Flashcards in Bacteria & Mycobacteria Dan Deck (356):
Discuss Cat scratch disease
Caused by Bartonella henselae
pt presents with unilateral tender lymphadenopathy 2-4 wks after scratch or bite - often single large node up to 10cm
most pts remain well
some get fever, malaise, headache, weakness
rare - encephalopathy, osteomyelitis, lung or liver infiltration
5% get occuloglandular syndrome of Parinaud (Unilateral granulomatous conjunctivitis w/ lymphadenoapthy - refer to ophthal urgently)
serology positive esp in 1st 2 wks of lymphadenopathy
otherwise LN biopsy shows typical intracellular gram neg bacilli
Rx w/ azithromycin or
doxy + rifampicin
may get Jarisch-Herxheimer-like rcn
List the slow growing mycobacteria
Take 2-3 wks to culture in lab
List the rapid growing mycobacteria
Rap(id) A Smeg For CHristmas
Take 3-5 days to grow
List the tuberculid reactions
PAPa Tubercle LIkes to NOD at the BAsin
Erythema induratum of Bazin
Erythema nodosum - not a classic tuberculid but can be due to tuberculosis
List the forms of cutaneous Tb
Tuberculous chancre (naieve host)
2 paucibacillary forms occur in pts w high immunity;
Warty Tb (tuberculosis verrucosa cutis) (high immunity)
Lupus vulgaris (high immunity)
Spread in infected host (MOST Laura Wheller)
*'MOST' four occur in pts w/ low immunity (multibacillary forms), LW forms in pts w/ high immunity;
Miliary Tb (haematogenous spread)
Orificial tuberculosis (autoinnoculation)
Scrofuloderma (contiguous spread)
Tuberculous gummata (haematogenous spread)
Lupus vulgaris (haem or contiguous in high immunity)
Warty Tb (autoinnoculation in high immunity)
Also (non infective reactions to TB); Tuberculids, Erythema nodosum
what are the key features of Buruli ulcer?
what is the organism and where is it found?
what is the method of diagnosis and treatment?
skin infection caused by M ulcerans
slow growing mycobac, grows at 32 degrees
AKA in Aus; Daintree ulcer or Bairnsdale ulcer
found in Daintree, coastal VIC and Capricorn coast
direct innocualtion or mosy/insect transmission
mainly kids esp under 15
2 month latent period
single firm nodule that ulcerates after 3 months, can involve bone and joint, not muscle as too warm
heals spontaneously - takes 9 months
Diagnose - swab/fluid/tissue for PCR. Can also culture
ABs 1st line - Rifampicin + Clarithromycin for 8 wks
Rx for 12 wks if severe or if paradoxical reaction
20% get paradoxical worsening - ensure compliance, extend AB course and add pred if necrosis
surgery 2nd line - wide excison or debridement + graft
heat therapy sometimes used
Which types of HPV cause warts and which cause cancer?
Which cause Bowenoid papulosis?
which are covered by gardasil vaccine?
Warts - 6, 11 - also cause Bowenoid papulosis
Cancer (cervix/anogenital SCC, VIN/PIN) - 16, 18, 31, 33
gardasil vaccine covers 6, 11, 16, 18
Latest Gardasil also covers 31, 33, 45, 52, 58
which vaccines are live?
intranasal infulenza (not flu jab)
What is Ramsay Hunt syndrome?
herpes reactivation (zoster) affecting the geniculate ganglion of the facial nerve causes the triad of;
Ipsilateral facial paralysis
vesicles in the auditory canal and auricle
When in the disease course is diagnostic testing for EBV useful?
Monospot is positive during 1st or 2nd week and VCA (viral capsid antigen) by 4 weeks
Cowpox is most commonly acquired from cows?
from doemstic cats
Herpes viruses are DNA viruses
HSV2 is responsible for >90% pf cases of genital herpes
Primary genital HSV is usually localised and unilateral
Primary is often widespread and can be pain and oedema
can cause AROU due to be paraesthesia of S2-4
Recurrences of genital HSV are usually localised and unilateral
Ulcers of genital herpes (HSV) are usually painful
antiviral prophylaxis should be provided for someone having 6 or more episodes of genital herpes per year
Microbiological conformation is always required to get antivirals on PBS for genital herpes
Streamlined PBS authority for initial infection – microbiology not required
Streamlined PBS authority for recurrent infection – microbiology required but ‘need not delay treatment’
What is rx ladder for genital warts?
1st line =
Immiquimod, Cryotherapy of Podophyllotoxin
Podophyllotoxin apply BD for 3 consecutive days of week for 4 wks (not if preg)
NB podophyllin (as opposed to Podophyllotoxin) can also be used
Cryo is safe in pregnancy
Excision or snip excision
Topical TCA (not if pregnant)
CO2 laser, can also use PDL
Imiquimod esp for for extensive or resistant lesions (avoid if pregnant or benign vulval apthous ulcers, caution if background vulval dermatitis – inflammation++)
Gonorrhoea causes pelvic inflammatory disease and never infects the vulva
PID can affect urethra, cervix or rectum + endometrium and follop tubes
Rarely involves vulva by infecting Bartholin’s glands and paraurethral glnds - either can cause abscesses
Usually due to abuse in children
What are the genital types of syphylis?
mucous patches - grey-white moist looking lesions
Chancre redux – recurrence of the primary chancre at its original site
gummas which are very rare on the vulva – single or multiple swellings or nodules
What organism causes chancroid?
what type of organism is it?
gram neg coccobacillus
Painful chancre - 'do cry' with ducreyi
as opposed to painless chancre of syphylis
chancroid presents as Single or multiple tender ulcers on lab maj, introitus, perineum or perianal area, can affect cervix and vagina
Women more likely to have multiple lesions. In men affects penis and surrounding area esp foreskin
50% get painful unilateral inguinal adenitis
Can cause buboes
What are buboes?
fluctuant lymph node lesions which rupture leaving wide ulceration
What is the histo of chancroid?
3 zones of inflammation below the ulcer on H+E
Superficial zone – neuts, fibrin, necrotic debris, organisms
Middle zone – granulation tissue
Deep zone – lymphocytes and plasma cells
use gram, Giemsa (blue) or Brown-Brenn (red) stain to see organisms in upper zone
H ducreyi organisms better seen on smears than histo even with special stains
What is the treatment for chancroid?
Azithro/Erythro, Ceftriaxone or cipro
Contact tracing of partners in 10 days prior to onset of symptoms – treat all
Chancroid has a long incubation period
Chancroid is common in developed world
sub Saharan Africa, India, SE Asia
What are the alternative names for Granuloma inguinale?
What is the organism?
AKA Granuloma venereum or Donovanosis
aka Calymmatobacterium granulomatis
(old name is Donovania granulomatis)
Granuloma inguinale doesnt occur in Australia
does occur esp in NT but rare
Also India, S Africa, Brazil, New guinea
Granuloma inguinale can be transmitted sexually or otherwise
LGV causes large beefy looking ulcers with rolled/overhanging edges
this is Granuloma inguinale
Granuloma inguinale can affect any part of the skin/mucosae or can be intra-abdominal or in the bones
Can be metastatic esp in women
Bones are most common non-skin site
Can be intra-abdominal - liver, spleen
Granuloma inguinale causes marked lymphadenopathy
Initial lesion of granuloma inguinales is most often on pubis, genitals, perineum, perianal or groin skin
inguinal lesions in 20%
Extra genital lesions in 5% esp nose and lips or elsewhere on face
can be on limbs
can be in mouth
How is diagnosis of granuloma inguinale made?
Swab for smear prep with Giemsa stain is best way to diagnose
– Donovan bodies in histiocytes (similar to inclusions seen in leishmaniasis, histoplasmosis and rhinoscleroma)
If biopsied silver stains may show organism as intracytoplasmic inclusions
- Donovan bodies – black oval or rod shaped structures with bipolar staining at their 2 ends in cytoplasm of histiocytes
serology is reliable to diagnose granuloma inguinale
no serology test
H+E of granuloma inguinale shows ulcer w/ granulation tissue and infiltrate of histiocytes, plasma cells and some neuts
What is treatment of granuloma inguinale?
Doxy 1st line
Azithro, erythro also effective.
Treat for 3 weeks minimum
Contact tracing – at least last 60 days before symptoms
What is the oragnism responsible for Lymphogranuloma venereum (LGV)
in tropical and subtropical countries
what type of organism is Klebsiella granulomatis?
gram negative intracellular bacillus
Klebsiella granulomatis cannot be cultured on growth media
never grown in pure culture
(grown in human blood or Hep 2 cells)
What are the features of Lymphogranuloma venereum (LGV)
3 letters (LGV) so all the 3s
Chlamydia trachomatis Serovars L1-3
Incubation time 3-13 days
Stage 1) Small papule occurs in 50% on vulva usually at fourchette or posterior vaginal wall in women and on coronal sulcus in men – heals quickly without scar
There is regional lymphadenopathy. Sometimes initial lesion is small ulcer, vesicle or urethritis/cervicitis
Stage 2) Weeks/months later there is striking unilateral lymphadenopathy
Stage 3) bubo formation
If untreated, after rupture and drainage of the bubo the site heals w/ scarring
Buboes are asociated with which infections?
Primary site of Lymphogranuloma venereum (LGV) can be anorectal or throat soemtimes
rectal proctocolitis which can cause ulceration and strictures. There is pain, discharge and tensemus (ano-genito-rectal syndrome)
Can affect oropharynx as primary site and cervical or submaxillary nodes
How is Lymphogranuloma venereum (LGV) diagnosed?
Swab sent for PCR (not culture as dificult and slow)
Histo of Lymphogranuloma venereum (LGV) shows 3 zones
3 zones in ulcers of chancroid
Histo in LGV is non-specific - abscesses, granulomatous inflammation, plasma cells
What is treatment of LGV?
Doxy 100mg BD 1st line
Erythro if pregnant
Need to treat for 3 weeks
Check for HIV and syphilis
Contact tracing – in 30 days pre symptoms
Acid fast mycobacteria cannot be treated with acids
Acid fast means once stained, not easily decolourized
->i.e. acid – fast
Most mycobacteria are harmless to human beings
After infection with TB 50% of pts develop clinical infection
Pts who develop symptomatic clinical primary TB infection will hav eno response to tuberculin skin test
will develop a necrotizing skin reaction
immunological hyper-reactivity may account for much of the lung tissue damage
Developmen tof protective immunity to TB is dependent upon T-cell mechanisms mediated by Th1 inflammatory cascade and IFN-γ
The Tuberculin skin test is looking for a cell-mediated response (Type IV delayed type hypersensitivity) to PPD (purified protein derivative)
Cell mediated immunity appears within 3-8 weeks of infection and is generally lifelong
The Tuberculin skin test or PPD are specific for M. tuberculosis
culture filtrate of tubercle bacilli containing over 200 antigens shared with BCG and many non-tuberculous mycobacterium
Positive Tuberculin skin test or PPD means immunity to TB
Means has been exposed to TB in past or to BCG or to another mycobacterial antigen in the PPD concentrate
may or may not have active or latent TB
BCG vaccine causes positivity on the Tuberculin skin test or PPD
Negative Tuberculin skin test or PPD means chance of prior exposure to TB is low, therefore chance of current active or latent infection is low
Interpretation of the Tuberculin skin test or PPD involves measuring the diameter of induration at 48 to 72 hrs
Regarding interpretation of the Tuberculin skin test or PPD;
≥5mm considered positive in;
Immunosuppressed patients (>15mg/d prednisone, TNF-alpha antagonists, other immunosuppressants)
Patients with fibrotic changes on CXR consistent with prior TB
Regarding interpretation of the Tuberculin skin test or PPD;
≥15mm considered positive in;
Immigrants from endemic areas
IV drug users
≥10mm for these groups
≥15mm considered positive in patients with no risk factors
What are the causes of false negative result on Tuberculin skin test or PPD?
Recent TB infection (within 8-10 weeks of exposure)
Very old TB infection (many years)
Very young age (less than 6 months old)
Recent live-virus vaccination (e.g., measles and smallpox)
Overwhelming TB disease
Some viral illnesses (e.g., measles and chicken pox)
Incorrect method of TST administration
Incorrect interpretation of reaction
The Quantiferon gold test meaures in vitro IFN-gamma released by the pts T-cells in response to antigens which are highly specific for TB but absent from BCG vaccine and most non-tuberculous mycobacteria
So BCG vaccine doesnt affect Qgold test
HIV infection is greatest known risk factor for progression from latent TB infection to TB disease
In HIV pts the lifetime risk of TB is 50% and 5% will die from disseminated TB.
In HIV pts in the developing world M. TB is more common than other mycobacterial infection
M avium complex most common
Other are M. TB, M kansasii and M. scrofulaceum
M. Bovis is pathological in humans and may gain access via gut or oropharynx when consumed in milk
Only 1-1.5% of isolates due to bovis
What is the 'primary complex' in TB?
Focal area of primary infcetion and regional enlarged LNs
Ghon focus and hilar lymph nodes
Skin chancre and superficial LNs
Primary innoculation of TB into the skin causes tuberculosis verrucosa cutis (warty TB)
Causes a TB chancre
Skin innocualtion in a previously sensitised pt causes tuberculosis verrucosa cutis (warty TB)
What are the features of tuberculoid granulomas?
Areas of caseation (looks like cheese macroscopically) necrosis (mass of tissue debris without nuclei, i.e. without live cells) surroudned by dense granulomas of hsitiocytes with giant cells
Can have Schuamann bodies or asteroid bodies in the giant cells
Dense infiltrate of lymphocytes surrounding the granulomas
Tuberculids have no mycobacteria in the skin lesions
TB has been found using PCR
Tuberculids have no tuberculoid granulomas
often do have tuberculoid granulomas
TB lesions with less caseation necrosis have more organisms
more organisms if more caseation necrosis - you find the most mycobacteria in these areas
The presence of perineural infiltration is helpful histologically to distinguish tuberculoid granulomas in TB from those in tuberculoid leprosy
What determines the type of clinical TB a person develops?
Route of infection (endogenous or exogenous, inhalation, innoculation etc)
Immune status of patient
Whether or not there has been previous sensitization with TB
Orificial, perioral, or perianal tuberculosis can occur following ingestion of mycobacteria from either swallowed respiratory secretions or from milk contaminated with M. bovis
Similar to leprosy, TB may be categorised as multibacillary or paucibacillary
Multibacillary forms (abundant mycobacteria)
- Tuberculous chancre
- Acute miliary tuberculosis
Paucibacillary forms (mycobacteria are difficult to isolate)
- Lupus vulgaris
- Tuberculosis verrucosa cutis
PCR is not of use in the diagnosis of skin manifestations of TB
should send tissue for PCR as well as histo and culture if TB suspected
Mycobacteria are gram negative
Mycobacteria are bacilli which cannot be fully gram stained although if anything they are gram positive as they take up the crystal violet which cannot be washed out with acid
The Tuberculin skin tests look for antibodies to mycobacteria
test of cell mediated immunity not antibodies
Qgold should not be used in children under 5
however most infections occur in first 5 years
Qgold is a useful rule out test for TB screening
as high sensitivity (80-90%)
But remember a good history is the best TB test
Qgold positivity cannot distinguish latent from active TB
Qgold becomes negative after TB is successfully treated
May or may not become negative
Qgold is more sensitive and specific than tuberculin skin test
esp it is more specific in BCG vaccinated population; 95-97% specificity
TST and Qgold have similar false negative rates in immunocompromised pts; 20-30%
Which histological stains are used for mycobacteria?
- Background pale blue, mycobacteria bright red
- Modification of ZN better for M leprae
Cutaneous TB is one of the least common types of extrapulmonary TB
BCG can cause tuberculosis of the skin
Scrofuloderma results from contiguous involvement of the skin overlying tuberculosis in a deeper structure
most commonly lymphadenitis, bone, or joint disease or epididymitis
Metastatic tuberculous abscesses (tuberculous gumma) can occur due to haematogenous spread from a primary focus (usually when host resistance is suppressed)
Infection with non-tuberculous mycobacteria can cause positive result on Qgold test
But only a few;
Marinum, Kansasii, Szulgai
A tuberculous chancre self resolves
Lupus vulgaris may develop at site of original lesion
May get erythema nodosum
Orificial TB is painless
What is lupus vulgaris?
what is clinical appearance?
A chronic, progressive, post-primary, paucibacillary form of cutaneous TB, occurring in a person with a moderate or high degree of immunity
A plaque composed of soft, reddish-brown papules, the appearance on diascopy is apple jelly (DD is sarcoidosis)
5 clinical types;
papular/nodular - disseminated form
BCC and SCC can develop in lesions of lupus vulgaris
risk is significant - 8%
lichen scrofulosorum is the most common tuberculid
Erythema induratum of Bazin most common - account for 90%
Tuberculids occur in pts with low immunity to TB
hypersensitivity reaction to M. tuberculosis or its products in a patient with significant immunity
lichen scrofulosorum clinicaly resembles lichen nitidus
Which areas of the body are affected by Erythema induratum of Bazin?
posterior aspect of the lower legs most common
Also thighs, buttocks, trunk, upper limbs
What are the histo findings of Erythema induratum of Bazin?
Focal or diffuse, lobular or septolobular, granulomatous panniculitis in association with neutrophilic vasculitis of either large or small blood vessels
Areas of coagulative and caseation necrosis and usually poorly developed granulomas
bacilli are absent but may be found on PCR in >75%
Positive histology is diagnostic for TB
Only culture or +ve PCR can confirm diagnosis of tuberculosis
How is TB managed?
Refer to ID
Notifiable disease - lab usually reports
screen for HIV in all cases
Standard regime is RIPE
Rifampicin (450-600mg daily) for 6 mths
Isoniazid (300mg daily) for 6 mths
Pyrazinamide (1.5-2g daily) for first 2 mths
Ethambutol (15mg/kg daily) for 2 mths
Can consider excision for lupus vulgaris or warty TB in additio to above therapy
BCG is an attenuated from of M bovis
BCG can reduce the risk of TB in children but no proven benefit in adults
BCG should not be given to immunosuppressed pts inclduing HIV
risk of generalized BCG infection
BCG can cause are lupus vulgaris, papulonecrotic tuberculid, lichen scrofolosorum
There are increasing presentations of mycobacteria in tattoos performed overseas
esp SE Asia
Pts present with an unusual papular rash in the tattoo area
Sarcoidal tattoo reaction is DD
Which mycobacteria cause sporotrichoid spread?
Mary and Gordon Kan Chew Spores
esp M. marinum (20% of cases have sporo)
but also M cholenaei, M kansasii and M gordonae
Mycobacterium cholenaei is associated at times with erythema nodosum
Mycobacterium scrofulaceum typically causes a scrofuloderma-like presentation
M marinum is found in both fresh and saltwater fish
M marinum can be contracted from swimming pools
esp if water not reguarly replaced and chemicals not used
Not killed by chlorine alone
Almost 1/3 of cases of skin M marinum get involvement of deeper structures
tendonitis, osteomyelitis, septic arthritis
Incubation period for M marinum is 10-12 weeks
but can be up to 9 months
Which mycobacteria grow best at 32 degrees?
- lesions on limbs usually
Other mycos grow best at 37 degrees
What are the histo findings of skin atypical myco infection?
suppurative granulomatous dermatitis
Tuberculoid granuloma’s with fibrinoid masses rather than caseation
AFB’s seen in only 10% (Z-N or W-F stains)
What is treatment for atypical mycobacterial infections?
Clarithromycin 500mg BD
Rifampicin 10mg/kg up to 300mg BD
suitable for all as first line usually for minimum 8 weeks often 12 weeks
What are second line agents for M marinum infection?
minocycline (100mg/day) > doxycycline
Co-trimoxazole (sulfamethoxazole + trimethoprim)
M kansasii is found in tap water worldwide
How is M kansasii treated?
Clarithro + rifampicin like other atypical myco
Kansasii additional ethambutol +/- pyridoxine
and longer Rx - for 9 mths in immunocompetent and 15-24 mths in immunocompromised
M ulcerans secretes a major virulence factor?
A lipid toxin
Causes local immunosupression and necrosis of fat and subcutaneous tissue
M ulcerans is the the 3rd most common mycobacterial infection in immunocompetent pts
after TB and leprosy
Where is M ulcerans found?
> 30 countries
in riverine areas (swamps, lakes, slow-flowing rivers) that have a humid hot climate
In Aus occurs in coastal victoria ‘Bairnsdale ulcer’
And between Mossman & Daintree region North of Cairns ‘Daintree ulcer’
Sometimes on Capricorn coast of QLD (near Rockhampton, Yeppoon) and in NT
How is M ulcerans transmitted?
Mode of transmission not known but probably directly from soil water through small breaks in skin.
New evidence in Aus that may be transmitted from possums by mosquitos and other biting insects
Occurs in outbreaks in affected areas but risk outside these areas is negligible
M ulcerans has a 2 month latent period
M ulcerans mainly infects children and younger teens
70% of pts
How is Buruli ulcer diagnosed?
PCR is mainstay now
- on swabs if ulcerated, or send fluid from FNA or tissue from biopsy
Can culture but slow growing
Burulin test has been used - tuberculin test using M ulcerans antigens
Histo supportive also
should take incisional biopsy for histo, culture and PCR
The classical buruli ulcer self heals after several months
heals with fibrosis and scarring
What are the clinical features of buruli ulcer?
single, asymptomatic, firm , non-tender nodule that ulcerates after 2-3/12
Ulcer extends rapidly reaching several cm over a few weeks
Classically undermined edges
Floor of ulcer formed of necrotic fat
Little constitutional disturbance
Heals over 6-9 months
How is Buruli ulcer treated?
Rif+clarithro 1st line and okay in kids and pregnancy
8 weeks if simple
12 weeks if bone or joint involved
Surgery second line
Heat therapy sometimes used as adjuvant as heat inhibits growth of organism – need 4-6 hrs per day for 4-8 weeks
You are treating buruli ulcer
There is initial improvement then wound deteriorates. Increased pain and discharge, new ulceration in lesion and new lesions appear
What is the diagnosis and course of action?
Paradoxical reaction most likely
occurs in 20%
Does not indicate Rx failure – should persist
Due to loss of the local immune suppression caused by mycolactone secreted by M ulcerans and resultant intense immunological response
If severe give high dose pred and taper over 4 weeks
Other DD is treatment failure or pt has been non-compliant
Ask about compliance to ensure not antibiotic failure Can also biopsy for H&E – intense inflammation typical of a responding treated infection
What are risk factors for paradoxical reaction when treating Buruli ulcer?
What are the indications for surgery in Buruli ulcer?
Surgery indicated if;
Antibiotics refused or not tolerated
Wide excision and direct closure with aim for complete removal of infected tissue
Dual antibiotics for 4 weeks prior reduces the risk of relapse post surgery
Lesions with significant tissue necrosis need debridement and antibiotics prior to grafting
M Fortuitum complex causes cold abscess
Chronic GVHD is a risk factor for non-tuberculous mycobacterial infection of the skin and other organs
What does pyoderma mean?
Any skin disease producing pus
E.g. abscess, furuncle, carbuncle, impetigo, ecthyma, foliculitis
Some use the terms pyoderma and impetigo interchangeably
Some use pyoderma to refer to strep impetigo only
What toxin-related conditions are due to staph infections?
Staphylococcal Scarlet fever
Staphylococcal scalded skin syndrome
Toxic shock syndrome
Recurrent toxin-mediated perineal erythema (Staph or strep)
What toxin-related conditions are due to strep infections?
Streptococcal toxic shock-like syndrome
Recurrent toxin-mediated perineal erythema (Staph or strep)
What are the derm complications of (group A) strep infections?
SssTREeP CK and infections
Scleredema (type 1)
Toxic shock syndrome
Reccurent toxin-mediated perineal erythema
Erythema nodosum, Erythema marginatum
Skin infections; Impetigo, cellulitis, perianal strep, erysipelas, perianal strep, nec facs, blistering distal dactylitis, ecthyma, vulvovaginitis
What are the non-derm complications of (group A) strep infections?
Other strep infection – sinusitis, pneumonia, septic arthritis, osteomyelitis, meningitis, vaginitis, necrotising fasciitis (type II)
Which Skin conditions are due to strep antigen hypersensitivity?
Erythema marginatum in rheumatic fever
Furunculosis is most common presenting infection of MRSA
Panton-Valentine Leukocidin is a pore-forming cytotoxin which can destroy WBCs and cause tissue necrosis
What is inducible resistance?
When a sensitive organism can turn into a resistant infection when treated with the antibiotic it is sensitive to
Because the antibiotic kills the sensitive organisms allowing the resisatnt ones to take over the infection
Staph resistant to erythro but sensitive to clindamycin have a variable risk of inducible resistance to clindamycin - how can this be tested?
In the lab using the D-test (double disk diffusion test)
result can guide whether clinda should be used
In a pt with a severe staph infection from an area where MRSA is high, clindamycin is first line empiric agent
strep is most common cause of impetigo
Staph most common, strep second
50% of impetigo cases are bullous
2 thirds of cases non-bullous (impetigo contagiosa, school sores), 1 third bullous
bullous impetigo is always caused by staph
What is the mechanism of bullae in bullous impetigo?
due to exfoliative toxins A & B (ETA & ETB) produced by staph aureus of phage group 2 which bind to dsg1 in the epidermal granular layer causing blister formation by disrupting desmosomes and resultant acantholysis
Desmoglein 3 is the target antign on bullous impetigo
Impetigo is highly contagious
Regarding impetigo; the bullous form is more likely to develop in intact skin than non-bullous form
pts with staph impetigo have risk if carriage of staph aureus in nose, pharynx, axilla or perianal regions
should swab and do eradication after treating impetgio if any remaining colonization and also swab and treat family if positive
What are the DDs of bullous impetigo?
Immunobullous Dx eg chronic bullous Dx of childhood
impetigo is self limiting but non-bullous form takes longer
self limiting but bullous form takes longer
Non-bullous 2 weeks
Bullous 3-6 wks
resolve quicker if treated
Impetigo can cause acute post-strep glomerulonephritis (APSGN) but is rarely a cause of acute rheumatic fever
Textbook says Impetigo does not cause rheumatic fever – however it is thought that strep ‘skin sores’ in aboriginal children do cause rheumatic feve
antibiotic treatment reduces the risk of strep impetigo causing APSGN
does not change risk
How is impetigo treated?
assess severity - is child well etc
Must swab to get organsim
If well can use condys or saltwater soaks and bactroban
If worse or widepsread oral ABs
If unwell or immunosuppressed admit for IVs and investigation etc– ceftriaxone 1st line IV while awaiitng sensitivities
If recurrent episodes check for nasal or other body site staph carriage and decolonize whole family
What is ecthyma?
Deep form of impetigo where infection extends into dermis – causes a shallow ulcer
Usually strep pyogenes, can be staph – either as a primary infection or infection of an insect bite etc
Who gets ecthyma?
What is ‘superficial folliculitis’?
When the infection only affects follicular ostium or slightly deeper
grouped pustules on erythematous background
heal w/out scarring
What organism most commonly causes folliculitis?
Who is at risk of gram neg folliculitis?
Acne pts treated with long courses of antibiotics or other pts on long terms ABs
Poorly treated hot tubs can cause pseudomonas folliculitis
What are risk factors for folliculitis?
occlusion, maceration ,overhydration, steroids, heat, humidity, shaving/waxing/plucking, diabetes, atopic eczema
Pustules of folliculitis can coalesce into plaques studded with pustules and crusts
What are the DDs of folliculitis?
acne, rosacea, chloracne, acne agminate, pseudofolliculitis barbae, sycosis, Pityrosporum folliculitis, steroid folliculitis, blastomycosis-like pyoderma, majocchis grnauloma, pyoderma faciale
What is pseudofolliculitis barbae?
ingrowing hairs and inflammation without infection in beard area
superficial folliculitis can be treated with topicals only
antibacterial wash – chlorhex or triclosan + topical antibiotics for 7-10 days – bactroban or clindamycin
If deeper need oral ABs as well as topical wash
What is sycosis?
chronic infection of the whole deep part of the follicle
Usually due to staph
Most often in beard are of men (sycosis barbae)
although there can be a confluent-looking area of involvement clinically, the deep follicles remain discrete unlike in a carbuncle
Can cause scarring destruction of the follicles = ‘Lupoid sycosis’ or ‘Ulerythema sycosiforme’
Scarring form is progressive scarring alopecia with advancing margin of papules and pustules and pink atrophic scar behind
Folliculitis de Calvans is Sycosis of the scalp
What is mycotic sycosis?
kerion of the cheek
acne necrotica is an infected form of acne
Not a variant of acne
cause unclear - possibly staph or p.acnes infection
What are the clinical and hsito findings of Acne necrotica (varioliformis)?
Affects face close to scalp margins, scalp and upper trunk – 2-5mm red itchy papules undergoe necrosis to form a haemorrhagic crust which detaches after 4 weeks leaving a (varioliform) scar
Histo - Lymphocytic folliculitis with necrosis of follicle and adjacent dermis and epi in older lesions
Eosinophilic pustular folliculitis (Ofuji’s disease) is more common in men
5x more men
Eosinophilic pustular folliculitis (Ofuji’s disease) occurs in adults and infants
expanding papulovesicles which become small annular lesions or plaques 3-5cm diameter on any body site
What are the associations of adult Eosinophilic pustular folliculitis (Ofuji’s disease)?
HIV, malignancy, drugs
Eosinophilic pustular folliculitis (Ofuji’s disease) occurs only in Japan and asia
Eosinophilic pustular folliculitis (Ofuji’s disease) is treated with systemic steroids or dapsone second line
resolve with hyperpigmentation
Eosinophilic pustular folliculitis (Ofuji’s disease) has a peripheral eosinohilia
an abscess is the same as a boil(faruncle)
Furuncle occurs in hair follicle; abscess can occur anywhere
Carbuncle is a loculated collection of contiguous furuncles
When should you think of staph carriage and eradication?
recurrent impetigo, folliculiits, abscesses or boils
or wound infections after skin surgery
Systemic symptoms rare in abscess and faruncles but common in carbuncles
cephalexin 1st line for abscesses and furuncles
Bactrim or doxy or clindamycin first line options as often MRSA
What are cellulitis, erysipelas and erysipeloid?
- Cellulitis is infection of deep dermis and subcut tissue most often due to staph or strep spp
- Erysipelasis a superficial type of cellulitis in upper dermis usually caused by group A strep but rarely staph or other organisms
- Erysipeloid is an acute bacterial infection of the skin +/- other organs caused by the microorganism Erysipelothrix rusiopathiae
Immunocompromised pts often get cellulitis from haematogenous spread of infection whereas immune competent pts usually have a break in the skin allowing microbes to enter
Lymphatic damage predisposes to recurrent cellulitis
e.g. LN dissection, Prior cellulitis, saphenous vein harvest
vesicles, pustules, bullae or necrotic tissue are not features of cellulitis - should look for another cause
these can all occur
celluliits affects head and neck most often in children
extremeties in adults (esp arms in IVDUs)
How is cellulitis managed?
past essay que
Make the diagnosis and exclude nec fasc or myositis by looking for signs of deeper infection
Assess severity and resucitate as required
Look portal of infection
Investigate as necesary - FBC, ELFT, CRP, ASOT, anti-DNAseB, swabs if weeping/wound, blood cultures etc
decide whether to admit
rest and elevate body part
supportive cares, fluids analgesia etc as indicated
NSAIDs are good painkillers for cellulitis
avoid NSAIDs as can mask signs of necrotizing infection
Who should be admitted for cellulitis?
Fail to respond
What antibiotics for cellulits?
Co-amoxiclav 625mg BD
bactrim, doxy or clindamycin if MRSA suspected
Benzyl penicillin 1.2g 6x/day + flucloxacillin 1g QDS
If diabetic or decubitus ulcer Piptaz or cipro+metronidazole
Vancomycin if MRSA
raised WCC can reliably differentiate cellulitis from causes of 'pseudocellulitis'
blood and swab cultures are also unreliable for diagnosis
DDs for cellulitis
Inflamed/infected venous stasis dermatitis – most common mimic
Discoid or other types of eczema
Contact dermatitis, phytophotodermatitis
Erythema chronicum migrans
Pannicuulitis e.g. EN, acute lipodermatosclerosis
Inflamed GA, interstitial granulomatous dermatitis
Toxic erythema of chemotherapy
(Infected) arthropod bite, papulonecrotic arachnoidism
Vaccine or injection site reaction
Periodic fever syndrome
Which organisms cause erysipelas?
group A strep or sometimes group B/C/D/G streps
Who gets erysipelas?
the young, old, debilitated those with lymphoedema or chronic ulcers
erysipelas affects boys more than girls and women more than men
The face is the most common site for erysipelas
face classical but leg most common
can be anywhere
In erysipelas there is sudden fever, rigors, malaise and nausea followed by the rash after hrs or a day
symptoms start after 2-5 day incubation period
What is natural Hx of erysipelas?
Erythematous plaque with sharp demarcation and ridged border, hot, tense and indurated with oedema
Can be pustules, vesicles, bullae or purpure or necrosis
Tender, can be burning pain
Usually lymphadenopathy, may be lymphangitis
Desquamates when resolving
What are gangrene and wet and dry gangrene?
Gangrene = irreversible tissue necrosis
Dry gangrene = end result of ischaemia without infection results in autoamputation. Low mortality.
Wet gangrene = ischaemia + infection with saprogenic (putrifying = denaturing proteins) bacteria esp clostridia and bacilli. Results in septicaemia and high mortality.
What is gas gangrene?
Infection caused by destructive organisms which produce gas as they digest tissues.
Most commonly alpha toxin producing strains of clostridium perfringens.
Rapidly progresses to septic shock and death.
Gas gangrene is a type of necrotizing fasciitis (type III)
What is necrotizing fasciitis?
Rapidly progressive necrosis of fat and fascia
Type I - polymicrobial (adults)
Type II – monomicrobial usually group A β-hameolytic strep (mainly kids)
Type III – gas gangrene usually due to C. perfringens
What are the clinical features of necrotizing fasciitis?
Starts as small very tender area of skin
Looks red and inflamed
Pain out of proportion to clinical appearance
Over 36 hrs rapid progression – turns purple then patchy blue-grey colour
May look haemorrhagic
There is a watery foul smelling discharge from necrosis of the fascia
Can feel woody hard on palpation
Destruction of dermal nerves causes anaethesia
Most often extremeties in adults or trunk in children
What is Fournier’s gangrene?
Nec fasc of scrotum/perineum/genitalia
What are clues to the diagnosis of necrotizing fasciitis?
Rapidly spreading tense/woody oedema
Foul smelling watery discharge
Imaging shows soft tissue air (in minority of cases)
MRI can confirm and delineate extent
What is Pyomyositis?
Primary bacterial infection of skeletal muscles most commonly due to staph aureus
Fever, pain and woody induration
DD for nec fas
What is Botryomycosis?
Rare chronic skin infection usually caused by staph aureus
Cutaneous and subcutaneous nodules with ulcers and verrucous plaques
Localized areas on extremeties
Often many draining sinus tracts
Histo has distinctive grain – 1-3mm granular bodies composed of bacteria, cells and debris
Rx with debridement or excision and antibiotics
What are SIRS criteria?
2 or more of;
Temp 38 degrees C
RR >20 or PCO2 12 x109/L or >10% immature forms
What are sepsis, severe sepsis and septic shock?
Sepsis (septicaemia) is;
- SIRS criteria + a source of infection
Severe sepsis (AKA ‘sepsis syndrome’) is;
- Sepsis + evidence of dysfunction of at least 1 organ system (includes skin)
Septic shock is;
- Severe sepsis + hypotension despite adequate fluid replacement (systolic BL
What are Osler's nodes?
Feature of staph or strep endocarditis
Tender red (subcutaneous) papules and nodules with white centre esp on finger pads and thenar or hypothenar eminances
What are Janeway lesions?
Feature of staph or strep endocarditis
Small, painless haemorrhagic macules or papules on palms or soles
Who gets Perianal strep cellulitis/dermatitis?
How is it treated?
Affects kids esp boys under 4
Can follow strep throat
Can be cause of acute guttate psoriasis
Pain, itch, painful bowel opening, blood streaked stool, anal leakage
7 days of cefuroxime
Strep pyogenes causes 10% of vulvovagintis in prepubertal girls
What is a Felon?
Localised abscess of distal finger pulp (volar fat pad)
Deeper infection than blistering distal dactylitis
Usually staph but sometimes strep
Needs I+D and antibiotics
What is Blistering distal dactylitis?
Localised infection of volar fat pad of a finger or toe
May involve nail or region of digit proximal to nailfold
Esp children age 2-16
Skin darkens for days – 1 week before blistering
Due to group A strep (pyogenes) most often but can be staph
Inoculation from trauma or nose picking
DD – Felon, paronychia, herpetic whitlow, burn, bullous impetigo, friction blister
Rx – drainage and 10 days systemic antibitoics
Either staph or strep can rarely cause sporotrichoid nodular lesions
Where is the focus of infection in staph scalded skin?
In children focus of infection is often nasopharynx or conjunctivae
In adults often staph pneumonia or other site
adults often immunosuppressed or renal failure
staph scalded skin is twice as common in males
at least 2:1
How is the toxin spread in staph scalded skin syndrome?
epidermolytic toxins (ET) A and/or B which bind to dsg1
Toxin diffused from a focus of infection and spreads haematogensouly
What are the typical clinicla features of staph scalded skin syndrome?
Prodrome of fever, malaise and tender skin
May have rhinorrea or other signs of local staph infection
Erythema starts on head and intertriginous sites then generalizes in 48 hrs
Flaccid blisters form – Nikolsky positive often start in flexures
Periorificial crusting and radial fissuring is classical
No mucosal involvement
staph scalded skin syndrome has a mortality of >50% in adults?
3% in kids
What are DDs of staph scalded skin syndrome?
sunburn, drug eruption, Kawaskis disease, toxic shock syndrome, viral exanthema, extensive bullous impetigo, acute GVHD, pemphigus folliaceus, SJS/TEN
What tests can help diagnose staph scalded skin syndrome?
Take swabs from site of infection – swabs from eroded skin will be negative
Histo on frozen section/urgent H&E of peeled skin may confirm the split is in the granular layer with acantholytic keratinocytes seen
Tzanck smear from freshly denuded skin will show epithelial cells but no inflammatory cells (in TEN there will be many inflammatory cells and few epithelial cells)
ELISA blood test may detect endotoxin
blood cultures are negative in adults with staph scalded skin syndrome
Blood cultures usually negative in kids but positive in adults
staph scalded skin syndrome resolves in 1-2 weeks without scarring
What is management of staph scalded skin syndrome?
Analgesia – paracetamol
Search for site of primary infection
Swab/investigate as needed
Oral or IV antibiotics – usually 48 hrs of IVs at least e.g. cephelx, diclox
Topical cares – dermeze etc
Monitor for secondary infection of eroded skin
Ensure temp and fluid balance closely controlled
Consider assessing pt and family for staph carriage and treating
Epidermolytic toxin A is the main cause for toxic shock syndrome
Mainly due to staph toxic shock syndrome toxin-1 (TSST-1) esp in menstrual cases
Can also be due to staph enterotoxins – enterotoxins A and B cause 50% of non-menstrual cases
Strep variant due to toxin producing group A strep;
e.g. strep pyrogenic exotoxins (SPE) SPE-A, B or C, strep mitogenic exotoxin Z (SMEZ), or streptolysin-O.
What kind of infections cause toxic shock syndrome?
retained tampon cases less common now
Can be nasal tampons, cutaneous pyodermas, postpartum infection, abscess, burns
affects healthy teens-young adults
soft tissue infection often triggers
affects healthy adults age 20-50
What are the clinical features of toxic shock syndrome?
High grade fever, headache, sore throat, myalgia, vomiting, diarrhoea
Blotchy macular erythroderma or scarlatiniform rash starting on trunk and spreading to extremeties
Swollen red palms, soles and oral mucosa
Hyperaemia of conjunctivae
Can get oedema from shock
Desquamation of hands and feet after 1-3 weeks is important clinical sign
The histo of toxic shock syndrome shows an infiltrate of lymphocytes and neutrophils in superficial dermis which affects hair follicles and sweat glands
and variable dermal oedema and epidermal spongiosis
What are the DDs for toxic shock syndrome?
Kawasaki disease main DD in kids
What are the laboratory criteria for toxic shock syndrome?
5 ‘clinical’ (includes bloods) and 2 ‘laboratory’ (culture & serology) criteria
Probable case if both laboratory and 4 clinical criteria
Confirmed case if both laboratory and all 5 clinical criteria
Positive blood or CSF culture for staph aureus
Negative serology for Rickettsia, leptospirosis and measles
The clinical criteria for toxic shock syndrome are;
Pyrexia 38.9 or above (high grade fever)
Systolic BP 2x normal
Liver – bili/AST/ALT >2x normal
CNS -confusion without focal neurology
IVIg may be used to neutralise the toxin in toxic shock syndrome
But removal of the source of infection, IV antibiotics and supportive cares are mainstay
A rise in CK due to myositis is seen in staph toxic shock syndrome but is unusual in strep Toxic shock-like syndrome and indicates nec fasc, myositis or muscle infection
in strep Toxic shock-like syndrome pt often has identifiable soft tissue infection e.g. nec fasc, myositis, gangrene
The staph and strep toxic shock syndromes present with an infection and clinical picture of septic shock but are due to toxins rather than the infection directly
desquamation is not a feature of strep Toxic shock-like syndrome
Blistering of skin more common than in staph TSS and desquamation of the generalised rash is part of diagnostic criteria
Only 20% get later desquamation of hands and feet which is common in staph TSS
Important DD for SJS/TEN
What are criteria for strep Toxic shock-like syndrome?
Strep isolation + Hypotension + >2 of 6 signs;
Group A Strep isolation
strep Toxic shock-like syndrome is rarer than staph TSS and has a lower mortality rate
strep TSS is rarer but much higher mortality; 30-60%
staph TSS has 3% mortality
Scarlet fever is due to SPE-A, B or C toxins from group A Beta haemolytic strep
(same toxins can cause strep TSS)
What are the clinical features of scarlet fever?
Mainly kids 1-10
Usually follows strep tonsillitis or pharyngitis (is a post strep syndrome) in winter
Sudden onset sore throat, headache, malaise, fever, rigors, anorexia, nausea
Can be vomiting, abdo pain or seizures esp in young kids
After 12-48hrs develop scarlatiniform rash - blanching erythema starting on neck and chest and in axillae; becomes generalised in 12 hrs forming tiny red papules (goosebumps + sunburn appearance)
Pastia’s lines – linear petechiae in axilla, groin and ACFs
Flushing of cheeks with circumoral pallor
Tongue is initially white w/ bright red papillae then becomes swollen and red – ‘strawberry tongue’
Pharynx red and develops exudates after 3-4 days
Desquamation of hands and feet esp; after 7-10 days can last 2-6 weeks
In scarlet fever you should give anti strep antibiotics for 10-14 days even if delayed diagnosis as can prevent rheumatic fever
Staph scarlet fever has the same clinical features as classical strep disease
Usually skin entry of bacteria and pt often an identifiable soft tissue infection e.g. abscess, furuncle etc
Generalised scarlatiniform rash
No pharyngitis, No strawberry tongue, No Pastias lines
Staph scarlet fever is due to the same toxins as bullous impetigo/SSSS?
Due to TSST-1 and enterotoxins - the same as TSS not the same as bullous impetigo/SSSS which are due to exfoliative toxins A & B
Recurrent toxin-mediated perineal erythema looks like erysipelas on the buttock
Can follow a staph or strep infection elsewhere
Responds to course of antibiotics
Clostridia are toxin-producing gram negative rods
toxin-producing gram positive rods
Spore-forming soil saprophytes
Clostridia are strict anaerobes
anaerobic cellulitis may have minimal symptoms but is high risk for necrotizing fasciitis
Present w/ minimal swelling and pain of affected skin and low grade temp. Often diabetic or IVDU
typically Clostridium perfringens
Can progress to gas gangrene (type III necrotizing fasciitis)
What are the clinical features of gas gangrene?
severe pain at site of infection and has low grade fever but is toxic with features of SIRS-septic shock spectrum
Dark yellow-bronze coloured skin, may be necrosis or bullae
May be ‘dirty dishwater’ discharge – thin, grey/brown and foul smelling
Usually crepitation as marked gas in subcutaneous tissues spreading along fascial planes
Hyperbaric oxygen may be helpful for the treatment of both anaerobic cellulitis and gas gangrene
as due to clostridia which are strict anaerobes
non-diphtheriae corynebacteria are known as ‘diphtheroids’
Corynebacteria are gram positive rods which make up half of normal skin flora
What organism causes erythrasma?
proliferating in the sratum corneum
is actually a complex of different species of fluorescent corynebacteria
the axillae is the most common site for erythrasma
Toe web spaces most common
erythrasma always occurs in skin folds
classic form usually in skin folds
Disciform variant – can occur anywhere on body esp if T2DM (looks a bit like discoid eczema)
Yellow fluoresence is characterisitic of erythrasma
coral pink fluoresence
due to porphyrins produced by bacteria
What are the treatments for erythrasma
Assess for and modify risk factors;
Whitfield’s ung – salycilic acid and benzoic acid
20% aluminium chloride (driclor)
Azole antifungal – esp miconazole (Daktarin)
if widespread or resistant – erythromycin or single dose 1g clarithromycin
What is the cause of pitted keratolysis?
usually kytococcus(micrococcus) sedentarius – produces 2 serine proteases which degrade keratin in SC releasing sulphur compounds which gives the smell
can be Corynebacteria, Actinomyces spp. etc
Rx the same as erythrasma
What are the causes of nodules or concretions on the axillary or other hair?
Trichomycosis axillaris (nodosa)
Hair casts (keratin)
Pediculosis capitis (knits)
What is the cause of Trichomycosis axillaris?
Corynebacteria coating the hairs – mainly axilla can be pubic
yellow, red or black nodules or cylindrical sheaths called concretions
Trichomycosis axillaris can cause pseudochromhidrosis
red coloured sweat
Trichomycosis axillaris fluoresces coral pink under Wood's lamp
How is Trichomycosis axillaris treated?
similar to erythrasma - can use topical erythro or clinda
Driclor helps to treat and prevent recurrence
Often best to shave area and use antibacterial wash to prevent recurrence
ecthyma diphthericum is an ulcer caused by
C. diphtheriae which occurs in poor tropical countries
which has black or grey pseudomembranous eschar esp on acral sites (inc face)
Acts as immunization as toxin slowly absorbed through skin
The ACTINOMYCETES class is composed of Actinomyces spp. and Nocardia Spp
and affect men more than women
Have branching filaments in vivo and in vitro so used to be classed as fungi
How does Actinomyces Israelii present as skin infection?
Cervicofacial actinomycosis (lumpy jaw)
important DD for dental sinus
A. Israelii is part of normal flora of mouth, GIT and female genital tract
Hx of poor dental hygiene, dental disease or dental surgery or facial trauma
Starts as bluish swelling in region of mandible – progresses to red-brown nodules which form sinus tracts to deep abscesses
Tracts drain pus with ‘sulfur granules’ – yellow grains which are clumps of bacteria
Other types of actinomycosis are Pulmonary and GI disease which rarely can form sinus tracts or fistulas to the skin surface
What is the treatment of Cervicofacial actinomycosis?
prolonged IV penicillin G or ampicillin (up to 6 weeks) followed by 3-12 months of oral penicillin if deep seated chronic lesions
I&D and shorter course suitable for less chronic/deep lesions
What is a mycetoma?
AKA Madura foot
chronic soft tissue (or sometimes involves bone) infection with a filamentous oragnism (mycet) causing a tumour like mass (oma) which is most often on the foot and characteristically drains granular exudate
Caused by species of actinomyctes including nocardia spp and actinomadura spp = Actinomycotic mycetoma or actinomycetoma
Or by various fungi such as madurella spp = Eumycetoma
Nocardia are filamentous gram positive acid fast bacteria found in soil worldwide and previously thought to be fungi
primary skin disease usually acquired by trauma to skin esp foot and contact with soil or soil-contaminated material
The types of skin infection with nocardia (nocardiosis) are
3 major types of primary cutaneous nocardiosis;
- Mycetoma (actinomycetoma, Madura foot)
- Lymphocutaneous nocardiosis
- Superficial nocardiosis
Also up to 10% of pts with systemic/pulmonary nocardiosis get (secondary) skin lesions
Lymphocutaneous nocardiosis presents with sporotrichoid spread
sulphonamides first line for nocradiosis e.g. bactrim
tetracycline if allergic
How does Listeriosis affect neonates?
Due to ubiquitus (soil, water, vegetation) motile gram positive bacteria lysteria monocytogenes
Mum acquires while pregnant
Vertical transmission to foetus causes neonatal septicaemia and meningitis
Skin shows petechiae, purpura, pustules or vesicles
What is the cause of erysipeloid and how is it acquired?
Non-motile, gram positive smooth or curved bacillus
Found in meat, poultry or fish
Skin infection due to traumatic inoculation e.g. fishermen, meatworkers
How is erysipeloid diagnosed and managed?
Can cause localised or generalised skin infection
Localised looks like cellulits and is most often on hand
- Classically involves finger webs and terminal phalanges
Generalized presents w/ fever, arthralgia, rash and widespread lesions; can be perifollicular papules, macular purpura, red plaques or necrotic lesions
Can get septic arthritis, endocarditis, abscesses of brain or other viscera
Hard to culture - send swabs for PCR
penicillin 1st line; also erythromycin, cephalosporins
The meningitis vaccine covers all strains of Neisseria Meningitidis
No vac for strain B
Human nasopharynx is the only known reservoir of Neisseria Meningitidis
Incubation period of 2-10 days
Most people develop a carrier state and may get mild URTI and transient bacteraemia. They are then immune to that strain
The clinical features of meningococcal septicaemia are due to massive bacterial load
Due to a potent endotoxin which triggers the massive inflammatory response resulting in shock, purpura fulminans and MOF
However the organism is also widespread
Neisseria Meningitidis is an aerobic gram negative diplococcus
With a polysaccharide capsule
In a biopsy from the inflamed skin of a patient with meningococcal septicaemia it is unusual to see the organism
In 70% of cases organisms seen with gram stain
How is suspected acute meningococcal septicaemia managed?
How are close contacts treated?
Resuscitate and admit
If suspected take full cultures – blood, skin, CSF and possibly other sites
Start antibiotics ASAP –
or 3rd gen cephalosporin- ceftriaxone, cefotaxime
2 day course of rifampicin as prophylaxis for close contacts
What is Fitz-Hugh-Curtis syndrome?
– RUQ pain and friction rub
N. Gonorrheoae is a gram negative diplococcus with a polysaccharide capsule
gram negative diplococcus
lacks polysaccharide capsule of N. Meningitidis so less virulent
gonorrhoea is often asymptomatic esp in women
genital disease asymptomatic in
10% of men
50% of women
Rectal disease is asymptomatic in 50% of cases in either sex (from anal sex)
How does gonorrhoea affect the eyes?
Auto-innoculation can acuse ‘gonococcal ophthalmia’ – can rapidly progress to keratitis and corneal opacification
vertical transmission from mother with active infection at time of parturition – neonatal conjunctivitis most common (ophthalmia neonatorum)
gonorrhoea can affect multiple sites and rarely can become disseminated
pneumonia in neonates
Disseminated; arthritis-dermatosis syndrome
Fever, rigors and painful swollen joint(s) and often skin lesions – pustules or haemorrhagic/necrotic pustules which heal in days with scarring
A high vaginal swab is used to diagnose gonorrhoea in women
urethral in men and endocervical in women
+/- rectal, pharyngeal, eyes, skin etc
gram stain is good for diagnosis but culture is gold standard to confirm and to determine resistance
gonorrhoea is a notifiable disease
How is gonorrhoea managed?
Can use cefixime, amoxicillin
Can also use erythromycin or doxycycline
Single dose for local disease (urethritis) - ceftriaxone/cipro/azithro/doxy
Must screen for other STIs – syphilis, HIV, Chlamydia
What gives the green colour in pseudamonas infection?
pseudamonas aeruginosa is a gram negative, anaerobic, motile bacillus
strictly aerobic - AERuginosa
gram negative, motile bacillus
pseudamonas green nail syndrome is often seen in pts with prolonged water contact, excessive hand washing, nail trauma or nail disease
Ubiquitus bacterium found in Soil, plants and water
How is pseudamonas green nail syndrome managed?
Avoid wet work
Vinegar soaks – 1:10 in water twice a day for 10 minutes for 1-2+ weeks
Octenidine dihydrochloride 0.1% soaks – 10min BD for 6 weeks
Topical quinolone (ciprofloxacin ear preparations) or aminoglycoside (tobramycin – Tobrex eye ung) for 1-4 months
Nail plate removal if refractory
What skin infections are caused by pseudomonas?
pseudomonas green nail syndrome
Otitis externa (Swimmer ear)
Hot tub folliculitis
Pseudomonas hot-foot syndrome
What is the appearance of Pseudomonal pyoderma or wound infection
Macerated and moth-eaten appearance with green tinge
Often mousy or grape-juice odor
Can occur on ulcer, burn or other skin break
Pseudomonal pyoderma classically occurs in toe web spaces and may be triggered by tinea pedis
IV piptaz if unwell, cipro orally, vinegar soaks
check for tinea and treat
What is Blastomycosis-like pyoderma?
Rare substantial skin infection often with pseudomonas but can also be caused by staph, strep, proteus or some other bacteria
usually in immunocompsomised
Presents with large verrucous plaque with elevated borders and pustules on surface
can be single or multiple
What is the histo of Blastomycosis-like pyoderma?
pseudoepitheliomatous hyperplasia with intraepidermal (neutrophil) microabscesses and diffuse mixed infiltrate with many neuts
In subtropical Aus cases histo may resemble a coral reef with solar elastosis++ so called a coral reef granuloma
How are pseudomonal skin infections treated?
Topical antiseptics – vinegar soaks, Octenidine dihydrochloride 0.1% etc
Silver sulphadiazine cream 1% (SSD, flamazine)
Topical quinolone (ciprofloxacin ear preparations) or aminoglycoside (tobramycin – Tobrex eye ung)
IV – gentamicin, piptaz, a carbopenem, ceftazidime
May need surgical debridement/excision/C&C/laser
1-2% of population have P. Auruginosa as colonizer in ear canal
But pseudomonas alos causes swimmers ear
often staph co-infection too
aural toilet, ciproxin drops, may need systemic ABs
Pseudomonal folliculitis can have widespread symptoms including systemic
E.g. itch, sore eyes, earache, headache, sore throat, fever, malaise, rhinorrhoea, nausea, painful swollen breasts, abdo pain
Usually no treatment as self limiting in 1-2 weeks
If pt at risk can give cipro
What is Pseudomonas hot-foot syndrome?
Rare infection of feet after wading in water with lots of pseudomonas
Soles diffusely red + red-purple tender 1-2cm nodules on sides and bottom of feet
rest and elevate - self limiting
What is ecthyma gangrenosum?
Ecthyma due to pseudomonas
Pt is often unwell with fevers and may have pseudomonas sepsis
Lesions on limbs or anogenital
infants may show grouped lesions in perioral and perianal areas
Purpuric macules evolve into haemorrhagic vesicles or bullae or pustule which rupture leaving necrotic ulcer with black eschar and surrounding erythema and slightly raised egde
Histo shows necrotizing vasculitis with gram neg rods in tunica media and adventitia of deeper vessels but characteristic sparing of the tunica intima, haemorrhage and necrosis
Need IVs e.g. gentamicin, piptaz, ceftazidime
Noma Neonatorum is due to vertical transmission of pseudomonas
Severe infection acquired in neonatal period esp prem or low birth wt in developing countries
Gangrene of nose, lips, mouth, perianal area + sometimes scrotum and eyelids
Fatal without prompt antibiotics
Bartonella are intracellular gram negative bacili
what disease are caused by bartonella spp?
3 species cause human disease;
1) B. bacilliformis - Bartonellosis/Carrion's Dx; Oroya fever or Veruga Peruana types
2) B. henselae - cat scratch Dx, bacillary angiomatosis
3) B. quintana - trench fever, bacillary angiomatosis
Only 50% of cases of cat scratch disease report a recent bite or scratch from a cat
Cat scratch disease is transmitted to humans by cat fleas
transmitted between cats by fleas
transmitted to humans by bite or scratch from cat but not from fleas
Cat scratch disease occurs typically in young teens and affects males and female pts equally worldwide
ave age 15
Cat scratch disease is the most common cause of prolonged lymphadenopathy in children and teens
lymphadenopathy lasts 2-6 months
What is the occuloglandular syndrome of Parinaud?
seen in 5% of cat scratch Dx cases
Unilateral conjunctivitis + ipsilateral preauricular lymphadenopathy
Which pts are most at risk of bacillary angiomatosis?
what are the organisms?
HIV pts esp if low CD4+ count
Caused by B. henselae or quintana
what are the features of bacillary angiomatosis?
multiple angiomatous vascular papules and nodules - look like pyogenic granulomas or kaposis sarcoma or angiosarcoma
can be eroded subcut nodules or indurrated plaque
can affect any organ e.g. liver/spleen (bacillary peliosis hepatis/splenis)
get fevers, rigors, night sweat, GI upset and hepatosplenomegally
send tissue sample for PCR to diagnose ??also serology
treat w/ azithro or doxy + rifampicin
can get jarisch-herxheimer-like rcn
what is a tropical ulcer?
ulcer on pts after minor trauma occuring in tropical locales such as PNG
due to synergistic infection of 2 or more organisms usually an anaerobe such as fusobacterium ulcerans and another is often a spirochete such as treponema spp
rapidly expanding ulcer with grey, foul-smelling base
treat w/ penicilin and metronidazole and supportive measures
Burkholderia mallei causes melioidosis
Glanders is transmitted from horses/mules and is a self limiting disease in humans
Is severe and has >90% mortality if untreated
rest is true
consider in a pt who is sick and has sporotrichoid lesions and has been in contact w/ horses/mules/donkeys in the 3rd world
Farcy buds and farcy pipes are features of glanders
farcy buds are subcut or intramuscular nodules
farcy pipes are thickened lymphatics like cords
Melioidosis is caused by Burkholderia pseudomallei
found in soil and water in N Aus, North of Rockhampton
What are the types of melioidosis skin disease?
Primary skin infection - pustule, ulcer, abscess, furuncle
Systemic melioidosis with secondary skin lesions - usually a generalised pustular eruption
The outcomes of primary skin infection are;
1) resolution with or w/out treatment and no latent disease
2) clinical clearance of infection but ongoing latent disease
3) ongoing clinical disease - cutaneous, systemic or both
If burkholderia pseudomallei is isolated from a well pt it should always be treated
the same is true if serology is positive and there is no clear history of treated disease
latent disease can reactivate systemically affecting the lungs, brainstem, bones, kidney, liver, spleen and other systems
Minimum 2 weeks IV piptaz or ceftazidime then 2-4 months of orals eg bactrim, doxy
resistant to macrolides, quinolones and aminoglycosides
Which organisms are best diagnosed on PCR?
LGV - chlamydia trachomatis (hard to culture)
Erysipeloid - erysipelothrix rhusiopthiae (hard to culture)
Bacillary angiomatosis - B henselae or quintana (culture v slow)
Chancroid - H ducreyi - can culture or PCR
Granuloma inguinale/donovanosis - swab for smear microscopy or serology; hard to culture and no PCR test
early in rickettsial disease (first 5 days) can do PCR on swab or biopsy from tick bite site eschar
Can do PCR for borellia from edge of lesions of erythema migrans
What is Tularemia?
rare gram neg infection from ticks in Northern hemisphere
causes ulcer on limb w/ marker lymphadenopathy -can suppurate, ulcerate or form buboes
can trigger EM, EN or morbilliform rash
Rhinoscleroma is caused by klebsiella rhinoscleromatis
this is a subspecies of K pneumoniae
a gram negative bacillus
Rhinoscleroma occurs in much of the developing world and in part of europe
What is Hebra nose?
destruction of nasal cartilages and granulomatous nodules seen in rhinoscleroma
What causes typhoid?
what are the skin features?
Typhoid fever caused by salmonella typhi
paratyphoid fever is similar and caused by S paratyphi
Non-typhoidal salmonella spp cause similar syndrome of diarrhoeal illness
rose spots - blanching pink papules on anterior trunk from 2nd week of illness - can culture Salmonella from lesions
erythema typhosum - generalized erythematous rash
EM, Sweets, pustues, haemorrhagic bullae
Rat bite fever causes an acral rash on palms and soles
this is typical
pts have been around rodents or contaminated food or water or raw milk
What infections are typically acquired from dog or cat bites?
e.g. P multocida or P.canis
gram neg coccobacilli
Other than rat bite fever what infections are acquired from rodents?
Plague - yersinia pestis
Leptospirosis (Weil's disease)
What type of organism are Vibrio?
what are the important infections caused by Vibrio spp?
gram neg anaerobic bacteria
main infections are;
Cholera - V cholera (others are called 'non-cholera vibrios')
V. vilnificus infection - most common cause of skin disease from Vibrio
What are the features of vibrio vilnificus infection?
due to contact with seawater or shellfish
typically men over 40 who are diabetic, immunsuppressed or have HIV, cancer or other comorbidities
can be a directly infected skin wound or systemic disease from ingested shellfish
get diarrhoeal illness if septicaemic
75% get skin signs - purpura, haemorrhagic bullae, necrotic ulcers
Rx w/ doxy, cipro or IV ceftazidime
what disease are caused by chlamydia trachomatis?
chlamydial urethritis or pelvic inflam disease
lymphogranuloma venereum (LGV)
Trachoma - causes blindness
Batemans syndrome consists of EM + EN + Psittacosis (chlaydia psittaci infection)
spirochetes are gram negative helically coiled organisms with a double membrane
Lyme disease acquired from Europe is usually caused by Borellia Burgdorferi
B burgdorferi found in N America
European lyme due to B afzelii or garinii
Lyme disease-causing borellia spp are transmitted from deers or mice to humans by ixodes ticks
the longer the tick is in the skin the higher the risk of transmission
what are the stages of Lyme disease?
what are the skin features of each?
Early localised - erythema chronicum migrans
Early disseminated - no typical skin findings
Chronic - acrodermatitis chronica atrophicans
erythema migrans develops at the site of the tick bite 1-2 wks after the tick has detached
seen in 60-90% of lyme cases
mostly trunk, axilla, groin or popliteal fossa
What is the appearance of erythema migrans?
starts as erythematous macule or papule
enlarges to >5cm diameter
can remain macular or may become annular with paler centre or targetoid with dark centre and pale inner ring
can be crusted or vesicular at edge
25% get disseminated erythema migrans with smaller lesions elsewhere appearing days or weeks after primary lesion
resolves in 4-6 weeks - european type lasts longer than US type
NB - an annular urticaria arising within hours of a tick bite should not be confused w/ erythema migrans which usually doesnt start until at least 1 week later
Other than erythema migrans what are the features of early localised lyme disease?
regional lymphadenopathy common
EU types have few other features
US types get fever, headache, malaise, fatigue, cough
early disseminated lyme Dx consists of fever, headache, arthralgia, arthritis, lymphadenopathy, cardiac and CNS complications, eye disease and orchitis
no major skin features
what are the features of chronic lyme disease?
Acrodermatitis chronica atrophicans
+ may have sequele from early disseminated disease
How is lyme disease diagnosed?
Need the following?
classical erythema migrans >5cm
+ either exposure to an endemic area (but Hx of actual tick bite not necessary) Or;
laboratory evidence; Serology or culture or PCR from edge of erythema migrans
NB serology peaks at 3-6 weeks after tick bite - most likely to be positive then
Borellial lymphocytoma is a blue-red firm nodule or plaque that may develop on the nipple/areaola or in kids on the earlobe in cases of european lyme disease
In 1% of early disseminated phase of european lyme
is a dense lymphocytic infiltrate resembling a lymphoid follicle - is a type of benign reactive lymphoid hperplasia
What is acrodermatitis chronica atrophicans?
Late manifestation of Lyme borreliosisInsidious onset of painless dull red nodules or plaques on the extremities (acro=acral), which slowly extend centrifugally leaving areas of central wrinkled atrophy and can be dyspigmentation or scale
May be pain, itch, numbness, hyperaesthesia
Due to Borrelia afzelii - N and C Europe, Italy and the Iberian Peninsula (rare in UK and USA)
rickettsiae are true bacteria
somewhere between bacteria and virus
gram neg, rod shaped, obligate intracellular growth
The genus rickettsia is part of the family of rickettsiae
other genus's are;
Rickettsia spp cause scrub typhus diseases
Rickettsia spp cause typhus and spotted fever diseases
Orienta spp cause scrub typhus group diseases
‘Typhus’ refers to several diseases caused by various members of the typhus group of rickettsial diseases
Rickettsiae have an invertebrate host such as ticks, fleas, lice etc and a vertebrate host (usually) other than humans such as rodents, marsuipials, lizards etc
Australian spotted fever is caused by R. australis
Aus Spotted fever is caused by R. honeii subgroup marmioneii
R. australis causes Qld tick typhus - another type of spotted fever
all australian endemic rickettsial diseases can be acquired in Qld
Flinder's island spotted fever is found in the region of Flinder's island including Tasmania, Victoria, SA and possibly NSW and ACT
All others are in Qld
Qld tick typhus is in the typhus group of rickettsial diseases
it is a spotted fever rickettsial disease caused by R. australis and transmitted by ticks