Chapter 27 Infections of the skin, soft tissue, muscle and associated systems Flashcards
Which factors control the skin’s microbial load?
- limited amount of moisture present
- acid pH of normal skin
- surface temperature (less than optimum for many pathogens)
- salty sweat
- excreted chemicals such as sebum, fatty acids and urea
- competition between different species of the normal flora
Which lines of attack result in microbial disease of the skin?
- breach of intact skin, allowing infection from the outside
- skin manifestations of systemic infections, which may arise as result of blood-borne spread from infected focus to skin or by direct extension (e.g. draining sinuses from actinomycotic lesions, or necrotizing anaerobic infection from intra-abdominal sepsis)
- toxin-mediated skin damage due to production of microbial toxin at another site in the body (e.g. scarlet fever, toxic shock syndrome)
What is impetigo, where in the skin is it found, and its common causative organism?
limited to epidermis, presents as bullous, crusted or pustular eruption of skin, Commonly caused by Staphylococcus aureus and/or Streptococcus pyogenes.
What is erysipelas and its common causative organism?
involves blocking of dermal lymphatics and presents as well-defined, spreading erythematous inflammation, generally on the face, legs or feet, and often accompanied by pain and fever. Commonly causes by Streptococcus pyogenes.
What is cellulitis and its common cause?
Diffuse form of acute inflammation with focus of infection in subcutaneous fat. Commonly caused by Streptococcus pyogenes and Staphylococcus aureus
What is the cause of Staphylococcal scalded skin syndrome and its effect?
strains of Staph. aureus producing toxin known as ‘exfoliatin’ or ‘scalded skin syndrome toxin.’ The toxin causes destruction of the intercellular connections in the stratum granulosum with strand separation of the top layer of the epidermis
What is toxic shock syndrome and its cause and treatment?
Toxic shock syndrome is caused by toxic shock syndrome toxin (TSST-1)-producing Staph. aureus
- Associated with tampon use by healthy women, but can occur as a result of Staph. aureus infection at non-genital sites (e.g. a wound).
- Toxic shock syndrome (TSS) involves multiple organ systems and is characterized by fever, hypotension and a diffuse macular erythematous rash followed by desquamation of the skin, particularly on the soles and palms.
- TSST1, which behaves as a superantigen (stimulating T-cell proliferation and cytokine release). Treatment: drain infected site, fluid replacement, antibiotics.
Which three genera of dermatophytes are important causes of disease?
Microsporum,TrichophytonandEpidermophyton.
What are dermatophytes?
keratin-loving organisms that invade keratinized structures of the body such as skin, hair and nails.
How do dermatophytes spread infection?
arthrospores adhere to keratinocytes, germinate and invade
What do dermatophytes produce and how does this help them adapt to life on the skin?
- proteases break down keratin
- Lys M proteins evade recognition by the host
- kinases and pseudokinases modulate host cell metabolism
What is the name for ringworm of the scalp? Describe the infection.
Tinea capitis is a highly contagious infection, most common in toddlers and school-age children
Which tool is useful to diagnose dermatophytes especially of tinea capitis in the clinic?
Wood’s lamp
Describe how two different reagents help diagnose tinea
KOH: dissolves hair, skin
calcofluor-white: fluorescent dye that binds to chitin in cell walls of fungi
How are dermatophyte infections treated?
Dermatophyte infections are treated topically if possible
A range of agents is available for topical treatment, both antifungals (e.g. miconazole-inhibit ergosterol synthesis) and keratolytic agents such as Whitfield’s ointment (a mixture of salicylic and benzoic acids).
In order to prevent relapse, treatment should be continued for 1-2 weeks after resolution of clinical signs.
Systemic therapy with oral antifungal drugs is required for scalp infection and is more effective than topical agents for nail infections.
Terbinafine or itraconazole are now used. These newer agents may give a cure rate of 70–80% for nail infections
What is a human dead-end host?
When an animal parasite is unable to complete its life cycle in humans, becoming trapped
Describe the life cycle of Guinea worm disease
TheCyclops (water flea)is dissolved by the gastric acid of the stomach and the Guinea worm larvae are released and migrate through the intestinal wall. After 100 days, the male and female meet and mate. The male dies in the tissues while the female moves down the muscle planes.
After about one year of the infection, the female worm emerges usually from the feet releasing thousands of larvae thus repeating the life cycle.
Very painful blister/ulcer, with fever, nausea, vomiting
Remove 2-3cm per day
How is Herpes Simplex Virus infection transmitted?
Infection is usually transmitted from the saliva or cold sores of other individuals and frequently by kissing and sexual intercourse.
After infection, the virus replicates in cells in the oral mucosa and forms virus-rich vesicles which ulcerate and become coated with a whitish-grey slough
Describe the pathogenesis of herpes simplex virus infection
During the primary infection, virus particles enter sensory nerve endings supplying the affected area of the skin and are transported to the dorsal root ganglion, where they initiate a latent infection.
The lesion resolves as antibody and CMI responses develop. The latent virus remains in the sensory ganglion for life, and under certain circumstances such as local trauma, can reactivate and spread down sensory nerves to cause cold sores at the site of the original infection
Describe how herpes simplex virus can manifest in different parts of the body
Primary infection can occur in various sites of the body and may be a result of inadvertent autoinoculation and include:
•in and around the mouth, lips and nose, causing painful, recurrent ulcers
•the eye, to cause conjunctivitis and keratitis, often with vesicles on the eyelids
•the finger, to cause herpetic whitlow
•the genital tract. Although HSV-2 arose as a sexually transmitted variant of HSV-1, the sites infected by the two types are now less clearly distinct.
What serious complications are associated with HSV infection?
•herpetic infection of eczematous skin areas leading to severe disease in young children, eczema herpeticum
The main treatment of eczema herpeticum is acyclovir.
- acute necrotizing encephalitis following either primary infection or reactivation (Ch. 25)
- neonatal infection acquired from the genital tract of the mother (seeCh. 24)
- primary or reactivating HSV infection in immunocompromised individuals, causing very severe disease
Describe HSV reaction, causes, detection, and treatment, if any.
In healthy individuals, HSV reactivation is provoked by:
certain febrile illnesses (e.g. common cold, pneumonia) direct sunlight stress trauma menstruation immunocompromised
-A sensory prodrome in the affected area may include feeling pins and needles, pain, burning, and itching which precedes the appearance of the lesion and is due to virus activity in sensory neurons
Large amounts of virus are shed from the lesion. Which usually heals in about a week.
Detection by PCR: to confirm HSV-1 or HSV-2
Treatment: If reactivation is often, acyclovir or valacyclovir (BID for 6-12 months)
What is fifth disease and what causes it?
erythema infectiousum, or ‘slapped cheek syndrome’ febrile illness caused by parvovirus B19 a single-stranded DNA virus.
What is unique about parvovirus B19 in its family?
Parvovirus B19 is the only member of the Parvoviridae family known to cause human disease and is tropic to erythroid progenitor cells and binds to the P antigen cellular receptor.
Where does the name ‘fifth disease’ caused by Parvovirus B19 come from?
Over 100 years ago, a group of characteristic childhood eruptions were described and numbered from one to six:
- measles
- scarlet fever
- Rubella
- Dukes disease
- erythema infectiosum
- roseola infantum.
