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 Infections
Staphylococcus aureus S. epidermidis

Gram-positive cocci and Gram-positive cocci and

coagulase-positive coagulase-negative
Leukocidin
Exfoliative toxin Slime layer
Enterotoxin
Nosocomial infection (surgical Transmitted thru medical
wound and breaks) procedure
Staphylococcus Streptococcus
Staphylococcal Biofilms

Figure 21.3
 Differential
Characteristics
S. aureus

Coagulase

Fibrinogen  Fibrin
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, Hexachlorophene

Antibiotics: 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

Toxicshock syndrome toxin

(TSST-1)
Super antigen
Produced by 5-25% isolates

Tampon or infected wound

Fever

Rash

Exfoliation of skin

Shock (death rate 3%)

 Staphylococcal Skin Infections
POE Skin , SURGICAL INCISION

s/sx Toxic Shock Syndrome

Fever
Rash
Exfoliative skin
Shock |(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 Fascitis
Extensive soft tissue destruction

MOT Direct contact

Tx Surgical removal of tissue

Antibiotics: Penicillin
 S. pyogenes
Necrotizing
Scarlet Fever fasciitis
 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:
 erythema
 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 dermatitis
Superficial rash

MOT Swimming water, hot tub, Endogenous infection

Tx Usually self limiting

Antibiotics:
 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 externa
Superficial 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 peroxide
Isotrenitoin , 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- NOTE: Double zone of hemolysis
positive bacilli

Inner beta-hemolysis = θ toxin Outer

alpha-hemolysis = α toxin
 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
Bacilllus anthracis
G+ and spore forming
Farm animals are major reservoir
Inhalation, GI, cutaneous

Day 7

Day 4
Day 5

Day 12
 Cutaneous Anthrax
Bacilllus anthracis
G+ and spore forming Day 4
Farm animals are major reservoir
Inhalation, GI, cutaneous
Virulence factors:
Capsules Day 5
Edema factor
Lethal factor
Vaccine
Toxoid (protective antigen) Day 7
Effective in short term but not
long term

Day 12
 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
• Staphylococcus epidermidis
Infections
– 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 cryotherapy

Electrodessication, 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
Distinguishing features of Smallpox from other
rashes

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.
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 vaccines

Anti-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 vaccines
Anti-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
 Human Herpesviruses
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
 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-2
HSV-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
 ROSEOLA
Agent 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 vaccines

No 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 vaccines

No treatment
 Rubella virus
Pathogenesis
•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
 RUBELLA
PATHOPHYSIOLOGY
• Transmission is by respiratory
droplets
• Respiratory tract -->cervical lymph
nodes-->hematogenous
dissemination
• Incubation period is 2 to 3 weeks
 RUBELLA
CLINICAL MANIFESTATIONS
• Malaise
• Headache
• Myalgias and arthralgias
• Post-auricular adenopathy
• Conjunctivitis
• NON-PRURITIC, ERYTHEMATOUS,
MACULOPAPULAR RASH
 RUBELLA
CLINICAL MANIFESTATIONS
 RUBELLA
CLINICAL 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
 Parvovirus pathogenesis

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
ERYTHEMA 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
 Anthropophilic
Associated 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 Distribution
Worldwide
 Dermatophytes
3 Genera

• Trichophyton
• Microsporum
• Epidermophyton
 Trichophyton
(19 species)
• Hair
• Skin
• Nails
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

• Skin
• Nails
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.
 SPOROTRICHOSIS
Agent 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
 Subcutaneous mycoses

•
Tinea
Subcutaneous
corporis
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.
 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.
 CANDIDIASIS
Agent 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

Thrush

Risk factors for candidiasis

Post-operative status
Cytotoxic cancer Chemotherapy
Antibiotic therapy
Burns
Drug abuse
Gastrointestinal damage.
Cutaneous
 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 & PEDICULOSIS
Agent Sarcoptes scabiei (mites)
Pediculosis humanus capitis (lice)
POE Skin

S/Sx Scabies- papules

Pediculosis – itching

MOT Scabies- direct contact

Pediculosis- direct contact, fomites
(beddings & combs)
Tx Scabies- Gamma benzene hexachloride,
permethrin
Pediculosis- 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 (38C) 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
Dis.
BACTERIAL INFECTION
Conjuctivitis Neonatal gonococcal
ophthalmia
Agent 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
Dis.
BACTERIAL INFECTION
Inclusion Conjuctivitis Trachoma
Agent Chlamydia trachomatis Chlamydia trachomatis
POE Conjunctiva Conjunctiva
S/Sx Swelling of the eyelid; Conjunctivi tis
mucus and pusChlamydia
formation
trachomatis

MOT Through birth canal; Direct contact, fomites and

swimming pools flies

Tx Tetracyline Azithromycin
 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
Trachoma

Figure 21.20a
 Viral Diseases of the Eye
• Conjunctivitis
– Adenoviruses
• Herpetic keratitis
– Herpes simplex virus 1 (HHV-1).
– Infects cornea and may cause blindness
– Treated with trifluridine
Dis.
VIRAL INFECTION
Viral conjunctivities Herpetic keratitis
Agent Adenovirus Herpes simplex type1
POE Conjunctiva Conjunctiva , cornea
S/Sx redness keratitis

MOT Direct contact, fomites and Direct contact, recurrent

flies latent infection

Tx None trifluveridine
 Protozoan Disease of the Eye
• Acanthamoeba keratitis
– Transmitted from water
– Associated with unsanitary contact lenses
Dis.
PROTOZOAN INFECTION
Achantamoeba keratitis
Agent Acantamoeba sp
POE Corneal abrasion,soft contact lenses
S/Sx keratitis

MOT Contact with freshwater

Tx Propamidine isethionate, miconazol

Guinea worm
 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.

222
 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. 224
 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. 226
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
228
 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.”
229
 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

230