ABTSI + Leprosy Dan Flashcards
T/F
More Aboriginal and Torres Strait Islander people live in urban areas than remote communities
True
T/F
some people find use of the word ‘indigenous’ offensive
True
it is vital that you confirm what is the locally-preferred term with the people you work with and use it
What is an aborigine?
A person who is of Aboriginal descent, who identifies as an Aboriginal person, and is accepted as such by the community in which he or she lives
What is a Torres Strait Islander?
A person who is of Torres Strait Islander descent, who identifies as a Torres Strait Islander and is accepted as such by the community in which he or she lives
T/F
The following principles are important when interacting with indigenous pateints;
Introduce yourself and say where you are from
Use simple language
Avoid jargon
Take consultation slowly and gently
Be non-judgemental
Avoid direct questioning
Allow for silences
Allow for reflection and confirmation
ABTSI may go silent when an uncomfortable subject is being discussed. Try a different approach, consider help from a health worker, consider offering a doctor of the same sex as the patient if available
Utilise aboriginal health worker to facilitate consultation if needed
Clearly illustrate principles of disease and management
True
T/F
The prevalence of systemic lupus erythematosus is the same in Aboriginal Australians and in European Australians.
False
2-3x (2-3.8 in latest AJD paper) more in aborigines and also more severe
affects 1:1000 – 1:1900 Aborigines
T/F
Lupus erythematosus affects females more than males
True
DLE 5x more common in females regrdless of race
other LE also more common in females
T/F
It is unknown if the prevalence of LE in aborigines is genetically or environmentally determined
True
Theories include
Inherited deficiency of complement component C4A
Induction of cross reactive anti-dsDNA antibodies by bacterial infections and
Super antigen effect
Genetic variants that offer resistance to infectious diseases such as malaria.
T/F
Lupus erythematosus in aborigines has a high morbidity and mortality and high frequency of renal disease
True
T/F
Autoantibodies to the Sm antigen are uncommon in Lupus erythematosus in aborigines
False
common
T/F
The majority of deaths in aboriginal patients with SLE are due to renal failure
False
The majority of deaths in aboriginal patients with SLE are due to infection - associatd with active disease and with steroids
Which sites are most affected by cutaneous lupus?
nose, cheeks and forehead
but the lips, scalp and trunk may be involved
T/F
cutaneous lupus lesions are darker in darker skin
True
What is the carpet tack sign in cutaneous LE?
follicular plugs covered with scale – may be removed when scale scraped off or tape-stripped like lifting a carpet with the tacks pointing out from underneath
T/F
Erythema at the edge of the hyperpigmented lesions is characteristic of cutaneous lupus
True
hypopigmentation and scarring come later - often permanent
What are the acute, subacute and chronic stages of lower lip lupus?
acute - the lip is red, friable and bleeds easily
chronic - hypopigmentation and scarring
subacute stage is transition between these two
T/F
It is difficult for the clinician and histopathologist to distinguish verrucous lupus from Squamous cell carcinoma on the lip
True
T/F
The main differential diagnosis of LE in aborgines is tinea faciei
True
What are the common and rare organism causes of sepsis in aboriginal SLE pts?
gram negative and staphylococci - same as other pts
But also risk of rare pathogens eg. CNS cryptococcocis and disseminated strongyloidiasis
T/F
In mothers of infants with neonatal lupus almost all sera contain IgG antibodies to the SSA(Ro), 60KDa protein
True
Often also antibodies to 52KDa SSA(Ro) and to SSB(La)
small proprotion have antibodies to U1-RNP
Ro52 Abs carry highest association with congenital heart block, then Ro60
Pts with U1-RNP Abs alone usually don’t get CHB
T/F
skin biopsy is always necessary in an infant with a rash and features suspicious for neonatal LE
False
Take blood for serology and investigate mother
Only biopsy if diagnosis in doubt after other investigations
T/F
>90% of infants with NLE develop skin lesions
False
approx 50%
T/F
Rash of NLE usually resolves in 1st year without scarring but can cause residual hypopigmentation, epidermal atrophy or telangiectasia
True
atrophy is rare
T/F
Rash of NLE is photosensitive
True
T/F
NLE is the most common cause of Congenital Heart Block (CHB) where the structure of the heart is normal
True
T/F
20% of neonates born to mothers with anti-SSA antibodies will develop NLE
False
2%
2% also quoted as risk of having a baby with CHB
T/F
congenital heart block usually presents in utero commonly at 18 – 24 weeks of gestation
True
Incomplete heart blocks can progress after birth and once complete heart block is present it is irreversible
What are the other cardiac manifestation sof NLE other than heart block?
cardiac malformations
cardiomyopathy
prolonged QT interval
sinus bradycardia
T/F
thrombocytopenia in NLE usually doesnt cause clinical problems
True
can also get
Anaemia, neutropaenia and recurrent pancytopaenia
T/F
1 third of pts with CHB require PPM
False
2 thirds
What are the 3 presenations of liver disease in NLE?
fulminant liver failure presenting at or shortly after birth
cholestasis a few weeks after birth
transient mild-moderate transaminase elevations occurring a few weeks or months after birth
T/F
maternal breastfeeding is fine in cases of NLE
disocouraged as may transfer more lupus antibodies
T/F
Topical steroids do not reduce the frequency of hypopigmentation, telangiectasia and atrophy.
True
sun avoidance and sunscreen are mainstay
TCS usually not needed but can use HCT
What is risk to mother of having a second baby with NLE?
25% of recurrence in later pregnancy
T/F
Disseminated strongyloidiasis should be considered in ill immunosupressed patients in the Northern Territory
True
T/F
Squamous cell carcinoma of the lower lip is a complication of cutaneous lupus in Aboriginals
True
T/F
Sepsis as a cause of death is associated with oral corticosteroid use
True
T/F
The reason for the increased prevalence of lupus in Aboriginals is unknown
True
T/F In indigenous Australians there are high prevalences of metabolic syndrome components: • glucose intolerance • dyslipidaemia • hypertension • insulin resistance
True
The important factors leading to metabolic syndrome components are:
• social disadvantage
• limited economic opportunity
• adoption of diets of poor nutritional qualit
• rapid weight gain
True
T/F
Blindness is the most frequent complication of T2 diabetes in aboriginals
False
nephropathy
T/F
T2 diabetes in aboriginals has an incidence of end-stage renal failure that is 20–30 times that observed in Caucasian type 2 patients
True
T/F
Aboriginal patients with diabetes die at a significantly younger age than their Anglo-Celt counterparts
True
T/F Aboriginals in homelands participating in caring for country activities have: • less abdominal obesity • less diabetes • lower systolic BP • lower HBA1c levels and • lower cardiovascular disease risk
True
T/F
Indigienous women ahve a prevalence of PCOS of >25%
False
>15%
T/F
Acanthosis nigricans is common in overweight Aboriginal people
True
T/F
Acanthosis nigricans is most easily appreciated at the posterior neck in Aboriginal people
True
May also present in the axillae, inguinal area, abdominal fat folds and sometimes the flexures of the limbs
T/F
painful leg ulceration in a 45 year old Aboriginal is more likely to be vascular in origin than pyoderma gangrenosum
True
Always think of the complications of diabetes, renal disease and vascular disease
T/F
Before European colonisation of Australia, obesity was rare in Aboriginals
True
T/F
Indigenous Australians have a high prevalence of metabolic syndrome components
True
T/F
Vascular disease is rare in Aboriginal Australians
False
prevalence ranges from 10% – 70%
T/F
Group A streptococcus is a comon cause of skin sores (pyoderma) in Aboriginal children in Australia’s northern tropical regions
True
but often staph also present
What are the complications of Group A streptococcus pyoderma?
acute rheumatic fever
rheumatic heart disease
Post strep glomerulomephritis
T/F
Pyoderma and poor outocmes are more common in household overcrowding
True
T/F
The prevalence of pyoderma in children is higher during the wet season
False
higher during dry season
Increased outdoor activity and a greater chance of minor trauma and children tend to avoid swimming during these months as the water is colder
T/F
scabies predisposes to pyoderma
True
T/F
There is no link link between skin infections in childhood and the extreme rates of end-stage renal failure in Aboriginal adults
False
strong link
Acquiring APSGN in childhood increases the risk of adult renal disease by six times
T/F
Episodes of acute post streptococcal glomerulonephritis (APSGN) are five times higher for children with skin sores
True
T/F
Episodes of acute post streptococcal glomerulonephritis (APSGN) are five times higher for children with scabies
False
twice as common with scabies
5x with skin sores
T/F
Acquiring APSGN in childhood increases the risk of adult renal disease by 10 times
False
6x increase risk of adult disease after childhood APSGN
T/F
Indigenous Australians to die from kidney failure with a frequency 5x higher than non-Indigenous Australians
True
T/F
Indigenous Australians have end-stage renal disease 21x more than non-Aboriginal Australians and doubling every four years
True
T/F
Acute rheumatic fever is 60x more common amongst aboriginal children than non-aboriginal children
True
300 per 100,000 Vs 5 per 100,0000
T/F
pharyngeal carriage rates of group A β-haemolytic streptococci are high amongst aboriginal children
False
Low
strep complications due to skin infection not pahryngeal
Recurrent skin infection may confer a degree of immunity resulting in lower risk of strep throat
T/F
ARhF and RhHD are classic diseases of social injustice
True
T/F
Rates of ARhF and RhHD in aboriginals in the NT are declining
False
little or no evidence of improvement over at least the past three decades.
T/F
skin sores are more common on the trunk
False
usually the result of trauma and are more common on the limbs
T/F
Pus is unusual in skin sores
False
may look dry but pus under scabs
What triggers skin sores?
Trauma
insect bites and scabies
T/F
skin sores are transient and heal without scars
False
not always
can be chronic and leave scars
T/F
community acquired MRSA is common in some aboriginal communities
True
T/F
The use of ASOT and anti-DNA’ase B serology is not recommended for the diagnosis of impetigo
True
a high background and persisting levels of antibody in Aboriginal populations
T/F
The use of ASOT and anti-DNA’ase B serology is not recommended for the diagnosis of acute post streptococcal glomerulonephritis
False
should check in cases of gn as if high supports the diagnosis
T/F
topical antibiotics are first line for skin sores
False
topical antiseptic + oral treatment or IM benzathine penicillin 1st line
bactroban TDS for 7 days good choice if above cannot be used
Which oral antibiotics are used for skin sores?
what doses?
phenoxymethylpenicillin (penicillin VK) for 10 days is 98% effective
- 250-500mg QDS in adults
Cephalexin 500mg 3 times per day is usually effective if S.aureus is predominant
- treat kids with Wt-based dosing
Roxithromycin daily for 10 days is usually effective in penicillin allergic patients
- 300mg/day adults
- 5 to 8 mg/kg/day kid in divided doses
T/F
avergae monthly prevalence of pyoderma in East Arnhem is 35%
True
T/F
Skin sores are usually purely steptococcal
False
ofetn staph also
T/F
antibiotics must be given for 10 days for cases of beta haemolytic strep infection
True
T/F
Multiple skin sores are treated with benzathine penicillin
True
Single injection of 900mg for adults
single injection of 675mg (900,000 units) for older children
single injection of 225 to 450mg (30-600,000 units) for infants and children under 27kg
T/F
In remote indigenous communities scabies is endemic and prevalence rates are up to 50% in children and 75% in adults
False
50% in children and 25% in adults
T/F
Scabies is responsible for a significant percentage of streptococcal pyoderma in Northern Tropical Australia
True
What is a core infector of scabies?
Individuals in the comunity with individuals with hyperinfestation (crusted or Norwegian scabies) who infect other community members
T/F
Canine and human scabies mites are morphologically indistinguishable and dog mites can produce itch on human skin
True
T/F
Dog scabies can cause mange
True
Mange is a skin disease of mammals caused by parasitic mites and occasionally communicable to humans
when due to scabies is called scabetic mange
T/F
cycles of scabies transmission in dogs and humans appear to significantly overlap in Aboriginal communities
False
dont significantly overlap
T/F Scabies transmission (photo of eggs) usually occurs through direct skin contact with infected persons
True
T/F
Dog scabies cause itch in humans but not established infection
True
T/F
Scabies mites may survive for 56 hours off the human host
True
T/F
scabies live longer off the host in dry environment
False
survival enhanced by humidity
T/F
Inadequate “health hardware” (washing machines, toilets, taps, showers) and chronic overcrowding contribute significantly to scabies transmission in Aboriginal communities
True
T/F
truncal eczematous eruption is typical of scabies
True
T/F
scabies affects the genotals in men and the nipples in women
True
T/F
Scabies in babies tends to produce a papular vesicular eruption on the palms and soles
True
T/F
Secondary infection with streptococcus pyogenes and/or staphylococcus aureus makes scabies lesions easier to identify
False
obscures lesions and produces deeper ulceration
T/F
With age and multiple chronic infestations, the individual may develop tolerance to the scabies mite with few signs or symptoms
True
T/F
In elderly or with HTLV-1 or HIV there can be crusted scabies with no itch
True
should check for HTLV-1 or HIV in cases of crusted scabies
T/F
Usually there is a single strain of scabies in a community
False
multiple overlapping epidemic cycles indicating a wide circulation of diverse strains of sarcoptes scabiei
What is the India Ink Test for scabies?
blue felt tipped pen is applied to the suspected Burrow and the superficial ink is removed with an alcohol swab. The ink stays in the Burrow
Scraped off burrow with a blade and examine under microscope after an application of potassium hydroxide
T/F
Topical 5% permethrin cream is the treatment of choice for scabies
True
2 treatments 7-14 days apart
T/F
In tropical regions, especially for children, the neck, head and scalp should also be treated with permethrin for scabies
True
T/F
Permethrin can be used by women in the early stages of pregnancy and children from 2 months of age and probably younger
True
ACD module
Permethrin is B3
T/F
Benzyl benzoate can be used for scabies although irritation often leads to non-compliance
True
Ascabiol lotion = 25% benzyl benzoate (B2)
take hot bath and scrub skin
apply otion all over below neck
after 24 hrs take another hot bath
1 Rx often sufficient, can repeat after 5 days
sometimes 5% tea tree oil is added
T/F
Infantile acropustulosis may be a persistant post-scabetic reaction
True
T/F
Preciptated sulphur can be used for scabies
True
traditional choice for pregnancy and children up to 2 months
6-10% in Aq cream BD
Use for 3 days then leave final application on for 24 hrs
Not mentioned in college module
T/F
Household conatcts who are not clinically infecetd should be reated with permethrin
False
not necessary unless share a bed
Household contacts should be treated with cleaning of clothing, bedding and simple cleaning of the house
T/F
Ivermectin is metabolized by the liver and excreted in the faeces over an estimated 12 days
True
so nursing mother should not breast feed for 2 weeks after last dose
T/F
10% of ivermectin is excreted in urine
False
What is the dose of ivermectin?
200 micrograms per kilogram (3mg tabs)
- NB Wt-based number of tablet dosing in MIMs up to 80kg body weight
1 dose on day 1 and another dose between day 8 and day 15
3 doses if severe
7 dose regime and topical keratolytic for crusted scabies
T/F
Hepatic transaminases may become elevated during ivermectin therapy
True
T/F
ivermectin is excreted in the breast milk
True
T/F
Ivermectin should not be used in children under 25kg
False
not if under 5 years old or under 15kg
T/F
Septicaemia is a common complication of crusted scabies and is frequently polymicrobial
True
Rx aggressively treated with broad spectrum antibiotics
How should crusted scabies be managed?
Admit pt to single hospital room - isolation + contact precautions
Provide clean clothes daily and clean room thoroughly daily
FBC, Lymphocyte subsets, ELFTs, CRP, BSL
Urine MC&S, protein and RBCs, glucose and ketones
check HIV, HTLV-I, strongyloides and hepatitis B and C
ANA, ENA, DNA,C3 and C4, immunoglobulins, RhF, serum protein EPP, antiphospholipid antibodies and lupus anticoagulant
Treat sepsis and any other complications or untreated conditions
Topical scabicide
- permethrin every 2-3 days
- or benzyl benzoate 25%
Topical keratolytic is vital eg 6% sal acid in Aq cream +/- coal tar
Ivermectin 7 doses over 1 month;
- days 0, 1, 7, 8, 14, 21, 28
Can also use Condys baths and TCS for itch
Assess and treat household contacts while pt in hospital - GP and/or aboriginal health worker
T/F
comunity-based scabies control programs successful in achieving an initial reduction in scabies and pyoderma but the prevalence often rises back to a pre-interventional level within one year
True
Regular follow-up is required for a sustained reduction
T/F
Community initiated clean-up days play an integral part in promoting personal and household hygiene in scabies-affected communities
True
T/F
Crusted scabies results from failure of the host immune response to control the proliferation of the scabies mite in the skin, with resulting hyperinfestation and concomitant inflammatory and hyperkeratotic reaction
True
T/F
crusted scabies is very common in south australian aboriginal comunities
False
rare in south although scabies is common
crusted scabies most comon in central and north australia
What are risk factors for crusted scabies?
what additional risk factors are found in aboriginals?
HIV HTLV-1 T-cell lymphoma and leukaemia immunosuppression esp transplant pts SLE rheumatoid arthritis diabetes malnutrition neurological disorders - neuropathy, spinal injury, leprosy Dementia Downs’s syndrome arthropathy
additional risk factors are found in aboriginals;
past history of lepromatous leprosy
heavy Kava use
heavy alcohol use
T/F
IgE and eosinophil count are often raised in crusted scabies
True
T/F
ANA often positive in crusted scabies pts
True
T/F
C3 and C4 are often high in crusted scabies pts
False
low
What is mode of action of Ivermectin?
Semi synthetic macrocyclic lactone antibiotic. It disrupts the function of a class of ligand-gated chloride ion channels However the target of this drug in the scabies mite has yet to be identified and only a pH-gated chloride channel that is sensitive to ivermectin has been described
T/F
It is thought that in vertebrates P-glycoprotein drug pumps exclude ivermectin from its potential site of action resulting in no effect
True
T/F
P-glycoprotein substrates such as cyclosporine and HIV protease inhibitors may theoretically increase risk of human ivermectin neurotoxicity by competition for P-glycoprotein binding sites
True
But this has not been seen in studies or clinical practice
What is the most likely reason for scabies recurrence after treatment?
The most likely reason for recurrence is reinfestation
resistance to Ivermectin in scabies mites is another possibility
T/F
Ivermectin is neurotoxic in collies
True
T/F
Scabies in babies involves the head and neck in tropical areas
True
T/F
Canine scabies produces significant infestation in Aboriginal communities
False
T/F
Resistance to ivermectin is developing in scabies
False
still extremely rare
T/F
Staphylococcus aureus is the most common bacteria in infected scabies in Aboriginals
False
strep
T/F
Patients with crusted scabies should be tested for HTLV-1
True
and HIV
Which populations are at risk of community associated MRSA (CA-MRSA)?
sporting teams incarcerated persons the military children in day care facilities men who have sex with men indigenous communities across the world
T/F
Crowded living conditions, poor hygiene and poor access to medical care are risk factors for CA-MRSA
True
T/F
CA-MRSA is largely from a single strain in Australia
False
diverse strains in different parts of the country which have almost certainly arisen from the local indigenous population
T/F
Aboriginal populations have higher incience of both MSSA and MRSA infections
True
T/F
Staph infection incidence rates strongly correlate with measures of remoteness and socio-economic disadvantage
True
T/F
CA-MRSA was first noted in Australia amongst aboriginal populations and these communities may provide the reservoir from which the infections emerge into the wider community
True
T/F
CA-MRSA is a “feral descendent” of health care associated MRSA strains that had escaped into the community
False
new strains emerging locally
T/F
Western Samoan Phage Pattern (WSPP) strain of MRSA arrived in Australia from PNG
False
arrived in Australia via Auckland in New Zealand and has probably arisen in Samoa
Found in QLD and NSW
T/F
The Panton-Valentine leukocidin (PVL) gene is an important virulence factor associated with more severe skin and soft tissue infections including necrotising fasciitis, necrotising pneumonia, abscesses and death
True
T/F
NT-MRSA and the original WA-MRSA clones are PVL positive
False
PVL negative
But recently pvl has been detected in some WA-MRSA strains
Which MRSA strains in Aus are PVL positive?
USA 300
UK MRSA (rare in Aus)
Queensland MRSA
Western Samoan Phage Pattern (WSPP)
T/F
When practising in an area with indigenous patients, it is essential to know the pattern of antimicrobial resistance of the local S. aureus isolates
True
T/F
antibiotics are essential for MRSA abscesses
False
The primary treatment for a CA-MRSA abscess is surgical drainage
Many patients respond to drainage alone.
Which antibiotics can be used for MRSA infections?
Clindamycin 300mg TDS - 450mg QDS (C. diff risk)
Bactrim
Vancomycin 1st line for severe infections requiring hospital treatment
T/F
For recurrent furunculosis, tetracyclines, particularly vibramycin, can be taken for a longer period of time in association with an anti-staphylococcal regime if practical
True
T/F
MRSA can be transmitted between dogs and humans
True
In both directions
Poor dog health and dog overpopulation are major problems in many an Aboriginal community
How is staph eradication performed?
Chlorhexidine 4% bodywash/shampoo or Triclosan 1 - 2%
daily as wash for 5 days to body
wash hair on days 1,3,5
Nasal mupirocin ung
Use matchstick head-sized amount (less for small child)
Apply 3 times day for 5 days with cotton bud to inner surface of each nostril.
Massage gently upwards.
If applied correctly, patient can taste Mupirocin at back of throat
T/F
The Panton-Valentine leukocidin is associated with necrotising fasciitis
True
T/F
The WSPP strain predominates in NSW
True
T/F
Trimethoprim-sulfamethoxazole is effective treatment for indigenous patients with moderately severe skin infections
True
T/F
CA-MRSA infections can be diagnosed clinically
False
T/F
Tinea of the skin and nails affects 5-15% of aboriginal children
True
T/F
tinea capitis with Trichophyton tonsurans can be very mild manifesting as scaling and without hair loss in a few patches
True
T/F
Geophilic fungi are the main cause of tinea of the skin, nails and hair
False
Anthropophilic fungi are the main cause of tinea of the skin, nails and hair
T/F
Tinea corporis in aborigines is usually caused by Trichophyton rubrum or Trichophyton tonsurans
True
In NT and NSW aboriginal studies
T/F
Trichophyton tonsurans is almost always isolated from tinea capitis in aborigines
True
T/F
superinfection with group A Streptococcus and Staphylococcus aureus occurs in dermatophyte infections
True
due to excoriations esp in infants
T/F
scaling is unusual in black skin affected by tinea corporis
False
Scaling may be prominent particularly in black skin
A circinate silvery scale may be the only manifestation
T/F
kerions may be secondarily infected with staph including MRSA
True
T/F
Woods light examination will show no fluorescence with anthropophilic fungi
True
T/F
Terbinafine is fungicidal and available on the PBS for Aboriginal or Torres Strait Islander patients where topical treatment has failed
True
T/F
topicals may be effective for small patches of tinea corporis
True
clotrimazole 1% cream twice daily for 4 weeks
terbinafine cream twice daily for 1-2 weeks
T/F
tinea capitis should always be treated
False
If localised scale only and no hair loss consider ketaconazole shampoo only as treatemnt likely to be ineffective or followed immedietely by reinfection in overcrowded hosuehild with poor hygeine and washing
T/F
For widespread tinea corporis oral terbinafine for 2 weeks is the treatment of choice
True Adults – 250mg Children >40kg – 250mg Children 20-40kg – 125mg Children
T/F
Terbinafine should be used with caution in patients with diminished renal function and the dosage may have to be reduced
True
T/F
terbinafine is fine in pts with liver disease
False
Oral teribinafine should only be used if absolutelty necessary in patients with liver disease
check FBC and LFTs and repeat fortnightly
T/F
There have been reports of agranulocytosis and hepatic failure with terbinafine
True
T/F
Terbinafine can precipitate or exacerbate subacute lupus erythematosus
True
How is tinea ungium treated?
Terbinafine (80% cure)
- 250mg daily (
6 wks for fingernails, 12-16 wks for toenails)
or pulse therapy of 500mg daily for 1 week per month for 3 mnths for fingernails and 4 mnths for toenails
T/F
Griseofulvin can precipitate DLE
True
and also SCLE
T/F
In tinea capitis topical therapy should be used as adjunctive therapy with either selenium sulphide or ketoconazole shampoo to reduce shedding of fungal spores. The shampoo should be applied 3 times per week and the lather left in the scalp for at least 5 minutes.
True
How is tinea capitis treated
Terbinafine – treat per weight for 4 weeks (best avoid for M. canis or need to double dose)
crush and add to light meal
Griseofulvin 20mg/kg/OD (up to 500mg) for 8-12 weeks (esp if M canis as terbinafine not recommended) - or can use 100mg per year of life up to age 5+
crush griseo tabs and put in ice cream (fatty)
T/F
Terbinafine and griseofulvin should not be used during pregnancy
True
T/F
Trichophyton tonsurans fluoresces under wood’s light
False
T/F
Trichophyton rubrum commonly causes tinea capitis
False
T/F
Griseofulvin is teratogenic
True
T/F
Mycobacterium leprae prefers to replicate in the hotter areas of the body
False
T/F
In polar tuberculoid leprosy there is a low bacillary load
True
T/F
In lepromatous leprosy there is a weak cell mediated immune response against mycobacterium leprae
True
T/F
In tuberculoid leprosy multiple nerves are affected
False
T/F
Madarosis is a feature of tuberculoid leprosy
False
T/F
If a patient has a positive skin smear treatment should be for multibacillary disease
True
T/F
Type 1 reaction is a delayed type hypersensitivity response to mycobacterium leprae
True
T/F
Erythema nodosum leprosum spares the testicles
False
T/F
M. pachydermatis is a common cause of pit versic in aboriginals
False
in dogs
Which species are responsible for pit versic?
Mlasezzia
mainly
M.furfur, M.globosa and M.symbodialis
What are the microscopic findings in scrapings of pit versic?
thick-walled, spherical yeast forms
budding from a narrow base and course septate mycelium often broken up into short filaments
What are predisposing factors for pit versic?
warm climate family history conjugal exposure (from partner) Cushing’s syndrome and possibly pregnancy.
Which age groups mainly get pit versic?
late teens and early twenties
rare in old age
T/F
The specific malassezia species causing pit versic has not been determined in Aboriginals
True
What is Kava?
Kava comes from the root of the pepper plant Piper methysticum. It is used in traditional ceremonies and for social occasions in many of the Pacific Islands. Kava is valued for its medicinal properties and is sold as a herbal preparation or medicine in many countries.
In the NT, Aboriginal people make a kava drink by mixing the dry, powdered root with water. Kava resin, suspended in water, contains active chemicals known as kava lactones. The strength of kava varies greatly and depends on the plant from which it is prepared and how it is prepared.
causes drowsiness, stupor, muscle relxation and ‘drunkeness’
T/F
Malazessia spp are hydrophilic yeasts
False
lipophilic yeasts
T/F
Malazessia spp are part of the normal skin flora
True
pityriasis versicolor in most cases represents a shift in the relationship between a human and his or her residential flora
What are colloquial names for pit versic among aboriginals?
“Darwin sunburn” - small and circular lesions
“white handkerchief” - extensive sheets
T/F
After Rx of pit versic the residual depigmentation may remain for many months without any scaling
True
Areas of Pit versic stand out more under Wood’s lamp. What colour do they fluoresce?
green-yellow
T/F
Pit versic may be moe extensive than usual in the tropics
True
Lesions in the axillae and groins, and on the thighs and genitalia occur and extension down the forearms and into the popliteal fossae may occur. Facial involvement occurs particularly in the tropics
T/F
culture of skin scarpings is helpful to diagnose pit versic
False not helpful malasezzia part of normal flora diagnose based on clinical appearance/Wood's lamp \+/- presence of typical microscopy
How is pit versic treated?
Azole antifungals
Topical
- Cream for localised area
- Ketoconazole (Nizoral) 2% daily for 10 days or leave on overnight and wash off then rpt after 7 days
- Econazole 1% (Pevaryl foaming lotion) nocte for 3 days leave on overnight then wash off + rpt at 1+3 months
- 2.5% Selenium sulphide shampoo (selsun gold) – leave on 20mins and wash off daily for 2 weeks – do not leave on overnight
- 50% propylene glycol in water
Systemics - off label use
- Fluconazole (diflucan) - less liver risk + cheaper
400mg single dose or
300mg/wk for 2-4 wks or
1-200mg/day for 3 weeks
- Itraconazole (sporonox) - v expensive, Incr risk
200mg/day for 1 week
Often need a once monthly rpt dose to maintain remission Flucon 300mg or Itra 200mg
T/F
All the systemically absorbed imidazole antifungal agents have the potential to induce hepatotoxicity
True
always ask about alcohol (and kava in aboriginals)
T/F
fatal hepatotoxicity can occur with itraconazole and ketoconazole
True
T/F
Itraconazole can also cause serious cardiovascular adverse events with concomitant administration of a number of drugs including erythromycin
True
check pts reg meds carefully for interactions
T/F
stretching the skin can help to see the fine white scale of pit versic
True
T/F
there is no way to speed up the recovery of depigmentation caused by pit versic
False
exposure to UV light from the sun speeds repigmentation
T/F Regarding Pit versic;
The diagnosis is usually made clinically
True
T/F Regarding Pit versic;
Topical treatments are usually curative
False
they help but reinfection is typical
T/F Regarding Pit versic;
Wood’s light examination helps distinguish it from tinea
True
T/F Regarding Pit versic;
Ketoconazole can be safely used with erythromycin
False
Avoid oral ketoconazole - too high risk
also avoid itraconazole with erythromycin and any other CYP3A4 inhibitor or metabolised drug including;
clarithromycin, erythromycin and indinavir, ritonavir, Rifampicin, phenytoin, rifabutin and isoniazid.
T/F
Trychophyton mentagrophytes is carried by kangaroos
True
T/F
The granular variant of T rubrum is endemic among aboriginal populations in tropical regions
True
but rarely causes tinea capitis
What are the causes of madarosis to consider in aboriginals?
= loss of eyebrows
Genetic
Trauma - burns, rubbing, trichotillomania
Hypothyroidism
Infection - lepromatous leprosy (NOT tuberculoid), secondary syphylis
What are the DDs of prominent forehead skin folds?
Cutis Verticus Gyrata • Essential type • Neurologic/ ocular type • Secondary type – Myxoedema, Acromegaly, Turners syndrome Leonine facies - many causes Extensive congential cerebriform melanocytic naevus Pachydermoperiostosis Acanthosis nigricans Dissecting cellulitis of scalp
What are the DDs of Leonine facies?
‘A lion PALMS you’ P – Pagets disease of bone A – Amyloidosis (systemic) L – Leishmaniasis, Lipoid proteinosis, lepromatous leprosy, lymphoma (B or T), leukaemia cutis M – Mastocytosis, MF S – Sarcoidosis, scleromyxoedema
T/F
Leprosy rates in Australia are more than 1 case per milion per year
False
less than 1 per million
T/F
Officially leprosy has been eliminated in Austalia but cases still occur
True
WHO defines elimination of eprosy as a prevalence of less than 1 per 10,000 population
which is true but there are still new cases each yr in Australia
T/F
New cases of leprosy in Australia mainly occur in Vic and SA?
False
mainly in the Kimberly and NT
T/F
Indegenous australians are the only ones who get leprosy in australia
False
not the only ones but mainly indegenous and recent arrivales from endemic countries
T/F
Leprosy has a short incubation time
False
long
2-5 yrs tuberculoid
9-12 yrs lepromatous
T/F
The doubling time for the M Leprae bacillus is 21 days
False
12 days
T/F
early treatment reduces the risk of onward transmission of leprosy
True
T/F
early treatment reduces the risk of NFI (nerve function impairment) in leprosy
True
Which 3 body regions are mainly affected by leprosy?
skin
mucous membranes of the nose
peripheral nerves
T/F
M Leprae replicates in macrophages
True
T/F
M Leprae replicates in peripheral nerves
True
T/F
There is a spectrum of disease type in leprosy between the two polar forms, tuberculoid and lepromatous leprosy
True
What steps are taken by the clincian in order to classify a case of leprosy?
Physical examination including neurology
skin smear
while skin biopsy may be useful for diagnosis it is of secondary importance in classification and used only if skin smear inconclusive
T/F
accurate classification of leprosy determines infectivity, prognosis, disease complications and treatment regimens
True
T/F
The WHO classification for leprosy is used most widely in developed countries
False
WHO used in resource limited countries
Ridley-Jopling system used in developed countries
T/F
In the Northern Territory an attempt is made to classify all leprosy patients by both the Ridley-Jopling classification (for prognosis) and the WHO classification (for reporting)
True
What are the categories of the Ridley-Jopling classification?
polar tuberculoid (TT) borderline tuberculoid (BT) borderline (BB) borderline lepromatous (BL) polar lepromatous (LL)
What are the categories of the WHO classification?
paucibacillary (PB) single lesion
paucibacillary (2 – 5 lesions)
multibacillary (6 or more lesions)
T/F Borderline leprosy (BB) is the most common type in the NT
False polar tuberculoid (TT) is most common
T/F polar tuberculoid (TT) leprosy pts have a poor cell-mediated immune response to the bacillus
False polar tuberculoid (TT) leprosy pts have a well developed cell mediated immunity and very low bacillary load and localised disease
T/F
In tuberculoid leprosy TH – 1 type cytokines such as interferon gamma and IL – 2 are the principle immune mediators of the disease
True
T/F
In lepromatous leprosy TH – 1 type cytokines such as interferon gamma and IL – 2 are the principle immune mediators of the disease
False
TH – 2 type cytokines such as IL – 4 and IL – 10 are the principal immune mediators in these lesions
T/F
In tuberculoid leprosy patients are typically smear negative
True
T/F
LL is less common than TT leprosy and these patients have a weak cell mediated immunity, high bacillary load and disseminated disease. They are smear positive
True
T/F
If skin smears are available and positive, the patient should be classified as multibacillary in the WHO system for leprosy
True
How is leprosy classified for treatment purposes in the NT?
In the Northern Territory leprosy is classified for treatment as either paucibacillary or multibacillary
No laternative Rx regime is used for single lesion paucibacillary type - they are treated the same as paucibacillary (2-5 lesions)
What are the keys teps in clinical examination of a leprosy patient?
history
skin examination inc neurosensory assessment
nerve palpation
eye examination
What is important in the history for leprosy pts?
Possible exposure - leprosy in contacts or time spent in endemic areas presence and duration of lesions nerve pain numbness and tingling weakness skin ulcers and injuries eye pain and worsening vision
T/F
In leprosy sometimes the only lesions are on the buttocks
True
Must examine the entire skin
T/F
Natural sunlight is the best light for detecting subtle skin changes of leprosy
True
T/F
Loss of sensation is a cardinal sign of leprosy
True
Usually accompanied by demonstrable nerve thickening and loss of temperature sensation
demonstration of this sign must be done systematically to accurately determine it’s presence
Other cardinal signs are;
- Hypo-pigmented or reddish localized skin lesions with definite loss of sensation (particularly of touch and temperature); OR
- Skin smear positive for AFB
T/F
M leprae prefers to multiply in vivo at a temperature of 27 – 30 degrees celsius
True
Which nerves are most affected by leprosy?
CRUMPS FTG Common peroneal Radial cutaneous Ulnar Median Posterior tibial Sural Facial and Trigemminal cranial nerves Greater auricular
How are nerves examined in leprosy assessment?
Examine the most commonly affected nerves (CRUMPS FTG)
examine the nerves on both sides together
palpate the nerve at its most superficial point
Use 3 fingers to roll the nerve gently against the bone
may be tender if inflamed
comapring to the contralateral nerve helps to appreciated thickening
T/F
In lepromatous leprosy only skin and nerves show clinical evidence of disease
False
this is true of tuberculoid leprosy
T/F
Tuberculoid leprosy may manifest as skin lesions alone, nerve findings alone or both together
True
T/F
In tuberculid leprosy The typical lesion is a plaque, with raised and clear cut edges sloping towards a flattened and hypopigmented centre
True
It may be erythematous, copper coloured or purple. Dark skins may not show erythema
It may be hypopigmented in dark skin
The surface is dry, hairless and insensitive
Where is the nerve palpated when a tuberculoid leprosy palque is present?
A thickened sensory nerve may be palpated beyond the outer edge of the lesion
T/F
Plaques are typical of lepromatous leprosy
False
lesions may be macules, papules, nodules or infiltration or all four
T/F
skin lesions of lepromatous leprosy are hairless and insensitive
False
this is true of lesions of tuberculoid leprosy
T/F Forehead thickening (cutis gyrata) and madarosis are typical features of lepromatous leprosy
True
T/F
lesions of lepromatous leprosy may be erythematous or hypopigmented and can become diffusely thickened and shiny
True
what are the mucosal complications of lepromatous leprosy?
Infiltration of the mucous membranes of the nose and mouth may produce stuffiness, epistaxis and atrophic rhinitis
The nasal septum can be destroyed
What are the extracutaneous findings in lepromatous leprosy?
Infiltration of the liver, spleen, eyes and testes may occur gynaecomastia
reactive amyloidosis
T/F
nerve involvemnt in tuberculid leprosy is symmetrical
False
symmetrical in lepromatous
associated with assymetrical plaques in tuberculoid
T/F
Reactional states are common in lepromatous leprosy
True
T/F
Borderline leprosy which changes to lepromatous leprosy is called ‘downgrading’
True
and change to tuberculoid is called upgrading
T/F
Borderline leprosy is the most common presentation
True
Skin lesions are intermediate between those of the two polar types
What is Indeterminate leprosy?
Early form manifesting as single or a few skin patches which are small, flat, hypopigmented or coppery with an irregular border
It occurs mainly in children
The majority of cases will heal spontaneously, some will persist in the indeterminate form and some will develop into one of the other forms
Histo shows Scattered nonspecific histiocytic and lymphocytic infiltration with some concentration about skin appendages. Occasionally AFB
T/F
ulcers and erosions or deformities of the extremeties and neuropathic joints occur in leprosy due to nerve involvement
True
T/F
can be easier to identify lack of sweating than lack of sensation in leprosy skin lesions in children
True
as may not be able to cooperate with testing
examine for sweating after running aroud outside
T/F
Light tough is tested by using a peice of rolled up cotton wool
True
can be normal, absent or reduced
if the touch is localised to a site >3cm away from the site of testing there is reduced sensation
How is the supraorbital nerve palpated?
Rub the thumbtips laterally just above the pts eyebrows, a thickened nerve may be felt 1cm from the medial end of the eyebrow
Can palpate preauricular region for branches of the facial nerve
How is the supraorbital nerve palpated?
Turn head to one side and feel along the SCM edge on the other side
How is the ulnar nerve palpated?
flex pts elbow to 90 degrees and feel medial to the point of the elbow
How is the median nerve palpated?
palpate at the distal wrist crease medial to the FCR tendon
How is the radial cutaneous nerve palpated?
lateral cutaneous nerve of the forearm
Roll fingers over the lateral side of the radius near the wrist crease
How is the common peroneal nerve palpated?
have the pt seated
Palpate 2cm distal and 1cm posterior to the head of the fubula
How is the posterior tibial nerve palpated?
Palpate 2cm below and 2cm posterior to the medial malleolus
T/F
In leprosy, Lagophthalmos may occur due to damage of the VIIth nerve
True
T/F
Pts with leprosy may be positive to the quantiferon gold test even though they do not have TB
True
T/F
PPD testing in pts with leprosy can trigger erythema nodosum leprosum
True
T/F
Pts with tuberculoid leprosy are highly infectious
False
probably never infectious
T/F
Leprosy is spread via nasal droplet discharge from lepromatous pts
True
What types of eye involvement may occur in leprosy?
Corneal hypoaesthesia, lagophthalmos, iridocyclitis, scleritis, ectropion, entropion, cataract
What are the features of the diffuse leprosy of Lucio and Latapi?
AKA (pure) diffuse leprosy, pretty leprosy, spotted leprosy of Lucio
diffuse non-nodular lepromatous leprosy
common in Mexico + costa rica
Get;
Diffuse infiltration of all the skin which never transforms into nodules
Complete alopecia of eyebrows and eyelashes and body hair
Anhydrotic and dysesthesic zones of the skin
Lepra reaction named Lucio’s phenomenon or necrotic erythema can occur
How is leprosy diagnosed?
A confirmed case requires definite laboratory criteria and one or more supportive clinical symptoms and signs
T/F Lab positivity for leprosy includes; M leprae on PCR of split skin smear, or; AFB on split skin smear, or; Histopath of skin or nerve confirming leprosy read by a laboratory experienced in leprosy diagnosis
True
But only the positive PCR is diagnostic alone
If other lab tests positive need one or more of the clinical evidence findings to make the diagnosis and call it a confirmed case
What is acceptable clinical evidence for leprosy diagnosis?
At least one of;
- compatible nerve conduction studies
- peripheral nerve enlargement
- loss of neurological function not attributable to trauma or other disease process
- hypopigmentated or reddish skin lesions with definite loss of sensation
From where may leprosy skin smears be taken?
both ear lobes, suspicious skin patches, thickened skin on the forehead above the medial eyebrows, knees or elbows and previous positive sites
T/F
AFB are often seen on histo of skin lesions in tuberculoid leprosy
False
usually not seen
How is the lab criteria for diagnosis met in pure neural leprosy?
nerve biopsy
What are the histo findings of tuberculoid and lepromatous leprosy?
In tuberculoid leprosy the tuberculoid granulomas collect into surrounding neurovascular elements. AFB are not seen
In lepromatous leprosy the typical diffuse leproma consists of foamy macrophages with a few lymphocytes and plasma cells and enormous numbers of AFB singly or in clumps.
What are the pre-treatment investigations in leprosy?
FBC, ELFT's, HIV antibodies glucose 6 phosphate dehydrogenase levels (dapsone) CXR Mantoux (PPD) or quantiferon gold
T/F regarding leprosy;
If a patient has a positive skin smear, regardless of clinical classification, or if the classification is in doubt, treatment should be MDT for multibacillary disease
True
How is paucibacillary leprosy treated?
Dapsone 100mg daily (self treated) +
Rifampicin 600mg monthly (DOT)
for 6 months
How is multibacillary leprosy treated?
Dapsone 100mg daily (self treated) +
Rifampicin 600mg monthly (DOT) +
Clofazimine either 50mg/day(self) or 300mg/month (DOT)
for 24 months
Can treat for 12 months only if pt has low bacterial index
T/F
Patients diagnosed with both leprosy and TB require full treatment for both diseases
True
T/F
In leprosy treatment Minocycline and ofloxacin may be necessary if there are severe side-effects caused by a drug in the first line regimens
True
T/F
Pts being treated for leprosy are typically seen every 4 weeks for DOT and clinical review
True
weekly initially then q4w
T/F
Immunological reactions in leprosy only occur after initiation of treatment
False
can be before, during or after Rx
treatment initiation is most common trigger
other infections or pregnancy can also trigger reactions
T/F
Type 1 lepra reaction is also called reversal
True
T/F
Type 2 lepra reaction is also called upgrading
False
Type 1 is called upgrading or reversal
T/F
HIV increases risk of leprosy
False
HIV does not increase risk or host response to leprosy
T/F
Type 1 reactions can occur in any type of leprosy
False
Most commonly borderline types (BB, BL, BT) but can be in tuberculoid or lepromatous. Not in indeterminate type
What are the features of Type 1 (reversal) reactions?
Inflammation of established lesions - Erythema, oedema or ulceration
Appearance of new (previosuly subclinical) lesions
Oedema of hands and feet
If severe can be Fever, malaise, peripheral oedema and symptomatic neuritis
Acute nerve damage – pain, tenderness (=neuritis) and loss of function (sens/motor)
Histo – tuberculoid granulomas, fibrinoid necrosis, oedema, granulomatous nerve destruction
What is the aetiology of Type 1 (reversal) reactions?
Is a Delayed-type hypersensitivity reaction
Enhancement of cell-mediated immunity with a Th1 cytokine pattern
T/F
Type 1 leprae reactions are terated with prednisolone?
True
1mg/kg
taper over 12 months but may need to continue for years
+/- NSAIDS, physio
Reports of steroid sparing w/ AZA, CsA, MTX
T/F
Erythema nodosum leprosum is the most common type of type 2 lepra reaction
True
What is the aetiology of Type 2 lepra reactions?
Excessive humoral immunity with a Th 2 cytokine pattern
formation of immune complexes
may be accompanied by increased cell-mediated immunity
Results in cutaneous and systemic small vessel vasculitis
T/F
Type 2 reactions mainly occur in lepromatous and BL cases of leprosy
True
T/F
Type 2 reactions mainly present shortly after initiation of treatment
False
mainly in second year on treatment
What are the features of type 2 rcn (erythema nodosum leprosum)?
Cropes of tender red nodules on legs (ENL) also arms, trunk and face
Systemic symptoms such as fever, myalgia, iridocyclitis, arthritis, neuritis, glomerulonephritis and orchitis may occur
Can be lymphadenopathy or hepatosplenomegally
Histo - Lobular panniculitis, oedema of dermis and subcutis, foamy macrophages containing many AFB (Virchow cells)
How is type 2 rcn (erythema nodosum leprosum) treated?
If mild and no neuritis - bed rest and aspirin
High dose oral pred often used initially if mod-severe cases
For severe cases;
Thalidomide 100-200mg/day + pred if neuritis
Clofazamine 300mg daily + pred if thalidomide contraindicated or ENL recurrent
What is Lucio phenomenon?
Type of lepra rcn occuring only in pts with Lucio type leprosy (diffuse non-nodular lepromatous leprosy)
Triggered by pregnancy, stress or infection
Necrotizing vasculitis of medium and small vessels of skin
Sudden appearance of painful blue/violaceous macules/plaques w/ surrounding erythema
Can progress to haemorrhagic infarcts or bullae which ulcerate and necrose esp lower legs, also forearms, buttocks. Painful but not tender. Also get subcutaneous nodules
Can progress to secondary infection and fatal sepsis
Hepatosplenomegally, lymphadenopathy, epistaxis, nasal septal perforation
Anaemia, neutrophilia and raised WCC & ESR
Histo shows abundant aggregates of AFBs in endothelial cells, thrombosis, fibrinoid necrosis of vessels and epidermal necrosis/ulceration, many macrophages
Treat with high dose pred, anti leprosy drugs (MDT regime), supportive care. Consider plasmapheresis
T/F in leprosy;
Nerve damage is more severe in tuberculoid form
True
T/F
In tuberculoid leprosy, bacillary multiplication is restricted to a few sites and bacilli are not readily found
True
How is a slit skin smear performed in leprosy?
Do on; - ear lobes/ forehead/ chin - suspicious skin patches - thickened skin grasp fold of skin between fingers and make longitudinal cut with 15 blade. Then turn the blade at 90 and scrape dermis. Then smear on slide, heat fix and stain. Note...any blood renders it useless so grip firmly
T/F
Melioidosis is infection with Burkholderia pseudomallei
True
AKA pseudo-glanders, Stratton’s disease, Whitmore’s disease
Burkholderia mallei causes glanders
T/F
Burkholderia pseudomallei is an environmental saprophyte found in soil and surface water in tropical regions
True
How is Burkholderia pseudomallei infection contracted
Inhalation or by skin/mucosal exposure when there is a portal of entry
T/F In melioidosis;
incubation time from exposure to clinical signs may range from a few days to over 20 years
True
T/F
Melioidosis can present as an acute, sub-acute or chronic form of disease
True
T/F
acute melioidosis is a life-threatening disease
True
acute septicaemic form causes death if untreated
survival is 50-80% if treated
T/F
Melioidosis can affect any organ system of the body
True
esp skin, joints, GU tract, lungs and brain stem
T/F
Burkholderia pseudomallei is facultative intracellular Gram positive motile bacillus
False
gram negative
T/F
Burkholderia pseudomallei grows in blood culture bottles and on standard lab media such as MacConkey, Chocolate or 5% sheep bloodagar
True
Ashdown’s media should be used for sub-culture when melioidosis is suspected
specific selective media developed in N QLD
contains gentamicin which inhibits most other Gram negative organisms
The colonies appear violet colour
T/F
Burkholderia pseudomallei takes weeks to grow in the lab
False
usually can be cultured within 48 hrs and defienitely identified within 72 hrs
If tissue is submitted with very low numbers of organisms or the patient was already been given antibiotics before microbiological sampling a “late” culture result will be positive
Cultures are often positive from skin, blood, soft tissue abscess aspiration, urine and sputum
Whic antibiotics is Burkholderia pseudomallei typically sensitive to?
Ceftazidime, Piptaz Ticarcillin/Clavulanate, Co-amoxiclav Meropenem Bactrim Doxycycline Chloramphenicol
T/F
On staining Burkholderia pseudomallei typically shows a bipolar “safety pin” appearance
True
not diagnostic but highly suggestive of the diagnosis in the correct clinical settling
Where is melioidosis seen in Australia?
North of Rockhampton
esp Townsville, Cairns and Darwin and surrounding rural areas inc Torres Strait, Cape York Peninsula
Endemic areas are usually between latitudes 20 degrees north and 20 degrees south
T/F
melioidosis occurs mainly in dry inland areas
False
mostly in coastal areas which are affected by the wet season
Esp during the wet season (Nov-March)/heavy rains when the organisms rise up from the soil/clay interface below the soil
T/F about 45-50 cases of melioidosis are diagnosed each year in Aus
True
slightly more in NT than FNQ
T/F
About 50% of Aus cases of melioidosis occur in indegenous pts
True
T/F
melioidosis is more likely to be caught from running than still water
False
still water more likely
rice paddies are a common source in South East Asia - Thailand has the most cases worldwide
T/F
In Northern Australia 10% of Aboriginals are sero-positive for past exposure to B pseudomallei
True
due to prior subclinical infection - common
the infection is completely cleared but they remain sero-positive
T/F
B pseudomallei is an intracellular pathogen and is therefore protected to a degree from the host immune system
True
T/F
Pts exposed to B pseudomallei can get sub-clinical infection that sequestrates in the body and may remain dormant or reactivate years after exposure in much the same way that tuberculosis can
True
often organisms are in the lungs or bowel
T/F
melioidosis cannot be transmitted person-person
False
rare reports of B pseudomallei transmission in this way
What are risk factors for development of clinical disease or more severe clinical disease following exposure to Burkholderia pseudomallei?
Immunosuppression, including neutrophil dysfunction
Cancer – haematologic and solid organ malignancy
Major Organ dysfunction (such as renal, hepatic or cardiac)
Renal stones
Splenectomy
Alcoholism
Diabetes
Cystic fibrosis and other chronic lung disease
Thalassemia
Kava consumption
Corticosteroid use
Chronic granulomatous disease
Poor nutrition
Males (perhaps due to more outdoor exposure)
Pregnancy
HIV
T/F
being aboriginal is an independent risk factor for severe melioidosis
False
no evidence for this
T/F
In Northern Australia approximately 75% of melioidosis cases are associated with diabetes
False
50%
T/F
In Northern Australia approximately 20-40% of melioidosis cases are associated with alcoholism
True
T/F
Melioidosis affects the skin in 60% of cases in Australia
False
9-28%
T/F
clinically cutaneous melioidosis can be categorized as primary or secondary, acute or chronic, localized or generalized
True
T/F
primary cutaneous melioidosis presenting as a single lesion is the most common presentation of cutaneous melioidosis
True The lesion can be; pustule, exudative purulent ulcer furuncle skin abscess +/- overlying skin fistula crusted erythematous plaque asymptomatic flat erythematous patch cellulitis
T/F
seropositivty for B pseudomallei always indicates latent disease
False
will be seropositive if had disease and cleared either spontaneously or with treatment or if have latent disease
T/F
Primary cutaneous melioidosis is unlikely to progress to severe systemic disease and death
True
but is possible
T/F
secondary cutaneous meioidosis is when skin lesions have occured after haematogenous spread
True
often in acute septicaemic form
What are the features of secondary cutaneous meioidosis?
commonest eruption is a generalized pustular eruption
Cellulitis, lymphadenitis, lymphangitis, necrotizing fasciitis, multiple ecthyma lesions and superficial skin abscesses may also occur
Papular eruptions similar to erythema multiforme can occur
sometimes there is primary and secondary skin disease together
Can culture Burkholderia pseudomallei from skin lesions or swabs of pus/exudate
What are the lesions of subacute and chronic cutaneous meioidosis?
Chronic/Subacute - subcutaneous draining abscesses are the hallmark of the disease, can be skin ulcers, fistulae
What are the features of acute systemic melioidosis?
Brain stem – cranial nerve defects, encephalomyelitis, cerebellar tract signs
Skeletal – septic arthritis, osteomyelitis
Genitourinary – kidney and collecting system, prostate
Pulmonary – upper lobe consolidation, cavitating and nodular lesions, pleural effusion, mediastinal lymphadenopathy
Other Organ Abscesses – parotid, liver, spleen, muscle, kidney, adrenal
T/F
Chronic systemic melioidosis often causes osteomyelitis or chronic septic arthritis
True
T/F
If Burkholderia pseudomallei is isolated from a “well” patient it should always be treated
True
T/F
In order to make the diagnosis of melioidosis cultures from every possible lesion/site are essential
True
swabs or ulcers, psutules etc, aspirates of deep abscesses, skin for histo and culture, blood culutres, urine and sputum cultures etc
T/F
Blood cultures should also be taken in a patient presenting with skin signs of melioidosis even if they appear “well”
True
T/F
Skin histo from pts with melioidosis may show different features in acute vs chronic disease
True
Acute shows necrotizing inflammation dominated by neutrophils but usually with macrophages and lymphocytes too. Bacilli are either absent or few in number but skin tissue culture is usually positive if the patient is antibiotic naïve
chronic lesions have loose granulomatous inflammation with giant cells and macrophages which contain globi (tangled clumps of bacilli).
T/F
Serological assessment of a patient for past exposure to melioidosis is helpful in the acute situation
False
no help
What methods are used for Serological assessment of a patient for past exposure to melioidosis?
ELISA Indirect haemagglutination (IHA)
T/F
Melioidosis hs a 10% relapse rate
True
T/F
B pseudomallei is usually resistant to macorlide, quinolones and aminoglycosides
True
What are the antibiotics of choice in melioidosis?
usually one of; Imipinem, meropenem ceftazidime Piptaz alone or in combination with bactrim for up to 4 wks depending on severity of disease for oral therpay for 2-4 months after acute Rx use; doxy or augmentin or bactrim
Outline the steps in clinical assessment of a suspected cellulitis
Assess vital signs and level of consciousness - resucitate if necessary
Systemic exam;
• pulse,
• temperature,
• respiratory rate,
• blood pressure.
• Carefully examine respiratory, abdominal, cranial nerves and musculoskeletal system
Rectal exam if GU or GI symptoms
Examine lymph nodes
Skin exam;
assess degree of pain on movement,
any evidence of anaesthesia,
assess reduced or absent pulses,
check capillary return in the nail folds,
assess for regional lymphadenopathy,
look for soft tissue abscess,
check for crepitation,
look for a portal of entry for infection at the site noted by the patient but also in between the toes and the soles of the feet.
Note the extent of the cellulitis and the degree of blistering
look at the rest of the skin for further clues.
T/F
Asymptomatic carriage of B pseudomallei can be ignored
False
T/F, Regarding Primary Cutaneous Melioidosis;
Multiple melioidosis risk factors are usually present
False
but should always check in history
T/F, Regarding Primary Cutaneous Melioidosis;
Multiple skin lesions are usually present
False
usually single lesion in primary disease
T/F, Regarding Primary Cutaneous Melioidosis;
Usually progresses to fulminant disease
False
T/F, Regarding Primary Cutaneous Melioidosis;
Usually responds to appropriate antibiotics
True
T/F, Regarding Primary Cutaneous Melioidosis;
Is endemic Australia wide
False
T/F
smoking is a risk factor for melioidosis
False
What is the Splendore Hoeppli phenomenon?
Formation of a sheath of deeply eosinophilic material around micro-organisms, usually fungal, bacterial or around parasites
Usually has a stellate or radiating appearance
Whic organismscan cause Splendore Hoeppli phenomenon?
Typical of zygomycosis caused by Basidiobolus ranarum also caused by; Fungi; zygomycosis - includes; mucormycoses and entomophthoromycoses sporotrichosis pityrosporum folliculitis candidiasis aspergillosis blastomycosis Bacteria; actinomycosis nocardiasis Parasites; schistomsomiasis
What are the DDs for chronic painless swollen limb?
filariasis, fungal and nocardial mycetoma, other subcutaneous mycoses, complicated dermatophyte infection, soft-tissue sarcoma, chronic lymphoedema, bacterial cellulitis, early subcutaneous (angioinvasive) mucormycosis (zygomycosis)
T/F
Most zygomycetes are sensitive to cycloheximide (actidione) and this agent should not be used in culture media
True
Zygomycetes are slow growing organisms and show white to grey or brownish, downy colonies with many radial folds
False
rapid growing
Which organisms cause chromoblastomycosis?
Phialophora verrucosa Fonsecaea pedrosoi F. compacta Cladophialophora carrionii Found in wood and soil
Which organisms cause phaeohyphomycosis?
Cladosporium Exophilia Wangiella Bipolaris Exserohilim Curvularia
Which organisms cause Mycotic mycetoma?
Pseudallescheria Madurella Acremonium Exophiala saprophytes in soil and on plants. It is common among agricultural workers
Which organisms cause subcutaneous zygomycosis, entomophthoromycosis type (Entomophthorales)?
Basidiobolus sp (esp B. ranarum) Conidiobolus sp (esp C. coronatus) V rare in Aus
Which organisms (genus) cause subcutaneous zygomycosis, mucormycosis type (Mucorales)?
Rhizopus Mucor Rhizomucor Absidia (myocladus) Saksenaea Cunninghamella Apophysomyces Cokeromyces Mortierella
What are zygomycoses?
subcutaneous mycosis caused by primitive, fast growing, terrestrial, largely saprophytic fungi with a cosmopolitan distribution
2 orders (genera);
Entomophthorales (the entomophthoromycoses)
Mucorales (the mucormycoses)
T/F
Mucorales type zygomycoses are angioinvasive causing embolization and subsequent necrosis of surrounding tissue
True
cause subcutaneous or systemic disease
typically involves the rhino-facial-cranial area, lungs, gastrointestinal tract, skin, or less commonly other organ systems
Have become more common in in patients undergoing treatment for haematological malignancy or stem cell transplantation
T/F
Entomophthorales type zygomycosis cause severe destructive disease
False
chronic, slowly progressive subcutaneous mycosis
Zygomycosis caused by B. ranarum are generally restricted to the subcutaneous tissue of the limbs, chest, back or buttocks. It presents as a massive, firm, indurated, painless swellings fixed to the skin. It is freely movable over the underlying muscle
T/F
Zygomycosis caused by Conidiobolus sp. is restricted to the nasal submucosa and characterised by polyps or palpable subcutaneous masses
True
What are the DDs for an aqcuired saddle nose/destructive nasal disease
Endemic/venereal syphilis esp congenital Leprosy Rhinoscleroma Mucocutaneous leishmoniasis (Tapir nose) Paracoccidiodomycosis Tuberculosis Glanders Zygomycosis due to Mucorales species (mucormycoses) Other infection e.g. pseudamonas Wegner’s granulomatosis Relapsing polychondritis NK/T-cell lymphoma, nasal type cocaine use
What is the treatment of Mucorales type zygomycoses?
1st line;
Liposomal amphotericin-B at 5 mg/kg/day
increased to 15mg/kg/day for severe and/or refractory disease
Posaconazole is an attractive alternative for patients who cannot tolerate or do not respond to amphotericin B products
What is the treatment of Entomophthorales type zygomycosis?
may eventually heal without treatment
Potassium iodide has been successfully tried in a few cases
amphotericin B, cotrimoxazole, fluclonazole
Itraconazole + terbinafine has been used successfully
Where does sporothrix schenkii grow?
North, South and Central America, Egypt, Japan, Australia and Africa
Fungus grows on in decaying vegetable material (timber in mines)
It may also occur in workers using straw as packing material, forestry workers, florists and gardeners
T/F
Basidiobolus ranarum occurs saprophytically in decaying vegetable material and soil and can be found in the dung of kangaroos and wallabies
True
Also in reptile dung
It has also been found in compost heaps, soil collected from a stream bed and its adjacent bank and from forests
What is Dermatosis papulosa nigra?
Small dark brown-black firm papules up to 5mm diameter Esp on face around eyes Scattered, not grouped or linear Asymptomatic Histo similar to seb k with horn cysts No risk of malignancy Can shave off
What is Chewing tobacco mucositis?
Due to contact with quid of sucked/chewed tobacco with oral mucosa
Oval 2-3cm asymmetrical lesion on buccal or labial mucosa with warty surface which may be pale, red or pigmented
DDs – LP, DLE, leukoplakia
T/F
More females than males use chewing tobacco in NT
True
What is Focal epithelial hyperplasia?
Benign oral papules, 2-8mm diameter
Single or multiple, painless, slightly pale
Often on inside of cheeks or lips, can be on tongue or gums
Larger lesions have a granular surface with red dots
Affects about 5% of aborigines esp younger age groups – children to 20s
May be due to HPV +/- genetic predisposition
Histo – para, acanthosis, dyskeratosis, vacuols in prickle cell layer, many mitoses, focal cellular necrosis with loosely textured fibrous tissue in core of the polyp
No significance, no treatment required
What is Residual ochre?
Leftover body paint made from natural ochres (clay + iron oxides)
Can resemble tinea capitis when on scalp
No significance
What are the major DDs for madarosis in aboriginals?
Genetic Trauma – rubbing, picking, burns Hypothyroidism Lepromatous leprosy Secondary syphylis
Wat causes Lateral malleolar bursitis in aboriginals?
Due to prolonged pressure from sitting cross-legged
M>F
Exclude neuropathic ulcers e.g. diabetes, leprosy and infections
What are sorry cuts?
Self inflicted wounds made at time of death or burial of close relative or friend
Men slash outer arms or thigh with a knife
Women use stone or wooden club to pound the skull
Also ‘Nice marks’ – cigarette burns on backs of hands and forearms made by adolescent girls in central Aus
Burning branch ritual – some aborigines have ceremonial ritual of touching the back of the shoulders with a burning branch
What are bush feet?
Reactive thickening of cornified layer on feet due to barefoot walking in bush
Looks like dried mud but doesn’t wash off
What is Kava dermopathy?
AKA crocodile skin Generalised white scale Starts on head, face and neck and extends over whole body to feet Develop thick keratotic plaques Aetiology unclear Resolves when kava drinking stops
