Lecture 4- skin infections Flashcards
what is mpox?
Discovered in monkeys 1958
Found in humans in 1970
Large outbreak in 2022
Usually self limiting,
Flu-like symptoms
Swollen lymph nodes
Rash – small pus filled blisters
Can be prevented with vaccine
JYNNEOS – approved in 2019
Two dose vaccine
66% effective
what is leprosy?
Caused by Mycobacterium leprae
Historically been feared and resulted in more social stigmatization than other infectious diseases.
Leprosy is still important worldwide
An estimated 6 million people have leprosy,
mainly in tropical, resource-limited countries, where the disease causes economic loss and human suffering.
what are the clinical features of leprosy?
Symptoms:
Patches of discoloured skin, lesions, progressive numbness
Most symptoms from nerve damage
Pathogenesis unknown
May be bacteria binding directly to Schwann cells
Incubation 5-20 years
Treatment with antibiotics
Multidrug regime for 6-12 months
what is chickenpox?
Caused by Varicella-zoster virus
Symptoms:
Disseminated rash with blisters
Fever
Flu-like symptoms
Self limiting, last 1-2 weeks
Effective vaccine available
what is shingles
Symptoms:
Stripe of blisters around one half of body
Intense localised pain
Headache
‘Feeling unwell’
Common in elderly (people who previously have had chickenpox)
Reactivation of virus from single motor nerve
Treatment – antivirals
Effective vaccine available
For >65 year old
what is poxviruses?
large DNA viruses that replicate in the cell cytoplasm
Infamous - Variola virus, which caused smallpox
Since 1977:
molluscum contagiosum and
zoonoses such as mpox, cowpox, orf virus, pseudocowpox, Yaba monkey tumour virus, and tanapox.
what are the clinical features of smallpox? and when was it eradicated?
Symptoms: High fever, Disseminated rash, followed by, blisters (infectious by contact), Vomiting/diarrhoea, Lifelong scarring
Mortality rate up to 40%
Treatment - None
No asymptomatic carriers, disease very easy to identify
Highly effective vaccines developed between 1890-1960s
Eliminated in Europe (1953) and US (1952)
WHO started worldwide eradication in 1959
Eradicated worldwide in 1977
what is Streptococcus pyogenes?
Causes range of disease
Mild skin infections (impetigo)
Systemic infections
Necrotising fasciitis
Scarlet fever
Only infects humans
Sensitive to penicillin
Can secrete Streptococcal chemokine protease
Kills neutrophils
what is scarlet fever?
Systemic S. pyogenes infection
Characteristic red blotchy rash
May have tongue rash - ‘strawberry tongue’
Rash due to toxin released by bacteria
Streptococcal pyrogenic exotoxin A
Specifically binds and activates T-cells
Up to 50% of all T-cells activated
T-cells produce inflammatory cytokines, leading to rash
Most common ages 2-6
Seasonal infection
Cases peak Dec-March
Approx. 20,000-60,000 cases/year
Treatment:
Penicillin
May require hospitalisation for high-risk people
pregnant women, <3 months, >75 years
what are types of Fungal infection - Dermatophytes
Septate branching hyphae
Anthropophilic, geophilic, zoophilic
Digest keratin – infect skin, hair and nails
Arthrospores in clinical specimens
microconidia and macroconidia in lab culture
Grow on Sabouraud’s within 7-14 days at 28C
Identify by surface appearance and colour of underside
Confirm by shape of macroconidia
Microsporum, Trichophyton, Epidermophyton
what is Staphylococcal scalded skin syndrome (SSSS)?
Requires presence of Exfoliative Toxins
Found in around 1% of strains
Proteases which only cleaves desmoglein 1 in desmosomes in skin
Allows spread of infection around body
Rare (25 in 100,000 babies under 1)
Most common between 1-2 months and 3 years
Newborns resistant due to different protein in desomsomes (desmoglein 3)
Treatment:
IV antibiotics every 6 hours
Emolients and dressings
Important that no secondary infections start
Pain relief
what is MRSA?
Methicillin-resistant Staphylococcus aureus
Resistant to a range of antibiotics including all penicillium-derivatives and cephlasporins
Vancomycin – drug of last resort
More common in hospitals, care homes, prisons, student halls
75% of infections localised to the skin
In addition to multiple drug resistance, also encodes arginine catabolic mobile element (ACME)
Provides resistance to innate immune system in the skin
what are the 3 general categories of skin infections?
Abscess formation:
Boil/furuncles – abscess involving hair follicle
Carbuncles – cluster of abscesses
Spreading infections:
impetigo - confined to the epidermis,
erysipelas - involving the superficial layers and dermal lymphatics,
cellulitis - major focus is the deeper layers of the skin, subcutaneous tissues and fat layer
Necrotizing infections: including fasciitis and gas gangrene (myonecrosis)
cell and tissue death
what are spreading responses?
impetigo, erysipelas and cellulitis
what is acne?
Cutibacterium acnes
Part of normal skin microbiome
Opportunistic pathogen
Blockage of pores promotes bacterial growth
Stimulates inflammation
Can be treated with antibiotics
Resistance increasing
how do pathogens enter the body?
From the outside - exogenous:
through cuts, wounds, insect bites, skin disease, burns or other breaks in the integrity of the stratum corneum
These organisms may also be part of the microbiome of the skin e.g Staphylococci
From within - endogenous:
through underlying tissue or carried by blood or lymph
Once microorganisms penetrate the skin, they spread locally and (may) invade the lymphatics or the bloodstream
As a result, infections originally confined to the skin and soft tissues may ultimately cause disease in other parts of the body.
Sepsis
what are exogenous infections? eg trauma
Resulting from direct invasion from the external environment
Trauma may be mild,
as in a torn hangnail or cracks in the skin caused by athlete’s foot
athletes foot is site of invasion for S. pyogenes
Major forms of trauma that place persons at risk for skin invasion include:
surgery (considered “organized trauma”)
Percutaneous (“through the skin”) catheters.
gunshot wounds, crush injuries (e.g., automobile accidents), or burns
Infections in surgical wounds are a major cause of morbidity in postoperative patients.
Infection also is the primary cause of mortality in burn victims.
what are endogenous infections?
The skin can become infected by microorganisms that spread from another infected internal site,
either by direct extension from an underlying focus or through the bloodstream.
Such secondary infections occur in both immunocompetent and immunosuppressed hosts, but with different degrees of incidence and severity.
what are sources of endogenous skin infections?
Direct Extension
Osteomyelitis
Lymphadenitis – TB, Streps, Staphs
Dental sepsis
Intrabdominal – necrotizing infections
Haematogenous (bloodstream) spread
Bacteraemia – meningococcal, staph
Endocarditis
Viraemia – measles, varicella zoster
Rickettsia - Rocky mountain spotted fever, epidemic or endemic typhus
differentiating characteristics in Staphylococci
vs Streptococci
similarities=
Gram positive cocci
Facultative anaerobes
Non-sporing, non-motile
Important pathogens
Pyogenic (pus forming) –suppurative infections
Commensals of mucous membranes and skin
differences
Staphylococci-
Opaque, creamy colonies
Produce catalase
Resistant to bile salts (grow on MacConkey agar)
Grow on simple media (Nutrient agar)
Generally survive well in the environment
Streptococci-
Translucent, greyish colonies
Don’t produce catalase
Sensitive to bile salts (don’t grow on MacConkey agar)
Don’t grow on simple media (Nutrient agar)
Generally survive poorly in the environment
what is the purpose of skin?
3 main functions: protection, regulation & sensation
Protection (physical and immunological)
Mechanical impacts/pressure
Temperature
Against micro-organisms
– prevents bacteria getting to deep tissue – compromised in burns
Radiation / chemicals
Physiological regulation
Body temperature via sweat and hair
Changes in peripheral circulation
Fluid balance via sweat (minor role)
Synthesis of Vitamin D
Sensation
Network of nerve cells that detect and relay changes in the environment (heat, cold, touch, and pain)
what is the spread and multiplication?
Pathogenic bacteria can express enzymes which help them spread
E.g. Haemolysins, lipases, collagenase, and elastases
The spread of some bacteria is associated with specific virulence factors;
E.g. hyaluronidase (also called spreading factor), an extracellular enzyme made by both Staph. aureus and Strep. pyogenes.
S. aureus infections tend to localize, forming abscesses,
S. pyogenes infections spread more extensively through tissues, causing cellulitis.
