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Aboriginal & Refugees Dan > ABTSI + Leprosy Dan > Flashcards

ABTSI + Leprosy Dan Flashcards

1
Q

T/F

More Aboriginal and Torres Strait Islander people live in urban areas than remote communities

A

True

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2
Q

T/F

some people find use of the word ‘indigenous’ offensive

A

True

it is vital that you confirm what is the locally-preferred term with the people you work with and use it

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3
Q

What is an aborigine?

A

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

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4
Q

What is a Torres Strait Islander?

A

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

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5
Q

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

A

True

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6
Q

T/F

The prevalence of systemic lupus erythematosus is the same in Aboriginal Australians and in European Australians.

A

False
2-3x (2-3.8 in latest AJD paper) more in aborigines and also more severe
affects 1:1000 – 1:1900 Aborigines

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7
Q

T/F

Lupus erythematosus affects females more than males

A

True
DLE 5x more common in females regrdless of race
other LE also more common in females

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8
Q

T/F

It is unknown if the prevalence of LE in aborigines is genetically or environmentally determined

A

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.

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9
Q

T/F

Lupus erythematosus in aborigines has a high morbidity and mortality and high frequency of renal disease

A

True

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10
Q

T/F

Autoantibodies to the Sm antigen are uncommon in Lupus erythematosus in aborigines

A

False

common

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11
Q

T/F

The majority of deaths in aboriginal patients with SLE are due to renal failure

A

False
The majority of deaths in aboriginal patients with SLE are due to infection - associatd with active disease and with steroids

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12
Q

Which sites are most affected by cutaneous lupus?

A

nose, cheeks and forehead

but the lips, scalp and trunk may be involved

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13
Q

T/F

cutaneous lupus lesions are darker in darker skin

A

True

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14
Q

What is the carpet tack sign in cutaneous LE?

A

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

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15
Q

T/F

Erythema at the edge of the hyperpigmented lesions is characteristic of cutaneous lupus

A

True

hypopigmentation and scarring come later - often permanent

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16
Q

What are the acute, subacute and chronic stages of lower lip lupus?

A

acute - the lip is red, friable and bleeds easily
chronic - hypopigmentation and scarring
subacute stage is transition between these two

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17
Q

T/F
It is difficult for the clinician and histopathologist to distinguish verrucous lupus from Squamous cell carcinoma on the lip

A

True

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18
Q

T/F

The main differential diagnosis of LE in aborgines is tinea faciei

A

True

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19
Q

What are the common and rare organism causes of sepsis in aboriginal SLE pts?

A

gram negative and staphylococci - same as other pts

But also risk of rare pathogens eg. CNS cryptococcocis and disseminated strongyloidiasis

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20
Q

T/F

In mothers of infants with neonatal lupus almost all sera contain IgG antibodies to the SSA(Ro), 60KDa protein

A

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

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21
Q

T/F

skin biopsy is always necessary in an infant with a rash and features suspicious for neonatal LE

A

False
Take blood for serology and investigate mother
Only biopsy if diagnosis in doubt after other investigations

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22
Q

T/F

>90% of infants with NLE develop skin lesions

A

False

approx 50%

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23
Q

T/F
Rash of NLE usually resolves in 1st year without scarring but can cause residual hypopigmentation, epidermal atrophy or telangiectasia

A

True

atrophy is rare

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24
Q

T/F

Rash of NLE is photosensitive

A

True

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25
Q

T/F

NLE is the most common cause of Congenital Heart Block (CHB) where the structure of the heart is normal

A

True

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26
Q

T/F

20% of neonates born to mothers with anti-SSA antibodies will develop NLE

A

False
2%
2% also quoted as risk of having a baby with CHB

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27
Q

T/F

congenital heart block usually presents in utero commonly at 18 – 24 weeks of gestation

A

True

Incomplete heart blocks can progress after birth and once complete heart block is present it is irreversible

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28
Q

What are the other cardiac manifestation sof NLE other than heart block?

A

cardiac malformations
cardiomyopathy
prolonged QT interval
sinus bradycardia

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29
Q

T/F

thrombocytopenia in NLE usually doesnt cause clinical problems

A

True
can also get
Anaemia, neutropaenia and recurrent pancytopaenia

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30
Q

T/F

1 third of pts with CHB require PPM

A

False

2 thirds

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31
Q

What are the 3 presenations of liver disease in NLE?

A

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

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32
Q

T/F

maternal breastfeeding is fine in cases of NLE

A

disocouraged as may transfer more lupus antibodies

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33
Q

T/F

Topical steroids do not reduce the frequency of hypopigmentation, telangiectasia and atrophy.

A

True
sun avoidance and sunscreen are mainstay
TCS usually not needed but can use HCT

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34
Q

What is risk to mother of having a second baby with NLE?

A

25% of recurrence in later pregnancy

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35
Q

T/F

Disseminated strongyloidiasis should be considered in ill immunosupressed patients in the Northern Territory

A

True

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36
Q

T/F

Squamous cell carcinoma of the lower lip is a complication of cutaneous lupus in Aboriginals

A

True

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37
Q

T/F

Sepsis as a cause of death is associated with oral corticosteroid use

A

True

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38
Q

T/F

The reason for the increased prevalence of lupus in Aboriginals is unknown

A

True

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39
Q 
T/F
In indigenous Australians there are high prevalences of metabolic syndrome components: 
•	glucose intolerance
•	dyslipidaemia
•	hypertension
•	insulin resistance
A

True

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40
Q

The important factors leading to metabolic syndrome components are:
• social disadvantage
• limited economic opportunity
• adoption of diets of poor nutritional qualit
• rapid weight gain

A

True

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41
Q

T/F

Blindness is the most frequent complication of T2 diabetes in aboriginals

A

False

nephropathy

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42
Q

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

A

True

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43
Q

T/F

Aboriginal patients with diabetes die at a significantly younger age than their Anglo-Celt counterparts

A

True

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44
Q 
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
A

True

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45
Q

T/F

Indigienous women ahve a prevalence of PCOS of >25%

A

False

>15%

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46
Q

T/F

Acanthosis nigricans is common in overweight Aboriginal people

A

True

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47
Q

T/F

Acanthosis nigricans is most easily appreciated at the posterior neck in Aboriginal people

A

True

May also present in the axillae, inguinal area, abdominal fat folds and sometimes the flexures of the limbs

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48
Q

T/F

painful leg ulceration in a 45 year old Aboriginal is more likely to be vascular in origin than pyoderma gangrenosum

A

True

Always think of the complications of diabetes, renal disease and vascular disease

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49
Q

T/F

Before European colonisation of Australia, obesity was rare in Aboriginals

A

True

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50
Q

T/F

Indigenous Australians have a high prevalence of metabolic syndrome components

A

True

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51
Q

T/F

Vascular disease is rare in Aboriginal Australians

A

False

prevalence ranges from 10% – 70%

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52
Q

T/F
Group A streptococcus is a comon cause of skin sores (pyoderma) in Aboriginal children in Australia’s northern tropical regions

A

True

but often staph also present

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53
Q

What are the complications of Group A streptococcus pyoderma?

A

acute rheumatic fever
rheumatic heart disease
Post strep glomerulomephritis

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54
Q

T/F

Pyoderma and poor outocmes are more common in household overcrowding

A

True

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55
Q

T/F

The prevalence of pyoderma in children is higher during the wet season

A

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

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56
Q

T/F

scabies predisposes to pyoderma

A

True

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57
Q

T/F
There is no link link between skin infections in childhood and the extreme rates of end-stage renal failure in Aboriginal adults

A

False
strong link
Acquiring APSGN in childhood increases the risk of adult renal disease by six times

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58
Q

T/F

Episodes of acute post streptococcal glomerulonephritis (APSGN) are five times higher for children with skin sores

A

True

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59
Q

T/F

Episodes of acute post streptococcal glomerulonephritis (APSGN) are five times higher for children with scabies

A

False
twice as common with scabies
5x with skin sores

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60
Q

T/F

Acquiring APSGN in childhood increases the risk of adult renal disease by 10 times

A

False

6x increase risk of adult disease after childhood APSGN

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61
Q

T/F

Indigenous Australians to die from kidney failure with a frequency 5x higher than non-Indigenous Australians

A

True

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62
Q

T/F
Indigenous Australians have end-stage renal disease 21x more than non-Aboriginal Australians and doubling every four years

A

True

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63
Q

T/F

Acute rheumatic fever is 60x more common amongst aboriginal children than non-aboriginal children

A

True

300 per 100,000 Vs 5 per 100,0000

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64
Q

T/F

pharyngeal carriage rates of group A β-haemolytic streptococci are high amongst aboriginal children

A

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

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65
Q

T/F

ARhF and RhHD are classic diseases of social injustice

A

True

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66
Q

T/F

Rates of ARhF and RhHD in aboriginals in the NT are declining

A

False

little or no evidence of improvement over at least the past three decades.

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67
Q

T/F

skin sores are more common on the trunk

A

False

usually the result of trauma and are more common on the limbs

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68
Q

T/F

Pus is unusual in skin sores

A

False

may look dry but pus under scabs

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69
Q

What triggers skin sores?

A

Trauma

insect bites and scabies

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70
Q

T/F

skin sores are transient and heal without scars

A

False
not always
can be chronic and leave scars

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71
Q

T/F

community acquired MRSA is common in some aboriginal communities

A

True

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72
Q

T/F

The use of ASOT and anti-DNA’ase B serology is not recommended for the diagnosis of impetigo

A

True

a high background and persisting levels of antibody in Aboriginal populations

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73
Q

T/F
The use of ASOT and anti-DNA’ase B serology is not recommended for the diagnosis of acute post streptococcal glomerulonephritis

A

False

should check in cases of gn as if high supports the diagnosis

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74
Q

T/F

topical antibiotics are first line for skin sores

A

False
topical antiseptic + oral treatment or IM benzathine penicillin 1st line
bactroban TDS for 7 days good choice if above cannot be used

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75
Q

Which oral antibiotics are used for skin sores?

what doses?

A

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

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76
Q

T/F

avergae monthly prevalence of pyoderma in East Arnhem is 35%

A

True

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77
Q

T/F

Skin sores are usually purely steptococcal

A

False

ofetn staph also

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78
Q

T/F

antibiotics must be given for 10 days for cases of beta haemolytic strep infection

A

True

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79
Q

T/F

Multiple skin sores are treated with benzathine penicillin

A

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

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80
Q

T/F

In remote indigenous communities scabies is endemic and prevalence rates are up to 50% in children and 75% in adults

A

False

50% in children and 25% in adults

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81
Q

T/F

Scabies is responsible for a significant percentage of streptococcal pyoderma in Northern Tropical Australia

A

True

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82
Q

What is a core infector of scabies?

A

Individuals in the comunity with individuals with hyperinfestation (crusted or Norwegian scabies) who infect other community members

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83
Q

T/F

Canine and human scabies mites are morphologically indistinguishable and dog mites can produce itch on human skin

A

True

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84
Q

T/F

Dog scabies can cause mange

A

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

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85
Q

T/F

cycles of scabies transmission in dogs and humans appear to significantly overlap in Aboriginal communities

A

False

dont significantly overlap

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86
Q 
T/F
Scabies transmission (photo of eggs) usually occurs through direct skin contact with infected persons
A

True

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87
Q

T/F

Dog scabies cause itch in humans but not established infection

A

True

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88
Q

T/F

Scabies mites may survive for 56 hours off the human host

A

True

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89
Q

T/F

scabies live longer off the host in dry environment

A

False

survival enhanced by humidity

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90
Q

T/F
Inadequate “health hardware” (washing machines, toilets, taps, showers) and chronic overcrowding contribute significantly to scabies transmission in Aboriginal communities

A

True

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91
Q

T/F

truncal eczematous eruption is typical of scabies

A

True

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92
Q

T/F

scabies affects the genotals in men and the nipples in women

A

True

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93
Q

T/F

Scabies in babies tends to produce a papular vesicular eruption on the palms and soles

A

True

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94
Q

T/F

Secondary infection with streptococcus pyogenes and/or staphylococcus aureus makes scabies lesions easier to identify

A

False

obscures lesions and produces deeper ulceration

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95
Q

T/F
With age and multiple chronic infestations, the individual may develop tolerance to the scabies mite with few signs or symptoms

A

True

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96
Q

T/F

In elderly or with HTLV-1 or HIV there can be crusted scabies with no itch

A

True

should check for HTLV-1 or HIV in cases of crusted scabies

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97
Q

T/F

Usually there is a single strain of scabies in a community

A

False

multiple overlapping epidemic cycles indicating a wide circulation of diverse strains of sarcoptes scabiei

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98
Q

What is the India Ink Test for scabies?

A

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

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99
Q

T/F

Topical 5% permethrin cream is the treatment of choice for scabies

A

True

2 treatments 7-14 days apart

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100
Q

T/F
In tropical regions, especially for children, the neck, head and scalp should also be treated with permethrin for scabies

A

True

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101
Q

T/F

Permethrin can be used by women in the early stages of pregnancy and children from 2 months of age and probably younger

A

True
ACD module
Permethrin is B3

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102
Q

T/F

Benzyl benzoate can be used for scabies although irritation often leads to non-compliance

A

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

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103
Q

T/F

Infantile acropustulosis may be a persistant post-scabetic reaction

A

True

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104
Q

T/F

Preciptated sulphur can be used for scabies

A

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

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105
Q

T/F

Household conatcts who are not clinically infecetd should be reated with permethrin

A

False
not necessary unless share a bed
Household contacts should be treated with cleaning of clothing, bedding and simple cleaning of the house

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106
Q

T/F

Ivermectin is metabolized by the liver and excreted in the faeces over an estimated 12 days

A

True

so nursing mother should not breast feed for 2 weeks after last dose

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107
Q

T/F

10% of ivermectin is excreted in urine

A

False

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108
Q

What is the dose of ivermectin?

A

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

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109
Q

T/F

Hepatic transaminases may become elevated during ivermectin therapy

A

True

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110
Q

T/F

ivermectin is excreted in the breast milk

A

True

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111
Q

T/F

Ivermectin should not be used in children under 25kg

A

False

not if under 5 years old or under 15kg

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112
Q

T/F

Septicaemia is a common complication of crusted scabies and is frequently polymicrobial

A

True

Rx aggressively treated with broad spectrum antibiotics

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113
Q

How should crusted scabies be managed?

A

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

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114
Q

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

A

True

Regular follow-up is required for a sustained reduction

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115
Q

T/F
Community initiated clean-up days play an integral part in promoting personal and household hygiene in scabies-affected communities

A

True

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116
Q

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

A

True

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117
Q

T/F

crusted scabies is very common in south australian aboriginal comunities

A

False
rare in south although scabies is common
crusted scabies most comon in central and north australia

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118
Q

What are risk factors for crusted scabies?

what additional risk factors are found in aboriginals?

A 
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

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119
Q

T/F

IgE and eosinophil count are often raised in crusted scabies

A

True

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120
Q

T/F

ANA often positive in crusted scabies pts

A

True

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121
Q

T/F

C3 and C4 are often high in crusted scabies pts

A

False

low

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122
Q

What is mode of action of Ivermectin?

A 
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
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123
Q

T/F
It is thought that in vertebrates P-glycoprotein drug pumps exclude ivermectin from its potential site of action resulting in no effect

A

True

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124
Q

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

A

True

But this has not been seen in studies or clinical practice

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125
Q

What is the most likely reason for scabies recurrence after treatment?

A

The most likely reason for recurrence is reinfestation

resistance to Ivermectin in scabies mites is another possibility

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126
Q

T/F

Ivermectin is neurotoxic in collies

A

True

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127
Q

T/F

Scabies in babies involves the head and neck in tropical areas

A

True

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128
Q

T/F

Canine scabies produces significant infestation in Aboriginal communities

A

False

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129
Q

T/F

Resistance to ivermectin is developing in scabies

A

False

still extremely rare

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130
Q

T/F

Staphylococcus aureus is the most common bacteria in infected scabies in Aboriginals

A

False

strep

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131
Q

T/F

Patients with crusted scabies should be tested for HTLV-1

A

True

and HIV

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132
Q

Which populations are at risk of community associated MRSA (CA-MRSA)?

A 
sporting teams
incarcerated persons
the military
children in day care facilities
men who have sex with men
indigenous communities across the world
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133
Q

T/F

Crowded living conditions, poor hygiene and poor access to medical care are risk factors for CA-MRSA

A

True

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134
Q

T/F

CA-MRSA is largely from a single strain in Australia

A

False
diverse strains in different parts of the country which have almost certainly arisen from the local indigenous population

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135
Q

T/F

Aboriginal populations have higher incience of both MSSA and MRSA infections

A

True

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136
Q

T/F

Staph infection incidence rates strongly correlate with measures of remoteness and socio-economic disadvantage

A

True

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137
Q

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

A

True

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138
Q

T/F

CA-MRSA is a “feral descendent” of health care associated MRSA strains that had escaped into the community

A

False

new strains emerging locally

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139
Q

T/F

Western Samoan Phage Pattern (WSPP) strain of MRSA arrived in Australia from PNG

A

False
arrived in Australia via Auckland in New Zealand and has probably arisen in Samoa
Found in QLD and NSW

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140
Q

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

A

True

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141
Q

T/F

NT-MRSA and the original WA-MRSA clones are PVL positive

A

False
PVL negative
But recently pvl has been detected in some WA-MRSA strains

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142
Q

Which MRSA strains in Aus are PVL positive?

A

USA 300
UK MRSA (rare in Aus)
Queensland MRSA
Western Samoan Phage Pattern (WSPP)

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143
Q

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

A

True

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144
Q

T/F

antibiotics are essential for MRSA abscesses

A

False
The primary treatment for a CA-MRSA abscess is surgical drainage
Many patients respond to drainage alone.

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145
Q

Which antibiotics can be used for MRSA infections?

A

Clindamycin 300mg TDS - 450mg QDS (C. diff risk)
Bactrim
Vancomycin 1st line for severe infections requiring hospital treatment

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146
Q

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

A

True

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147
Q

T/F

MRSA can be transmitted between dogs and humans

A

True
In both directions
Poor dog health and dog overpopulation are major problems in many an Aboriginal community

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148
Q

How is staph eradication performed?

A

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

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149
Q

T/F

The Panton-Valentine leukocidin is associated with necrotising fasciitis

A

True

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150
Q

T/F

The WSPP strain predominates in NSW

A

True

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151
Q

T/F

Trimethoprim-sulfamethoxazole is effective treatment for indigenous patients with moderately severe skin infections

A

True

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152
Q

T/F

CA-MRSA infections can be diagnosed clinically

A

False

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153
Q

T/F

Tinea of the skin and nails affects 5-15% of aboriginal children

A

True

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154
Q

T/F

tinea capitis with Trichophyton tonsurans can be very mild manifesting as scaling and without hair loss in a few patches

A

True

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155
Q

T/F

Geophilic fungi are the main cause of tinea of the skin, nails and hair

A

False

Anthropophilic fungi are the main cause of tinea of the skin, nails and hair

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156
Q

T/F

Tinea corporis in aborigines is usually caused by Trichophyton rubrum or Trichophyton tonsurans

A

True

In NT and NSW aboriginal studies

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157
Q

T/F

Trichophyton tonsurans is almost always isolated from tinea capitis in aborigines

A

True

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158
Q

T/F

superinfection with group A Streptococcus and Staphylococcus aureus occurs in dermatophyte infections

A

True

due to excoriations esp in infants

159
Q

T/F

scaling is unusual in black skin affected by tinea corporis

A

False
Scaling may be prominent particularly in black skin
A circinate silvery scale may be the only manifestation

160
Q

T/F

kerions may be secondarily infected with staph including MRSA

A

True

161
Q

T/F

Woods light examination will show no fluorescence with anthropophilic fungi

A

True

162
Q

T/F
Terbinafine is fungicidal and available on the PBS for Aboriginal or Torres Strait Islander patients where topical treatment has failed

A

True

163
Q

T/F

topicals may be effective for small patches of tinea corporis

A

True
clotrimazole 1% cream twice daily for 4 weeks
terbinafine cream twice daily for 1-2 weeks

164
Q

T/F

tinea capitis should always be treated

A

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

165
Q

T/F

For widespread tinea corporis oral terbinafine for 2 weeks is the treatment of choice

A 
True
Adults – 250mg
Children >40kg – 250mg
Children 20-40kg – 125mg
Children
166
Q

T/F

Terbinafine should be used with caution in patients with diminished renal function and the dosage may have to be reduced

A

True

167
Q

T/F

terbinafine is fine in pts with liver disease

A

False
Oral teribinafine should only be used if absolutelty necessary in patients with liver disease
check FBC and LFTs and repeat fortnightly

168
Q

T/F

There have been reports of agranulocytosis and hepatic failure with terbinafine

A

True

169
Q

T/F

Terbinafine can precipitate or exacerbate subacute lupus erythematosus

A

True

170
Q

How is tinea ungium treated?

A

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

171
Q

T/F

Griseofulvin can precipitate DLE

A

True

and also SCLE

172
Q

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.

A

True

173
Q

How is tinea capitis treated

A

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)

174
Q

T/F

Terbinafine and griseofulvin should not be used during pregnancy

A

True

175
Q

T/F

Trichophyton tonsurans fluoresces under wood’s light

A

False

176
Q

T/F

Trichophyton rubrum commonly causes tinea capitis

A

False

177
Q

T/F

Griseofulvin is teratogenic

A

True

178
Q

T/F

Mycobacterium leprae prefers to replicate in the hotter areas of the body

A

False

179
Q

T/F

In polar tuberculoid leprosy there is a low bacillary load

A

True

180
Q

T/F

In lepromatous leprosy there is a weak cell mediated immune response against mycobacterium leprae

A

True

181
Q

T/F

In tuberculoid leprosy multiple nerves are affected

A

False

182
Q

T/F

Madarosis is a feature of tuberculoid leprosy

A

False

183
Q

T/F

If a patient has a positive skin smear treatment should be for multibacillary disease

A

True

184
Q

T/F

Type 1 reaction is a delayed type hypersensitivity response to mycobacterium leprae

A

True

185
Q

T/F

Erythema nodosum leprosum spares the testicles

A

False

186
Q

T/F

M. pachydermatis is a common cause of pit versic in aboriginals

A

False

in dogs

187
Q

Which species are responsible for pit versic?

A

Mlasezzia
mainly
M.furfur, M.globosa and M.symbodialis

188
Q

What are the microscopic findings in scrapings of pit versic?

A

thick-walled, spherical yeast forms

budding from a narrow base and course septate mycelium often broken up into short filaments

189
Q

What are predisposing factors for pit versic?

A 
warm climate
family history
conjugal exposure (from partner)
Cushing’s syndrome 
and possibly pregnancy.
190
Q

Which age groups mainly get pit versic?

A

late teens and early twenties

rare in old age

191
Q

T/F

The specific malassezia species causing pit versic has not been determined in Aboriginals

A

True

192
Q

What is Kava?

A

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’

193
Q

T/F

Malazessia spp are hydrophilic yeasts

A

False

lipophilic yeasts

194
Q

T/F

Malazessia spp are part of the normal skin flora

A

True
pityriasis versicolor in most cases represents a shift in the relationship between a human and his or her residential flora

195
Q

What are colloquial names for pit versic among aboriginals?

A

“Darwin sunburn” - small and circular lesions

“white handkerchief” - extensive sheets

196
Q

T/F

After Rx of pit versic the residual depigmentation may remain for many months without any scaling

A

True

197
Q

Areas of Pit versic stand out more under Wood’s lamp. What colour do they fluoresce?

A

green-yellow

198
Q

T/F

Pit versic may be moe extensive than usual in the tropics

A

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

199
Q

T/F

culture of skin scarpings is helpful to diagnose pit versic

A 
False
not helpful
malasezzia part of normal flora
diagnose based on clinical appearance/Wood's lamp 
\+/- presence of typical microscopy
200
Q

How is pit versic treated?

A

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

201
Q

T/F

All the systemically absorbed imidazole antifungal agents have the potential to induce hepatotoxicity

A

True

always ask about alcohol (and kava in aboriginals)

202
Q

T/F

fatal hepatotoxicity can occur with itraconazole and ketoconazole

A

True

203
Q

T/F
Itraconazole can also cause serious cardiovascular adverse events with concomitant administration of a number of drugs including erythromycin

A

True

check pts reg meds carefully for interactions

204
Q

T/F

stretching the skin can help to see the fine white scale of pit versic

A

True

205
Q

T/F

there is no way to speed up the recovery of depigmentation caused by pit versic

A

False

exposure to UV light from the sun speeds repigmentation

206
Q

T/F Regarding Pit versic;

The diagnosis is usually made clinically

A

True

207
Q

T/F Regarding Pit versic;

Topical treatments are usually curative

A

False

they help but reinfection is typical

208
Q

T/F Regarding Pit versic;

Wood’s light examination helps distinguish it from tinea

A

True

209
Q

T/F Regarding Pit versic;

Ketoconazole can be safely used with erythromycin

A

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.

210
Q

T/F

Trychophyton mentagrophytes is carried by kangaroos

A

True

211
Q

T/F

The granular variant of T rubrum is endemic among aboriginal populations in tropical regions

A

True

but rarely causes tinea capitis

212
Q

What are the causes of madarosis to consider in aboriginals?

A

= loss of eyebrows
Genetic
Trauma - burns, rubbing, trichotillomania
Hypothyroidism
Infection - lepromatous leprosy (NOT tuberculoid), secondary syphylis

213
Q

What are the DDs of prominent forehead skin folds?

A 
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
214
Q

What are the DDs of Leonine facies?

A 
‘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
215
Q

T/F

Leprosy rates in Australia are more than 1 case per milion per year

A

False

less than 1 per million

216
Q

T/F

Officially leprosy has been eliminated in Austalia but cases still occur

A

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

217
Q

T/F

New cases of leprosy in Australia mainly occur in Vic and SA?

A

False

mainly in the Kimberly and NT

218
Q

T/F

Indegenous australians are the only ones who get leprosy in australia

A

False

not the only ones but mainly indegenous and recent arrivales from endemic countries

219
Q

T/F

Leprosy has a short incubation time

A

False
long
2-5 yrs tuberculoid
9-12 yrs lepromatous

220
Q

T/F

The doubling time for the M Leprae bacillus is 21 days

A

False

12 days

221
Q

T/F

early treatment reduces the risk of onward transmission of leprosy

A

True

222
Q

T/F

early treatment reduces the risk of NFI (nerve function impairment) in leprosy

A

True

223
Q

Which 3 body regions are mainly affected by leprosy?

A

skin
mucous membranes of the nose
peripheral nerves

224
Q

T/F

M Leprae replicates in macrophages

A

True

225
Q

T/F

M Leprae replicates in peripheral nerves

A

True

226
Q

T/F

There is a spectrum of disease type in leprosy between the two polar forms, tuberculoid and lepromatous leprosy

A

True

227
Q

What steps are taken by the clincian in order to classify a case of leprosy?

A

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

228
Q

T/F

accurate classification of leprosy determines infectivity, prognosis, disease complications and treatment regimens

A

True

229
Q

T/F

The WHO classification for leprosy is used most widely in developed countries

A

False
WHO used in resource limited countries
Ridley-Jopling system used in developed countries

230
Q

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)

A

True

231
Q

What are the categories of the Ridley-Jopling classification?

A 
polar tuberculoid (TT)
borderline tuberculoid (BT)
borderline (BB)
borderline lepromatous (BL)
polar lepromatous (LL)
232
Q

What are the categories of the WHO classification?

A

paucibacillary (PB) single lesion
paucibacillary (2 – 5 lesions)
multibacillary (6 or more lesions)

233
Q 
T/F
Borderline leprosy (BB) is the most common type in the NT
A 
False
polar tuberculoid (TT) is most common
234
Q 
T/F
polar tuberculoid (TT) leprosy pts have a poor cell-mediated immune response to the bacillus
A 
False
polar tuberculoid (TT) leprosy pts have a well developed cell mediated immunity and very low bacillary load and localised disease
235
Q

T/F
In tuberculoid leprosy TH – 1 type cytokines such as interferon gamma and IL – 2 are the principle immune mediators of the disease

A

True

236
Q

T/F
In lepromatous leprosy TH – 1 type cytokines such as interferon gamma and IL – 2 are the principle immune mediators of the disease

A

False

TH – 2 type cytokines such as IL – 4 and IL – 10 are the principal immune mediators in these lesions

237
Q

T/F

In tuberculoid leprosy patients are typically smear negative

A

True

238
Q

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

A

True

239
Q

T/F
If skin smears are available and positive, the patient should be classified as multibacillary in the WHO system for leprosy

A

True

240
Q

How is leprosy classified for treatment purposes in the NT?

A

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)

241
Q

What are the keys teps in clinical examination of a leprosy patient?

A

history
skin examination inc neurosensory assessment
nerve palpation
eye examination

242
Q

What is important in the history for leprosy pts?

A 
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
243
Q

T/F

In leprosy sometimes the only lesions are on the buttocks

A

True

Must examine the entire skin

244
Q

T/F

Natural sunlight is the best light for detecting subtle skin changes of leprosy

A

True

245
Q

T/F

Loss of sensation is a cardinal sign of leprosy

A

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

246
Q

T/F

M leprae prefers to multiply in vivo at a temperature of 27 – 30 degrees celsius

A

True

247
Q

Which nerves are most affected by leprosy?

A 
CRUMPS FTG
Common peroneal
Radial cutaneous
Ulnar
Median
Posterior tibial
Sural
Facial and Trigemminal cranial nerves
Greater auricular
248
Q

How are nerves examined in leprosy assessment?

A

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

249
Q

T/F

In lepromatous leprosy only skin and nerves show clinical evidence of disease

A

False

this is true of tuberculoid leprosy

250
Q

T/F

Tuberculoid leprosy may manifest as skin lesions alone, nerve findings alone or both together

A

True

251
Q

T/F
In tuberculid leprosy The typical lesion is a plaque, with raised and clear cut edges sloping towards a flattened and hypopigmented centre

A

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

252
Q

Where is the nerve palpated when a tuberculoid leprosy palque is present?

A

A thickened sensory nerve may be palpated beyond the outer edge of the lesion

253
Q

T/F

Plaques are typical of lepromatous leprosy

A

False

lesions may be macules, papules, nodules or infiltration or all four

254
Q

T/F

skin lesions of lepromatous leprosy are hairless and insensitive

A

False

this is true of lesions of tuberculoid leprosy

255
Q 
T/F
Forehead thickening (cutis gyrata) and madarosis are typical features of lepromatous leprosy
A

True

256
Q

T/F

lesions of lepromatous leprosy may be erythematous or hypopigmented and can become diffusely thickened and shiny

A

True

257
Q

what are the mucosal complications of lepromatous leprosy?

A

Infiltration of the mucous membranes of the nose and mouth may produce stuffiness, epistaxis and atrophic rhinitis
The nasal septum can be destroyed

258
Q

What are the extracutaneous findings in lepromatous leprosy?

A

Infiltration of the liver, spleen, eyes and testes may occur gynaecomastia
reactive amyloidosis

259
Q

T/F

nerve involvemnt in tuberculid leprosy is symmetrical

A

False
symmetrical in lepromatous
associated with assymetrical plaques in tuberculoid

260
Q

T/F

Reactional states are common in lepromatous leprosy

A

True

261
Q

T/F

Borderline leprosy which changes to lepromatous leprosy is called ‘downgrading’

A

True

and change to tuberculoid is called upgrading

262
Q

T/F

Borderline leprosy is the most common presentation

A

True

Skin lesions are intermediate between those of the two polar types

263
Q

What is Indeterminate leprosy?

A

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

264
Q

T/F

ulcers and erosions or deformities of the extremeties and neuropathic joints occur in leprosy due to nerve involvement

A

True

265
Q

T/F

can be easier to identify lack of sweating than lack of sensation in leprosy skin lesions in children

A

True
as may not be able to cooperate with testing
examine for sweating after running aroud outside

266
Q

T/F

Light tough is tested by using a peice of rolled up cotton wool

A

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

267
Q

How is the supraorbital nerve palpated?

A

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

268
Q

How is the supraorbital nerve palpated?

A

Turn head to one side and feel along the SCM edge on the other side

269
Q

How is the ulnar nerve palpated?

A

flex pts elbow to 90 degrees and feel medial to the point of the elbow

270
Q

How is the median nerve palpated?

A

palpate at the distal wrist crease medial to the FCR tendon

271
Q

How is the radial cutaneous nerve palpated?

lateral cutaneous nerve of the forearm

A

Roll fingers over the lateral side of the radius near the wrist crease

272
Q

How is the common peroneal nerve palpated?

A

have the pt seated

Palpate 2cm distal and 1cm posterior to the head of the fubula

273
Q

How is the posterior tibial nerve palpated?

A

Palpate 2cm below and 2cm posterior to the medial malleolus

274
Q

T/F

In leprosy, Lagophthalmos may occur due to damage of the VIIth nerve

A

True

275
Q

T/F

Pts with leprosy may be positive to the quantiferon gold test even though they do not have TB

A

True

276
Q

T/F

PPD testing in pts with leprosy can trigger erythema nodosum leprosum

A

True

277
Q

T/F

Pts with tuberculoid leprosy are highly infectious

A

False

probably never infectious

278
Q

T/F

Leprosy is spread via nasal droplet discharge from lepromatous pts

A

True

279
Q

What types of eye involvement may occur in leprosy?

A

Corneal hypoaesthesia, lagophthalmos, iridocyclitis, scleritis, ectropion, entropion, cataract

280
Q

What are the features of the diffuse leprosy of Lucio and Latapi?

A

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

281
Q

How is leprosy diagnosed?

A

A confirmed case requires definite laboratory criteria and one or more supportive clinical symptoms and signs

282
Q 
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
A

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

283
Q

What is acceptable clinical evidence for leprosy diagnosis?

A

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
284
Q

From where may leprosy skin smears be taken?

A

both ear lobes, suspicious skin patches, thickened skin on the forehead above the medial eyebrows, knees or elbows and previous positive sites

285
Q

T/F

AFB are often seen on histo of skin lesions in tuberculoid leprosy

A

False

usually not seen

286
Q

How is the lab criteria for diagnosis met in pure neural leprosy?

A

nerve biopsy

287
Q

What are the histo findings of tuberculoid and lepromatous leprosy?

A

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.

288
Q

What are the pre-treatment investigations in leprosy?

A 
FBC, ELFT's, 
HIV antibodies
glucose 6 phosphate dehydrogenase levels (dapsone)
CXR 
Mantoux (PPD) or quantiferon gold
289
Q

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

A

True

290
Q

How is paucibacillary leprosy treated?

A

Dapsone 100mg daily (self treated) +
Rifampicin 600mg monthly (DOT)
for 6 months

291
Q

How is multibacillary leprosy treated?

A

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

292
Q

T/F

Patients diagnosed with both leprosy and TB require full treatment for both diseases

A

True

293
Q

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

A

True

294
Q

T/F

Pts being treated for leprosy are typically seen every 4 weeks for DOT and clinical review

A

True

weekly initially then q4w

295
Q

T/F

Immunological reactions in leprosy only occur after initiation of treatment

A

False
can be before, during or after Rx
treatment initiation is most common trigger
other infections or pregnancy can also trigger reactions

296
Q

T/F

Type 1 lepra reaction is also called reversal

A

True

297
Q

T/F

Type 2 lepra reaction is also called upgrading

A

False

Type 1 is called upgrading or reversal

298
Q

T/F

HIV increases risk of leprosy

A

False

HIV does not increase risk or host response to leprosy

299
Q

T/F

Type 1 reactions can occur in any type of leprosy

A

False

Most commonly borderline types (BB, BL, BT) but can be in tuberculoid or lepromatous. Not in indeterminate type

300
Q

What are the features of Type 1 (reversal) reactions?

A

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

301
Q

What is the aetiology of Type 1 (reversal) reactions?

A

Is a Delayed-type hypersensitivity reaction

Enhancement of cell-mediated immunity with a Th1 cytokine pattern

302
Q

T/F

Type 1 leprae reactions are terated with prednisolone?

A

True
1mg/kg
taper over 12 months but may need to continue for years
+/- NSAIDS, physio
Reports of steroid sparing w/ AZA, CsA, MTX

303
Q

T/F

Erythema nodosum leprosum is the most common type of type 2 lepra reaction

A

True

304
Q

What is the aetiology of Type 2 lepra reactions?

A

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

305
Q

T/F

Type 2 reactions mainly occur in lepromatous and BL cases of leprosy

A

True

306
Q

T/F

Type 2 reactions mainly present shortly after initiation of treatment

A

False

mainly in second year on treatment

307
Q

What are the features of type 2 rcn (erythema nodosum leprosum)?

A

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)

308
Q

How is type 2 rcn (erythema nodosum leprosum) treated?

A

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

309
Q

What is Lucio phenomenon?

A

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

310
Q

T/F in leprosy;

Nerve damage is more severe in tuberculoid form

A

True

311
Q

T/F

In tuberculoid leprosy, bacillary multiplication is restricted to a few sites and bacilli are not readily found

A

True

312
Q

How is a slit skin smear performed in leprosy?

A 
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
313
Q

T/F

Melioidosis is infection with Burkholderia pseudomallei

A

True
AKA pseudo-glanders, Stratton’s disease, Whitmore’s disease
Burkholderia mallei causes glanders

314
Q

T/F

Burkholderia pseudomallei is an environmental saprophyte found in soil and surface water in tropical regions

A

True

315
Q

How is Burkholderia pseudomallei infection contracted

A

Inhalation or by skin/mucosal exposure when there is a portal of entry

316
Q

T/F In melioidosis;

incubation time from exposure to clinical signs may range from a few days to over 20 years

A

True

317
Q

T/F

Melioidosis can present as an acute, sub-acute or chronic form of disease

A

True

318
Q

T/F

acute melioidosis is a life-threatening disease

A

True
acute septicaemic form causes death if untreated
survival is 50-80% if treated

319
Q

T/F

Melioidosis can affect any organ system of the body

A

True

esp skin, joints, GU tract, lungs and brain stem

320
Q

T/F

Burkholderia pseudomallei is facultative intracellular Gram positive motile bacillus

A

False

gram negative

321
Q

T/F
Burkholderia pseudomallei grows in blood culture bottles and on standard lab media such as MacConkey, Chocolate or 5% sheep bloodagar

A

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

322
Q

T/F

Burkholderia pseudomallei takes weeks to grow in the lab

A

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

323
Q

Whic antibiotics is Burkholderia pseudomallei typically sensitive to?

A 
Ceftazidime, 
Piptaz
Ticarcillin/Clavulanate, 
Co-amoxiclav 
Meropenem
Bactrim
Doxycycline 
Chloramphenicol
324
Q

T/F

On staining Burkholderia pseudomallei typically shows a bipolar “safety pin” appearance

A

True

not diagnostic but highly suggestive of the diagnosis in the correct clinical settling

325
Q

Where is melioidosis seen in Australia?

A

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

326
Q

T/F

melioidosis occurs mainly in dry inland areas

A

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

327
Q

T/F about 45-50 cases of melioidosis are diagnosed each year in Aus

A

True

slightly more in NT than FNQ

328
Q

T/F

About 50% of Aus cases of melioidosis occur in indegenous pts

A

True

329
Q

T/F

melioidosis is more likely to be caught from running than still water

A

False
still water more likely
rice paddies are a common source in South East Asia - Thailand has the most cases worldwide

330
Q

T/F

In Northern Australia 10% of Aboriginals are sero-positive for past exposure to B pseudomallei

A

True
due to prior subclinical infection - common
the infection is completely cleared but they remain sero-positive

331
Q

T/F

B pseudomallei is an intracellular pathogen and is therefore protected to a degree from the host immune system

A

True

332
Q

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

A

True

often organisms are in the lungs or bowel

333
Q

T/F

melioidosis cannot be transmitted person-person

A

False

rare reports of B pseudomallei transmission in this way

334
Q

What are risk factors for development of clinical disease or more severe clinical disease following exposure to Burkholderia pseudomallei?

A

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

335
Q

T/F

being aboriginal is an independent risk factor for severe melioidosis

A

False

no evidence for this

336
Q

T/F

In Northern Australia approximately 75% of melioidosis cases are associated with diabetes

A

False

50%

337
Q

T/F

In Northern Australia approximately 20-40% of melioidosis cases are associated with alcoholism

A

True

338
Q

T/F

Melioidosis affects the skin in 60% of cases in Australia

A

False

9-28%

339
Q

T/F

clinically cutaneous melioidosis can be categorized as primary or secondary, acute or chronic, localized or generalized

A

True

340
Q

T/F

primary cutaneous melioidosis presenting as a single lesion is the most common presentation of cutaneous melioidosis

A 
True
The lesion can be;
pustule, 
exudative purulent ulcer 
furuncle 
skin abscess +/- overlying skin fistula 
crusted erythematous plaque 
asymptomatic flat erythematous patch 
cellulitis
341
Q

T/F

seropositivty for B pseudomallei always indicates latent disease

A

False

will be seropositive if had disease and cleared either spontaneously or with treatment or if have latent disease

342
Q

T/F

Primary cutaneous melioidosis is unlikely to progress to severe systemic disease and death

A

True

but is possible

343
Q

T/F

secondary cutaneous meioidosis is when skin lesions have occured after haematogenous spread

A

True

often in acute septicaemic form

344
Q

What are the features of secondary cutaneous meioidosis?

A

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

345
Q

What are the lesions of subacute and chronic cutaneous meioidosis?

A

Chronic/Subacute - subcutaneous draining abscesses are the hallmark of the disease, can be skin ulcers, fistulae

346
Q

What are the features of acute systemic melioidosis?

A

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

347
Q

T/F

Chronic systemic melioidosis often causes osteomyelitis or chronic septic arthritis

A

True

348
Q

T/F

If Burkholderia pseudomallei is isolated from a “well” patient it should always be treated

A

True

349
Q

T/F

In order to make the diagnosis of melioidosis cultures from every possible lesion/site are essential

A

True
swabs or ulcers, psutules etc, aspirates of deep abscesses, skin for histo and culture, blood culutres, urine and sputum cultures etc

350
Q

T/F

Blood cultures should also be taken in a patient presenting with skin signs of melioidosis even if they appear “well”

A

True

351
Q

T/F

Skin histo from pts with melioidosis may show different features in acute vs chronic disease

A

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).

352
Q

T/F

Serological assessment of a patient for past exposure to melioidosis is helpful in the acute situation

A

False

no help

353
Q

What methods are used for Serological assessment of a patient for past exposure to melioidosis?

A 
ELISA
Indirect haemagglutination (IHA)
354
Q

T/F

Melioidosis hs a 10% relapse rate

A

True

355
Q

T/F

B pseudomallei is usually resistant to macorlide, quinolones and aminoglycosides

A

True

356
Q

What are the antibiotics of choice in melioidosis?

A 
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
357
Q

Outline the steps in clinical assessment of a suspected cellulitis

A

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.

358
Q

T/F

Asymptomatic carriage of B pseudomallei can be ignored

A

False

359
Q

T/F, Regarding Primary Cutaneous Melioidosis;

Multiple melioidosis risk factors are usually present

A

False

but should always check in history

360
Q

T/F, Regarding Primary Cutaneous Melioidosis;

Multiple skin lesions are usually present

A

False

usually single lesion in primary disease

361
Q

T/F, Regarding Primary Cutaneous Melioidosis;

Usually progresses to fulminant disease

A

False

362
Q

T/F, Regarding Primary Cutaneous Melioidosis;

Usually responds to appropriate antibiotics

A

True

363
Q

T/F, Regarding Primary Cutaneous Melioidosis;

Is endemic Australia wide

A

False

364
Q

T/F

smoking is a risk factor for melioidosis

A

False

365
Q

What is the Splendore Hoeppli phenomenon?

A

Formation of a sheath of deeply eosinophilic material around micro-organisms, usually fungal, bacterial or around parasites
Usually has a stellate or radiating appearance

366
Q

Whic organismscan cause Splendore Hoeppli phenomenon?

A 
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
367
Q

What are the DDs for chronic painless swollen limb?

A 
filariasis, 
fungal and nocardial mycetoma, 
other subcutaneous mycoses, 
complicated dermatophyte infection, 
soft-tissue sarcoma,
chronic lymphoedema, 
bacterial cellulitis, 
early subcutaneous (angioinvasive) mucormycosis (zygomycosis)
368
Q

T/F

Most zygomycetes are sensitive to cycloheximide (actidione) and this agent should not be used in culture media

A

True

369
Q

Zygomycetes are slow growing organisms and show white to grey or brownish, downy colonies with many radial folds

A

False

rapid growing

370
Q

Which organisms cause chromoblastomycosis?

A 
Phialophora verrucosa
Fonsecaea pedrosoi
F. compacta
Cladophialophora carrionii
Found in wood and soil
371
Q

Which organisms cause phaeohyphomycosis?

A 
Cladosporium
Exophilia
Wangiella
Bipolaris
Exserohilim
Curvularia
372
Q

Which organisms cause Mycotic mycetoma?

A 
Pseudallescheria
Madurella
Acremonium
Exophiala
saprophytes in soil and on plants. It is common among agricultural workers
373
Q

Which organisms cause subcutaneous zygomycosis, entomophthoromycosis type (Entomophthorales)?

A 
Basidiobolus sp (esp B. ranarum) 
Conidiobolus sp (esp C. coronatus)
V rare in Aus
374
Q

Which organisms (genus) cause subcutaneous zygomycosis, mucormycosis type (Mucorales)?

A 
Rhizopus
Mucor
Rhizomucor
Absidia (myocladus)
Saksenaea
Cunninghamella
Apophysomyces
Cokeromyces
Mortierella
375
Q

What are zygomycoses?

A

subcutaneous mycosis caused by primitive, fast growing, terrestrial, largely saprophytic fungi with a cosmopolitan distribution
2 orders (genera);
Entomophthorales (the entomophthoromycoses)
Mucorales (the mucormycoses)

376
Q

T/F

Mucorales type zygomycoses are angioinvasive causing embolization and subsequent necrosis of surrounding tissue

A

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

377
Q

T/F

Entomophthorales type zygomycosis cause severe destructive disease

A

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

378
Q

T/F
Zygomycosis caused by Conidiobolus sp. is restricted to the nasal submucosa and characterised by polyps or palpable subcutaneous masses

A

True

379
Q

What are the DDs for an aqcuired saddle nose/destructive nasal disease

A 
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
380
Q

What is the treatment of Mucorales type zygomycoses?

A

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

381
Q

What is the treatment of Entomophthorales type zygomycosis?

A

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

382
Q

Where does sporothrix schenkii grow?

A

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

383
Q

T/F
Basidiobolus ranarum occurs saprophytically in decaying vegetable material and soil and can be found in the dung of kangaroos and wallabies

A

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

384
Q

What is Dermatosis papulosa nigra?

A 
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
385
Q

What is Chewing tobacco mucositis?

A

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

386
Q

T/F

More females than males use chewing tobacco in NT

A

True

387
Q

What is Focal epithelial hyperplasia?

A

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

388
Q

What is Residual ochre?

A

Leftover body paint made from natural ochres (clay + iron oxides)
Can resemble tinea capitis when on scalp
No significance

389
Q

What are the major DDs for madarosis in aboriginals?

A 
Genetic
Trauma – rubbing, picking, burns
Hypothyroidism
Lepromatous leprosy
Secondary syphylis
390
Q

Wat causes Lateral malleolar bursitis in aboriginals?

A

Due to prolonged pressure from sitting cross-legged
M>F
Exclude neuropathic ulcers e.g. diabetes, leprosy and infections

391
Q

What are sorry cuts?

A

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

392
Q

What are bush feet?

A

Reactive thickening of cornified layer on feet due to barefoot walking in bush
Looks like dried mud but doesn’t wash off

393
Q

What is Kava dermopathy?

A 
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

Aboriginal & Refugees Dan (3 decks)

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