Skin infection .pdf

Pathogens Causing Skin Infections
Will Discuss
Common Bacterial
Common Viral Infections
Fungal infections will be discussed
separately
2

How skin infections occur ?
1- There is a breach
2- Long term steroid therapy
3- Long term anti-biotic therapy
4- Disease induced
5- Drug induced
5

Skin Breaches range from microscopic to major trauma
6

Direct entry into skin of bacteria and fungi
Skin structure involved Infection Likely pathogen
Keratinized epithelium ringworm Dermatophyte fungi
Epidermis impetigo S.Pyogenes and /or S.Aureus
Dermis erysipelas S.Pyogenes
Hair follicles follicutlitis,
boils & carbuncles
S.Aureus
Subcutaneous fat cellulitis S.Pyogenes and /or S.Aureus
Fascia Necrotising faciitis Anaerobes and aerobes; usually
mixed pathogens
Muscle Myonecrosis/gangrene Clostridium perfringens
7

Bacterial infections of skin, soft tissue & muscle:
The classification depends upon the layers of skin
and soft tissue involved, although some infections
may involve several components of the soft tissues
(see table below)
The common causative organisms include :
Streptococcus pyogenes, Staphylococcus
aureus
8

Bacterial infections of skin, soft tissue &
muscle:
Can be classified as:
Abscess formation e.g. boils, carbuncles
Spreading infections e.g. impetigo, cellulitis,
erysipelas, wound infections, diabetic foot
infections.
Necrotizing infections e.g. fasciitis, gangrene
9

Folliculitis: is the inflammation of hair follicles due to
an infection, injury, or irritation
Infective folliculitis is the infection of hair follicles.
It starts when hair follicles are damaged by friction from clothing,
blockage of the follicle, or shaving.
The damaged follicles are then infected with the pathogen.
Commonly the causative pathogen is Staph.aureus. Sometimes
Strep. Pyogenes.
10

Folliculitis:
It is characterized by tender, swollen
areas that form around hair follicles.
This can occur anywhere on the skin or
scalp ; but often on the neck, breasts,
buttocks, and face.
Usually there is some itch, sometimes a
little soreness i.e. a mildly itchy
pustules on an erythematous base.
It is more common in hot weather, and
often occurs in macerated areas,
including under wet dressings. It may
be associated with shaving.
11

Folliculitis:
Other pathogens can cause folliculitis, so it is important is that
the pathogen is confirmed by culture if possible. Examples of
other causative pathogens include:
- Pseudomonas aeruginosa (usually acquired from
contaminated water supplied in hot tubs and spas)
- Malassezia yeasts, dermatophytes and herpes simplex
virus may also cause the condition.
12

Folliculitis: treatment
Sterile folliculitis is usually due to maceration, especially in
obesity, persons that sweat heavily, where there is contact with
occlusive substances (such as oils), shaving and waxing.
Treatment includes looking at the causes and using antiseptic
washes (e.g. triclosan 1%, chlorhexidine 2%) to reduce the
overgrowth of skin flora.
For pseudomonal folliculitis- you need to identify where the
patient was exposed to the pathogen (e.g. hot water tank, spa) .
Patient needs to avoid contact with the water source, until the
water supply has been treated to eliminate the bacteria.
13

Folliculitis- treatment
Mild forms of folliculitis can be managed with warm
compresses.
In severe cases of folliculitis a bacterial swab for
cultures and susceptibility should be taken. If S. Aureus,
is confirmed then topical preparation of mupirocin 2%
ointment or cream can be used twice daily for 5 days.
1
4

BOILS (Furuncles) :
Boils are abscesses–associated
with hair follicle, that extend into
the subcutaneous tissue.
Boils usually start as red, tender lumps.
The lumps (firm)quickly fill with pus,
growing larger and more painful until they
rupture and drain.
Although some boils disappear a
few days after they occur, most take
about two weeks to heal.
Boils can occur anywhere on the skin, but
appear mainly on the face, neck, armpits,
buttocks or thighs — hair-bearing areas
where person’s are most likely to sweat or
experience friction.
15
Image taken from Dermatology Image Atlas.
http://www.dermis.net/dermisroot/en/26817/image.htm

Carbuncles:
A carbuncle is a cluster of boils
that often occurs on the back of
the neck, shoulders or thighs,
especially in older men.
Carbuncles cause a deeper and
more severe infection than a
single boil. They also develop and
heal more slowly and are more
likely to leave a scar.
Symptoms include: fever, extreme
pain, increase white blood cell
count (WBC),exhaustion.
1
6
Image taken from Dermatology Image Atlas

Boils & Carbuncles:
The causative organism is usually Staphylococcus aureus,
occasionally in combination with Streptococcus pyogenes.
Most lesions are able to be treated with incision and drainage;
without the use of antibiotics
17

Boils & Carbuncles- treatment
If lesions are associated with spreading cellulitis or there systemic symptoms
are present……..
THEN
the patient requires antibiotic treatment; together with surgical incision and
drainage of the lesions.
Also, microscopy and cultures should be performed on the lesions
if ABs are going to be used.
For empirical therapy (adult):
di/flucloxacillin 500 mg orally, 6-hourly for 5 days
OR
1
8
Ref- e Therapeutic Guidelines - Antibiotic Version 15- Accessed 3/8/17

Boils & Carbuncles- treatment
For patients hypersensitive to penicillin (excluding
immediate hypersensitivity),use:
cephalexin 500mg orally,6 hourly for 5 days.
OR
For patients with immediate penicillin hypersensitivity,
use:
clindamycin 450 mg orally, 8-hourly for 5 days.
OR
trimethoprim+sulfamethoxazole 160+800 mg orally,
12-hourly for 5 days
19

Impetigo:
Impetigo is superficial infection of the skin (epidermal layer)
Most often seen in children.
Impetigo has TWO distinct presentations/types:
1. crusted or non bullous impetigo
OR
2. bullous impetigo
In affluent communities (non –remote) the common pathogen is Staph. aureus
and less commonly by Strep. pyogenes (or both together).
2
0

Impetigo- crusted or non-bullous:
It is a contagious superficial infection of
the skin due to Streptococci,
Staphylococci or both.
Characterized by superficial vesicular
lesions that later become pustular then
crusted, the resultant crusts being often
honey colored.
Lesions occur predominately on face, legs,
arms of infants and children.
21
http://www.dermis.net/bilder/CD067/550px/img0033.jpg

Bullous Impetigo:
It is a contagious superficial infection of the
skin associated with Staphylococci.
It is characterized by small vesicles or
pustules that develop into thin walled bullae
which rupture easily.
The resulting erosions maybe covered by a
yellow or brown crust.
The face, trunk and extremities of infants
and children are mainly affected.
2
2

Impetigo- treatment:
Non-remote community settings:
Usually suspect S. aureus as the pathogen.
Antibiotic therapy that is active against S. aureus also will also
cover S. pyogenes.
For localised skin sores, use:
• mupirocin 2% ointment or cream topically to crusted areas, 8-
hourly for 7 days.
2
3

Impetigo- treatment:
Non-remote community settings:
For multiple skin sores or recurrent infection, use:
di/flucloxacillin 500 mg (child: 12.5 mg/kg up to 500 mg) orally, 6-hourly for up to 10
days (stop therapy earlier if infection has resolved).
In patients with no immediate penicillin allergy:
cephalexin 500mg (child: 12.5 mg/kg up to 500 mg) orally, 6-hourly for 10 days (stop
therapy earlier if infection has resolved).
For patients with immediate penicillin hypersensitivity, use:
trimethoprim+sulfamethoxazole 160+800 mg (child 1 month or older: 4+20
mg/kg up to 160+800 mg) orally, 12-hourly for 5 days.
24

Impetigo- treatment cont’d:
In remote community settings in central and northern Australia
S. pyogenes is usually the causative pathogen of impetigo.
Use:
1. benzathine penicillin 900 mg (child 3 kg to 6 kg: 225 mg; 6 kg to 10 kg: 337.5 mg;
10 kg to 15 kg: 450 mg; 15 kg to 20 kg: 675 mg; 20 kg or more: 900 mg) IM, as a single
dose
OR
1. trimethoprim+sulfamethoxazole 160+800 mg (child 1 month or older: 4+20 mg/kg
up to 160+800 mg) orally, 12-hourly for 5 days
OR
1 .trimethoprim+sulfamethoxazole 320+1600 mg (child 1 month or older: 8+40
mg/kg up to 320+1600 mg) orally, daily for 5 days
25

Impetigo- treatment cont’d:
Impetigo that has not responded to usual empirical therapy
may possibly be caused by community-associated
methicillin-resistant S. aureus [CA-MRSA]).
Then try :
trimethoprim+sulfamethoxazole 160+800 mg (child 1 month
or older: 4+20 mg/kg up to 160+800 mg) orally, 12-hourly for
5 days.
If the above does not work then treatment should be guided
by the results of cultures and susceptibility tests
26

Erysipelas:
Erysipelas is a superficial form of cellulitis; a bacterial infection
affecting the dermal layer of the skin.
It particularly affects infants and the elderly, but can affect any
age group.
Unlike cellulitis, almost all erysipelas is caused by Group A beta
haemolytic streptococci (Streptococcus pyogenes)
27

Erysipelas:
Erysipelas usually involve the face
It can have a characteristic butterfly
distribution on the cheeks and bridge
of the nose.
If face is affected ,there may be an
underlying facial sinus or dental
infection. Dental examination and
imaging of sinuses is recommended.
It can also affect the skin of the lower
limbs.
28

Erysipelas
Affected skin is distinguished from other forms of cellulitis by a
well-defined, raised border between affected & non-affected skin.
The affected skin is red, swollen and may be finely dimpled (like
an orange skin). It may be blistered.
Bleeding into the skin may cause purpura(purple patches).
Symptoms and signs of erysipelas are usually abrupt in onset and
often accompanied by general illness in the form of fevers, chills
and shivering.
Treatment is the same for mild early cellulitis (see slides below).
2
9

Cellulitis:
Cellulitis is a common infection of the skin (usually bacterial),
which can affect all ages; more common among infants, young
children and older adults.
A cellulitic infection extends more deeply than an erysipelas, and
involves subcutaneous tissues.
The infection occurs because the cutaneous layer of skin has been
damaged in some way, which allows bacteria to enter.
The diagnosis of cellulitis is based on the clinical features(see slides
below). Investigations are rarely needed or useful.
30

Cellulitis:
The most common infecting organisms are Streptococcus pyogenes
(two thirds of cases) and Staphylococcus aureus (one third).
Cellulitis caused by S.aureus is usually associated with wounds,
trauma or ulcerations. Spontaneous rapidly spreading cellulitis is
almost always caused by S.pyogenes
In immunosuppressed patients, a wide variety of organisms
including Gram-negative bacteria, fungi and mycobacteria may also
be responsible.
Cellulitis may also complicate wounds (eg cuts, abrasions), insect bites
or scabies.
3
1

Cellulitis- Clinical features:
Some or all of the following features may be seen over the
affected skin:
redness (tender erythema)
swelling
increased warmth
tenderness
as rash progresses blistering may occur
if there is no increased warmth over the skin it is unlikely to be cellulitis.
People working at farms at a higher risk/ hygiene is one of the main issue.
32

Cellulitis- Clinical features
It usually affects a limb but can occur
anywhere on the body. It is most often
unilateral. Cellulitis in adults most often
affects the lower legs.
Symptoms and signs are usually localised
to the affected area but patients can
become generally unwell with fevers,
chills and shakes, increased WBC.
3
3

Cellulitis- Clinical features
Other features seen less commonly include swollen
lymph glands draining the affected area (e.g. in the
groin with a leg cellulitis), or abscess formation
within an area of cellulitis.
After successful treatment, the skin may flake or
peel off as it heals.
3
4

Predisposing factors for Cellulitis:
Problems with venous or lymphatic drainage of the area
Previous injury to the limb (e.g. trauma, radiotherapy, surgery)
Diabetes
Fissured dermatitis
Alcoholism
Obesity
Swelling of the legs
Pregnancy
Tinea Pedis in the toes of the affected limb
35

Question:
Looking at the major causative pathogens for
cellulitis & erysipelas
which antibiotics would be the likely ones used
for treatment ?
3
6

Erysipelas& Cellulitis- Mild early cellulitis and erysipelas
Treatment:
To cover Staphylococcus aureus and Streptococcus pyogenes, use in adults:
di/flucloxacillin 500 mg (child: 12.5 mg/kg up to 500 mg) orally, 6-
hourly for 5 to 10 days.
If S. pyogenes is confirmed, or suspected due to clinical presentation (see
above) or local susceptibility patterns use
1. phenoxymethylpenicillin 500 mg orally, 6-hourly for 5 to10 days
OR
1. procaine penicillin 1.5 g IM, daily for at least 3 days.
37

Erysipelas & Cellulitis- Mild early cellulitis and erysipelas
Treatment:
For patients hypersensitive to penicillin (excluding immediate
hypersensitivity), in adults, use :
cephalexin 500 mg orally, 6-hourly for 5 to 10 days.
For patients with immediate penicillin hypersensitivity, in adults ,
use:
clindamycin 450 mg orally, 8-hourly for 5 to 10 days.
38

Severe cellulitis is when patient has significant systemic
features that have not responded to 48 hours of oral
therapy.
Treatment :
requires IV antibiotic therapy.
rest and elevation of the affected area are advisable.
nonstick dressings if skin is eroded
other treatment could include:
 surgery
 debridement of dead tissue
 incision & drainage of abscesses
 removal of clots and foreign bodies
3
9

Severe cellulitis- IV Antibiotic treatment:
To treat infection with either streptococci or staphylococci, use:
Flucloxacillin IV 2 g (child: 50 mg/kg up to 2 g) IV, 6-hourly.
For patients hypersensitive to penicillin (excluding immediate hypersensitivity), use:
Cephazolin IV 2 g (child: 50 mg/kg up to 2 g) IV, 8-hourly.
For patients with immediate penicillin hypersensitivity, use
1st line - Vancomycin IV OR 2nd line - Clindamycin IV
clindamycin 600 mg (child: 15 mg/kg up to 600 mg) IV, 8-hourly
IV therapy should be continued until the patient is afebrile and systemic features
have improved. The patient can then change to oral therapy for
a total of up to 2 weeks treatment.
40

What preventive measures can be taken
to reduce the risk of recurrent cellulitis?
41

Preventative measures for patient’s with
recurrent cellulitis:
Examine patients hands & feet for___tinea_____, and if present treat it.
Avoid trauma/injury to skin , wear _long sleeves and pants in high risk
activities e.g. gardening .
Keep skin _clean____and well _moisturized______ with nails well
tended.
If appropriate, use compression stockings (e.g. patients with leg oedema,
venous insufficiency or ulcers)
42

Preventative measures for patient’s with recurrent
cellulitis:
Keep swollen limbs _elevated__ during rest periods to aid lymphatic
circulation.
In cases of frequent recurrence, continuous prophylaxis can be considered .
Use :
phenoxymethylpenicillin 250 mg orally, twice daily for 6 months initially.
Patients with recurrent cellulitis should be referred to an infectious diseases
physician for assessment.
43

Necrotising skin and soft tissue
infections:
•Necrotising fasciitis
•Gas Gangrene
44

Necrotising fasciitis is a (usually
bacterial) infection of the soft
tissue and the fascia (which covers the
muscle).
It is potentially fatal, if not treated
promptly.
The bacteria enter , multiply and
release toxins and enzymes that
result in thrombosis (clotting) in
the blood vessels; eventually
resulting in destruction of the soft
tissues and fascia… i.e. necrosis.
45
Image taken from New Zealand Dermatological Society
Incorporated. Published online at: http://www.dermnetnz.org.
http://www.dermnet.org.nz/bacterial/necrotising-fasciitis.html

Necrotising fasciitis:
The aetiology of necrotising fasciitis is not fully
understood and in many cases there is no identifiable
cause.
Patients usually have some history of trauma to the skin;
which can be minor (e.g. insect bite, small cut, scratch, iv
drug use/site) or major (e.g. bed sore, post-operative
wound, crush injury).
46
Reference: Hasham S Matteucci P, et al. Necrotising fasciitis Clinical review
BMJ 2005;330:830-833 (9 April).
http://bmj.bmjjournals.com/cgi/content/full/330/7495/830

Necrotizing fasciitis:
Also most patients who develop necrotising fasciitis have pre-
existing conditions that render them susceptible to infection for
example:
peripheral vascular disease
diabetes mellitus
drug misuse
immunosuppression
chronic renal failure
seem to be risk factors .
47
BMJ 2005;330:830-833 (9 April).

There are two types of necrotising fasciitis:
Type I monomicrobial >>>>due to one organism e.g:
 Haemolytic group A S. pyogenus ( flesh eating disease)
 Clostridium perfringens (gas gangrene) -G+ve anaerobic rods
 S. aureus (G+ve cocci)
Type 2 polymicrobial >>>>>synergistic gangrene i.e. more than on
bacteria involved.
Pathogens include mixed aerobic and anaerobic bacterial flora eg. E. coli,
B.fragilis, Streptococci & staphylococci
Use MCS of tissue sample to identify pathogen.
4
8
BMJ 2005;330:830-833 (9 April).

Necrotising Fasciitis – Sign & Symptoms
The diagnosis is based on clinical signs & symptoms (i.e. a clinical one).
The information from all the investigations should be taken into account.
Symptoms appearing usually within 24 hours of an skin injury or surgery:
Pain in the affected area of the injury, which increases over time.
Cellulitic-type rash.
Patient can display /report nausea, fever, diarrhea, dizziness and general
malaise.
Patient reports an intense thirst (dehydration).
49

Necrotising Fasciitis – Sign & Symptoms:
Within 3-4 days of the initial symptoms the
following may occur:
Swelling of the affected area; purplish rash may
appear.
The skin darkens and this progresses into blisters
filled with dark fluid (haemorrhagic bullae).
Skin starts to die and area appears necrotic. At
this point in time the patient experiences severe
pain.
5
0
Image taken from (New Zealand
Dermatological Society Incorporated.
Published online at:
http://www.dermnetnz.org).
http://www.dermnet.org.nz/bacterial/necr
otising-fasciitis.html

Necrotising Fasciitis – Sign &
Symptoms
If allowed to progress……by about days 4-5 the patient:
is acutely unwell and may require intensive care support
will likely have a very low blood pressure
has tachycardia
has high temperature
high WCC
Increased serum creatinine
↓↓ albumin
gas in the soft tissues (detected by palpation or imaging)
THEN
51

Necrotising Fasciitis – Sign &
Symptoms
The infection has spread into the bloodstream
leading to toxic shock, renal failure (multi organ
failure)
may have altered levels of consciousness or become
totally unconscious.
Death
52

Treatment of necrotising fasciitis involves the
following key strategies:
surgical removal of dead tissue (sometimes even
amputation)
plus
the prompt initiation of IV antibiotics
(broad spectrum for empirical therapy)
supportive therapy (e.g. IV fluids and inotropes where
necessary)
and a possible skin graft at a later date.
53

Necrotising fasciitis :Treatment
For empirical therapy, where the diagnosis is uncertain and
until tissue and blood culture results are available, use initially:
meropenem IV PLUS vancomycin IV PLUS clindamycin IV
(clindamycin (or lincomycin) is recommended to reduce bacterial toxin production)
Therapy is then modified (directed) according to gram stain and
culture and susceptibilities of a surgical deep tissue specimen.
Duration of IV treatment is usually a minimum of 5 days….but this
depends on the patient's response and the ongoing need for
surgery. Patient should be switched to oral therapy only after there
has been a significant improvement in their condition.
54

Necrotising fasciitis :Treatment
For proven Streptococcus pyogenes necrotising fasciitis, use:
Benzylpenicillin IV PLUS clindamycin IV
PLUS (consider after expert advice) normal immunoglobulin
up to 2 doses during the first 72 hours.
For patients hypersensitive to penicillins (excluding immediate
hypersensitivity) you can replace the benzylpenicillin with cephazolin 2 g
IV .
IV antibiotic treatment is usually for minimum of 7 days but this depends on
the patient's response and the ongoing need for surgery.
55

Clostridial infection-> gas gangrene/myonecrosis :
Clostridium bacteria produce many different toxins, four of
which(alpha, beta, epsilon, iota) can cause potentially fatal
syndromes.
In addition, they cause: tissue death (necrosis), destruction of
blood (hemolysis), local decrease in circulation
(vasoconstriction),and leaking of the blood vessels (increased
vascular permeability).
These toxins are responsible for both the local tissue
destruction ,therefore maintaining anaerobic environment
and the systemic symptomS.
5
6

Gas gangrene/ Myonecrosis
Gas gangrene is a potentially deadly form of tissue death.
The condition is most often caused by a bacteria called
Clostridium perfringens. It occurs when clostridia invade
healthy muscle from adjacent traumatized muscle or soft
tissue.
This bacteria under anaerobic (low oxygen) conditions,
produces gas as a result of anaerobic fermentation and
toxins that cause tissue death and associated symptoms.
5
7

Gas gangrene
Clostridial infection can progress to gas gangrene
/myonecrosis. This is a fast-spreading infection of
muscle tissue that quickly leads to death if untreated.
Gas gangrene generally occurs at the site of trauma or a
recent surgical wound. About a third of cases occur
spontaneously.
Patients who develop this disease spontaneously, often
have underlying blood vessel disease (atherosclerosis or
hardening of the arteries), diabetes, or colon cancer.
58

Gas gangrene : Local sign & symptoms
Onset of gas gangrene is sudden and
dramatic.
There is moderate to severe pain around a
skin injury.
There is progressive swelling around the
injury.
Skin color is initially pale, later dusky
progressing to dark red or purple
Vesicle formation; coalescence (combine into
large blisters); blisters fill with brown-red
fluid.
59
Image taken from
http://anaerobicinfections.blogspot.com/p/cutaneou
s-soft-tissue-and-muscle.html

Gas gangrene : Local sign & symptoms
If tissue is drained - there is foul-
smelling brown-red or bloody fluid
(serosanguineous discharge).
Air under the skin – subcutaneous; gas
may be felt in the tissue as a crackly
sensation when the swollen area is
pressed with the fingers.
60
Plain X-ray often shows gas in the
subcutaneous tissue and fascial plains
Pictures From ref : 2

Gas gangrene - Systemic signs &
symptoms:
develop early in the infection.
consist of sweating, moderate to high fever and increased heart rate .
if untreated or treatment is delayed, the individual can
develop a shock -like syndrome with decreased blood
pressure (hypotension), kidney failure, delirium,
coma………and can progress to death.
if patient survives they may be left with disfiguring or disabling
permanent tissue damage.
6
1

Clostridial infection-> gas gangrene-> diagnosis & treatment
The initial diagnosis of gas gangrene is based on the person's
symptoms and a physical examination, i.e. it is a clinical diagnosis.
Gas bubbles found in muscle on x- ray may increases a doctor's
suspicion of a clostridial infection.
Examination of secretions from the wound under a microscope may
reveal the clostridia, and cultures can confirm their presence - but
because gas gangrene is so rapidly fatal, treatment is always begun
before the culture results are available.
6
2

Clostridial infection-> gas gangrene->
Treatment includes:
immediate surgery to remove dead , damaged or infected
tissue (sometimes amputation is necessary to contain the
infection)
intravenous antibiotic therapy
analgesia for pain
supportive therapy (intensive care , iv fluids, etc)
+/- hyperbaric oxygen (especially for severe infections)
and later …..skin grafting will most likely be necessary.
6
3

Clostridial infection-> gas gangrene-> Antibiotic Treatment :
For Clostridial infection with or without myositis/myonecrosis
(gas gangrene), in adults, use:
benzylpenicillin 2.4 g IV, 4-hourly.
For patients with penicillin hypersensitivity, use:
metronidazole 500 mg IV, 8-hourly.
Note: high doses
64

Viral infections that cause skin manifestations:
Herpes simplex
Herpes Zoster
6
5

Herpes simplex:
a viral infection with a skin manifestation caused by herpes simplex virus (HSV) ;
a blistering rash; blisters localised.
there are two main types of HSV:
- Type 1- mainly associated with facial infections
(cold sores or fever blisters, oral ulcers).
- Type 2- mainly genital (more likely sexually transmitted).
when you get an “attack of herpes” the virus has grown down the
nerves and onto skin and mucous membranes>>> multiplies>>>>blistering rash.
6
6

Herpes simplex:
HSV is spread is by direct contact with infected secretions.
The virus is shed in saliva and genital secretions, during a clinical
attack and for some days or weeks afterwards; more of virus
secreted in active lesion.
Post “attack” the virus travel back up the nerve and becomes
dormant ;both type 1 and type 2 HSV can lie dormant in nerves.
67

Herpes simplex:
HSV infections look like clustered vesicles on an
erythematous (red/inflamed) base.
Itching or burning at site precedes lesions.
Can often progress to pustular or ulcerated
lesions, and they eventually form a crust.
Systemic symptoms, such as fever, malaise, and
enlarged lymph nodes , may accompany the
lesions, especially in primary infections.
Diagnosis is usually clinical one BUT if in doubt it
can be confirmed microbiologically.
68
Images taken from (New Zealand Dermatological
Society Incorporated. Published online at:
http://www.dermnetnz.org

Herpes simplex: Recurrent infection
HSV lesions tend to recur at or near the same location within the distribution of
a sensory nerve; not necessarily exactly the same site.
The appearance of a recurrent infection usually differs from primary; smaller
vesicles ,grouped closer.
HSV Type 1 infection can re- occur on any site but more often on the face,
especiallyparticularly on the lips (‘herpes simplex labialis’).
HSV Type 2 infection may also re-occur on any site but most often affect the
genitals or buttocks.
Triggers for reoccurrence can include: stress, trauma to affected site,
sun exposure, operations/procedures performed on the face.
6
9

HSV oral mucocutnaeous treatment:
Cases of minor primary episodes of oral mucocutaneous HSV
infection can be treated symptomatically with systemic
analgesic, antipyretics, and topical anaesthetic drugs
(e.g. lignocaine gel +/- Chlorhexidine in preparation).
Chlorhexidine mouthwash can be used to prevent
secondary infection and aid oral hygiene. Can be used in
combination with benzydamine, a topical analgesic (see
lozenge preparations).
70

attack/episode:
Oral antiviraltherapy is recommended in severe herpes simplex virus infections on any part of the skin or oral
mucosa. Start treatmentpromptly.
Use:
1. aciclovir 400 mg orally, 5 times a day for 7 days
OR
1. famciclovir 500mg orally, 12-hourly for 7 days
OR
1. valaciclovir 1g orally, 12-hourly for 7 days.
If the patient is immunocompromised or is unable to take oral antivirals, then IV
antivirals need to be given, with the consultation of an infectious diseases expert.
71
Ref- e Therapeutic Guidelines– Dermatology 2015- Accessed 3/8/17

HSV oral mucocutnaeous - Recurrent episodes
As mentioned previously, HSV Type 1 infection can re- occur on any
site but more often on the face, especiallyparticularly on the lips
(‘herpes simplex labialis’).
If a minor recurrence- use: topical aciclovir (adult and child) at the
first sign of the lesion:
Aciclovir (adult and child) _5__ % cream topically, _4__ times
daily (every 4 hours while awake) for _5__ days at the first sign
of recurrence.
72
.

HSV oral mucocutnaeous - Recurrent episodes
If infrequent but severe recurrence of oral mucocutaneous HSV infection, Start
treatment ASAP when symptoms occur; it is effective if started within 48 hours
of symptom onset.
Use: 1. famciclovir 1500 mg orally, as a single dose
OR
1. valaciclovir 2 g orally, 12-hourly for 1 day
OR
2. aciclovir 400 mg (child: 10 mg/kg up to 400 mg) orally,
5 times daily for 5 days
73
If the patient is immunocompromised or is unable to take oral antivirals, then IV antivirals
need to be given, with the consultation of an infectious diseases expert.
Note: would expect you to know which drugs; no need to memorise doses .

Herpes Zoster or Varicella Zoster (Shingles):
A viral infection with a skin manifestation, that causes a
blistering rash which is painful.
Caused by reactivation of the varicella-zoster (VCZ) virus
(chicken pox, the primary infection).
After the primary infection the VCZ virus lies dormant in the
nerve cells in the spinal cord, usually of nerves that supply
sensation to the skin.
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4

Herpes Zoster or Varicella Zoster (Shingles):
If the VCZ virus is reactivated it travels down the nerves to the
skin to cause the blistering rash= SHINGLES.
Occurs more commonly in adults and can occur in
anyone who has previously had chickenpox. More
common and more severe in patients with poor immunity.
75
Image s taken from Dermatology Image Atlas
http://www.dermis.net/

Herpes Zoster- Signs & Symptoms:
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6
Image s taken from Dermatology Image
Atlas http://www.dermis.net/
• Usually the first sign is pain (+/- severe)which
occurs along the pathway of the sensory
nerves emerging from the spine.
• The chest (thoracic), neck (cervical), forehead
(ophthalmic) and lumbar/sacral sensory nerve
supply regions are most commonly affected.
• Pain be localized or may be spread.
• 1-3 days post occurrence of pain, the
SHINGLES rash appears, where the pain on
skin occurred previously; the rash appears as
a “crop” of closely grouped raised red lesions.

Herpes Zoster- Signs & Symptoms :
The rash is like a “band”/”stripe” on the
skin supplied by one, occasionally two,
and rarely more neighbouring spinal
nerves.
New lesions continue to appear for
several days; they blister>become
pustular> then crust.
The rash is usually unilateral – one side
of body affected.
The patient usually unwell with fever
and headache.
7
7
http://www.dermis.net/

Lymph nodes draining the affected area are often enlarged and tender. Pain and
general symptoms subside gradually as the eruption disappears.
Note- pt. in the vesicular stage is infective and can infect non immune contacts
with Varicella.
In uncomplicated cases recovery is 2-4 weeks; recovery time longer in elderly.
After resolution of the shingles, some patients (~10%) are often
left with post herpetic neuralgia (pain for >4 weeks after crusting of
vesicular lesions); occurs more often in elderly.
78

Postherpetic neuralgia:
◦ pain is usually severe
◦ pain sensation can be: burning, aching, boring, stabbing.
◦ patient almost always has an atypical response (allodynia) of severe
pain to a light stimulus, such as gentle brushing of the skin.
◦ it may be prolonged and difficult to manage.
◦ severity of rash or scarring has no bearing on degree of post herpetic
pain.
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9

Herpes Zoster : Management & Treatment
Antiviral treatment should be prescribed for any patient seen
within 72 hours of the onset of vesicles/rash AND all
immunocompromised patients.
USE:
1. famciclovir 250 mg orally, 8-hourly for 7 days
OR
1. valaciclovir 1 g orally, 8-hourly for 7 days
OR
2. aciclovir 800 mg (child: 20 mg/kg up to 800 mg) orally,
5 times daily for 7 days.
80
Note: would expect you to know which drugs; no need to memorise doses

Lesions should be bathed with saline 3 times a day to remove
crusts and exudate.
Use non adherent dressings to cover lesions, protect and reduce
infectivity.
Use analgesics for pain; ice packs or cold compresses.
If there is an ocular involvement ophthalmic herpes zoster (refer to
ophthalmologist).
81
Herpes Zoster : Management & Treatment

Skin infection .pdf

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