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Transcript of 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