Infective diseases Flashcards
primary infection with HSV usually occurs when? what symptoms will they present with?
in childhood - asymptomatic or gingivostomatitis
herpes simplex infection occurs when there is reactivation of the HSV from a __ __ __ or __ __ __
dorsal root ganglion
cranial nerve ganglion
T/F: after initial infection with the herpes simplex virus, HSV becomes dormant and lies in the dorsal root ganglia of the spinal nerves for life
true
characteristic lesion with HSV?
localised painful vesicular rash preceding by tingling (esp if recurrent)
HSV-1 is most commonly associated with ___ lesions, whereas HSV-2 is most commonly associated with ___ lesions
1- oral
2- genital
Presentation of herpes labialis?
(aka coldsore)
Prodromal burning/ itching > small crop of vesicles arise on lips/ perioral > burst to leave a crust
Presentation of herpes genitalis?
Prodromal burning/ itching > small crop of acutely painful vesicles arise on the genitalia (+ rarely anal)
Presentation of herpetic whitlow?
paronychia
most common in dentists and other healthcare workers
diagnosis of HSV?
clinical diagnosis
management of HSV infection?
topical aciclovir
oral if widespread/ systemic upset
complications of HSV infection?
eczema herpeticum (pt with atopic eczema - urgent IV therapy + hospitalisation)
erythema multiforme
herpes simplex encephalitis
what virus causes chicken pox
varicella zoster virus (90% of population infected before adolescence)
transmissions of varicella zoster virus?
via airborne droplets and/ or direct contact with the lesions of an infected person
Varicella zoster virus:
1) Once in contact with pt, the virus travels where to replicate?
2) after several days, virus spreads to the __ and __ and continues to multiply
3) 1-2 weeks later, migrates to skin and mucous membranes causing characteristic ____ rash
4) on exposure to virus, large number of ___ are released throughout the body
5) the virus becomes dormant in the __ __ __
6) it can then reactive in later life as ____
1) regional lymph nodes (primary viraema)
2) spleen and liver
3) vesicular (vesicles are filled with highly contagious viral fluid)
4) Abs (providing lifelong immunity - chicken pox for 2nd time v rare)
5) dorsal root ganglia of the spine
6) shingles (herpes zoster)
presentation of chicken pox?
1) prodrome (1-2 days before cutaneous features): pyrexia, HA, malaise, abdo pain
2) widespread vesicular rash: begins on trunk, quickly spreads to the rest of the body. Extreme pruritis, vesicles burst leaving a crust.
diagnosis of chicken pox?
clinical diagnosis
Rx of chicken pox?
self-limiting. Supportive treatment (paracetamol, NSAIDs, emollients)
aietology of shingles?
reactivation of varicella zoster virus from DRG or CNG
shingles
1) T/F: can arise in anyone
2) more common in elderly
3) more common in patients who are _____
1) as long as they’ve been preivously infected with varicella zoster
2) true (unsuual in children)
3) immunocompromised
differentiating shingles from chickenpox?
shingles: arises in a single dermatome (relating to the ganglion the virus has reactivated in)
3 stages of shingles?
1) pre-eruptive: prodromal pruritis or burning for 1-2 days
2) eruptive: maculopapular rash developing in a single dermatome. Clusters of small vesicles >burst and form crust. Severe neuritic pain and allodynia.
3) chronic: post-herpetic neuralgia. Can be recurrent/ last >1 month after the rash has cleared
diagnosis of shingles?
clinical diagnosis (vesicular rash confined to single dermatome)
if uncertain > viral swab for PCR
Rx shingles?
aciclovir (early oral therapy may reduce length of illness and risk of post-herpetic neuralgia)
symptomatic: rest, paracetamol, NSAIDs
prevention: shingles vaccine. If infection = avoid contact with pregnant women and immunocompromised
Complications of shingles?
Ramsay hunt syndrome
Herpes zoster opthalmicus
what is ramsay hunt syndrome?
aka herpes zoster oticus
virus reactivates in geniculate gangloin, causing it to migrate down CNVII and VIII
Rash/ vesicles develop in the auditory canal and throat. Facial palsy, deafness, vertigo, tinnitus.
what is herpes zoster opthalmicus
virus reactivates in the ophthalmic division of the trigeminal nerve (CN V1). +ve Hutchinson sign: indicates involvement of the nasociliary branch + potential ocular complications - keratitis, uveitis, conjuncitivis, iritis, optic neuritis
what is impetigo
contagious bacterial infection common in childhood (2-5)
can occur later in life if pts are immunocompromised
most commonly develops during what sort of weather?
hot and humid
most common pathogens in impetigo
most often s. aureus.
Less commonly strep pyogenes or MRSA
2 types of impetigo?
impetigo (non-bullous)
bullous impetigo
how does impetigo form
small breaks in skin/ minor abrasions allow bacteria to enter skin from another infected individual
presentation of impetigo
most often the face (esp around mouth+ nose)
erythematous macules > small crop of vesicles/ pustules > rupture releasing exudate > dries forming golden yellow/ brown crust (honey comb)
impetigo infection lasts how long?
2-3 weeks
diagnosis of impetigo?
clinical diagnosis
swab if uncertain
Rx of impegito?
wound care: regular cleaning, topical antiseptic or Abx
Oral fluclox if infection extensive
Measures to reduce spread (not sharing towels etc)
what is this describing:
a pyogenic infection of the s/c fat and lower dermis
cellulitis
causative pathogen in cellulitis?
step pyogenes (2/3) staph aureus (1/3)
risk factors for cellulitis?
prev cellulitis venous stasis lymphodema obesity elderly IVDU alcoholism inflammatory dermatoses insect bites pregnancy immunosupression
how does cellulitis form?
bacteria penetrate the skin through disruptions to the normal barrier
they make their way to the deep dermal and s/c layers where they proliferate
presentation of cellulitis?
often unilateral, affecting a limb
localised, painful, erythematous and swollen
systemic features (fever, rigors, malaise)
diagnosis of cellulitis
clinical diagnosis
confirm with: raised WCC, raised CRP, swab and culture causative organism
Rx of cellulitis?
analgesia (WHO ladder)
fluclox 1st line Abx
what is molluscum contagiosum
viral skin infection that presents as cluster of papules (mollucsa)
who gets molluscum contagiosum?
almost exclusively childhood infection (1-4)
what causes molluscum contagiosum?
infection with Poxvirus
methods of transmission: direct skin-skin contact, indirect (fomite), autoinucolation (scratching, shaving), sexual transmission
presentation of molluscum contagiosum?
clusters of small, shiny, round, umbilcated papules most often on limbs
usually flesh coloured (can be white, pink or pigmented)
diagnosis of molluscum contagiosum?
clinical (skin biopsy if unusual presentation - rare)
Rx of molluscum contagiosum?
no treatment to eradicte the virus
self limiting mostly, not actively treatment (often lasts 12-18 months)
To speed up disappearance of each papule: squeeze out the soft, white core of the papule, cryothereapy, gentle curettage, antiseptics, wart paints/ salicylic acid
what is pityriasis versicolor?
a common cutaneous yeast infection
pityriasis versicolor more common in what climate?
hot/ humid
what causes pityriasis versicolor?
infection with the fungus Malassezia (makes up part of normal cutaneous flora)
> changes from its usual form to a pathological form that proliferates and causes infection
pityriasis versicolor presentation:
1) most commonly presents on the ___ initially
2) describe the lesions
3) are the lesions symptomatic?
1) trunk
2) multiple hypopigmented macules with a fine scale
4) may be slightly pruritic
diagnosis of pityriasis versicolor?
clinical
if uncertain: wood’s lamp (yellow/ green fluorescence). Skin scraping for microscopy.
Rx of pityriasis versicolor?
topical anti-yeast e.g. clotrimazole or ketoconazole
what is this describing:
Also known as slapped cheek/ fifths disease.
A common infective paediatric condition.
erythema infectiosum
erythema infectiosum - most common in who? and when?
children
winter months
what causes erythema infectiosum?
infection with parovirus B19/ erythrovirus
- spread via respiratory droplets
presentation of erythema infectiosum?
non-specific prodrome (HA, malaise, fever)
biphasic rash
- erythema over cheeks, sparing nasal bridge and periorbital region. 1-4 days.
- pink, lace-like rash trunk and limbs. 5-9 days. Can recur in the following months following trigger e.g. sunlight, stress etc
when are pts with erythema Infectiosum no longer infectious?
when erythematous rash over cheeks forms
complications of erythema Infectiosum?
small joint polyarthropathy
spontaneous abortion (hydrops foetalis)
aplastic crisis
chronic anaemia
diagnosis of erythema Infectiosum?
clinical
if uncertain -Ab testing (paravirus B19 IgM)
rx of erythema infectiosum?
self-limiting
supportive Rx
hand, foot and mouth disease occurs following infection with what?
cocksackie virus A16, cocksackie virus A10, enterovirus 71 (usually more severe)
transmission of hand, foot and mouth disease?
often faecal-oral route
presentation of hand, foot and mouth disease?
non-specific prodrome: HA, malaise, fever
painful oral lesions (vesicles and ulcers)
vesicles on palms of hands, soles of feet and in between fingers (grey in colour, have tendency to ulcerate/ crust. Typically resolve in 10 days. May be painful
complications of hand, foot and mouth disease?
neuro involvement/ meningitis risk - usually when enterovirus 71 is the causative virus
Rx of hand, foot and mouth disease?
self-limiting
supportive treatment as required
what is Pitted Keratolysis?
a bacterial skin infection mainly affecting the feet
Pitted Keratolysis
1) more common in what weather?
2) high incidence in what occupations?
1) hot and humid
2) farmers, athletes, industrial/ construction workers
causative organism in Pitted Keratolysis?
Corynebacterium infection.
Pitted Keratolysis risk factors?
- hot, humid weather (bacteria proliferative)
- poorly breathable footwear
- excessive perspiration
- poor hygeine
- immunosupression
Pitted Keratolysis pathophysiology
1) bacteria rapidly proliferative in optimum conditions
2) they produce protease enzymes that work to destroy the __ __
3) ____ compounds released by the bacteria cause a potent malodour
2) stratum corneum (>characteristic pitted appearance)
3) sulfur
Pitted Keratolysis almost always affects where?
plantar aspect of foot (+ rarely the hands)
how does Pitted Keratolysis present?
extremely unpleasant, malodorous feet
multiple small pits covering the feet. Usually asymptomatic, may rarely cause pain or itching. May coalesce to form a large crater-like lesion
diagnosis of Pitted Keratolysi?
clinical
skin scraping to rule out fungal infection
Rx of Pitted Keratolysi?
encourage breathable, light footwear and foot hygeine
topical fusidic acid
oral Abx therapy if severe erythromycin)
lice are obligate ____ found living on the human body
how are they spread?
ectoparasites
spread via human contact
what are the names for
1) head louse
2) body louse
3) pubid louse
1) Pediculus capitis
2) Pediculus corporis (aka Vagabond’s disease when chronic)
3) Phthirus pubis
presentation of lice
intense pruritis
often visible lice and eggs
diagnosis of lice?
clinical
Rx of lice?
malothion lotion of other insecitide
hygeine to avoid spread/ reinfection
what is tinea?
a fungal infection with a dermatophyte
aka ringworm of the skin
subtypes of tinea?
Tinea capitis = Scalp. Tinea barbae = Beard. Tinea corporis = Body. Tinea manuum = Hands. Tinea unguium = Nails. Tinea cruris = Groin. Tinea pedis = Feet.
how is tinea spread?
can be human contact (most common) animal contact, soil contact
organism responsible for tinea?
trichophyton rubrum (>70%) and Trichophyton mentagraphytes (>20%) spread by human contact
Microsporum canis spread through animal contact (cats and dogs)
presentation of tinea?
expanding lesions with central clearing and red scaly serpignous edge, thickened and crumbling nail
diagnosis of tinea?
clinical
skin scraping/ nail clippings for microscopy and culture
Rx of tinea?
small and localised infection: clotrimazole cream
extensive/ stubborn infection: oral terbinafine or intraconazole
affecting nails: oral terbinafine
what is the most common fungal infections affecting the skin?
candida skin infection
most common type of yeast infection
candida infection of the skin is most often with candida _____
albicans
risk factors for candida infection?
extremes of life warm, humid climate immunodeficient broad-spec Abx certain underlying skin conditions Fe deficiency COCP use/ pregnancy
Candida makes up part of the normal flora of the human ___ ___ and ____.
digestive tract
vagina
T/F: candida is a commensal of the skin
not typically, but can colonise areas temporarily
Candida skin infection presentation?
typically affects the folds of the skin (groin, under breasts, abdo skin folds etc - candida intertrigo)
Skin in red, can look shiny in skin folds and there are often spotty ‘satellites’ around the edges
Also commonly affects the oral cavity (white plaques on buccal mucosa/ tongue)
diagnosis?
clinical
if uncertain skin swabs and scrapings for microscopy and culture
Rx of candida skin infection?
clotrimazole cream
oral fluconazole
what causes scabies
infection with a parasitic mite Sarcoptes scabiei, variety hominis
transmission of scabies?
skin-skin contact between individuals
scabies:
Mite burrows through the epidermis and lies in the ___ ____
Here, it lays 2-4 eggs each day.
The symptoms experienced by infected individuals are due to what?
stratum corneum
the host immune response
presentation of scabies?
extreme pruritus (worse at night, often distrurbing sleep)
affects whole body, almost always scalp-sparing
burrows: irregular tracks, usually grey. Most often in webspaces. Also around waist, axillae and groin.
Erythematous papules, vesicles and excoriations
diagnosis of scabies?
clinical
microscopic examination of scabies burrow
Rx of scabies?
permethrin cream (malothion as alternative) antihistamines, crotamiton cream and hydrocortisone cream to reduce pruritis avoid contact with others
what is necrotising fasciitis?
acutely life-threatning infection of one of more of the deep soft tissue compartments (dermis, adipose tissue, fascia, muscle)
T/F: necrotising fasciitis has a high mortality rate
true
risk of serious complications
type 1 vs type 2 nec fascitis?
1) polymicrobial infection. Both anaerobic and aerobic bacteria. Most common in patients who are immunocomprimised/ chronically ill
2) infection with strep pyogenes (GAS)
how does nec fas form?
Bacteria enter skin through sites of trauma (small puncture wounds, surgical incisions…etc).
Often the primary site is not identified.
The infection spreads along the fascial plane to infect the deep soft tissues.
presentation of necrotising Fasciitis?
severe pain out of proportion to what is seen
erythema with well-defined edge
oedema
skin surface may appear relatively normal (while underlying tissue is extremely necrotic)
systemic upset
what signs/ symptoms would suggest necrotising Fasciitis with streptococcal infection?
ulceration, haemorrhagic bullae, lymphangitis
what signs/ symptoms would suggest necrotising Fasciitis with anaerobe infection?
foul smelling wound
diagnosis of necrotising Fasciitis?
‘dishwater fluid’ on wound washout
bloods: FBC, CRP, U&E, CK, lactate
blood and wound cultures
surgical exploration ASAP
treatment of necrotising Fasciitis?
urgent surgical debridement
broad spec abx
admission to ICU
what is Orf
a viral skin infection transferring to humans from sheep and goats
relatively common in sheep/ goat farmers
Orf causative pathogen?
parapox virus: contracted through direct contact with infected sheep/ goats
Orf presentation?
development of a single lesion at the site of inoculation
- mutiple lesions rare
- most often on hands/ forearm
- lesion arises as small, firm papule which is initially very tender and irritating
- the lesion enlarges to become a flat-topped pustule/ blister with a white centre and red periphery
Orf diagnosis?
clinical
Orf treatment?
self-limiting (6 weeks)
What is lyme disease
rare bacterial infection contracted from ticks
lyme disease is most common in what region?
temperate - scottish highlands most common in UK
peak incidence in summer
what causes lyme disease?
infection with bacteria, Borrelia (spirochete bacterium)
Ixodes ticks act as a vector for the bacteria
presentation of lyme disease?
erythema migrans
- 1-2 weeks post bite
- ‘bulls eye’
- usually painful
- possible associated malaise, myalgia, pyrexia
- resolves within 3-4 weeks
disseminated disease, days-weeks post bite
- arthritis, cardiac complications, nerve palsies, rheum complications
chronic lyme disease
- chronic arthritis/ pain
diagnosis?
high clinical suspicion required
blood sample for ELISA testing
Rx of lyme disease?
oral antibiotic therapy (amox/ doxy)
cure rate decreases as treatment delayed
