULITIS, FURUNCLE OR CARBUNCLE
cause by staph and MRS
-carbuncles are more serious can get deeper with moe bacteria
-need to be surgically drained
folliculitis vs furuncle vs carbuncle
folliculitis - pustular inflammation of hair follicles
furuncle - painful, firm, abscess from hair follicle
carbuncle - furuncles connected by sinus tracts
CELLULITIS
-Acute spreading inflammation of superficial skin & subcutaneous fat tissues.
- legs and face.
-S. aureus, GAS, other BHS enter skin from mild trauma or a wound, burn, or surgical incisions
-Can be serious if organism gets into lymphatics & bloodstream.
ERYSIPELAS
-cellulitis affects mostly legs & face.
- more superficial, upper dermis & superficial lymphatics.
-S. aureus & GAS (but can also be caused by other organisms).
HUMAN OR ANIMAL BITES ***know the bacteria for CSMLS
Infection is due to normal mouth flora & is often polymicrobial (mix of O2 & ANO2 bacteria).
-can cause cellulitis or go deeper
Common pathogens from dog or cat bites:
Pasteurella, Streptococcus, Staphylococcus + other oral flora including anaerobes.
Common pathogens from human bite
Mouth flora like Streptococcus anginosis, (other Strep), S. aureus, Eikenella, Fusobacterium & Prevotella.
DIABETIC FOOT INFECTION
-Due to nerve damage & compromised circulation.
-Infections seen as cellulitis, or acute/chronic ulcers that can cause to osteomyelitis & gangrene.
need debridement or if severe, amputation.
-starts as Staph or Strep infection
Becomes polymicrobial-mix of bacteria including GN & anaerobes
DECUBITUS ULCER (PRESSURE /BED SORE)
Injury to skin (buttocks, back & ankles)due to long period of constant pressure
-bedridden, wheelchair or elderly.
-due to decreased blood flow
-Starts as pressure sore then progresses to decubitus ulcer (bed sore).
NECROTIZING INFECTIONS
-infections that lead to tissue necrosis.
-starts off infecting skin, fascia & subcutaneous fat –& progresses to muscle tissue.
-quick and life threatening needs debridement or amputation
-classification by # of bacteria & type causing the infection
Types of NECROTIZING INFECTIONS
Type I: polymicrobial infection- may include GAS, S. aureus, Enterobacterales & anaerobes.
Type II: GAS alone or 2nd most commonly by S. aureus alone or very rarely, by both together
Type III: includes marine bacteria V. vulnificans & Aeromonas & Gas Gangrene (Clostridial myonecrosis): Clostridium spp
S. aureus SKIN/SOFT TISSUE MANIFESTATIONS
Causes most community & healthcare acquired SSTIs.
Seen as folliculitis, furuncles, carbuncles, impetigo, cellulitis, bullous & abscesses.
Infections typically a pyoderma meaning pus-filled.
-causes various toxin related soft tissue infections that are much more serious.
S. aureus TOXIN RELATED SSTI
Scalded skin syndrome:
-SA produces Exfoliative or Epidermolytic toxin
- blistering & peeling of skin localized or spread to 90% of body
-Affects mostly children <6 (primarily in newborns) -can happen in immunocompromised adults.
S. aureus TOXIN RELATED SSTI
Toxic Shock Syndrome TSS:
-rare could become fatal multisystem disease
-starts with fever, sun burn like rash, peeling skin.
-Progresses quickly to hypotension, organ failure, shock & death.
-S. aureus produces TSST-1(superantigen) exotoxin – elicits massive proinflammatory response
S. aureus TOXIN RELATED SSTI
Toxic Shock Syndrome TSS:
2 types:
Menstruating associated: high absorbency tampon use in women who have S. aureus as normal flora in vagina or on hands.
Non menstruating associated: associated with any S. aureus infection especially post-surgical ones.
MRSA SKIN & SOFT TISSUE INFECTIONS
Hospital acquired (HA), community acquired (CA) & livestock acquired (LA).
-Begin as small red bump that looks like spider bite ,fever or rash.
-Becomes larger boil that leads to abscess.
-Can also cause cellulitis.
-May spread to other areas of skin or to other people by skin-to-skin contact (hospital outbreaks).
-People can become colonized & infections can be recurring.
-Difficult to treat
Can sometimes spread to bone, organs or blood
S. aureus TYPE IINECROTIZING INFECTION
rare mostly in sick ppl
-mostly due to community acquired MRSA
-Rapid & serious - affects skin, fascia, subcutaneous and muscle tissue.
- occur without a defined portal of entry or through an open skin wound or after surgery.
-Large # of exotoxins cause decreased coagulation & fluid leakage in tissue.
-Results in swelling and blister formation.
with blockages in blood vessels that lead to tissue death - person goes into shock and dies.
S. pyogenes (GAS) SKIN &
SOFT TISSUE INFECTION
Scarlet fever:
-Causes impetigo, cellulitis, erysipelas & wound infections.
-causes toxin related soft tissue infections.
-Infection with GAS producing pyrogenic exotoxin
-Damages plasma membranes of capillaries
-Seen as diffuse red rash on upper chest - spreads to trunk & extremities
-Followed by peeling of skin.
-fever, sore throat & strawberry tongue
If untreated, can result can affect the kidneys or heart or cause arthritis.
S. PYOGENES (GAS) SKIN &
SOFT TISSUE INFECTION
GAS Toxic Shock Syndrome:
-rare,multisystem disease caused by GAS that makes pyrogenic exotoxin- SpeA, B or C.
-Organism enters after minor bruise, injury, surgery or respiratory infection
-Portal of infection can be unknown.
-Children with chicken pox & elderly more at risk.
-Toxin acts as a superantigen initiates massive proinflammatory response.
-Same symptoms as Staph TSS - rapid multiorgan failure leads to shock & death.
S. pyogenes (GAS) SKIN &
SOFT TISSUE INFECTION
. GAS Necrotizing fasciitis Type II
-GAS is most common cause
-Due to strains with M proteins & pyrogenic exotoxin A.
-Enters thru surgical wound or trauma – sometimes no obvious point of entry.
-starts as redness, swelling and pain out of proportion to signs of skin infection.
-quickly progresses to fever, skin discoloration & swelling.
Decreased blood supply= severe tissue damage & necrosis.
Person goes into shock & dies.
PSEUDOMONAS SKIN & SOFT TISSUE INFECTIONS
primary skin manifestation
due to direct inoculation of bacteria in skin.
-mild skin infection, like folliculitis or more severe like skin and soft tissue infections
-Infects burns, bed sores & wounds due to injuries or surgery gets directly into blood to cause bacteremia
PSEUDOMONAS SKIN & SOFT TISSUE INFECTIONS
Secondary skin manifestations
as a result of
Pseudomonas bacteremia.
-Ecthyma gangrenosum.
-Lesion due to bacterial invasion of dermal veins leading to hemorrhage & necrosis of skin.
-Sore has purple-black center and is surrounded by a band of red
CoNs TO CONSIDER IN SKIN/SOFT TISSUE INFECTIONS
S. lugdunensis:
-can be harmless or be life threatening causing infective endocarditis
-Mostly causes skin/soft tissue, bloodstream, & prosthetic device infections.
-can be virulent & cause serious infections exactly like S. aureus
-In superficial wounds – full ID with AST only if pure or predominating numbers
-In deep wounds or sterile site- full ID with AST regardless of amount growing in culture
CHARACTERISITICS OF S. lugdunensis
-Small-med, white, NH or weak BH.
-GPC clusters, Catalase pos
Staphaurex neg (may be positive), Tube coagulase neg (gold standard for lug)
PYR pos, ORN pos (COMMOM CSMLS)
-Use Vitek OX MIC result or KB with cefoxitin disk (30ug) as a surrogate to report oxacillin – Do not do OX screen - not reliable because CONS wont grow on media with salt
-CLSI uses same interpretation breakpoints as S. aureus
VIBRIO
SOFT SKIN INFECTIONS
Vibrio vulnificus: Type III necrosis
-Exposure of open wound/or a wound obtained in seawater with organism.
-Skin lesions with hemorrhagic bullae that progress to necrosis, septicemia and death.
AEROMONAS
SOFT SKIN INFECTIONS
Aeromonas: Type III necrosis
-Found in brackish or fresh water -enters skin through open wound.
-or if leeches used therapeutically because leeches have aeromonas in their gut
-Starts with pain, swelling, hemorrhagic bullae, necrosis, gangrene with gas production, septicemia and death.
CHARACTERISTICS OF VIBRIO ** exams
-pathogens arent always looked for but more so pt history
Curved GNB/comma”- facultative anaerobe
-MAC: V. vulnificus is LF, others are NLF
-Oxidase pos, reduce nitrates to nitrites
-Salt loving (halophilic) – can grow on media with high salt
-MALDI, Vitek, API, Tube biochemicals
Characteristics of Aeromonas: *examsss
GNB (small coccobacilli)– facultative anaerobe
Oxidase pos
MAC: LF - Can’t grow on media with high salt
MALDI, Vitek, API, Tube biochemicals
Pasteurella multocida SKIN/SOFT TISSUE INFECTIONS
-Facultative, GNB or GNCB
-Cause SSTIs after animal bite- dogs & cats.
5 serotypes but A & D cause disease
=Virulence due to production of capsule & toxins
-starts with redness & swelling then cellulitis with purulent discharge.
-Rarely, becomes necrotizing infection.
- osteomyelitis, septic arthritis, septicemia or endocarditis –but more in those with co-morbidities.
Does not grow on MAC
Oxidase pos, spot indole pos- ID by MALDI OR VITEK
CLOSTRIDIUM GAS GANGRENE
TYPE III NECROTIZING FACIITIS
Large gpb with spores, strict ANO2
-spontaneous with abdominal diseases – usually due to Clostridium septicum.
-More often from severe traumatic wound –usually Clostridium perfringens
-Produces multiple toxins- alpha toxin most virulent.
-Causes clots in veins = decrease blood/O2 to tissue and pores in tissue cells so they lyse.
-Produces DNAse, hyaluronidase, & hemolysin - all breakdown tissue -accompanied with foul smelling gas – gas gangrene
Leads to shock & death unless treated or amputation.
Neisseria meningitidis SKIN/SOFT TISSUE INFECTIONS
-GNDC, can colonize the nose.
-Rarely a direct cause of cellulitis
- cause of indirect skin manifestation following septicemia or meningitis.
- skin rash or Purpura fulminans (PF).
-PF causes dermal micro clots in blood vessels leading to hemorrhagic skin necrosis, peripheral gangrene & shock
Amputation & death may result.
OTHER PATHOGENS IN SKIN & SOFT TISSUE INFECTIONS
Enterobacterales
Acinetobacter spp.
Stenotrophomonas maltophilia
Enterococcus spp. (if predominating or pure)
Anaerobes (from deep wounds or bites only)
SPECIMEN COLLECTION
Superficial Swabs
Superficial Swabs (not optimal) – only when tissue or aspirate can’t be obtained. like when wounds wont close and can lead to unnecessary treatment
-clean wound by irrigating with sterile saline to remove debris
-roll swab 5 times focusing on pus or inflamed tissue
-swab in Amies or Stuarts
-NOT FOR ANO2
SPECIMEN COLLECTION
best samples
-Aspirates of pus or abscess fluid by needle or syringe.
-Biopsies of infected wound tissue.
-Both good for aerobic or anaerobic culture.
-Portion of specimen placed in sterile empty container for aerobic culture.
-Portion of specimen placed in an anaerobic transport tube.
-For bite wounds best sample is aspirate pus from infected wound.
-Don’t take specimens from fresh bite wounds- will have normal oral/resp flora introduced from bite but cultures can’t predict if these will cause infection.
SPECIMEN COLLECTION INTRAVASCULAR TIPS
-detection of IV catheter-associated bloodstream infections.
-Short section of catheter that has been under the skin is aseptically cut off.
-Collected into sterile container & sent to lab ASAP
-Cultured by rolling tip across the agar surface using sterile forceps
direct GRAM STAIN
done on all skin/wound specimens.
-Quantitate & report pus, epithelial cells & any organisms seen because your workup is based on the # of these seen on the gram
-epithelial cells indicates contamination of specimen with NSF.
-WBCs is good indicator of infection.
-Information regarding type of wound (surgical, traumatic pressure ulcer etc.) & location of wound important & should be on requisition.
What are some less common causes of skin infections
where mycobacteria, zoonotic bacteria, fungus, virus, or parasites directly affect skin
- Or organisms where skin manifestation of disease due to complications of a disseminated infection caused by that organism
CUTANEOUS DIPTHERIA INFECTION
less common
-due to Corynebacterium diphtheriae or Corynebacterium ulcerans
-dipthe transmitted p/p or surface very contagious
-Ulcerans from infected animals/animal products
*Only strains that acquire tox gene from bacteriophage cause respiratory form of Diphtheria.
*Both toxigenic & non-toxigenic strains cause cutaneous form.
-seen as a vesicle that becomes an ulcer with grey membrane
both gpb clubbed
dipth- urea neg
ulcer- urea pos
CUTANEIOUS DIPTHERIA LAB TESTING
you can use Swabs, aspirate, biopsy or skin membranous material
-culture to media from bacterial isolation
-ID with gram, colo morph and MALDI
-PCR to detect dipth tox gene if ID is any cornye
-if pos for tox gene- sent to National Microbiology Laboratory for confirmation by PCR and Modified Elek test
CHLAMYDIA Lymphogranuloma venereum (LGV)
less common
serovars L1 to L3 of Chlamydia trachomatis infects lymphatics Transmission = Sexual
1st stage- ulcers - painless - heals
2nd stage - moves to lymph nodes > puss filled buboes. they burst
3rd stage - Strictures/obstruction of lymph vessels -possible necrosis of genital tissue
testing for Lymphogranuloma venereum (LGV)
based on history , clinical presentation and lab testing
-men :Urine, urethral, throat or rectal swab, lesion swab bubo fluid
-women-Urine, cervical, vaginal, throat or rectal swab, lesion swab, bubo fluid
test with NAAT, any pos NAAT send to national laboratory to confirm for LGV genotype
-culture not routinely done maybe at PHL
Syphilis SKIN MANIFESTATIONS
Treponema pallidum subspecies pallidum (not all treponema are pathogenic)
-ANA corkscrew, motile GNB - hard to stain
-transmitted sexually or mother-baby
-2 stages: primary, 2ndary, latent and tert
1-chancres
2. red brown rash
3. gumma formation
Haemophilus ducreyi
sexually transmitted
-forms lesion with soft edge = cancroid
-if untreated becomes ulcer and causes lymph node buboes
-tan yellow that you can push on agar
-GNCB = school of fish
*Oxidase: pos, Only X factor needed
*MALDI or PCR
ACTINOMYCETES SKIN & SOFT TISSUE INFECTION
-branched beaded GPB
-lung infection , skin and soft tissue
-common one infecting SST - Actinomyces & Nocardia
Actinomyces spp
Anaerobic, NOT acid fast
Causes Actinomycoses: abscess of face & jaw that goes into deeper tissue.
*Draining sinuses + yellow orange sulfur granules
Nocardia spp
strict aerobe, modified acid fast
-Crumbly and looks like a molar tooth
-Branching beaded GPB
Causes Nocardiosis: Skin ulcer
*Or Mycetoma-little abcesses under skin if on foot =Madura foot
-black granules if fungus
-red granules if Nocardia
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
rickettsiae
BSL3
Small GNB
Rocky mountain spotted fever
-maculopapular rash with petechiae
-ticks, mites, lice, fleas
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
leptospira interrogans
leptospirosis
maculopapular rash that becomes hemorrhagic
rodents and mammals
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
bartonella henselae and bartonella quintana
GNB
Bartonellosis - Cat Scratch disease
papule , lesions
cat bites, sandflies, lice
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
streptobacillus monilformis
Spirillum minus
streptobacillus monilformis GNB
Spirillum minus GNB Spiral
rat bite fever
maculopapular or pustular rash on palms and soles
rodent bites or contact with their feces
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
francisella tularensis
BSL3
Tularemia
maculopapular or vesicular rash
ulceroglandular
painless ulcer and painful swelling of the lymph node
rabbits, rodent,
bite from infected tick, flea , deerfly
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
eryripelothrix rhusiopathiea
small gpb
erysipeloid
painful red lesion with raised borders
animals, animal meat, hides, saltwater fish
handlers of above also at risk
ZOONOTIC INFECTIONS w SKIN MANIFESTATIONS
baclluss, anthracis
BSL3
Large GPB with spores
anthrax cutaneous form
starts a painless papules on face or arms, then they become vesicles leading to necrotic lesions with black centers
coming in contact with animal or animal products with the spores
DIAGNOSIS OF ZOONOTIC SKIN DISEASES
specimens for zoonotic orgs
- Swabs from skin lesions or ulcers
*Fluid, abscess aspirates
*Tissue biopsy or Blood sample
testing of growing organisms in BLS3 labs only
-gram and histo direct stains
-immunology /serology
-PCR - single org or multiplexing
-grow in culture and then MALDI
MYCOBACTERIA SKIN MANIFESTATIONS
-Transmitted person-person or environment, food, animal or vector transmission
*Organism seeds skin directly
*Or as it travels through blood or lymphatics
*Also, if travels from nearby area of infection
4 Types of Mycobacterial Skin disease
1.Cutaneous manifestations due to Mycobacteria in MTB complex
2.Buruli ulcer caused by Mycobacterium ulcerans & other ulcers caused by slow growing NTM
3.Leprosy caused by Mycobacterium leprae &Mycobacterium lepromatosis
4.Cutaneous infections caused by rapidly growing NTM
UNGROUPEDMYCOBACTERIUM SKIN DISEASES
M. ulcerans
M. ulcerans: Buruli ulcer (Africa),Bairnsdale ulcer (Australia)
-*In environment –transmitted by skin trauma.
Causes nodular lesions with or without ulceration
.Produces necrotizing immunosuppressive toxin – mycolactone.
*able to infect underlying bone to cause osteomyelitis
uNGROUPEDMYCOBACTERIUM SKIN DISEASES
M. leprae (Hansen’s bacilli): Leprosy
strictly human pathogen and armadillo
-droplet spread but only 5% carry leprosy
-Chronic infection of skin, peripheral nerves & mucous membranes.
*Paucibacillary form: < #s of organism & infected skin patches
*Multibacillary form: > #s of organisms & infected skin patches
MYCOBACTERIAL SKIN INFECTION LAB TESTING
specimen
and tests
Swab of lesion, vesicle or ulcer in Amies or Stuarts
.Aspirate of fluid from infected tissue.
*Tissue samples are best sample.
* blood
Microscopy: acid fast stains ZN, Kinyoun, Auramine rhodamine
Culture: To both Solid agar (LJ egg based or Middlebrook agar based) + broth (Middlebrook broth or broth included with automated instruments
Identification: Biochemical tests, MALDI, PCR
Common viral skin manifestations are
Rashes (different types)
*Lesions
*Warts
*Vesicles
Virus Specimen Collection
take sample from spot where virus causes infection
-SST lesion secretions Dacron/Rayon swabs -plastic or wire
-all else use cell scrapings, tissue biopsy, body fluids
-swab and tissue go in VTM/Universal UTM transport media (sucrose, proteins, antibiotics, buffers, gelatin & phenol red)
-otherwise you would dilute
.fluid samples in sterile screw top that will not break when frozen & thawed
-Do not use UTM/VTM for these because will dilute the virus.
*Place specimens for PCR – in its own manufacturer media
VIRUS SPECIMEN TESTING
Process culture immediately
*If there is a delay <72 hrs., store at 4, ship on a gel pack.
*If delay is >72 hrs., freeze at -70oC.
*Never freeze at -20oC because ice crystals form which damage the virus
*Never freeze and thaw numerous times can damage the virus
4 Main ways to diagnose viral infections:
1.Direct microscopic detection (direct fluorescence)
2.Molecular testing like PCR, multiplexing
3.Serological assays to detect viral Ags or Abs to the virus
4.Isolation of virus in cell culture with evidence of specific cytopathic effect
SUPERFICIAL MYCOSES
what
lab diagnosis
Tinea Versicolor due to Malassezia furfu
-NF on skin
-needs fat /oil to grow found around sebaceous gland
-opportunistic causing dry patches
-dandruff
Lab Diagnosis:
-Shine fluorescent woods lamp on skin & fungus will fluoresce
*Microscopic exam of skin/hair specimen in 10%KOH shows“spaghetti & meatballs” = budding yeast & hyphae.
*Won’t grow on culture media unless covered with oil – w/o oil cultures look negative
CUTANEOUS MYCOSES
*Infections of keratinized tissue–skin, hair and nails
*Dermatophytes or Candida spp. *Symptoms: redness, itching, scaling & ring like lesion (ringworm)
*Named Tinea followed by the site where lesion is found. Tinea pedis = feet, Tinea capitis = hair, Tinea corporis = body skin
-Transmission: direct/indirect contact with infected host.
*Three genera infect different areas Microsporum infects skin and hair (not nails)
Epidermophyton infects skin and nails (not hair)
Trichophytoninfects hair, skin & nail
LAB DIAGNOSIS OF DERMATOPHYTES
specimen and lab testing
BSL2 in CL 2 Lab with PPE & Class II BSC Specimens:
*Skin scraped from margin of lesion
*Hair plucked, not cut, from edge of scalp lesion
*Nails scrapings of nail bed
:1. Microscopic exam directly on specimen: 10%KOH or Calcofluor white fluorescent stain
*Look for 2 sizes of asexual reproductive cells-each a distinct shape Macroconidia & or Microconidia
2. Culture specimen on fungal media
3. Describe front and back of colony growing on plates
4. Lactophenol cotton blue of colony & examine microscopically for characteristic macro & or microconidia.
CUTANEOUS CANDIDIASIS
Yeast skin infection caused by Candida spp.- C. albicans
.Affects warm, moist areas, especially in folds.
seen in infant diaper rash
.Can infect nails.
*Causes red, itchy rash, skin can crack or blister.
*Increased risk in diabetes, obesity, on antibiotics or immunocompromised.
SUBCUTANEOUS MYCOSES
Chronic infection of deep skin layers -may spread to muscle & bone but not usually blood or organs.
*Environmental fungus in tropical areas enters skin trauma
*Cause progressive non healing ulcers, draining sinus & tissue destruction
*Eumycotic Mycetoma = mycetoma caused by fungus (examples: Madurella or Fusarium spp.)
Actinomycetoma=mycetoma caused by Actinomycetes, like Nocardia
.Fungal form causes black melanotic granules.
*Are microcolonies of fungus discharged onto skin surface through sinus tracts.
*Granules are expressed from draining lesions.
SYSTEMIC MYCOSES
Fungal infection that spreads throughout the body.
*affects organs, blood, CSF.
* fatal in immunocompromised.
*caused by dimorphic fungus, Aspergillus or a yeast.
IMORPHIC SYSTEMIC MYCOSES w SKIN MANIFESTATIONS
Transmitted by inhaling spores, ingestion or inoculation of spore into skin
-starts as a lung infection and rash
-healthy people can overcome
-immuno ppl get get chronic pulmonary infection - leads to granulomatous skin lesions which lead to systemic infections
LAB DIAGNOSIS OF DIMORPHIC FUNGUS
BSL3 organisms use proper PPE & class II biological safety cabinet when processing
.*Growing cultures only worked on in CL3 Lab
Specimens: tissue biopsy, body fluid, sputum, blood
Lab testing:*Antigen or Antibody detection: serological or immunodiagnostic techniques.
*Molecular tests like PCR:
*Direct Specimen Microscopy: detect yeast form in tissue.
*Culture on fungal media 25C & 35C: may take weeks to grow (“Yeast in beast mold in cold”)
*Microscopy of colony with LPCB to see characteristic dimorphic yeast or mold structures.
ACANTHAMOEBA
Free-living protozoan amoebae in soil and fresh water
*Can cause Granulomatous Amebic Encephalitis (infects CSF & brain, when breathed in thru nose), Amebic Keratitis (Eye) & Cutaneous Acanthamoeba (Skin)
-infection through open wounds
-seen as abscesses, ulcers, nodules
Staining skin biopsy by H & E, Periodic acid-Schiff (PAS), or calcofluor white.
*Molecular can be done as well
HELMINTH PARASITE SKIN MANIFESTATIONS
Nematode round worms
Hookworm: *Larvae gets in skin & burrows.
*Visible under skin as a winding, threadlike, raised trail.
*Rash, small bumps & blisters may also occur
.Trematode flat worms like Schistosoma
:*Cause irritation of skin where larval form enters through the persons skin.
ECTOPARASITIC SKIN INFECTIONS
Beg bugs
Genus Cimex spp
.Feed on blood, at night. Bites =skin rash & allergic reactions.
Scabies
Sarcoptes scabiei mite
Burrows in surface skin.
Causes itching & rash
Lice
Head Louse Pediculus
Groin Louse Phthirus pubis
Spread by close contact
Causes itching, & sores
common viral skin manifestation
Parvo
oral herpes
Papillomas
Roseola
varicella
rubeola (measles)- paramyxovirus
Rubella - german measles
Monkeypox
Parvo - slapped cheek rash
Oral Herpes - cold sores
Papillomas - plantar warts, filiform warts
Roseola - cold followed by a rash 3-5 days later
varicella chickenpox
rubeola (measles)- paramyxovirus
rubella - german measles nonpruritic
Monkeypox othropoxvirus - rash with blisters
Ebola, Marburg, Dengue
Zoonotic viruses that cause severe bleeding under skin
