Infection of skin and soft tissue Flashcards

1
Q

Where is colonisation by microbes most evident on skin

A
  • Forearms and back = low –> low diversity, Gram +ve bacteria and yeast
  • Armpits and groin = high –> high diversity, Gram +ve and -ve bacteria, yeast
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2
Q

How does the transmission of skin infections occur?

A

3 lines of attack

  • Breach of the skin
  • Skin manifestation from systemic infection
  • Toxin-mediated skin damage

Direct introduction of bacteria or fungi into the skin is the most common route of infection

  • Infections range from mild, often chronic conditions such as ringworm
  • to acute and life threatening fasciitis and gangrene
  • relatively few species are involved in the common infections
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3
Q

What is staphylococcus aureus? What are its microbe features, and what the major types ofs skin infections associated with it

A
  • Gram-positive coccus, form clusters –> facultative anaerobe
  • Common resident of nose, respiratory tract and skin
  • “Golden Staph” – large, round, golden-yellow colonies
  • Some virulent type cause mild to severe disease
  • Now Gram-negative also major concern

> major Gram-positive - Staph. aureus

> major Gram-negative – E. coli, P. aeruginosa

Transmission

  • Self-contamination into wound, person to person
  • Contamined hands, items such as towels, clothing

Skin Pathologies

Boils - most common cause of boils

  • begins as superficial infection in and around a hair follicle
  • Intense immunological response: pus, abscess

Scalded skin sydrome –> Caused by S.aureus producing toxin Exfoliatin

  • destruction of connection of upper layers of the epidermis: large blisters containing clear fluid, within 1 or 2 days, the overlying areas of skin are lost
  • Normal skin underneath, may require fluid treatment, antibiotic treatment

Toxic shock syndrome - rare

  • Affecting multiple organ systems
  • Toxin acting as superantigen: stimulating T cell proliferation and cytokine release; desquamation of hands and feet
  • Can be fatal
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4
Q

What is streptococcus pyogenes? What are its microbe features, and what the major types of skin infections associated with it?

A

Gram-positive coccus, forms chains

  • Aerotolerant, anaerobic
  • Occasional resident of nose, respiratory tract and skin
  • Common cause of sore throat and skin infections
  • Surface proteins M and T associated with certain infections: M, inhibits opsinisation; T, pili
  • Group A Streptococcal infections (GAS), β-haemolytic
  • Transmission – same as for S. aureus

Skin Pathologies

Impetigo = mostly children, pick at sores, infected hands and nails

  • S.pyognes produces a number of toxic products and enzymes, allows it to invade tissue
  • Can cause erysipelas (an acute deeper infection)

Cellulitis: extends deeper than erysipelas, usually originates either from boils or ulcers or following trauma, rarely bloodborne – infection of the sub-cutaneous fatty layer

  • Disease has a rapid progression - particularly when mixed: strep. pyogenes and staph. aureus
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5
Q

What is gangrene? Describe its transmission, pathogenesis and clinical features

A

Caused by mixture of organisms; low oxygen streptococci and staph aureus

  • Rare but most commonly follows surgery in the groin or genital area, starting at the site of a drain or suture
  • Progresses rapidly (within hours), leaving a black necrotic centre
  • Condition is often fatal, and treatment requires radical excision of the necrotic area and systemic antibiotic therapy

Also caued by clostridiym species –> gas gangrene/clostridial myonecrosis

  • Most comomnly caused by clostridium perfringens
  • Gram positive, bacillus, anaeroobic
  • Found in soil and in human and animal faeces
  • Infection through traumatized tissues

> develops in areas with poor blood supply: buttocks, perineum are common sites, ischaemic vascular disease or peripheral arteriosclerosis

  • C. perfringens produces toxin lecithinase/alpha toxin (hydrolyses lipids in cell membranes –> cell lysis and death)

Pathogenesis: organisms multiply in the subcutaneous tissues, producing gas and an anaerobic cellulitis

  • Deep tissue invasion, to muscle
  • Myonecrosis –> produce bubbles of gas
  • Proceeds very rapidly and causes acute pain
  • Compromises the blood supply, organisms multiply and produce more toxin and more damage

Treatment: immediate amputation/excision of infected sites, hyperbaric oxygen chamber, penicillin

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6
Q

What is leprosy(hansens disease) ? Describe its micorbe features, transmission, pathogenesis, clinical features and treatment

bacterial infection of the skin that tends to occur on the lower legs and in areas that are damaged or inflamed.

A

Caused by mycobacterium leprae (leprosy)

Gram-positive, rod, intrcellular

  • Acid fast stain (ziehel-neelsen) characteristic waxy coating, slow growing
  • Found in warm tropical countries
  • Rare in developed countries but still significant problem in SE asia, africa and the americans

Transmission

  • Direct contact and aerosol , mostly nasal secretions, children more susceptible, low rate of transmission
  • Slow incubation period, average 5 years
  • M.leprae grows intracellularly: in skin histocytes (dendritic), endothelial cells and the schwann cells of peripheral nerves
  • Immune response is important in deciding the type of disease: TT and LL

Clinical Features

  • Gradual tissue destruction, numb areas from nerve destruction, LL results in deformation of face and loss of finger/toes, TT may progress to LL

Treatment

  • multidrug therapy over extended period (up to 2 yrs); vaccine in countries with high incidence
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7
Q

What is cutaneous mycoses? Describe its general transmission and clinical features, fungi that cause tinea at different body sites

A

Mycoses (fungal infection0 that cause superficial infections of the epidermis, hair, and nails

Caused by dermatophytes: keratin-loving organisms, ‘Tinea’

  • Invade the keratinized skin, hair and nails

Transmission: spread by contact with arthrospores

  • the thick-walled vegetative cells formed by dermatophyte hyphae

Clinical features: lesion in ring shape

  • main symptom is itching but varies in degree
  • Skin is often dry and scaly and sometims cracks

Sources:humans, animal, soil, tinea pedis, tinea corporis

Treatmen: For skin infections usually topical treatment (anti-fungals miconazole) and keratolytic agents such as whitfields ointment

For nails and hair: oral antifungal drugs

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8
Q

What is papillomavirus: viral features, pathogenesis, treatment

A
  • Papillomaviruses
  • Small (55 nm) diameter, icosahedral, non-enveloped, double-stranded DNA viruses
  • 70 different types that can infect humans
  • cause skin papillomas (warts)
  • At least 40 types, including HPV 6, 11, 16 and 18, can infect the anogenital tract and other mucosal areas and are sexually transmitted.
  • HPV 1 and 4 tend to cause plantar warts
  • HPV 2, 3 and 10 cause warts on the knees and fingers • 4% of cancers associate with papillomavirus infection

Pathogenesis

  • Papillomaviruses are usually transmitted by direct contact; breach in the skin or mucosa
  • Infect basal cells, activated by cellular cornification process
  • Cell tropism, do not infect other tissues
  • Causes over-proliferation of cell mass (immortalise), takes 1-6 months to protrude

Treatments: application of keratolytic agents such as salicylic acid and destruction of wart tissue by cryotherapy (dry ice or liquid N)

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9
Q

What is the herpes simplex virus? Discuss its viral features, transmission, pathogenesis and treatment

A
  • dsDNA virus of the herpesvirus group, enveloped
  • Two types: HSV-1 and HSV-2 (also called Human herpesvirus-1 and -2) are distinguishable antigenically
  • They cause a wide variety of clinical syndromes, the basic lesion being an intraepithelial vesicle, from which the virus is shed: HSV-1, cold sore; HSV-2, genital herpes.
  • Infection is usually transmitted from the saliva or cold sores of other individuals and frequently by kissing.
  • Neonatal infections can occur from birth canal, if mother has lesions, and can lead to blindness.
  • Primary or reactivating HSV infection in immunocompromised individuals can causing very severe disease.

Pathogenesis

  • During the primary infection, virus particles enter sensory nerve endings in the lesion and are transported to the dorsal root ganglion → initiate latent infection (for life)
  • Lesion resolves as antibody and CMI responses develop

Reactivation in healthy individuals provoked by certain febrile ilnesses (fever) (e.g. common cold, pneumonia), direct sunlight , stressm trauma, immunocompormised

Treatment: Aciclovir revolutionized treatment of HSV infection can be used either topically or systematically

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10
Q

What is the varicella-zoster virus? Describe its viral features, transmission, pathogenesis and treatment

A

Varicella = chickenpox, Zoster = shingles

  • dsDNA virus of the herpesvirus group, Human herpesvirus-3 (HHV-3)
  • Infection – inhalation of droplets from respiratory secretions and saliva, or by direct contact from skin lesions
  • Primary infection causes chicken pox, reactivation causes shingles

Vaccine = monovalent and combination available

MMRV vaccine at 18 months

  • Live attenuated varicella-zoster virus, injection

Pathogenesis

  • Primary infection, the virus passes across epithelium in the respiratory tract to infect mononuclear cells, and is then carried to lymphoid tissues.
  • no symptoms and no detectable lesions at site of entry
  • The virus slowly replicates in lympho-reticular tissues for about 1 week,.
  • Then enters the blood in association with mononuclear cells and is seeded out to epithelial sites:
  • ainly the respiratory tract and the skin, but also include the mouth, often the conjunctiva
  • The virus reaches the surface and is shed to the exterior to infect other individuals about 2 weeks after initial infection.

Varicella clinical features

  • Patient remains well until a day or two before the rash: may be slight fever and malaise, but the illness is usually mild and often unnoticed.
  • The vesicles appear on the trunk, face and scalp, and less commonly, on the arms and legs •
  • They often come in ‘crops’ over the course of several days and all stages of lesions occur simultaneously, then develop into pustules, break down, and scab over.
  • Scarring is common and mouth lesions may be painful
  • The skin lesions can become infected with staphylococci or streptococci to produce secondary impetigo

Zoster (shingles) clinical features

  • Later in life, reactivation can occur to cause zoster in the dermatome (area of skin supplied by that nerve)
  • Pain may be severe and precedes the development of the blistering rash in which virus-rich vesicles appear
  • Fever and malaise may accompany the rash

Treatment for varicella-zoster

Chickenpox – often considered a mild infection that causes little discomfort in children; calamine lotion to relieve itching and to prevent scratching and secondary infection

Zoter = acyclobir, famciclovir

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11
Q

What is small pox? what are its viral features, clinical features and dicuss its eradication

A

Poxvirus, Poxviridae family, dsDNA, enveloped •

  • A major scourge to humanity over last 3000 yrs •
  • Highly contagious with high mortality, up to 40% •
  • Transmitted from person to person by contact with skin lesions and via the respiratory tract
  • Upper respiratory tract infection, the virus reached the skin, where it replicated to cause a widespread vesiculopustular rash, with later scarring, especially on the face
  • Eradication by mid-1900’s, last case 1977, possible due to:

> No subclinical infections, and symptoms could be readily identified

> The virus was eliminated from the body on recovery

>Humans were the only host (no animal reservoir)

>An effective vaccine was available

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