Ch 19: Infections of the Skin and Eye

Skin

• The largest human organ

• 16-22 square feet

• effective barrier for blocking microbial access to deeper tissues

Epidermis

• Superficial

• Five layers

• Consist of dead keratinocytes

• Keratinocytes make the structure protein—keratin

Dermis

• deep layer

• connective tissue

• blood vessels, nerves, hair follicles, sweat glands

Skin rash

• change in color and texture of the skin

• usually caused by an infectious agent, such as a virus, and represent a reaction to a toxin produced by the organism, damage to the skin by the organism, or an immune response

Exanthem

Widespread skin rash accompanied by systemic symptoms (fever, malaise, headache)

Enanthem

Rash on mucous membranes

Macular rash

• flat and red

• less than 1 cm in diameter

Papular rash

small, solid, and elevated lesion called a papule

Pustular rash

a papule filled with pus

Maculopapular rash

a reddened papule

Vesicular rash

small blisters are formed

Mucous membranes

• epithelial

• serve as a barrier (protection)

• Line the inside of the body

• Continuous with the skin in several places

• Not all produce mucous

External structures of the eye

• eyelids, cornea, lens, iris, pupil, sclera

• covered with conjunctiva

Internal structures of the eye

retina, macula, vitreous humor

Measles/Rubeola/first disease

• Viral infection of the skin

• Negative-sense, single stranded RNA virus

• very contagious (8-10 day incubation period)

Measles/Rubeola/first disease portal of entry

• respiratory or conjunctiva

• Replicates in the lungs

  • moves to regional lymph nodes

  • produces a viremia (virus in blood) that spreads throughout the body

Measles/Rubeola/first disease symptoms

• prodromal period starts with cold/flu-like symptoms

• high fever (104 F)

• Koplik’s spots: white spots on the buccal mucosa (inner cheeks), only in measles

• maculopapular rash

• tiredness, low appetite, conjunctivitis, descending rash

German Measles/Rubella/Third Disease

• Viral infection of the skin

• Also called 3-day measles, rash similar to measles

• pronounced eliminated from the US in 2004 but still endemic in many parts of the world

German Measles/Rubella/Third Disease portal of entry

• inhalation of aerosolized respiratory particles

• replicates in the cytoplasm of cells lining the nasopharynx and nearby lymph nodes

• viremia ensues during the 12-23 day incubation period

German Measles/Rubella/Third Disease symptoms

• Pinpoint maculopapular pink rash caused by host immune response

  • appears on head and spreads to the body and extremities

  • does not darken or scab over

  • spreads fast

  • short duration of 1-3 days

• Low grade fever

• enlargement of head and neck lymph nodes

• mild, subclinical, and self limiting

  • more difficult in adults and can lead to joint pain, bacterial superinfections, birth defects

• MMR vaccine

Fifth Disease/Erythema Infectiosum

• Viral infection of the skin

• Human parvovirus B19

Fifth Disease/Erythema Infectiosum portal of entry

• respiratory tract

• viral attachment to and replication in erythrocyte progenitor cells

• viremia within 7-10 days

• bind P antigen (globoside, on the surface of RBCs and their progenitors

• The body responds by producing antibodies and cytokines (TNF-a, IFN-y, and interleukins 2-6)

Fifth Disease/Erythema Infectiosum Symptoms

• Prodromal symptoms coincide with viremia

  • mild fever, flu-like symptoms, arthralgia (joint pain)

• initial rash is pathogenomic (specific to fifth disease)

• Often described as a slapped-cheek rash

• rash followed by a red or gray papular enanthem on the palate or throat

• Third stage is a maculopapular rash that forms on body and limbs

  • looks like lace (reticular rash)

Roseola Infantum/Sixth Disease

• viral infection of the skin

• human herpes virus 6/7 (HHV-6; HHV-7)

• young children usually under 3 years

Roseola Infantum/Sixth Disease Transmission

• respiratory secretions or saliva

Roseola Infantum/Sixth Disease Symptoms

• 3-5 days of very high fever (over 104 F)

• Fever followed by sudden macular or maculopapular red rash that blanches (turns white) when touched

• Latent (hidden) in most people

Chickenpox

• viral infection of the skin

• Herpesviridae family

• Varicella-Zoster virus (VZV)

• initial exposure=chickenpox

  • virus remains latent in the dorsal root ganglia and re-emerges later in life in about 20% of patients which causes shingles (herpes zoster)

• Shingles occurs more often in older people because their cell-mediated immunity decreases

• Chickenpox and shingles are usually diagnosed clinically, but antibody and DNA tests can also be used to detect the virus

Chickenpox portal of entry

• inhalation of infected particles from skin lesions

• virus replicates in nasopharynx and infects the regional lymph nodes, leading to viremia

• 2nd round of replication occurs in liver and spleen followed by a secondary viremia 14-16 days postinfection

• VZV invades capillary endothelial cells in the deepest layer of epidermis which produces fluid accumulation and vesicle formation

Chickenpox symptoms

• usually no prodromal symptoms

• itchy rash on the face, back, chest, and belly

• maculopapules, vesicles, pustules, and scabs

Chickenpox latency

• can be life-threatening in immunocompromised patients

• latency established when viral DNA integrates into host DNA

• can last for decades

• virus infects the nerve endings of the skin

• travel along nerves to the ganglia where they lie in a dormant state

• Latent Virus reactivation: virus particles travel along the sensory nerves of the skin to produce a localized, painful, dermatomal rash known as shingles

Chickenpox treatment

• antihistamines, oatmeal baths, and calamine lotion to reduce intense itching

• acetaminophen to reduce pain and fever

• Acyclovir: used to treat shingles and severe cases of chickenpox

• Varicella vaccination: routine immunization in childhood, live attenuated form of VZV

• People 60 years and older should be vaccinated with zoster vaccine to prevent shingles

Cold sores and genital herpes

• viral infection of the skin

• Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2)

• infects skin and mucous membranes

  • able to infect CNS and occasionally the visceral organs

Cold sores and genital herpes transmission

• direct contact and replicates in mucosal surfaces or epidermis

  • final destination is the neuronal cell in the ganglia where the virus becomes latent

• Primary infection may be subclinical or symptomatic

• reactivation of the latent virus always results in symptoms

• severity and recurrence is dictated by the immune status of the person infected

Cold sores

• primarily caused by HSV-1 which is very contagious

• Is present in the active or latent form in 60-90% of older adults

• No vaccine for HSV-1

• Spread from person to person contact

Genital herpes

• primarily caused by HSV-2

• sexually transmitted disease

• Tissue distribution of HSV-1 and 2 is not absolute: HSV-1 can infect genital skin and mucosa and HSV-2 can infect the oral tissue

Cold Sores and genital herpes treatment

• Antiviral medications

  • acyclovir, valacyclovir, and famciclovir used during primary infections

  • reduce pain and duration of lesions

  • decrease viral shedding (passing it to someone else)

  • reactivation can be treated with a topical antiviral

Warts

• viral infection of the skin

• caused by human papilloma virus (HPV) of the family Papillomaviridae

• tissue controlled: not same on hands and feet

Warts transmission

• transmitted by contact

• enters cell via an endosome by a receptor-mediated mechanism

• HPV DNA leaves endosome and enters the nucleus

• Viral proteins interfere with cell proliferation controls

  • infected cell replicates uncontrollably, producing warts

Warts treatment/prevention

• freezing, burning, surgical removal

• vaccines are available, must be administered before recipient is sexually active to ensure effectiveness

Warts subtypes

• HPV-6 and HPV-11 infect mucous membranes of ano-genital region

  • 90% of genital warts (condyloma acuminata)

• HPV subtypes 16 and 18 have more serious consequences

  • linked to 70% of human cervical cancers

Smallpox (Variola)

• viral infection of the skin

• only known reservoir is humans

• eradicated from population in 1979

• Member of Poxviridae family

• Virus is divided into two variants

  • Variola major: severe, 30% fatality

  • Variola Minor: 1% fatality rate

• Variants very similar to each other and to another virus called the vaccinia virus (cowpox)

  • used to make a vaccine against smallpox

Smallpox (Variola) treatment/prevention

• Diagnosis can be made based on viral cultures and serology

• No FDA approved treatments

• We no longer vaccinate against smallpox

  • government officials have stockpiled vaccine in strategic centers across U.S.

Staphylococcal skin infections

• staphylococcus epidermis

• staphylococcus aureus

  • normal inhabitant of the nares (nose)

  • Can infect a cut and gain access to dermis via a hair follicle

• Require surgical drainage and antibiotic therapy

Staphylococcus aureus

• possess enzymes that contribute to disease

  • Coagulase

• Exotoxins damage host tissue and weaken host defenses

  • Toxic shock syndrome toxin (TSST)

  • Exfoliative toxin

Coagulase

• enzyme in Staphylococcus aureus

• coats the bacteria with fibrin and walls off the infection from the immune system and antibiotics, promoting abscess formation

Toxic shock syndrome toxin (TSST)

• a strain of Staphylococcus aureus

• superantigen causes toxic shock syndrome

• Superantigen can cause serious disease

Exfoliative toxin

• a strain of Staphylococcus aureus

• superantigen causes a blistering condition in children called scalded-skin syndrome

Folliculitis

• Staphylococcus aureus infection of hair follicles

• superficial

• resolve on their own

Boil or furuncle

• Staphylococcus aureus infection of hair follicles

• deep

• red, painful, swollen skin mass

• Carbuncles: boils joined together

  • need surgery/antibiotics

Methicillin-resistant S. aureus (MRSA)

• Staphylococcal bacterial skin infection

• strain that has emerged over the past decade

• resistant to antibiotic methicillin (interfering with cell wall synthesis)

Methicillin-resistant S. aureus (MRSA) treatment

• Vancomycin

• first appeared as a nosocomial infection (originating in a hospital)

• Today, MRSA is no longer confined to the hospital; “community acquired infections”

Streptococcus pyogenes

• streptococcal bacteria skin infections

• human nasopharynx and parts of the skin are the natural reservoir for S.pyogenes

Necrotizing fasciitis (flesh-eating disease)

• streptococcal skin infection

• Type 1: polymicrobial

• Type 2: one microorganism, usually S.pyogenes, sometimes S.aureus

Necrotizing fasciitis (flesh-eating disease) treatment

• therapy includes antibiotics

  • clindamycin, metronidazole, and gentamicin

• incidence has risen recently due to increased use of NSAIDS

Streptococcus pyogenes virulence factors

• capsule: helps organism avoid phagocytosis

• Pilus-like M protein: Binds complement regulatory protein (factor H)

• Lipoteichoic acid: cell wall component that facilitates adherence to host cells

• Streptolysins: lyse blood cells

• Enzymes that degrade: DNA (DNAse), fibrin (streptokinase), and connective tissue (hyaluronidase), making pus less viscous

• Peptidoglycan: activates the alternative complement pathway and a MAMP that binds NOD-like receptors, causing inflammation

Streptococcal pyogenic exotoxins (SPEs)

• superantigens; massive amounts of cytokines released in response to SPEs can produce high levels of inflammation and lead to shock

• SPEs are associated with scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis

Hemolysin

• Lyses RBCs

• These streptococci are subclassified into groups A-O according to cell wall antigens

• S. pyogenes is the main pathogen among group A streptococci (GAS)

Rheumatic fever

• Can develop after the resolution of a primary GAS infection

• Sequela is the result of immunological cross-reactivity between specific GAS M protein antigens and host antigens

• Autoreactive B cells activated by the bacterial M protein antigen make antibodies against cardiac antigen

  • trigger an inflammatory reaction that damages those tissues

Fungi

• includes molds and yeasts

• Eukaryotic microbe

• Filamentous or single-celled

Dermatophytes

• love human skin

• Cool, moist, keratinized tissues (skin, hair follicles, nails)

• enter epidermis and cause inflammatory response

• Epidermophyton, Trichophyton, and Microsporum cause the majority of infections

Fungal infections of the skin

• Named after location in the body

• Tinea-gnawing worm

• Tinea capitis: scalp

• Tinea corporis: body

• Tinea cruris: jock itch

• Tinea pedis: foot

• Tinea unguium: nails

Candida

• fungal infection of the skin

• candida species

• dimorphic yeasts

• part of normal flora of the GI tract, vaginal tract, oral cavity, and skin

• immunocompromised are more susceptible

Candida albicans

• can infect:

  • the skin

  • mucous membranes

  • body organs

Candidal intertrigo

• fungal infection of skin

• infected areas where the skin touches and rubs together such as between fingers, under the arm, or groin

Fungal infections diagnosis

• clinical appearance

• microscopic examination of potassium hydroxide (KOH) preparations of skin flakes or hair

  • the KOH destroys skin cells but not the more resilient walls of mycelia or spores, which can be seen under a light microscope

• Fungi can also be cultures on a special selective medium called Sabouraud agar

Fungal infections treatment

• antifungal medications

• imidazole compounds such as clotrimazole are most common and can be purchased over the counter

Conjunctivitis

• just describing the appearance

• “pink eye”

• inflammation of conjunctiva

• can be due to infection, trauma, or an allergic reaction

Keratitis

• inflammation of the cornea

• corneal destruction by a bacterial infection

• can be sight threatening

Endophthalmitis

• infection of inner structures

• uncommon and almost always results from direct spread of a superficial eye infection or seeding the infection with bacteria carried by blood

Herpes Zoster Opthalmicus

• outbreak of shingles along the ophthalmic division (eye to tip of nose) of the trigeminal nerve

• Results in eruption of vesicular lesions on forehead, eyelids, nose, and may even spread to eye itself

• Causes corneal inflammation, eye pain, and sensitivity

Herpes Zoster Opthalmicus treatment

treated with oral medications such as acyclovir, valacyclovir, and famciclovir

Bacterial conjunctivitis

• affects one eye and is acute, painful, and purulent (pus being formed)

• Pyogenic bacteria such as staph and strep cause marked irritation and a stromgy, opaque, grayish or yellowish mucopurulent discharge that may caue the lids to stick together

• Chlamydia trachomatis and Neisseria gonorrheae cause serious infections of the reproductive system; also cause the majority of acute bacterial conjunctivitis