Infestations and infections of the skin Flashcards
Session Plan
Differential diagnosis and investigation
Skin in systemic disease, no matter what presentation, always take a categorical approach of possibilities on left.
In terms of diagnostic approach for infectious etiology, a lot of the important investigations are serology, so bloood tests for viruses and bacteria, swabs of vesicle, fluid or pus for bacterial and viral studies, you can also take tissue cultures and send them for culture or PCR, you can also send them for histology.
Bacterial Infections
Slide shows how heterogeneous they can be in their manifestations
Bacterial Infections-Staphylococcus
So staphylococcus aureus has a number of virulence factors, including receptors that allow it to bind to fibrin in wound surfaces and in dermatitis. It also expresses a particular virulence factor called Panton Valentine Leukocidin (PVL). Only some strains, thankfully, express this virulence factor. And other strains of staphylococcus express different virulence factors such as Toxic shock syndrome toxin one (TSST1), and exfoliative toxins. So each strain has different clinical manifestations. And those are things that we’re going to talk about.
So some of the more common manifestations in skin infections are those of cellulitis, impetigo and folliculitis, it can also cause Ecthyma. And it can also cause staphylococcal scolded skin syndrome (SSSS) and it can get involved in other dermatoses, such as eczema, herpes and leg ulcers.
Bacterial Infections-Streptococcus
Streptococcus is also one of the more common causes of skin infections, and streptococcus pyogenes has receptors that allow it to bind to epithelial surfaces. And also different factors that allow it to evade phagocytosis, such as its hyaluronic acid capsule and M protein. It also produces some different virulence factors that account for some of the clinical manifestations, such as exotoxins that produce erythema. Similar to Staphylococcus aureus. It’s a frequent cause of impetigo, and cellulitis. It can also cause erysipelas, ecthyma, necrotising fasciitis, and similar to Staphylococcus aureus, it can also superinfect other skin problems.
(Erysipelas is a superficial form of cellulitis, a potentially serious bacterial infection affecting the skin. Erysipelas affects the upper dermis and extends into the superficial cutaneous lymphatics.)
Folliculitis
So folliculitis refers to inflammation of the hair follicle unit, which is a part of sebaceous unit, and folliculitis may be infectious folliculitis or it may be non-infectious. Non-infectious examples to include frictional folliculitis, and also eosinophilic folliculitis, which is associated with the immune dysregulation seen in HIV.
And in terms of infectious causes, Staphylococcus aureus is a very common cause of this. And PVL expressing Staphylococcus aureus also expresses it too. Staphylococcus aureus, can colonise the nasal cavity, so there can be a reservoir there and that can cause distant manifestations on the skin. So you can get folliculitis anywhere as a result of a nasal carriage or a reservoir of Staphylococcus aureus.
In terms of infectious, staphylococcal mediated folliculitis. Think back to your differential diagnosis. So we feel already thought of non-infectious variants of folliculitis, so those would be classed as inflammatory, frictional, you could categorise that under trauma.
So how would you tell the difference? So taking a swab for bacterial microscopy and culture and sensitivity of this pus.
And it’s treated with antibiotics. And if there’s a nasal reservoir, how will you tell? = you’ll take a nasal swab, and if there is positive nasal carriage of Staphylococcus, you can treat that with nasal Mupirocin.
Folliculitis can become complicated into furuncles and carbuncles:
•What is the difference between a furuncle and a carbuncle?
Top right=carbuncles
Remember previously mentioned that you can develop nasal carriage or reservoir of staphylococcus aureus, and that can lead to recurrent staphylococcal infections, so that’s an important thing to check for.
Immunodeficiencies is another cause for recurrent infection
Panton Valentine Leukocidin Staphylococcus Aureus
So Panton Valentine leukocidin, the mechanism by which it expresses virulence, is by forming pores. So the consequence of that is destruction of leukocytes. So it’s a more aggressive infection. And tissue necrosis. So strains of staphylococcus that express this toxin have higher morbidity, mortality and transmissibility. And it causes the different manifestations of Staphylococcus aureus.
But the difference is that it’s often more than one site, it’s often painful, it’s often recurrent, and it’s often present in contact simply because basically it destroys the white cells that are trying to kill it, so it’s going to cause more and more widespread infections and more transmissibility as a result.
Is can cause complications outside the skin. So in the lungs, it can cause a necrotising pneumonia by forming pores in that tissue. Similarly, it can cause necrotising fasciitis, which is seen at the top right. And Purpura fulminans, which is where you develop widespread clotting and bleeding in the context of an infection. And it’s a form of disseminated intravascular coagulation and it has a high mortality.
Panton Valentine Leukocidin Staphylococcus Aureus
Risk of acquiring:
Panton Valentine Leukocidin Staphylococcus Aureus
•Consult local microbiologist / guidelines
So PVL, because of its increased morbidity and mortality, needs to be treated very, very precisely and effectively. And with any infection, it’s important to ensure that you’re treating as per guidelines. Guidelines are based on evidence and they help ensure effective treatment of infections. And where guidelines don’t exist or where there’s any doubt, it’s important to discuss with the microbiologists who generally will be notified once PVL is demonstrated on growth of a swap.
Generally speaking, we treat it with tetracyclines and we also decolonise the body by giving people chlorhexidine body wash, (Hibiscrub) for seven days and Nasal mupirocin ointment. Of course Microbiology guidelines may vary by different areas. So it’s important to follow the ones that apply to whichever area you are practising in.
Not only to you have to treat the person who has grown this organism, but you have to treat any of their close contacts as well, because it’s so transmissible. They may be also carrying it, but not manifesting any of the clinical diseases as a result.
Pseudomonal Folliculitis
- Many organisms can cause folliculitis, Pseudonomas is one of them
- People who go to spa together might all erupt in rash, or if use dirty wet suit.
- Rarely can develop into furuncles, abssess or lymphangitis but usually it is self limiting and gets better by itself.
Cellulitis
- Tender blanching area (blanches when you press on it ie turns white), it is not well defined at the edge
- if you have oedema, such as elderly people, or people with venous stasis, swollen lower limbs or people with lymphadema, these are people who are at higher risk of cellulitis.
- When someone has cellulitis, you need to look for a portal of entry, so how did that organsism get into the body? So it is worthwhile checking for Staph in the nose, check between the toes to see if there’s athlete’s foot, these may serve as a port of entry so if there’s athletes foot or nasal carriage, treat that.
- You’ll see that in cellulitis there is no pus, there is usually no exudate, so you can’t swab it, so generally you treat it on clinical grounds.
Impetigo
-of course you should always swab this for a culture and sensitivity and microscopy, but you can actually tell on clinical grounds which organism it may be, because Staphylococcus causes bullous (blistering impetigo), it does this by the exfoliative toxins, these split the epidermis by targeting a cell adhesion molecule called desmoglein 1, which is in the epidermis so this gives a superficial, easily breaking blister.
Strep doesn’t express that virulence factor therefore it doesn’t cause that manifesation, so it just causes the crusts. It is always important to swab anyway as it helps you to identify the sensitivities.
Impetigo typically affects the top part of body, especially the face and head.
It is important to treat it topically, sometimes it doesn’t respond so well to systemic antibiotics because it’s so superficial, so its important to treat topically as well as oral antibiotics.
Impetiginisation
When impetigo happens in the context of atopic eczema=impetinisation
Remember people with eczema are usually already colonised by staphylococcus aureus
You don’t necessarily see the blistering that you see in the bullous impetigo caused by Staph, because the strain that causes bullous impetigo which expresses exfoliative toxins, doesn’t need to express those exfoliative toxins in atopic eczema because the skin is so abnormal with the barrier defect.
Ecthyma
This is a more severe form of impetigo. Remember in impetigo you have these stuck on crusts with a small erosion, so in ecthyma it is a some what deeper erosion, still an erosion, maybe an ulceration. So it’s a relatively superficial infection, but just a bit deeper.
Staphylococcal Scalded Skin Syndrome
Bullous impetigo is caused by exfoliative toxins. So what happens if you have that organism but that exfoliative toxin builds up in your system eg due to kidney impairment or in an infant whose kidney doesn’t work that well yet. So then you’ll get a lot of exfoliative toxin in you system and you’ll get a different manifestation.
You get widespread denudation of the skin and shedding of the superficial layers because you’ve got so much of that exfoliative toxin in your system. And this is a serious condition as you can get skin failure-so skin is so compromised it can’t perform function eg thermoregulation and defence barrier etc.
Agrssive treatment with antibiotics and support for skin function
Looks similar to SJS but in SJS the entire epidermis comes off but in this it is only the top superficial layer so they are not quite as ill and it doesnt have the same consequences as SJS.
Toxic Shock Syndrome – Group A S. aureus
This isn’t a skin infection in itself, it simply manifests in the skin.
This is where you are infected by Group A Staphylococcus aureus strain, which produces a virulence factor called Toxic Shock Syndrome Toxin 1 (TSST-1)
- Associated with leaving tampon in for too long which can be portal of entry
- Causes widespread rash especially of mucous membranes, you get erythema.
- See peeling off of dead superficial layers eg palms and soles when recovering.
Erythrasma
This is another very superficial infection
Affects intertriginous areas ie places where skin meets skin eg armpits
Pitted Keratolysis
Skin looks really white and macerated (wet appearing skin) with very distinctive pits.
This organism is fastidious (fussy in conditions in which it grows) so wont grow on a swab so have to rely on clinical judgement.
treated with topical antibiotics
Erysipeloid
Looks a bit like cellulitis but it is very slow spreading, it extends over weeks
Associated with handling raw fish and meat
Treatment involves consulting local microbiology guidelines
Anthrax
Here is an ulcer with surrounding swelling and purpura and this implies necrosis. This ulcer looks dramatic but is painless, but it is associated with painful surrounding lymphaenopathy. If see this think of cutaneous anthrax.
Blistering Distal Dactylitis
Superficial blisters on volar aspect of digit. Toes can be affected, but usually fingers.
Think what causes blisters-categorical approach: could it be friction, could it be cancerous-no, drug-induced blisters (eg fixed drug eruptions-rare in children), herpetic blister eg herpetic Whittlow etc.
Take a swab and consider wider clinical picture.
Erysipelas
Remember how cellulitis affects dermis and subcutaneous tissue, well Erysipelas is quite similar, and it’s caused by similar organisms, it’s also tender, patients are generally quite unwell.
Difference between Erysipelas and cellulitis in practical terms, is that Erysipelas is more likely to affect upper extremeities and characteristically it is more clearly demarcated-there is this so called cliff drop edge, and it more often blisters, so not only does it affect the deep dermis and subcutaneous, but it can affect the more superficial layers as well. Patients are typically more unwell, and you can get streaks of redness along the lymphatic channels and local lymphadenopathy.
Like with cellulitis-look for portal of entry eg athletes foot
Treat this aggressively with IV Antibiotics, as people can become unwell.
Scarlet Fever
Not a skin infection, but has dramatic manifestations on the skin, similar to TSS which isn’t primarily a skin infection.
Primarily in children. Fast moving. Start with fever and then they get blanching red spots on upper body and within hours this spreads to rest of body with sandpaper texture. Important to recognise as can lead to complications which may have longterm implications eg rheumatic fever damage to heart valves, glomerulonephritis causing kidney falure and various other organs.
Can be treated if caught early, so important to recognise.
Necrotising Fasciitis
Infection not just of skin but of underlying connective tissue and muscle. Doesn’t respect anatomical boundaries
Usually more than one organism and can be fungal progresses quickly and can be fatal
Doesn’t look dramatic at beginning so if patient seems unwell and is in a lot of pain but just has dusky discolouration you need to consider necrotising fasculitis. MRI can support diagnosis.
Start with empirical ABs and once have results form tissue and blood culture can tailor the diagnosis
Fornier’s gangrene is when it affects scrotum
Atypical Mycobacterial Infection
-Take full history eg travel history, do they work with animals, do they have a fish tank, social history, occupational history
Sarcoidosis=great mimicker
So take think of taking skin biopsy for microbiological PCR studies, histological study, culture
AKA fish tank granuloma
It follows this very unusual manifestation called sporotrichoid spread, where you get lesions along the lymphatic channels.
Mycobacterium Chelonae is associated with getting a tattoo or having surgery with contaminated instruments
Mycobacterium ulcerans is a tropical infection.
Borreliosis (Lyme Disease)
Mannifests as annular redness around tick bite.
May see targetoid appearance like a bulls eye, but often just circular redness.
Borreliosis (Lyme Disease)
If untreated can progress to lots of smaller secondary red areas that are similar to the primary erythematous annular rash, but smaller.
This organism can progress to affect other organ systems such as the heart, nervous system and the joints.
Borreliosis (Lyme Disease)-diagnosis
Can see on the neck it is not a very obvious bullseye
The serology isn’t accurate enough
Can take a biopsy but it is often not specific so just treat
Tularaemia
Manifests in a PAINFUL ulcer and is also associated with painful regional lymphadenopathy
Thinking back to categorical diagnosis for painful ulcers, cancer can cause it- Squamous cell carcinoma can cause painful ulceration, other infections-this is an example of an infection, cutaneous antrax doesn’t, it causes painless ulceration, pyoderma gangrenosum is an inflammatory cause of painful ulceration, obviously you can also get vasculitis, that can also cause ulceration, impaired vascular supply so peripheral vascular disease can cause painful ulceration.
This is an infectious cause from handling infected animals
May have malaise, rigor fever and headache
Ecthyma Gangrenosum
So we saw ecthyma earlier, which is a deeper version of impetigo. This is another form of it called Pseudomonas. In people who are neutropenic they are vulnerable to pseudomonas infections.
red spot becomes oedematous and then becomes a bruising blister, so this is another lesion with a blackened scab ie an Eschar
Escharotic Lesions
Another example of a disease causing a black scab-Eschar. Don’t need to remember all these differential diagnoses
Skin Disorders
Left-non specific rash
Top Middle-dusky pink patches
Bottom-scaley violacious papules
Right-scaley erythema
Skin Disorders
Warty lesions in anogenital lesion, superficial ulcers of the tongue, erosions on inner mucosa, and again warty lesions in genital region.
Skin Disorders
Ulcers in genitals
What could this be?=syphylis
The pictures before were: Syphilis
Painless ulcer typically of genital region but could be anywhere, wherever sexual contact occured. Like cutanous anthrax it is non painful.
Syphilis-secondary Syphilis (this is a great mimicker like sarcoidosis, it could look like a lot of other things)
heterogenous in presentation, so well worth checking serology
Syphilis-Lues maligna
This is another thing to think of in terms of seeing black scab ie Escharotic lesions
Caused by the organism simply blocking the blood vessels.
Tertiary syphilis
Gummas spread in a circumferential manner, the central areas heal, albeit with scarring and thinning and those can destroy underlying cartilage.
Syphilis diagnosis and treatment:
In primary syphilis serology isn’t as important, it is important just to treat it. Like with lymes, if there is a possibility just treat.
Differential diagnosis and investigation
Leprosy
This prodominantly targets skin and nerves but it can affect any organ.
Pic on top left and bottom shows lepromatous leprosy where you have lots of nodules with a deep component and macules. Lepromatous-where you have lots of the organism and not much of an immune response against it, and normal sensation. Same organism, it’s just the body isn’t reacting against it.
Tuberculoid Leprosy, which is at the far end of the continuum, is where body has mounted a strong response and there is hardly any orgnaism in the body, so you only get one or maybe a few lesions which are numb. Similarly to tertiary syphilis you get a scarred centre while it spreads outwards.
Can get manifestations in between these=dimorphous leprosy
Tuberculosis
Can affect any organ and can affect skin as well
There are different ways you can catch it-primary innoculation into skin, haematological or lymaphatic spread into the sight or you can get spread in from an underlying structure.
Under armpit we see scrofuloderma, where maybe an underlying infected lymph gland has spread into the skin. That looks a little bit like hidradenitis suppurativa, which is the condition where you get nodules and absesses in the intertrigenous areas.
Tissue for PCR, tissue for culture, tissue for histology (there is a stain called ziehl neelsen stain, which can identify mycobacteria, and the interferon gamma release assay.
Tuberculosis-Cutaneous manifestations
Tuberculous Chancre-primary innoculation
Lupus Vulgaris-scarring and peripheral spreading little bit similar to tuberculoid leprosy in clinical manifestation, and similar to tertiary syphilis in that you have central healed scarring and circumferential spread. Usually of face in lupus vulgaris.
Differential diagnosis and investigation
Viral Infections
Show how varied viral infections can be
Skin Disorders
Molluscum Contagiosum
Usually harmless and don’t need to treat as will resolve, but if in doubt do biopsy.
Tiny dot in centre
Skin Disorders
See blistering on lips, superficial erosions on trunk, oral ulceration
Blister in armpit, ulcers on penis, blisters on digits
Herpes Simplex Virus
Herpes comes in 2 types and both can affect anywhere
Generally sexual contact is more likley to result in HSV-2, but it can be any type.
You can spread this if you have this without you seeing any abnormalities, so someone’s fingers or lips or genitals that look normal can be shedding the virus, so this is why it spreads so efficiently.
80% of population have Herpes and once you ave it, you have it forever. It travels towards the dorsal root ganglia and that’s why it can come back and cause recurrent infections, so that’s why people get recurrent cold sores.
Herpes Simplex Virus-symptoms
Often get tenderness or burning before you see blisters
They may be asymptomatic or they may be really painful
Systemic effects like viral meningitis are possible but not common
Herpes Simplex Virus-Eczema herpeticum
Remember people with eczema have staphylococcus colonising the skin universally because of the abnormalities of the skin barrier
Monomorphic ie lesions are all the same size
Herpes spreads really rapidly across skin of people with eczema and this is an emergency.
Need usually IV antibiotics as otherwise can get encephalitis and die.
Herpes Simplex Virus-Herpetic whitlow
Swabs and viral PCR swabs to make distinction and if in doubt treat for both. This is usually in children as well just as the bacterial one is
Herpes Simplex Virus-Herpes gladiatorum
Neonatal HSV infection
Caused by acquition of HSV 1 or 2 soon after birth
Children’s immune system are quite vulnerable at that time so can develop permanent consequence neurological deficits if they develop encephalitis, so this needs aggressive treatment with IV antivirals.
Herpes Simplex Virus-Severe or chronic
Can also get wart like manifesations and can spread into internal organs too.
HSV-diagnosis and treatment:
Or treat immediately and don’t wait if suspicious
Varicella Zoster Virus aka Herpes Zoster as it is in Herpes family
Take bacterial and viral swabs although can be known clinically.
Can cause blindness if near eye so treat Intravenously if the case.
Can effect several dermatomes
Hand Foot and Mouth Disease
Mostly caused by Coxsackie, sometimes Echo 71
Spread by oral oral contact or faecal oral route
No specific treatment but usually self limiting, Echo virus is more likely to result in encephalitis and other neurological consequences though
Which viruses cause morbilliform (measles-like) eruptions?
What other agents cause morbilliform rashes?
Whenever see this macular papular or morbiliform rash (ie measles like rash), think DRUG or BUG!
•Which disorders mimic morbilliform eruptions?
•What causes petechial/purpuric eruptions?
Just remember meningiococcus as this can be fatal, and endocarditis can cause it as well
Think could it be vasculitis, could it be menginococcus, could it be endocarditis or could it be coagulation abnormalities?
Sometimes you get skin eruptions that are not due to the infectious organism itself, it’s due to the body’s response:
Symmetric eruption of red bumps. It’s self limiting and resolves, but may be worth checking serology as HEP B can have longer term consequences.
Erythema Infectiosum
Usually self limited, can cause crises in sickle cell disease, and loss of pregnancy in pregnant women.
This is slower progression than Scarlet fever
Roseola infantum
Few days of high fever than get eruption of tiny pink raised lumps
Orf
Caused by zoonotic infection from goats or sheep. Self limited
These are also umblical blisters but are a lot more wet and blistering, with purpura content as well.
Umbilicated= having a small depression that resembles a navel umbilicated vesicles.
Warts
Fungal Infections
We define disseminated fungal infection as the presence of a fungal pathogen in the blood (fungemia) and/or any other sterile deep-seated structure because of hematogenous seeding
Superficial Fungal Infections-Pityriasis versicolor
These are part of our commensual, but they can become active in immunosuppressive states or heat or high humidity etc.
Hard to demonstarte malassezia on diagnostic states as it is fussy where it grows so relies on clinical judgement.
Superficial Fungal Infections
Superficial Fungal Infections-Tinea pedis
Tinea often presents as redness and scales
Superficial Fungal Infections
Id reaction
Not itself a reaction but is the body’s hypersensitivity reaction to the fungal infection.
Treat with topical steriods if looks like eczema or histamine in looks like uticaria
Majocchi granuloma
Eats through the dermis
Candidiasis
In immunosuppressed people it can become systemic, but it is often superficial.
Predisposition where skin meets skin as thrives in warm humid environment
Deep Fungal Infections
Very difficult to treat
Remember Sporotrocoid spread (eg in some atypical mycobacterium infections) where you see infection spreading along the lympatics, this was originally described in sporotrichosis but it is also found other conditions eg bacterial infection
Systemic Fungal Infections-sometimes you have fungi that don’t primarily target the skin, but the skin can be targeted similarly.
These are endemic to specific areas so taking a travel history is important and taking a skin biopsy, histology and culture and particularly checking if they’re immunosuppressed or not, eg check HIV status.
Opportunistic Fungal Infections
Black appearance surrounded by dusky erythema suggesting necrotysing infection
Aspergillosis
Again don’t respect anatomical boundaries eg invade blood vessels, cartilage and bone
Require aggressive treatment and early recognition
Mucormycosis
People with diabetes esp diabetic ketoacidosis are particularly at risk
Can’t always rely on diagnostic as progresses too quick to take sample, will be losing too much tissue.
Infestations
Scabies
Itchy eruption, typically worse at night-clue that it is scabies, other clue=contact might be itchy
In item C can see these burrows
In bottom right have patient with crusting. This is an example of norwegian scabies where you get this hyperkeratinosis. Same scabies species but norwegian just refers to hyperkeratinosis.
Most places recommend 2 cycles of treatment to kill the eggs
Treat topically with permethrin
Lice
Treat topically or orally. Don’t need to treat skin, just clean clothes.
Bedbugs
Don’t need to treat patient, just need to fumigate the home.
