Microbiology Chapter 19 - PowerPoint Presentation

Slide1

Microbiology

Chapter 19

Microbial Diseases of the Skin and Wounds

Slide2

Function and Components

of the

Integumentary System

Physical

Epidermis – stratified squamous epithelium

Dermis –

sweat glands, oil

glands with hair follicles, sensory nerve endings, capillaries

Immunological

Macrophages, Dendritic cells

Microbiological – resident microbiota

Staphylococcus, Micrococcus,

Malassezia

,

Corynebacteria

,

P

ropionibacteria

, Pseudomonas

Slide3

Defensive Mechanisms in the Skin

Multiple layers of dead skin (

stratum

corneum

) makes a barrier to penetration

The stratum

corneum

is continuously produced and shed off (turnover time is one month)Perspiration (watery secretions)salt, urea, lysozyme, ferritin, non-fatty acids, anti-microbial peptides, IgASebae (oily secretions)Fats and fatty acidsHowever, the sweat and oily secretions of the glands can contribute to infection of the skin (see next slide)

Slide4

Eccrine glands (sweat or sudoriferous glands)

merocrine secretion; empties to skin surface

standard watery sweat glands – no cellular components

contain

NaCl

(up to 10% after evaporation)

Also contain hydrophilic (lactic, citric, pyruvic, uric) and hydrophobic (fatty) acids

Secrete antimicrobial proteins (lysozyme, ferritin, IgA, anti-microbial peptides)They support microbial growth in apocrine and sebaceous glands by diluting their contentsWhy would many mammals (e.g., dogs, cats) evolve to not contain sweat glands?Apocrine glandsapocrine secretion; resemble eccrine gland, but empty to hair shaft (or skin surface of balded skin)oily secretion in primates and non-sweating mammals ; oily and watery in other sweating mammalsContains fats/fatty acids, proteins, steroids and pheromones, lubricants, pinched-off cell fragmentsSebaceous glandsholocrine secretion; integrated with hair shaftwax (cholesteryl fatty esters), fats and fatty acids, dead cells and cell debrisPreferred site of growth for skin microbiota, and most common site for microbial tissue damage

The Integumentary Glands – the good and the bad

Slide5

Resident Microbiota of the Skin

Normal biota live:

On skin

surface

In hair

follicles

In outer portion of eccrine and apocrine glands

They feed off of dead cells, cell debris, and secretory productseccrine glands - mucus secretionapocrine glands - mucus secretion, bioorganic moleculesSebaceous glands - bioorganic secretionsmicrobiota create body and “underarm” odor as they degrade lipids, glycogens and proteins

Slide6

Normal

microbiota

of the skin

Mostly aerobic

Most commonly observed

Staphylococcus epidermidis

Corynebacteria

Variably observedDependant on genetics, diet, and medical history Bacteria – Staphylococci (esp. aureus), Pseudomonas, Lactobacillus, Haemophilus sp., PrevotellaFungi – Malassezia

,

Candida

Anaerobic bacteria deep within hair follicles and sweat glands

Propionibacterium acnes,

Bacterioides

sp.,

Slide7

How microbes infiltrate the skin, and how the skin is healed

How microbes infiltrate the skin:

They can grow in hair follicles

They invade when the skin is compromised

How the skin is healed

If blood vessels are broken, the blood clotsIf hole in the skin forms, clotted blood fills the new spaceThe wound initiates an inflammatory responseInfection results in additional “danger” inflammatory responses

Any infections must be cleared out before repair beginsChronic infection/inflammation – healing stops hereCell debris (damaged tissue,

clot) removedNew cells and vasculature arrive – original tissue or scar

Slide8

Acute Inflammation and proper wound healing

1 - Blood clot forms quickly

2,3 - Pathogens are killed within days

NOTE! Repair does not continue until this finishes

4 - Epithelial

tissues spread under clot4,5,6 - Fibroblasts infiltrate to rebuild dermis (healthy tissue or scar tissue)

Not displayed - Mesenchymal

stem cells turn into blood vessels and adipose tissues

Slide9

Granuloma – How our skin fights chronic infection/inflammation

Arriving fibroblasts that normally help repair tissue instead make a spherical wall around the chronic infection

G

ranuloma

a.k.a. “the sac” – this scar-like wall and the three inflammatory layers within it

Deepest layer is pathogen, dead/dying cells, neutrophils

Degranulation occurs here

Calcification occurs to “turn everything to stone”

Surrounded by interdigitating macrophages and inflammatory macrophages

dendritic cells cycle between lymphocytes and “garbage”

Outermost layer composed of lymphocytes (B cells, T cells, NK cells

Slide10

Granuloma – wall off an infection to keep it from spreading

Epidermoid cysts are chronic infections, always encased within a fibrous “sack” to keep the infection from spreading further.

Failure to remove sack can cause the cyst to re-grow or return.

Disrupting the sack can cause the infection to spread.

Have you ever heard of cysts getting hard and calcified??

Slide11

Most common smaller

s

kin lesions

– FOR REFERENCE ONLY

To differentiate between these, note the following differences:

Is the fluid clear/yellow, or is it filled with dead cells (white)?

It is in the epidermis or the dermis?

Is there fluid being made or not?Did a break in the skin make it easier for an infection to start?

Slide12

FOLLICULITIS

Inflammation of hair follicle due to (most often) pathogen growth

Redness and pus formation

Commonly known as

pimples

Most common cause –

S. aureus

Treatment – topical

muriprocin

after follicle openings unclogged

and

all pimples

drained

Prevention -

Vaccine under

development

Slide13

Staphylococcal Scalded

Skin Syndrome

Mediated by

S.

aureus

Common in newborns

Exotoxin-mediated separation of stratum granulosum from stratum spinosum throughout body

Susceptible to other topical infectionsResembles burnt skin or systemic impetigoEpidermis regrows in 7-10 days after infection clears

Slide14

S

treptococcal Skin diseases – SUMMARY SLIDE

Impetigo

80% Staphylococcus aureus

20%

S

treptococcus pyogenes

Infection usually limited to the epidermis; localCellulitisSame agents as impetigoInfection spreads to the dermis; systemicErysipelasMost cases involve S. pyogenesInfection spreads into the dermis and progresses through the lymph nodes; systemicNecrotizing fasciitisMost cases involve S. pyogenesInfection spreads to underlying tissues; systemic

Slide15

Impetigo

Affects 2% of world population

80% caused by

Staphylococcus aureus

20% are

Streptococcus pyogenes

Most commonly seen near the mouth

Very contagiousAt risk: young, incomplete immune development, poor nutrition, uncleanRed patches become vesicular and pus-filledDiagnosis – microscopic analysis of pus; only epidermal layersTreatment – topical antibiotics (mupirocin, penicillin), frequent washing, good hygiene; usually resolves without treatment in 3 weeksPrevention – good hygiene, cleanliness; previous exposure to strep throat yields some immunity

Slide16

Cellulitis

Same infectious agents as impetigo, but infection is in dermis and

in subcutaneous tissues; requires penetration of epidermis

Spreads quickly; inflammatory, potential bacteremia

Increased incidence in immunocompromised and opportunistic

(poor integumentary innate system?)Common secondary infection after dermatophytes

Slide17

Erysipelas

Can present with impetigo

Most common cause is

substrains

of

Streptococcus pyogenes

with increased virulenceMigration into dermis and into lymph nodesShiny red, well-defined zones of infectionHigh fever, pain, sorenessIf left untreated:Risk of development into acute glomerulonephritisMortality can approach 2-17% (higher if young, old, or immuno-compromised)Diagnosis – microscopic analysis of skin cultures; wide-spread rednessTreatment – oral clindamycin or doxycycline; usually resolves in a weekPrevention – good hygiene, cleanliness; previous exposure to strep throat yields some immunity

Slide18

Necrotizing fasciitis

A.k.a. flesh-eating [bacterial] disease

Most common cause is

substrains

of

Streptococcus pyogenes

with greatly increased virulence and poor immunitySudden onset diseaseRapid migration into subdermal tissuesHigh fever, pain, soreness progresses into septic shockMedical emergency or death is certainDiagnosis – microscopic analysis of skin cultures; necrotic tissueTreatment – extensive surgery and broad-spectrum combination antibiotics (clindamycin and penicillin)Prevention – good hygiene, cleanliness; early treatment of impetigo or erysipelas

Slide19

ACNE

G

rowth of bacteria in hair follicles, causing a visible lesion

Most commonly found bacterium is

Propionibacterium

acnes

P. acnes

is not necessarily the cause, just the end result

Slide20

Classifications of

Acne

Based on severity of acne; problems additive

Comedonal

(mild)

acne

Growth of bacteria under anaerobic conditionsPore clogged with skin; fully anaerobic – comedo “whitehead”Pore “open” to air but clogged with sebum – open comedo “blackhead” Inflammatory (moderate) acneLymphocytes recruited to comedo; redness (pimples)Cystic (severe) acneComedo expands to deeper skin; called cystBecomes painful and medically dangerous (internal rupture)

Slide21

Comedonal

Acne

Treatment

Topical agents –

azelaic

acid

Salicyclic

acid preparationsRetinoids (tretinoin, tazarotene, adapalene)

Slide22

Inflammatory Acne

Treatment

Preventing sebum formation (

isotretinoin

/

accutane

- teratogen)

Antibiotics (clindamycin, erythromycin)Benzoyl peroxide to loosen clogged folliclesVisible (blue) light (kills Proprionibacterium acnes)

Slide23

Cystic

Acne

Inflammatory acne that is no longer localized to single hair follicles; scarring through granulomas more likely

Treatment is with antibiotics (clindamycin, erythromycin)

Frequent washing loosens epidermis and unclogs follicles

Benzoyl peroxide to kill

S. aureus

, loosen clogged follicles

Slide24

Boils

Resembles acne in that hair follicles are infected, but…

most common agent:

Staphylococcus aureus

(chronic)

furuncle (one hair follicle; surface)

carbuncle (many hair follicles; deeper)

greater chance of systemic infection and more contagiousmore medically serious than acne

Slide25

Catscratch

Disease

Caused by

Bartonella

henselae

g

ram negative rod, facultative intracellular parasites (RBCs and endothelial cells)Primary portals of entry: skinCan be delivered by scratches or bites by kittens or cats (asymptomatic carriers) or can be delivered by flea bitePapules at site of infection – clear in a few days usuallySymptoms usually clear from lymph nodes in a few weeksSymptoms aggravated in immunocompromised or AIDS patientsTreatment: azithromycin most commonly used

Slide26

Pseudomonas

infection

Caused by

P

seudomonas aeruginosa

most commonly

g

ram negative rod, facultative anaerobePrimary portals of entry: skinDoes not colonize skin or mucous membranesCause of 10% of nosocomial infectionsParenteral entry into deep tissues – very hard to kill and removeSymptoms - fever, chills, creation of a blue dye in culture or sometimes in woundsTreatment – sulfadiazine and piperacillinPrevention – aseptic technique (lives in soil)

Slide27

Rickettsial

Spotted

Fevers

Also called

Rocky Mountain spotted fever

Caused by

Rickettsia

rickettsiiMeasles-like rash, except that the rash also appears on palms and solesSpread by a wood tick, dog tick, Lone Star tick

Slide28

Rocky Mountain Spotted Fever, 1997–2002

Slide29

Cutaneous anthrax

Most common way to be infected by

Bacillus

anthracis

Less severe than inhaled infection

Both routes equally possible by biowarfare

Endospores enter skin through abrasions/lesions

Skin become necrotic and erupts into painless eschar {es-KAR}Mortality 20%; Cipro/doxycycline/penicillin treatment reduces to 1%Vaccination for military and biowarfare researchers/first responders; civilian vaccination NOT recommended

Slide30

Gas gangrene

a.k.a.

clostridial

myonecrosis

Caused by

Clostridium

perfringens, a gram-positive, endospore-forming obligate anaerobic rod(inactive) spores found in soil, skin, intestines, vaginaRequires parenteral entry to maintain anaerobicityhighly fastidious; needs dead tissues to germinategrows anaerobically in muscle tissue, produces necrosis and noxious gases; bacteria spread to newly killed cellsGas formation and exotoxins disrupt muscle tissueTreatment – antibiotics (penicillin, clindamycin), frequent wound cleansing, hyperbaric oxygen chambers, amputationMedical emergency; mortality can be 40%

Slide31

Gas gangrene

Anaerobic

cellulitis

necrosis

is

localized

does

not infect healthy tissue

Myonecrosis

systemic infection

Higher mortality rate

Slide32

Viral skin diseases – SUMMARY SLIDE

Poxviruses

Herpesviruses

Papillomaviruses

Chickenpox/Shingles

RubellaMeaslesOther childhood diseases Erythema

Infectiosum Roseola

Slide33

Smallpox Viruses

Smallpox (

variola

)

Smallpox virus (

orthopox

virus)

Variola major has 20% mortalityVariola minor has <1% mortalityEradicated by vaccination by 1979Pre-2001, last vaccinations done in 1970sACAM 2000 is military-only vaccine for smallpox biowarfare responders; significant side effectsMonkeypoxMonkey version of small poxTransmitted through prairie dogs and African ratsPrevention by smallpox vaccination

Slide34

Smallpox Lesions

Slide35

HSV-1/HHV-1 infection

Oral Herpes

Signs and symptoms

Presence of cold

sores near lips, where nerve density is highest and skin flexing greatest

Pathogen and pathogenesis80% by human herpesvirus 1 (HHV-1); remainder HHV-2

Virions form syncytia to avoid host’s immune system

Latency established in the trigeminal nerve ganglionEpidemiologyInfections occur by casual contact in childhood (parent to child most often)80% of population has HHV-1 antibodies by age 2Later onset usually due to HHV-2Primary infections are usually asymptomatic; subsequent reinfections are less symptomatic

Slide36

Figure 23.12

Oral herpes

lesion.

Slide37

Figure 23.13 Latency and reactivation of oral herpesviruses.

Slide38

Viral Diseases of the Digestive System

Oral Herpes

Diagnosis

, treatment, and prevention

Diagnosis is based on characteristic lesions

Topical penciclovir, acyclovir, or valacyclovir limits duration of lesionsAvoid direct contact with infected individualsAcute breakouts usually self-resolve

Stress or immunosuppressive drugs can promote herpetic breakouts

Slide39

Figure 24.10 Sites of events in genital herpesvirus infections.

Note that the virus causing each of these diseases can be

the same

It only varies based on which nerve ganglion it resides

It spreads to other ganglia only though skin-to-skin contact

dentists/oral hygienists working without gloves

Thumb-sucking/nail biting

Rubbing eyes or skin without hygiene

Slide40

Figure 24.11 Herpes lesions of the eyes and skin.

Slide41

Warts,

a.k.a

papillomas

Usually r

estricted to squamous epithelium

Papillomaviruses (< 100

types now known)Seen in plantar warts, genital warts, cervical polyps and carcinomas, oral, esophageal, and penile carcinoma, and possibly acrochorda (skin tags)Prevention – vaccination for 10 subtypesTreatmentRemoval – Cryotherapy, Electrodessication, Salicylic acidImiquimod (stimulates interferon production)BleomycinTime – warts usually self-resolve

Slide42

Various appearances of HPV infections

Can appear anywhere on body

Slide43

Chickenpox

Varicella-zoster virus (human

herpesvirus

3)

Transmitted by the respiratory route

Causes

pus-filled vesicles10-20 day incubation, contagious until pustules clear in 2-3 more weeks

Before vaccination in 1995, “chickenpox parties” were held to get children sick early (less painful earlier in life)Virus infects sensory nerve endings near pox and remains there for lifeRemains dormant unless “aggravated” or immune system “forgets”Prevention: Live attenuated vaccine (95% effective)Vaccination highly recommended for adults that acquired infection naturally as children (before 1984)

Slide44

Latent Chickenpox

Breakthrough

varicella

in vaccinated

people from incomplete protection (artificial vs. natural immunity)

Improperly stored vaccine; immunodeficiency; vaccine protection wore out (> 6 years)

Attenuated virus used for vaccine (Oka strain) less immunogenic than fully active virus

Because vaccine is still partially effective, breakthrough varicella is less severe than chickenpoxVirus reactivation and reemergence in later life known as shinglesBooster now recommended even in adults who were exposed naturally to chickenpox to prevent re-emergenceProQuad = Oka + MMR for children, MMRV, young adultsZostavax for adults 60+

Slide45

Shingles

Reactivation of latent HHV-3 releases viruses that move along peripheral nerves to

skin

Semi-localized pattern corresponds to sensory innervation (dermatomes)

Painful vesicles; nerve pain

Months to resolve

Postherapeutic

neuralgiaPrevention: Live attenuated vaccine (Zostavax)Acyclovir may lessen symptoms

Slide46

Rubella (German Measles)

Rubella virus

Macular rash and fever

Congenital rubella syndrome

causes severe fetal

damage; deformities

Prevented by

vaccination (MMR)Must ensure pre-expectant mothers are vaccinated, not recommended for expectant mothers (why?)

Slide47

Measles (

Rubeola

)

Measles virus

Transmitted by respiratory route

Koplik's

spots (oral lesion), then macular-to-systemic rash

Prevented by MMR vaccination (95-97% response; second immunization is a back-up)Re-infection very rareAlmost gone from the USA; resurgences due to international travellers and refusals to vaccinate

Slide48

Complications from Measles

With improved diet and overall health in last 100 years, complications and fatalities from measles became very uncommon (pneumonia, encephalitis from cytokine response to infection in 1:100 cases)

Secondary infection –

H. influenza

,

S. pneumonia

– leads to pneumonia, URI

Subacute sclerosing panencephalitis in 1 in 1,000,000 cases – relapse by defective virus that is fatal

Slide49

Reported U.S. Cases of

Measles

1944–2005

vaccine

licensed

2° vac.

rec’d

1995

Slide50

Resurgence

of

Measles

2001–2019

2019 cases expected to peak over 1500

2019 data is January to April

Slide51

Fifth

Disease – Erythema

infectiosum

Name derived from a 1905 list of skin rashes,

that

included

1. Measles

2. Scarlet fever3. Rubella4. Filatov Dukesdisease (now known to be mild scarlet fever)5. Fifth disease, or erythema infectiosumCaused by Human parvovirus B19

B19 discovered

only in 1989

Highly contagious; placental

transmissionProduces mild flu-like symptoms and facial rash

More common in children, elderly, and

immunocompromised

Can cause stillbirths

Slide52

Roseola

,

a.k.a

exanthema

subitum

Caused by human

herpesvirus 6 (HHV-6) and 7 (HHV-7, 5-10% of cases)High fever and (afterward) rash lasting for 1–2 daysNearly 100% of population infected by adulthood, most before 5 y.o.Both viruses present in saliva of most adults

Disseminated rash caused by HHV-6 or HHV-7 can present in AIDS patients and in the immunocompromised

Slide53

Cutaneous

Mycoses

a.k.a.

dermatophytes

Dermatomycoses

Also known as

tineas

or ringwormMetabolize keratin; some can feed on sebaeDisease NAMES are in Latin – these are NOT species names!Tinea capitis – ringworm of the scalp – bald patchesTinea cruris – ringworm of the groinTinea pedia – athlete’s footTinea unguium

-

(under finger/toenails

)Tinea

barbae – barber’s itch (from animals nowadays unless you go to an unsanitary barber)Tinea

versicolor

– (

Malasezzia

yeast species) – never penetrates beyond stratum

corneum

; aggravates dandruff

or psoriasis?

Slide54

Dermatomycoses

Tinea

versicolor

Tinea

cruris

Tinea capitis

Slide55

Dermatomycoses

(c)

Tinea

unguium

(d)

Tinea

barbae

Slide56

Cutaneous Mycoses

Genera of fungi

involved in most cases (except tinea versicolor)

Trichophyton

:

Infects hair, skin, and nails

Epidermophyton: Infects skin and nailsMicrosporum: Infects hair and skinTreatmentTopical miconazole, tolnaftate, itraconazole, allylamine, terbinafine, hydrogen peroxideKeep it dry

Slide57

Protozoan skin disease -

Leishmaniasis

Caused by at least three species of

Leishmania

(

kinetoplasmid

)Transmitted by sand flies; endemic in equatorial regionsMultiplies in macrophagesRed papule in skin becomes a large ulcerTreated by chemicals or some antimicrobials to prevent secondary infections

Slide58

Scabies

Mite infection of skin tissues

Larvae feed on epidermis and trigger inflammatory response

Person-to-person spreading through sharing clothes, bedding or towels

More common in concentrated and dirty areas

May also be spread through insect bites (mechanical vector)Diagnosis – difficult – very few microscopic (0.3 mm length) adultsPrevention – clean clothing, hygiene, vaccination not possible