Skin

MICROBIAL DISEASES OF THE SKIN AND EYES

Skin

Salt inhibits microbes.

Lysozyme hydrolyzes peptidoglycan.

Fatty acids inhibit some pathogens.

Defensins are antimicrobial peptides.

Figure 21.1

Mucous Membranes

Line body cavities. The epithelial cells are attached to an

extracellular matrix. Cells secrete mucus. Some cells have cilia.

Normal Microbiota of the Skin Gram-positive,

salt-tolerant bacteria Staphylococci Micrococci Diphtheroids

Malassezia furfur

Figure 14.1a

Microbial Diseases of the Skin Exanthem: Skin rash arising from another

focus of the infection.

Enanthem: Mucous membrane rash arising from another focus of the infection.

Microbial Diseases of the Skin

Figure 21.2

Staphylococcal Skin InfectionsStaphylococcus aureus S. epidermidis

Gram-positive cocci and coagulase-positive

LeukocidinExfoliative toxinEnterotoxin

Gram-positive cocci and coagulase-negative Slime layer

Nosocomial infection (surgical wound and breaks)

Transmitted thru medical procedure

StreptococcusStaphylococcus

Staphylococcal Biofilms

Figure 21.3

S. aureus

Coagulase

Fibrinogen Fibrin

Differential Characteristics

Mannitol Salts Agar (MSA)

Staphylococcus aureus

Staphylococcal Skin Infections

POE Skin , hair follicle

s/sx Folliculitis: Infections of the hair follicles.Sty: Folliculitis of an eyelash.Furuncle (Boil): Abscess; pus surrounded by inflamed tissue.Carbuncle: Inflammation of tissue under the skin

MOT Direct contact, fomite and endogenous infection

Tx Drainage Antibiotics: Penicillin

Clinical Manifestations/Disease

SKIN folliculitis boils (furuncles) carbuncles

Folliculitis

Furuncles (boil)

Staphylococcal Skin Infections

POE Skin (Nursery)

s/sx Impetigo Thin walled vesicles that ruptures and later crust over

MOT Direct contact, fomites

Tx Potassium Iodide Solution, HexachloropheneAntibiotics: Penicillin

Clinical Manifestations/Disease

impetigo (bullous & pustular)

scalded skin syndrome• Neonates and children under 2years

Impetigo

Staphylococcal Skin Infections Scalded skin

syndrome Bright red lesions

that easily peels off in sheets

Exfoliative toxin Antibiotic tx Part of Toxic Shock

Syndrome TSS

Figure 21.4

Staphylococcal scalded skin syndrom (SSSS)

Dermonecrotic toxin (exfoliative toxin)Bullous exfoliative dermatitis

Clinical Manifestations/Disease Other infections

Primary staphylococcal pneumonia Food poisoning vs. foodborne disease Toxic shock syndrome

Toxic shock syndrome

Toxic shock syndrome toxin (TSST-1)

Super antigenProduced by 5-25% isolatesTampon or infected wound

FeverRashExfoliation of skinShock (death rate 3%)

Staphylococcal Skin Infections

POE Skin , SURGICAL INCISION

s/sx Toxic Shock SyndromeFever RashExfoliative skinShock |(3% death rate)

MOT Endogenous infection (tampoons and infected wound)

Tx Antibiotics: Penicillin

Metastatic Infections

•Bacteremia

•Osteomyelitis disease of growing bone Pulmonary and cardiovascular infection

Streptococcal Skin Infections Streptococcus

pyogenes Group A beta-

hemolytic streptococci

M proteins

Figure 21.5

Streptococcus pyogenes

Local infections Impetigo Erysipelas Cellulitis Necrotizing fasciitis (flesh-eating bacterium)

Systemic effect Streptococcal toxic shock-like syndrome

(STSS) Spe (similar to TSS by S. aureus)

Scarlet fever (pyrogenic toxin by lysogenized ) Post-infection

Rheumatic fever (associated with pharyngitis) Glomerulonephritis

Invasive Group A Streptococcal Infections

M protein Streptokinases Hyaluronidase Exotoxin A, superantigen Cellulitis Necrotizing fasciitis

Figure 21.8

Virulence factors

Adhesins M protein (fibrillar Ag) Fibronectin binding proteins (Protein F) Lipoteichoic acid (LTA)

Hyaluronic acid capsule Invasins

Streptolysins (S & O) Hyaluronidase Streptokinases

activates blood clot dissolving protein-plasminogen (human specific)

Dnase

Exotoxins Pyrogenic (erythrogenic) toxin - Spe

Scarlet fever Toxic shock syndrome

Streptococcal Infections

POE Skin abrasion

s/sx Necrotizing FascitisExtensive soft tissue destruction

MOT Direct contact

Tx Surgical removal of tissue Antibiotics: Penicillin

S. pyogenesNecrotizing

fasciitisScarlet Fever

Streptococcal Infections

POE Skin and mucous mebrane

s/sx Erysipelas reddish pathes on skin, often with high fever

MOT Endogenous infection

Tx Antibiotics: Penicillin

Streptococcal Skin Infections Erysipelas

Impetigo

Figures 21.6, 21.7

Erysipelas

NOTE:

Ö erythema

Ö bullae

Erysipelas

Caused by group A streptococci, is characterized by raised, bright-red plaques with sharply defined borders.

Cellulitis

Pseudomonas Infections

POE Skin abrasion

s/sx Pseudomonas dermatitisSuperficial rash

MOT Swimming water, hot tub, Endogenous infection

Tx Usually self limitingAntibiotics:

Infections by Pseudomonads

Pseudomonas aeruginosa Gram-negative, aerobic rod Pyocyanin produces a blue-green pus

Pseudomonas dermatitis Otitis externa Post-burn infections

Pseudomonas Infections

POE ears

s/sx Otitis externaSuperficial infection of external ear; reddish, tender and swelling

MOT Swimming water

Tx Antibiotics: Flouroquinolones

Acne

Comedonal acne occurs when sebum

channels are blocked with shed cells.

Inflammatory acne

Propionibacterium acnes

Gram-positive, anaerobic rod

Treatment

Preventing sebum formation (isotretinoin)

Antibiotics

Benzoyl peroxide to loosen clogged follicles

Visible (blue) light (kills P. acnes)

Propionibacterium Infections

POE Sebum channels

s/sx Acne Inflammatory lesion originating with accumulation of sebum that rupture a hair follicle

MOT Direct contact

Tx Benzoyl peroxideIsotrenitoin , azelaic acid

Acne

Inflammatory acne (continued) Nodular cystic acne

Treatment: isotretinoin

Skin and other infections

Staphylococcus aureus Skin, food poisoning, osteomyelitis, kidney

abscess, endocarditis Streptococcus pyogenes

Skin, pharyngitis and blood stream Botulinum

Wound, food & infant C. perfringens

Skin and diarrhea Anthrax

Cutaneous, respiratory & GI

Gas gangrene (Clostridium perfringens)

Alpha toxin (phospholipase C)

Zinc metallophospholipase hemolysis and bleeding

Gas formation

Myonecrosis, shock, renal failure and death

Clostridial Cellulitis

Micro & Macroscopic C. perfringens

NOTE: Large rectangular gram-positive bacilli

Inner beta-hemolysis = θ toxin Outer alpha-hemolysis = α

toxin

NOTE: Double zone of hemolysis

Alpha toxin

Treatment Debridement and excision Antibiotics (prevent further spreading) Hyperbaric oxygen therapy

Inhibit or kill the anaerobic bacteria

Epidemiology of Bacillus anthracis Rare in the US (1974-1990, 17 cases

reported by CDC) Enzootic in certain foreign countries (e.g.,

Turkey, Iran, Pakistan,and Sudan) Anthrax spores infectious for decades

• Biologic warfare experiments (annual tests for 20 years)

Three well-defined cycles• Survival of spores in the soil• Animal infection• Infection in humans

Epidemiology of Bacillus anthracis (cont.)

• Primarily a disease of herbivorous animals

• Most commonly transmitted to humans by direct contact with animal products (e.g., wool and hair)

• Also acquired via inhalation & ingestion• Increased mortality with these portals of

entry

Epidemiology of Bacillus anthracis (cont.)

• Still poses a threat• Importing materials contaminated with

spores from these countries (e.g., bones, hides, and other materials)

• Usually encountered as an occupational disease

• Veterinarians, agricultural workers

Cutaneous Anthrax

Day 4Day 5

Day 7

Day 12

Bacilllus anthracisG+ and spore formingFarm animals are major

reservoirInhalation, GI, cutaneous

Cutaneous Anthrax

Day 4

Day 5

Day 7

Day 12

Bacilllus anthracisG+ and spore formingFarm animals are major

reservoirInhalation, GI, cutaneous

Virulence factors:CapsulesEdema factorLethal factor

VaccineToxoid (protective antigen)Effective in short term but not

long term

Clinical Presentation of Anthrax 95% human cases are cutaneous infections

1 to 5 days after contact –

Small, pruritic, non-painful papule

hemorrhagic vesicle & ruptures

Slow-healing painless ulcer with black eschar surrounded by edema

Infection may spread -- Septicemia -- 20% mortality

Other Skin and Mucus Membrane Infections Staphylococcus epidermidis

Catheters and prostheses Vibrio vulnificus

From shellfish and salt water Obligate anaerobes (usually polymicrobic and foul

smelling) Puncture wounds Deep wounds Impaired blood supply

Gram negative bacteria Decubitus ulcer (bed sores) After intestinal “spill”

Pseudomonas aeruginosa Catheters and prostheses Burns and Surgical wounds

VIRAL SKIN INFECTION

Warts

Papillomaviruses Treatment

Removal Imiquimod (stimulates interferon production) Interferon

WART

agent

Viral- Papilloma sp.

POE Skin

s/sx Horny projection of the skin formed by proliferation of skin

MOT Direct contact

Tx Liquid nitrogen cryotherapyElectrodessication, acids and lasers

HPV and skin warts

(From Fields Virology, 4th ed, Knipe & Howley, eds, Lippincott Williams & Wilkins, 2001, Table 66-3.)

Poxviruses

Smallpox (variola)

Smallpox virus

(orthopox virus)

Variola major has 20%

mortality

Variola minor has <1%

mortality

Monkeypox

Prevention by smallpox

vaccination Figure 21.9

SMALLPOX

agent

Viral- Smallpox (variola) sp.

POE Respiratory tract

s/sx Pustules that may be nearly confluent on skin

MOT Aerosol

Tx None

Note in this slide that the density of the rash is greater on the face than on the body.

Pocks are usually present on the palms of the hands and on the soles of the feet.

Distinguishing features of Smallpox from other rashes

Monkeypox an emerging disease

Monkeypox – an indigenous virus of

equatorial Africa Although not a virus of humans, the clinical

symptoms are indistinguishable from smallpox.

Lethality is only slightly less than smallpox. Although not as efficient as smallpox,

Human to human transmission has been well documented

Monkeypox should perhaps be considered a bioterrorist agent

In smallpox, fever is present for 2 to 4 days before the rash begins, while with chickenpox, fever and rash develop at the same time.All the pocks of the smallpox rash are in the same stage of development on any given part of the body and develop slowly. In chickenpox, the rash develops more rapidly, and vesicles, pustules, and scabs may be seen at the same time.

Herpesviruses•Herpes simplex I & II (cold sores, genital herpes)

•Varicella zoster (chicken pox, shingles)

•Cytomegalovirus (microcephaly, infectious mono)

•Epstein-Barr virus (mononucleosis,Burkitt’s lymphoma)

•Human herpesvirus 6 & 7 (Roseola)

•Human herpesvirus 8 (Kaposi’s sarcoma)

Herpesviruses

Varicella-zoster virus (human herpes virus 3)

Transmitted by the respiratory route

Causes pus-filled vesicles

Virus may remain latent in dorsal root ganglia

Figure 21.10a

CHICKENPOX (VARICELLA)

agent

Viral- Varicella zoster

POE Respiratory tract

s/sx Vesicles ; face, throat and lower back

MOT Aerosol

Tx Pre- exposure vaccinesAnti-viral agents Acyclovir for immunocompromised patients

Zoster

Neonatal Varicella

Varicella Vaccine

•Prevents 40 - 70% of chickenpox occurrence

•Greatly reduces the severity in the rest

•Attenuated virus

•Can still establish latency and reactivate

SHINGLES (HERPES ZOSTER)

agent

Viral- Varicella zoster

POE Endogenous infection of peripheral nerves

s/sx Vesicles on one side of the waist, face, scalp and upper chest

MOT Recurrence of latent chickenpox infection

Tx Preventive vaccinesAnti-viral agents Acyclovir for immunocompromised patients

Shingles

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

Figure 21.10b

Zoster

Virus Subfamily Disease Site of Latency

Herpes Simplex Virus I a Orofacial lesions Sensory Nerve Ganglia

Herpes Simplex Virus II a Genital lesions Sensory Nerve Ganglia

Varicella Zoster Virus a Chicken Pox Sensory Nerve Ganglia Recurs as Shingles

Cytomegalovirus b Microcephaly/Mono Lymphocytes

Human Herpesvirus 6 b Roseola Infantum CD4 T cells

Human Herpesvirus 7 b Roseola Infantum CD4T cells

Epstein-Barr Virus g Infectious Mono B lymphocytes, salivary

Human Herpesvirus 8 g Kaposi’s Sarcoma Kaposi’s Sarcoma Tissue

Human Herpesviruses

Herpes Simplex 1 and Herpes Simplex 2 Human herpes virus 1 and HHV-2 Cold sores or fever blisters (vesicles

on lips) Herpes gladiatorum (vesicles on

skin) Herpes whitlow (vesicles on fingers) Herpes encephalitis (HHV-2 has up

to a 70% fatality rate)

Herpes Simplex 1 and Herpes Simplex 2 HHV-1 can remain latent in

trigeminal nerve ganglia. HHV-2 can remain latent in sacral

nerve ganglia. Acyclovir may lessen symptoms.

Tissue tropism of HSV-1 and HSV-2HSV-1:

•Causes 95% of orofacial herpes (remainder caused by HSV-2)

•Causes 10 - 30% of primary genital herpes (but seldom recurs there)

HSV-2:

•Causes primary and recurrent genital herpes infections

•May cause primary oral herpes but, like HSV-1 in genital area, it seldom recurs there

HERPES SIMPLEX INFECTION

agent

Viral- Herpes simplex virus type 1

POE Skin mucous membrane

s/sx Vesicles around mouth; can also affect other areas of skin and mucous membranes

MOT Initial infection by direct contact, Recurrent latent infection

Tx Anti-viral agents Acyclovir may modify symptoms

Cold Sores

Eczema/Herpes

Herpes Simplex Virus type 2

•Infects the genital tract

•Is sexually transmitted

•Complicates childbirth

ROSEOLAAgent

Human Herpes virus 6, 7

POE Respiratory tract

S/Sx High fever followed by a macular body rash

MOT Aerosol

Tx No treatment

Roseola

Measles (Rubeola)

Measles virus Transmitted by respiratory

route. Macular rash and Koplik's

spots. Prevented by vaccination. Encephalitis in 1 in 1,000

cases. Subacute sclerosing

panencephalitis in 1 in 1,000,000 cases.

Figure 21.14

MEASLES (RUBEOLA)

agent

Measles virus

POE Respiratory tract

s/sx Skin rash of reddish macules first appearing in the face and spreading to the trunk and extremities

MOT Aerosol

Tx Pre exposure vaccinesNo treatment

Measles induced syncytia

Formation of giant cells (syncytia) in measles pneumonia. Notice the eosinophilic inclusions in both the cytoplasm and nuclei. (From Schaechter’s Mechanisms of Microbial Disease; 4th ed.; Engleberg, DiRita & Dermody; Lippincott, Williams & Wilkins; 2007; Fig. 34-3)

Measles pathogenesis

Mechanisms of spread of the measles virus within the body and the pathogenesis of measles. CMI, Cell-mediated immunity; CNS, central nervous system. (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-3.)

Measles time course

Time course of measles virus infection. Characteristic prodrome symptoms are cough, conjunctivitis, coryza, and photophobia (CCC and P), followed by the appearance of Koplik's spots and rash. SSPE, Subacute sclerosing panencephalitis. (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-4.)

Koplik’s spots

Koplik's spots in the mouth and exanthem. Koplik's spots usually precede the measles rash and may be seen for the first day or two after the rash appears. (Courtesy Dr. J.I. Pugh, St. Albans; from Emond RTD, Rowland HAK: A color atlas of infectious diseases, ed 3, London, 1995, Mosby.) (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-5.)

Measles rash

Measles rash. (From Habif TP: Clinical dermatology: Color guide to diagnosis and therapy, St Louis, 1985, Mosby.) (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-6.)

Rubella (German Measles)

Rubella virus Macular rash

and fever Congenital

rubella syndrome causes severe fetal damage.

Prevented by vaccination

Figure 21.15

GERMAN MEASLES (RUBELLA)

agent

Rubella virus

POE Respiratory tract

s/sx Mild macular lesion with a rash resembling measles, but less extensive and disappear in 3days or less

MOT Aerosol

Tx Pre exposure vaccinesNo treatment

Rubella virusPathogenesis• respiratory transmission• replication in cytoplasm; budding• Viremia • Mild rash in adults; congenital rubella

syndrome (CRS) after infection in first trimester when virus passes the placenta and infects fetus

• CRS- deafness, blindness, mental retardation

RUBELLAPATHOPHYSIOLOGY

Transmission is by respiratory droplets

Respiratory tract -->cervical lymph nodes-->hematogenous dissemination

Incubation period is 2 to 3 weeks

RUBELLACLINICAL MANIFESTATIONS Malaise Headache Myalgias and arthralgias Post-auricular adenopathy Conjunctivitis NON-PRURITIC, ERYTHEMATOUS,

MACULOPAPULAR RASH

RUBELLACLINICAL MANIFESTATIONS

RUBELLACLINICAL MANIFESTATIONS

A 1905 list of skin rashes included (1)measles, (2)scarlet fever, (3)rubella, (4)Filatow-Dukes (mild scarlet fever), and (5)Fifth Disease: Erythema infectiosum

Human parvovirus B19 produces milk flu-like symptoms and facial rash.

Roseola Human herpesvirus 6 causes a high fever and

rash, lasting for 1-2 days.

Parvovirus

Structure Small (5 kb) linear ssDNA genome, naked capsid

Pathogenesis respiratory transmission replication in nucleus, very host dependent, needs S phase cells or

helper virus viremia antibody important in immunity targets erythroid lineage cells; fifth disease (symptoms

immunological); transient aplastic crisis; hydrops fetalis Diagnosis

serology, viral nucleic acid Treatment/prevention

none

FIFTH DISEASE(ERYTHEMA INFECTIOSUM)agent

Human Parvovirus B19

POE Respiratory tract

s/sx Mild disease with a macular facial rash

MOT Aerosol

Tx No treatment

From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 56-3.

Parvovirus pathogenesis

A "slapped-cheek" appearance is typical of the rash for erythema infectiosum.(From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 56-5.)

Parvovirus pathogenesis

PARVOVIRUSERYTHEMA INFECTIOSUM

Coxsakie Viral infection

Hand and mouth disease

FUNGAL SKIN INFECTION

Cutaneous Mycoses

Dermatomycoses: Tineas or ringworm Metabolize keratin Trichophyton: Infects hair, skin, and nails Epidermophyton: Infects skin and nails Microsporum: Infects hair and skin Treatment

Oral griseofulvin Topical miconazole

TINEA

Ringworm (moth)

RINGWORM (TINEA)Agent

Microsporium, Trichophyton, Epidermophyton

POE Skin

S/Sx Highly varied lesion on scalp that may cause local hair loss

MOT Direct contact, fomites

Tx Griseofulvin(orally), Miconazole, Clorimazole(topically)

Tinea corporis(the body)

Tinea pedis(feet)

Tinea unguium(nails)

Tinea capitis(scalp)

Tinea cruris(jock itch)

Tinea barbae(bearded area)

Tinea versicolor

(Spaghetti and meatballs)

Ecology of Dermatophytes

To determine the source of infection Anthropophilic

Zoophilic Geophilic

ANTHROPOPHILICAssociated with humans only. Person -to-person transmission through contaminated objects (comb, hat, etc.)

ZOOPHILIC

Associated with animals. Direct transmission to humans by close contact with animals.

GEOPHILIC

Usually found in soil. Transmitted to humans by direct exposure.

GEOGRAPHIC DISTRIBUTIONWorldwide

Dermatophytes3 Genera

TrichophytonMicrosporumEpidermophyton

Trichophyton (19 species)

Hair SkinNails

Trichophyton species

Large, smooth, thin wall, septate, pencil-shaped

TRICHOPHYTON RUBRUM

Causes a chronic infection in patients with a cell-mediated immune defect.(most common in SC blacks)

Microsporum(13 species)

Skin Hair

Microsporum species

Thick wall, spindle shape, multicellular

MICROSPORUM CANIS

.

Most common etiologic agent of tinea in SC whites

Epidermophyton floccosum

SkinNails

Epidermophyton floccosum

Bifurcated hyphae with multiple, smooth, club shaped macroconidia (2-4 cells)

Therapy

Griseofulvin Tinactin Clotrimazole Miconazole Ketoconazole Itraconazole Terbinafine

Dermatophytid Reaction(ID)

Dermatophyte infection on feet (not clinically evident)

Ringworm Lesion on hand

(usually the dominant side)

Dermatophytid Reaction(ID)

Culture skin scrapings from feet

Treat the tinea pedis

The hand lesion (ID phenomenon) will respond to therapy of the foot.

Dermatophyte Culture

Cutaneous Mycoses

Figure 21.16

Subcutaneous Mycoses

Sporotrichosis Sporothrix schenckii enters puncture wound Treated with KI

SPOROTRICHOSIS

Primarily a disease of the cutaneous tissue and lymph nodes. Recently, pulmonary disease.

SPOROTRICHOSISAgent

Sporothrix schenckii

POE Skin abrasion

S/Sx Ulcer at site of infection spreading into nearby lymphatic vessels

MOT Soil

Tx Potassium iodide solution (orally)

PORTALS OF ENTRY

Inhalation Inoculation

ECOLOGICAL ASSOCIATIONS

Rose thorns Sphagnum moss Timbers Soil

SPOROTRICHOSIS

Tinea corporis Subcutaneous

infections - produce chronic inflammatory disease of subcutaneous tissues and lymphatics.

sporotrichosis - ulcerated lesions at site of inoculation followed by multiple nodules - caused by a dimorphic fungus: Sporotrix schenckii.

Subcutaneous mycoses

DRUGS OF CHOICE

CUTANEOUS OR SYSTEMIC FORM

Itraconazole

Candidiasis

Candida albicans (yeast) Candidiasis may result from suppression

of competing bacteria by antibiotics. Occurs in skin; mucous membranes of

genitourinary tract and mouth. Thrush is an infection of mucous

membranes of mouth. Topical treatment with miconazole or

nystatin.

CANDIDIASISAgent

Candida albicans

POE Skin, mucous membrane

S/Sx Infected skin bright red

MOT Direct contact, endogenous infection

Tx Miconazole, Clorimazole(topically)

Candidiasis

Figure 21.17

Candidiasis

Risk factors for candidiasisPost-operative statusCytotoxic cancer

ChemotherapyAntibiotic therapyBurnsDrug abuseGastrointestinal damage. Cutaneous

Thrush

Chronic mucocutaneous candidiasis

• given to a group of overlapping syndromes that have in common a clinical pattern of persistent, severe, and diffuse cutaneous candidal infections.

• These infections affect the skin, nails and mucous membranes.

SCABIES & PEDICULOSISAgent

Sarcoptes scabiei (mites)Pediculosis humanus capitis (lice)

POE Skin

S/Sx Scabies- papulesPediculosis – itching

MOT Scabies- direct contactPediculosis- direct contact, fomites (beddings & combs)

Tx Scabies- Gamma benzene hexachloride, permethrinPediculosis- Topical insecticide solution

Scabies

Sarcoptes scabiei burrows in the skin to lay eggs

Treatment with topical insecticides

Figure 21.18

Pediculosis

Pediculus humanus capitis (head louse)

P. h. corporis (body louse) Feed on blood. Lay eggs (nits) on

hair. Treatment with

topical insecticides.

Figure 21.19

Macular Rashes

A 9-year-old girl with a history of cough, conjunctivitis, and fever (38C) has a mcular rash that starts on her face and neck and is spreading to the rest of her body. Can you identify the cause of her symptoms Measles Rubella Fifth disease Roseola Candidiasis

BACTERIAL INFECTIONDis. Conjuctivitis Neonatal gonococcal

ophthalmiaAgent

Haemophilus influezae

Neisseria gonorrhea

POE Conjunctiva Conjunctiva

S/Sx Redness Acute infection with much pus formation

MOT Direct contact and fomites

Through birth canal

Tx None Silver nitrate, tetracycline, Erythromycin for prevention

Bacterial Diseases of the Eye Conjunctivitis (pinkeye)

Haemophilus influenzae

Various microbes

Associated with unsanitary contact lenses

Neonatal gonorrheal ophthalmia Neisseria gonorrhoeae

Transmitted to a newborn's eyes during passage

through the birth canal.

Prevented by treatment of a newborn's eyes with

antibiotics

BACTERIAL INFECTIONDis. Inclusion Conjuctivitis Trachoma

Agent

Chlamydia trachomatis

Chlamydia trachomatis

POE Conjunctiva Conjunctiva

S/Sx Swelling of the eyelid; mucus and pus formation

Conjunctivi tis

MOT Through birth canal; swimming pools

Direct contact, fomites and flies

Tx Tetracyline Azithromycin

Chlamydia trachomatis

Bacterial Diseases of the Eye Chlamydia trachomatis

Inclusion conjunctivitis

Transmitted to a newborn's eyes during passage

through the birth canal

Spread through swimming pool water

Treated with tetracycline

Trachoma

Leading cause of blindness worldwide

Infection causes permanent scarring; scars

abrade the cornea leading to blindness

Figure 21.20a

Trachoma

Viral Diseases of the Eye

Conjunctivitis Adenoviruses

Herpetic keratitis Herpes simplex virus 1 (HHV-1). Infects cornea and may cause blindness Treated with trifluridine

VIRAL INFECTIONDis. Viral conjunctivities Herpetic keratitis

Agent

Adenovirus Herpes simplex type1

POE Conjunctiva Conjunctiva , cornea

S/Sx redness keratitis

MOT Direct contact, fomites and flies

Direct contact, recurrent latent infection

Tx None trifluveridine

Protozoan Disease of the Eye

Acanthamoeba keratitis Transmitted from water Associated with unsanitary contact lenses

PROTOZOAN INFECTIONDis. Achantamoeba keratitis

Agent Acantamoeba sp

POE Corneal abrasion,soft contact lenses

S/Sx keratitis

MOT Contact with freshwater

Tx Propamidine isethionate, miconazol

Guinea worm

222

What is MRSA?

Easily transmitted and drug resistant, MRSA can survive on hands, clothing, environmental surfaces, and equipment.

About 126,000 hospitalized patients develop MRSA infections each year.

Over 5,000 of those patients die.

224

More about MRSA

Staphylococcus aureus is commonly carried on healthy people’s skin, nares, and perineum.

It may cause superficial skin infections treatable with beta-lactam inhibitors (such as methicillin).

Over time, some strains have become resistant.

First cases of MRSA in the United States occurred in the 1960s.

Today, 46 out of 1,000 patients have MRSA.

226

Controlling the spread of MRSA in a health care facility

Improve hand hygiene. Make fastidious environmental cleaning

and disinfection a priority. Consider performing active surveillance

cultures. Identify colonized patients and

implement contact precautions. Implement and perform all interventions

from the central line bundle and the ventilator bundle.

228

Stopping antimicrobial drug resistance Using antibiotics appropriately is key.

Encourage cultures before antibiotics are started, and, if necessary, narrow the spectrum of antibiotics based on culture results.

Review all culture reports to ensure that bacteria are sensitive to the prescribed antibiotics.

Teach the patient how to use antibiotics: Take as prescribed Finish the course of treatment Don’t take someone else’s prescribed

medication

229

Two types of MRSA

Community-associated MRSA (CA-MRSA) Causes skin and soft-tissue infections, such as boils,

blisters, abscesses, folliculitis, and carbuncles Also, fever and local warmth, swelling, pain, and purulent

drainage

Health care-associated MRSA More highly drug resistant Causes more invasive infections, such as surgical site

infection, endocarditis, osteomyelitis, bacteremia, pneumonia

“According to the Centers for Disease Control and Prevention definition, a diagnosis of CA-MRSA requires that the patient have

no medical history of MRSA or colonization and no risk factors associated with

health care–associated MRSA.”

230

MRSA transmission

CA-MRSA Person-to-person by sharing personal items

(clothing and towels) Close contact

Health care-associated MRSA Contaminated environmental surfaces Staff members