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Medical dermatology Dan > Parasitic diseases Dan > Flashcards

Parasitic diseases Dan Flashcards

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1
Q

T/F

The main parasites are Helminths (worms) and Protozoa

A

True

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2
Q

What are the main Helminth groups?

A

Nematodes (round worms, pinworms and hook worms)
Cestodes (flatworms/tapeworms)
Trematodes (flukes)

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3
Q

What are the main Protazoal diseases?

A

Leishmaniasis (most important for derm)
Amoebiasis
Trypanosomiasis
Toxoplasmosis

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4
Q

What are the main Nematode diseases?

A

larva migrans, onchcerciasis, gnathostomiasis, filiariasis, Loiasis, Drancunculiasis, Strongyloidiasis
Enterobiasis (Pinworm/threadworm)
Ancylostomiasis (Hook worm)

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5
Q

What are the main Cestode diseases?

A

Cysticercosis and echinococcosis

Sparganosis

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6
Q

What are the main Trematode diseases?

A

Schistosomiasis
Paragonimiasis
Fascioliasis
Cercarial dermatitis(swimmer’s itch)

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7
Q

what organism is responsible for cutaneous larva migrans?

A

Ancylostoma spp; (BCC)
braziliense, caninum or ceylanicum
hookworms which can infect domestic dogs or cats as well as foxes, wolves, wild dogs and cats etc. The larvae is what infects humans

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8
Q

where is cutaneous larva migrans acquired and how?

A

In North, C and S America and parts of asia
pts walks barefoot/lies in outdoors; sandy area etc
hook worm eggs have been passed in feaces from infected animal and hatch into filariform larvae in sandy soil so are present on the ground and penetrate skin

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9
Q

T/F

The incubation time for cutaneous larva migrans is approx 2 weeks

A

False

1-6 days

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10
Q

T/F

some pts with cutaneous larva migrans get systemic symptoms including cough and wheeze

A

True
small percentage
rarely can get Loefller’s syndrome - eosinophilic pneumonia due to parasite infection

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11
Q

T/F

Creeping eruption and ground itch are other names for cutaneous larva migrans

A

True

also sandworms and Plumbers itch

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12
Q

what are the clinical features of cutaneous larva migrans?

A

starts as dermatitis at site of entry of larva - often feet or buttocks from standing or sitting on affected ground
can stay like that for wks-months before typical meandering serpiginous trail of erythema begins or can begin very quickly
dermatitis can be raised and vesicular
trail moves slowly 1mm-3cm per day
is 3mm wide and up to 15-20cm long
can be single or many
self limiting - usually resolves in 4-8 weeks when nematode dies
can be secondary impetiginisation - 10%
can get hookworm folliculitis with up to 200 follicular papules and pustules confined to one part of the body
Can get EM

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13
Q

How is cutaneous larva migrans diagnosed?

A

A typical eruption in a pt with a consistent Hx is adequate for a clinical diagnosis
If tests required can take biopsy of folliculitis showing nematode larvae but often larvae have migrated by the time the biopsy is taken
or skin scrapings from serpiginous trail showing larvae and dead nematodes

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14
Q

T/F

Humans are a dead end host for the dog or cat hookworm

A

True
cannot penetrate basement membrane of skin as lack specific collagenases
nematode dies in 4-8 weeks

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15
Q

How is cutaneous larva migrans treated?

A

No Rx - self limiting
can treat to alleviate symptoms
single dose ivermectin - preferred Rx for adults and children over 15kg
3 day course of albendazole - 400mg for adults and children over 10kg or 200mg for children under 10kg
both taken with fatty food
Can use topical thiabendazole 10%; Grind up two 500mg tablets into 10g of WSP and apply bd for 1 week

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16
Q

How does cutaneous larva migrans differ clinically from larva currens?

A 
Migrans; 
well defined narrow, often raised train
Moves slowly max 3cm/day often few mm only
Currens;
Poorly defined urticated trail
Moves quickly, 5-15cm per hour
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17
Q

T/F

Oncherciasis is caused by Onchocerca volvulus, a filarial nematode

A

True

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18
Q

T/F

Oncherciasis is also called sleeping sickness

A

False

Oncherciasis is also called River blindness

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19
Q

Which organs/systems are most affected by Oncherciasis?

A

Skin
Eyes
Lymphatics

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20
Q

T/F

Oncherciasis is transmitted by the female sandfly

A

False

Oncherciasis is transmitted by the female black fly (Simulium damnosum)

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21
Q

T/F

onchocercomas are the first and most characteristic skin finding of Oncherciasis

A

True

subcutaneous nodules over bony prominences esp skull which are fibrous tissue surrounding coiled adult worms

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22
Q

What are the skin manifestations of Oncherciasis?

A

Onchocercomas
Acute papular onchodermatitis on trunk and limbs
Chronic papular onchodermatitis on buttocks, hips, shoulders
Lichenified onchodermatitis - usually one thickened and lichenified area on a limb
Atrophy around waist, butocks and thighs and Hanging groin
Depigmentation known as leopard skin

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23
Q

T/F
Microfiliarae in Oncherciasis cause conjunctivitis, sclerosing keratitis, uveitis, optic atrophy, and glaucoma which can lead to blindness

A

True

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24
Q

T/F

Oncherciasis is the most common infective cause of blindness

A

False

second most common infective cause of blindness

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25
Q

How is Oncherciasis diagnosed?

A

Pt has typical clinical features and Hx of travel to endemic area; sub-saharan mainly and occasionally in Central and South America (Mexico -> Venezuela) and middle east
Tests;
excison of onchocercoma - see adult worm
skin or sclera snip test - very superficial shave left on slide in saline for 20mins then examined for released microfilariae

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26
Q

T/F

Oncherciasis is treated with Ivermectin 200mcg/kg as single dose and repeated at 6 and 12months

A

True
Ivermectin 1st line
Can use doxy 100mg OD for 6 weeks – kills a bacteria the worms live on
and must refer to ophthalmology

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27
Q

T/F

Gnathostomiasis is a nematode infection caused by worms of the genus Gnathostoma

A

True
Dogs and cats are usual host
throughout SE Asia + Japan, S Africa and C and S America
worms wander in humans in the SC fat and muscles causing deep tunnels which are the sites of inflammation or abscess formation resulting in migratory sucutaneous inflammatory swellings

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28
Q

What is the classic diagnostic triad of Gnathostomiasis?

A

History of travel to an endemic area
Intermittent migratory swellings/nodules
Eosinophilia

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29
Q

T/F

Gnathostomiasis histo shows dense eosinophilia and flame figures and may see the worm

A

True

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30
Q

T/F
Gnathostomiasis is treated with Albendazole 400mg daily for 1 month or ivermectin 200 mcg/kg single dose or surgical extraction of the worm

A

True

Treatment important to prevent ocular involvement

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31
Q

T/F

What is tropical elephantiasis?

A

Another term for filiariasis
The clinical finding of elephantiasis indicates lymphatic and skin changes are no longer fully reversible despite treatment

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32
Q

T/F

The nematode Wucherera bancrofti is responsible for >90% of cases of filiariasis

A

True

called Bancroftian filiariasis

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33
Q

What is Malayna?

A 
Less common form of filiariasis due to 
Brugia malayi (South and East Asia) or
B. timori (limited to islands in Indonesia - timor)
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34
Q

T/F

filiariasis is the same as mossy foot

A

False
But they are DDs for each other
Mossy foot is podoconiosis, a non-infectious elephantiasis chnage due to barefoot walking on alkali volcanic soil

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35
Q

T/F
In filiariasis the nematode worms acquired via mosquitos mature into adults in the lymphatics where they cause obstruction and recurrent inflammation when they die and eventually permanent damage

A

True

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36
Q

T/F
The most common acute manifestation of
lymphatic filariasis is acute adenolymphangitis
(ALA). ALA is characterized by episodes of fever
attacks, inflamed lymph nodes in the groin and
axillae, and localized areas of warmth, swelling,
redness, and pain

A

True
response to worms dying
Also get lymphangitis, fever, and orchitis

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37
Q

T/F

filiariasis can only be diagnosed by blood smear for microfilariae

A

False
serology also
for detection of circulating filarial antigen

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38
Q

What are the chronic manifestations of

lymphatic filariasis?

A

lymphoedema (reversible), elephantiasis (irreversible), hydroceles, chyluria
massive swelling of legs or scrotum common

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39
Q

T/F

filariasis is treated with Diethylcarbazine (DEC)

A

True
Can use;
Doxycycline 200mg OD for 6-8 weeks (kills Wolbachia bacterium necessary for worms to reproduce)
Ivermectin 400mcg/kg reported

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40
Q

T/F

Onchocerciasis is treated with Diethylcarbazine (DEC)

A

False
Oncherciasis is treated with Ivermectin 200mcg/kg as single dose and repeated at 6 and 12months
Dont give DEC in Onchocerciasis as can worsen eye disease

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41
Q

T/F

Loiasis is treated with Diethylcarbazine (DEC)

A

False
Loiasis is treated with albendazole or surgical removal
DEC should also be avoided in patients with loiasis because can cause encephalopathy or death

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42
Q

What are Calabar swellings?

A

transient localized subcutaneous swellings on the extremeties which occur in 50% of pts with Loiasis
Itchy not painful
‘Lu lu (Loa Loa) rocks the Calabar!)

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43
Q

T/F

Loiasis is cause by Loa Loa filarial nematode

A

True

Both the nematode and the disease are known as the ‘African eyeworm’

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44
Q

What are the features of Loiasis?

How is it diagnosed and treated?

A

1 year after infection adult worms cause calabar swelling and can cross the eyeball under the conjunctivae
there is a crawling sensation in the skin and significant eye irritation
can also present as recurrent migratory focal angioedema caused by adult filariae
Can diagnose by daytime blood smear (giemsa) or serology for PCR
Or by demonstrating adult worm removed from conjunctival or subcutaneous tissue
Treat with Ivermectin standard dose

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45
Q

T/F
Migration of the adult worm across the
conjunctiva of the eye occurs in approximately
30% of Loiasis patients

A

False

70%

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46
Q

T/F

Dracunculiasis is caused by the guinea worm

A

True
Dracunculus Medinensis
Both the nematode and the disease are known as ‘guinea worm’

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47
Q

T/F

In Loiasis the female worm may be seen protruding from an ulcer on the lower leg

A

False

This is a feature of Dracunculiasis

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48
Q

T/F

systemic metronidazole or thiabendazole are curative for Dracunculiasis

A

False
metronidazole or thiabendazole are given to aid worm removal which is the cure
Also need antibiotics + tetanus shot
Extract worm w/out breaking - wrap around a stick and pull out over several days

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49
Q

What is the organism responsible for Pinworm/threadworm infection?
How is diagnosed and treated?

A

Enterobius vermicularis a nematode
= Enterobiasis
diagnose by seeing worms at anal margin at night or +ve stool OCP
Rx;
mebendazole 100mg stat (combantrin) and rpt in 2-4 weeks or
pyrantel 10mg/kg (anthel)
Also treat entire family and launder linen + clean kids fingernails and dont let them scratch!
Sometimes mebendazole 100 bd for 3 days + rpt at 2 weeks is required if resistant

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50
Q

What are the clinical features of Enterobiasis?

A

Pinworm/threadworm infection
mainly affects children
nocturnal pruritus ani is main symptom
worms migrate to perianal region at night to lay eggs - kids scratch and then eggs go back into mouth from fingernails
Infection self limiting if good hygeine to prevent reinfection

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51
Q

T/F

Enterobius vermicularis is the commonest human parasite

A

True

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52
Q

T/F

The human hookworm does not occur in Australia

A

False
Ancylostoma duodenale is found across Northern Aus and has a high prevalence among indiginous peoples in rural communities w/ poor sanitation

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53
Q

What causes human hookworm

A

The nematodes
Necator americanus - Africa, S Asia, Americas
and
Ancylostoma duodenale - Aus, Europe, N and C Asia
Their filiform larvae penetrate the skin the same as dog/cat hookworms in larva migrans but are able to go to the lungs where they are coughed up and swallowed

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54
Q

What is ‘ground itch’

what causes it?

A 
pruritic papular or papulovesicular rash and may be accompanied by a general urticaria
Causes are;
Cutaneous larva migrans
Strongyloides
Hook worms - N americanus or A duodenale
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55
Q

What are the symptoms of human hookworm?

A 
ground itch
GI upset
anaemia - pallor, lethargy, reduced exercise tolerance
cough, wheeze, SOB
Can get Loeffler’s syndrome
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56
Q

How is hookworm diagnosed and treated?

A

send stool for OCP
Mebendazole 100mg bd for 3 days
or;
albendazole 200mg bd for 3 days

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57
Q

How is strongyloides treated?

A

Ivermectin standard dose repeated after 1 week

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58
Q

What is the lifecycle of strongyloides stercoralis?

A

filiform larve penetrate skin to start infection
get into blood stream and go to lungs
penetrate alveoli and are coughed up and swallowed
larvae mature in gut an drelease eggs which mature into new flarvae in gut
gut larvae are excreted in stool but also can become filiform and penetrate lower bowel wall or perianal skin to reinfect host
excreted larvae can live full lifecycle and reproduce as free-living worm s outside an animal host or can reinfect another host

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59
Q

T/F

Pts with strongyloides are often symptomatic

A

True

may or may not have a persistant eosinophilia

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60
Q

T/F

Urticaria occurs in 2/3 of strongyloidiasis cases

A

True
always include in urticaria screen in Aus
Typically larva currens is a serpiginous urticaria on the buttocks thighs and abdo

61
Q

T/F

strongyloides stercoralis can complete its lifecycle inside or outside a human host

A

True

62
Q

T/F

Feocal multiplex PCR can detect bowel helminths

A

False
Detects bacteria and protozoa only
Need OCP for helminths

63
Q

What are acute symptoms of strongyloides infection?

A

Ground itch
abdo pains, diarrhoea
cough, wheeze, SOB
usuallly no rash

64
Q

T/F

Larva currens is a feature of chronic and self perpetuating strongyloidiasis

A

True
allergic response to the migrating larvae as they travel through the skin from the anus so typically nipples to knees area of skin
a fast moving migration where a linear wheal and flare response covering 5-15cm/hr

65
Q

What are severe forms of strongyloidiasis?

A

Hyperinfection
Disseminated strongyloidiasis
both occur in immunocompromised

66
Q

What is Strongyloides Hyperinfection?

A

there is excessive worm burden within small intestine due to an acceleration of their normal life cycle which can lead to profuse diarrhoea, electrolyte changes, fever, hemoptysis, dyspnoea, mental confusion and petechial ‘thumbprint’ purpura radiating from the periumbilical area.
Occurs in immunocompromised and there is shock, sepsis and high mortality

67
Q

What is Disseminated strongyloidiasis?

A

occurs when patients with chronic strongyloidiasis become immunosuppressed
larvae spread to other organs (e.g. heart, urinary tract, CNS) that are not normally part of the parasitic life cycle

68
Q

How is strongyloides diagnosed?

A

serology (ELISA for specific IgG)
feaces for OCP examination
also high IgE and eosinophilia

69
Q

T/F
Leishmaniasis is caused by the Leishmania spp of protozoa transmitted by the bite of infected female phlebotomine sandflies

A

True

The sandflies inject the infective stage (ie, promastigotes) from their proboscis (salivary glands) during blood meals

70
Q

T/F

Leishmania transform and replicate inside human macrophages and other phagocytic cells

A

True

71
Q

T/F

Old and new world leishmaniasis are trasnmitted by the same species of sandlfies worldwide

A

False
all are phlebotomine sandflies in the subfamily phlebotominae;
Phlebotomus (genus) sand flies in Old World
Lutzomyia (genus) and Psychodopygus (genus) in the New World

72
Q

T/F

Sandflies are large flies which bite during the daytime

A

False
This is true of horseflies
Sandflies are only 1/3 the size of a mosy and silent, active at night

73
Q

T/F

children are more susceptible to leishmaniasis

A

True

kids affected > adults

74
Q

T/F

Schistosomes are obligate intracellular parasites that exist in 2 forms (dimorphic), amastigote and promastigote forms

A

False
This is Leishmania spp;
Promastigote from is extracellular and flagellated
Amastigote form is intracellular and non-flagellated

75
Q

T/F

kangaroos are reservoirs for leishmania spp

A

True
but this form doesnt seem to infect humans
Other reservoirs are man, dogs, leopards, hyenas, rodents, bats, and baboons

76
Q

How do leishmania spp evade the immune system?

A

By inhibiting phagolysosome biogenesis and altering phagosome degradative properties

77
Q

T/F

Leishmanaisis is the second top cause of death from tropical parasite infection after malaria

A

True

78
Q

T/F

Leishmanaisis is self limiting

A

True
some forms are
particularly cutaneous leishmaniasis esp old world types

79
Q

T/F

Leishmanaisis incubation time is >12 months

A

False
Several weeks to two months for cutaneous lesions
Three to nine months for mucucutaneous lesions or visceral involvement

80
Q

T/F

Clinical manifestations of leishmaniasis depend on the host’s cell-mediated immune response and the species involved

A

True
Robust Th1 response (i.e. production of IL-2 and IFN-gamma) leads to cell mediated immune response and inflammation which is associated with a quicker resolution
Lack of Th1 response or development of a Th2-type response leads to antibody-medicated immune response and is associated with progression of the disease

81
Q

T/F

Leishmaniasis is endemic to all continents except Australia and Antarctica

A

False
is a kangaroo variant in Aus
only absent from antarctica
although this statement is in JAAD paper

82
Q

T/F

There are 2 species of leishmania - old and new world

A

False

>20 species - some old and some new world

83
Q

T/F

L infantum is found in both old and new world and can cause cutaneous or visceral disease

A

True

dog is main reservoir

84
Q

T/F

Cutaneous leishmaniasis is more common in the old world

A

True

85
Q

T/F

Mucocutaneous leishmaniasis is more common in the old world

A

False

exclusively New world

86
Q

T/F

Diffuse cutaneous leishmaniasis is more common in the new world

A

True

87
Q

T/F

Visceral leishmaniasis only occurs in New world

A

False
Old or new
Mucocutaneous leishmaniasis only occurs in New world

88
Q

T/F

>90% of cutaneous leishmaniasis infections occur in Middle East, Brazil, and Peru

A

True

89
Q

T/F

clinical manifestations of leishmaniasis depend on the species of leishmania and the hosts cell mediated immune response

A

True

90
Q

T/F

L infantum is found in both old and new world

A

True

91
Q

T/F

the promastigote is the intracellular form of leishmaniasis

A

False
promastigote is extracellular, flagellated form
amastigote is intracellular, non-flagellated form
leishmaniasis is dimorphic = 2 forms

92
Q

what are the clinical forms of leishmaniasis?

A

cutaneous leishmaniasis
diffuse/disseminated cutaneous leishmaniasis
mucocutaneous leishmaniasis
visceral leishmaniasis = kala azar (black fever)

93
Q

T/F

The new world species of leishmania are generally named after regions or countries in central and south america

A

True
2 main groups are
laishmania braziliensis also called leishmania viannia
and leishmania mexicana
in the braziliensis group are L braziliensis, gyanensis, panamensis and peruviana
In the mexicana group are L mexicana, amazonensis and venezuelensis which has 2 subgroups; pifanoi and garnhami (these and L Chagasi are the 3 new world names which are not obvious new world regions)
all the other leishmania species are old world except L infantum is both old and new world
the main old world groups are leishmania donovani and leishmania tropica

94
Q

what is the incubation period for leishmaniasis?

A

weeks to months for skin disease

3-9 months for mucocutaneous or visceral disease

95
Q

what is the natural history of cutaneous leishmaniasis?

A

after weeks to months a small papule appears at innoculation site - usually extremeties or face or neck
enlarges to nodule or plaque then ulcerates or becomes verrucous
has a raised violaceous border
may have satellite lesions
may have regional LNs
most cases heal spontaneously over months and leave a depressed scar
clinical variants;
Old world;
localized - as above
lupoid - resembles lupus vulgaris/pernio, often chronic
recidivans - chronic relapsing
diffuse - disseminated disease
New world;
sporotrichoid - esp L gyanensis or panamensis
pustular, impetigo-like, sarcoidosis-like, eczematoid, erysipeloid
Chiclero’s ulcer - L Mexicana on ear
Uta - L peruviana self healing lesions can spread to adjacent mucosa
Pianbois - L guyanensis w/ sporotrichoid spread of lesions; Rx resistant
Ulcera de Bejuco - L panamensis shallow ulcers w/ sporotrichid spread

96
Q

what is the recidivans form of cutaneous leishmaniasis?

A

also called chronic relapsing type
the cutaneous lesion heals but there is recurrence at the edge which occurs repeatedly
due to failure of cell mediated immunity to completely clear the disease

97
Q

what is the lupoid form of cutaneous leishmaniasis?

A

a clinical descriptive variant
infiltrated erythematous plaque w/out pustules or ulceration which resembles lupus vulgaris or lupus pernio and less so DLE
can be more persistent than other cutaneous forms

98
Q

what is disseminated cutaneous leishmaniasis?

A

pts develop multiple painless keloid-like nodules
ears, face and limbs esp knees and elbows - can be widespread
can be leonine facies
may be hypopigmented lesions mimicking tuberculoid leprosy
30% get nasal infiltration and may get laryngeal or pharyngeal ulceration
occurs in pts with poor Th2 response esp HIV

99
Q

what important risk factor should be considered in pts with disseminated cutaneous leishmaniasis?

A

HIV/AIDS

esp with immune reconstitution inflammatory syndrome after starting HAART

100
Q

what organisms cause disseminated cutaneous leishmaniasis?

A

mainly;
L aethiopica in old world
L mexicana amazonensis in new world

101
Q

T/F

mucocutaneous leishmaniasis is only seen in old world

A

False

only new world

102
Q

what species is most commonly responsible for mucocutaneous leishmaniasis?

A

L braziliensis

103
Q

T/F

mucocutaneous leishmaniasis affects 20% of those with cutaneous disease

A

False
3-5%
up to 20% in some areas
onset usually after resolution of cutaneous disease

104
Q

T/F

mucocutaneous leishmaniasis usually starts within 2 years of infection

A

True

but rarely up to 30 yrs later

105
Q

T/F

only one species of leishmaniasis causes mucocutaneous leishmaniasis

A

False

usually L braziliensis but can be amazonensis, panamensis or guyanensis

106
Q

What is a Tapir nose?

A

result of mucocutaneous leishmaniasis

nasal infiltration causes convex swelling of the nose like a tapir - later there is ulceration and nasal destruction

107
Q

T/F

bone is destroyed by mucocutaneous leishmaniasis

A 
False
bone is spared
rarely involves cartilage
usually spares nasal septum but can perforate this as well as laryngeal cartilage and soft palate
can destroy vocal cords
108
Q

T/F

mucocutaneous leishmaniasis may be caused by a virus rather than the leishmania protozoa itself

A

True

this is a theory

109
Q

What is kala azar?

A

Visceral leishmaniasis
involves liver, spleen and bone marrow
causes fever, cough, lymphadenopaty, hepatosplenomegally and anaemia then wasting/emaciation
high mortality if untreated

110
Q

T/F

visceral leishmaniasis affects children more in new world and adults in old world

A

True

111
Q

T/F

HIV pts are at increased risk of visceral leishmaniasis

A

True
risk is increased by between 100 and 2000 times
also of diffuse cutaneous disease

112
Q

T/F

leishmania causes SCC or BCC esp in HIV pts

A

False
can be found inside these lesions but not causative
can also find protozoa inside kaposis sarcoma

113
Q

How does HIV/AIDS impact on leishmaniasis

A

increased risk of mucocutaneous and visceral disease
also atypical presentation, poor Rx response and increased mortality
leish can also cause progression of AIDS

114
Q

What is post kala-azar dermal leishmaniasis (PKDL)?

A

uncommon sequele of treated or untreated visceral leishmaniasis - can occur during Rx for kala azar or up to 20yrs later
seen in africa and asia esp sudan not in new world
resembles diffuse cutaneous leishmaniasis - skin coloured papules or nodules, hypopigmented macules and malar erythema

115
Q

T/F

dual infection with leishmaniasis and another infection is unusual

A

False
not uncommon
lesions can have secondary bacterial or viral infection
pts may have 2 species of leishmania at once
may also have TB, leprosy or other mycobacterial infection

116
Q

T/F

L donovani is a common cause of visceral leishmaniasis

A

True

also L infantum in old world and L chagasi in new world

117
Q

What is the diagnostic finding in tissue smears or biopsy specimens for leishmaniasis?

A

Amastigotes in dermal macrophages known as

Leishman-Donovan bodies

118
Q

T/F

PCR is most sensitive tool for diagnosing cutaneous leishmaniasis

A

True

119
Q

T/F

leishmaniasis serology is useful for diagnosing cutaneous disease

A

False
useful for visceral disease
but cross reacts with Chagas disease

120
Q

T/F

multiple diagnostic methods are recommended when investigating for cutaneous leishmaniasis

A 
True
take biopsy across edge of new lesion
divide and use portions for;
histo w/ special stains
smear on glass slide - giemsa stain
culture - Nicolle-Navy-MacNeal medium
PCR
121
Q

Whats special stains are used for histology for leishmaniasis?

A

Giemsa, Wright and Feulgen

122
Q

T/F

topical and physical therapy are useful for cutaneous leishmaniasis

A

True
esp old world as resource poor and good cure rates with these modalities
topical 15%paromycin + 12%methylbenzethonium chloride daily for 20 days has 76% cure rate
can use topical paromycin alone or with gentamicin
immiquimod
topical amphotericin B
intralesionals; sodium stibogluconate, meglumine antimoniate or pentamidine
LN2 cryo
CO2 slush Rx
radiofrequency heat Rx

123
Q

In which leishamniasis pts should systemic therapy be used?

A

lesions likely to heal with disfiguring scars
hand sores or those on lower legs or over joints
lesions >4cm
multiple lesions
mucocutaneous leishmaniasis/lesions
immunosuppressed pts
infections due to l braziliensis or panamensis

124
Q

T/F

pentavalent antimonials are 1st line for new world leishmaniasis

A

True

esp IM/IV sodium stibogluconate for 2-3 weeks

125
Q

Aside from antimonials what systemic Rx is used for leishmaniasis?

A

miltefosine
itraconazole
allopurinol
others

126
Q

T/F

after recovery from leishmaniasis pts are completely immune to future infections

A

False

only immune to reinfection with same species

127
Q

T/F

mosy nets and window screens are effective at preventing sand fly bites

A

False

128
Q

What is the treatment of strongyloides stercoralis?

A

Ivermectin - second dose 1-2 weeks after first
albendazole is an alternative but less effective
for hyperinfection give ivermectin daily until symptoms resolve

129
Q

T/F

Praziquantel is the treatment for all trematode infections

A

False

all except fascioliasis - treated with triclabendazole

130
Q

T/F

kala azar is systemic schistosomiasis

A

False

kala azar is systemic leishmaniasis

131
Q

T/F

Bilharziasis is schistosomiasis

A

True

same thing

132
Q

what organism is responsible for schistosomiasis?

A

The schistosoma sp of trematode

S mansoni, japonicum or haematobium

133
Q

T/F

schistosomiasis is the most prevalent trematode infection worldwide

A

True

second most important tropical disease after malaria in terms of public health problem

134
Q

T/F

free swimming cercariae of schistosomiasis live in salt water in endemic regions

A

False
fresh water
endemic in >60 countries

135
Q

T/F

schistosome worms live in the biliary tree

A

False

mature in the portal vessels and lay eggs in pelvic veins

136
Q

T/F

adult schistosoma worms replicate in the vessels of the human GI tract

A

False lay eggs here but these disseminate so do not replicate there

137
Q

T/F

the first stage of schistosomal infection is the same as swimmers itch

A

True
the cercariae enter the skin in the same way but in schistosomiasis they go on to establish infection. In swimmers itch due to cercariae of non-human flukes the larvae die and symptoms resolve (may be a flare in symptoms as larvae die)

138
Q

What is katayama fever?

A

Acute schistosomiasis
onset 2-8 weeks after penetration of larvae
lasts 4-6 weeks
fever, chills, headache, abdo cramps, diarrhoea, arthralgia
may be hepatosplenomegally
may be purpura or urticaria and oedema of extremeties, genitals and trunk

139
Q

What is bilharziasis cutanea tarda?

A

skin lesions in pts with chronic visceral schistosomiasis
granulomatous-looking infiltrated plaques and fistulous tracts esp in groin and perineal region
lesions can resemble warts, condylomata lata or bowenoid papulosis
rarely truncal lesions

140
Q

How is schistosomiasis diagnosed?

A

stool and urine test for ova
serology for anti-schistosomal Abs
plasma schistosomal antigen blood test
skin biopsy of cutaneous lesions - ova and surrounding granulomatous inflammation
also - eosinophilia, high ESR, deranged LFTs in acute infection

141
Q

T/F

prednisolone is given in katayama fever

A

True

along with praziquantel

142
Q 
T/F
swimmers itch (cercarial dermatitis) can be acquired from fresh or salt water
A

True
fresh water type common in many parts of world - avian spp
salt water avian sp seen on atlantic coast of USA
other type is fresh water mammalian spp - usual host is water buffalo

143
Q

T/F

the skin signs of both echinococcosis and cystericosis are firm, painless subcutaneous swellings

A

True
1-2cm
although skin involvement rare in both cases

144
Q

T/F

imaging of the brain is important in pork tapeworm infection

A

True
Taenia solium - cystericosis
treatment not necessary for skin disease but need MRI brain and if CNS disease need praziquantel and steroids

145
Q

T/F

trichomonal vaginosis is a common protozoal infection

A

True
organism is called Trichomonas vaginalis
infection is called trichomoniasis or trichomonal vaginosis

146
Q

T/F

trichomonal vaginosis is treated with azithromycin

A

False

metronidazole

147
Q

What are the types of trypansomiasis?

A

African = sleeping sickness; Trypansoma gambiense

american (south american) = Chagas disease; trypansoma cruzi

148
Q

T/F

american trypansomiasis has more cutaneous features than african type

A

False
african type more
get chancre at bite site within days; heals in weeks
followed by acute disease with fever, oedema and rash/urticaria - if invades CNS get coma and death

Medical dermatology Dan (41 decks)

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