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Dermatology Board Prep > DERM (11) Infections, Infestations, and Bites > Protozoa and Worms > Flashcards

Protozoa and Worms Flashcards

1
Q

What type of organism are the Leishmania species?

A

Obligate intracellular

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2
Q

What two forms do the Leishmania species exist in?

A

Promastigote (long-elongated flagellated infective form that gets transmitted with bite) and amastigote (protist cell that has no visible external flagella or cilia and is intracellular. replication occurs)

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3
Q

What is the vector of leishmania species?

A

Sandfly

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4
Q

What are the reservoirs of leishmaniasis?

A

Rodents and canines

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5
Q

What is the pathogenesis of leishmaniasis?

A

Within the gut of the sandy the organism proliferate and turn into the flagellated promastigotes, then when the sandfly bites a human these then are transferred. Then the histocytes engulf these promastigotes and then they transform into amastigotes and multiply inside of macrophages. Clinical signs of leishmaniasis develop after weeks to months/years later

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6
Q

What are the old world leishmaniasis organisms and what is their vector?

A

L. major, L. tropica>L. aethiopica, L. infantum, and others

Vector: Phlebotomus sandflies

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7
Q

What are the new world leishmaniasis organisms and what is their vector?

A

L. mexicana, L. braziliensis, L. amazonensis, and others

Vectors: Lutzomyia sandflies

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8
Q

What other diseases are spread by lutzomyia sand flies?

A

Vector for B. Bacilliformis (verruga peruana, Carrion disease, Bartonellosis, Oroya fever

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9
Q

What are the 4 clinical classifications of leishmaniasis?

A
  1. Cutaneous
  2. Diffuse cutaneous
  3. Mucocutaneous
  4. Visceral
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10
Q

What are the most common causes of old world cutaneous leishmaniasis?

A

More common in old world (90% occur in Middle East, Brazil and Peru)

L. Major, L. Tropica (>L. infantum)

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11
Q

Clinical appearance of cutaneous old world leishmaniasis?

A

It begins as a solitary, small, erythematous edematous nodule at the bite site (usually exposed skin sites – arms face, legs) that ulcerates or becomes verrucous. It can later develop sporotrichoid like spread and with satellite lymphatic nodules and lymphangitis.

It does heal with scarring over months to years

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12
Q

Most common causes of new world cutaneous leishmaniasis?

A

L. Mexicana (>l. braziliensis)

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13
Q

What is the clinical presentation of new world cutaneous leishmaniasis?

A

Can have a more varied presentation than old world cutaneous. Ulcerations (chiclero ulcer = ear lesion in workers who harvest chicle gum in the forest), impetigo appearing lichenoid, sarcoid-like vegetating miliary and nodular

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14
Q

What are the most common organisms involved diffuse cutaneous leishmaniasis?

A

More widespread cutaneous lesions; usually arises in immunosuppressed pts

  • L. amazonesis (americas), L. aethiopica (Africa)
  • Can look like multiple keloidal lesions of the face, especially can be prominent on the nose and the extremities
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15
Q

Most common organisms associated with mucocutaneous leishmaniasis?

A

Almost always New World leishmaniasis: L. braziliensis (>L. amazonesis, L. panamenis, and L. guyanesis

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16
Q

Clinical presentation of diffuse cutaneous leishmaniasis?

A

More widespread cutaneous lesions; usually arises in immunosuppressed pts

  • L. amazonesis (americas), L. aethiopica (Africa)
  • Can look like multiple keloidal lesions of the face, especially can be prominent on the nose and the extremities
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17
Q

Clinical presentation of mucocutaneous leishmaniasis?

A

Presents w/ lip, nose, and oropharyngeal infiltration and ulceration.

  • Leads to the destruction of the nasopharyngeal area (airway obstruction, mutilation of mouth and perforation of nasal septum which gives the “tapir face”
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18
Q

What are the most common organisms to cause visceral leishmaniasis?

A

Due to systemic infection of bone marrow liver, spleen; Old World > New World; long incubation time months to years

L. donovani (India, Sudan, Bangladesh; most common cause in adults), L. infantum (Europe often a/w HIV), L. Chagasi

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19
Q

What is the clinical presentation of visceral leishmaniasis?

A

Fever, weight loss, diarrhea, abdominal tenderness, LAD, hepatosplenomegaly, nephritis, intestinal hemorrhage, and death in 2 years if not treated

specific skin findings: papules, ulcers at the bite site, then they can have non-specific purpura, hyperpigmentation (that’s why it is called black fever), kwashiorkor changes (brittle hair)

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20
Q

What are the skin lesions that can occur after visceral leishmaniasis?

A

Post-kala-azar dermal leishmaniasis: this is a new-onset cutaneous leishmaniasis that arises in up to 20 years after recovery from untreated viscera leishmaniasis

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21
Q

What is the best test for leishmaniasis?

A

PCR

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22
Q

What culture medium is needed for leishmaniasis?

A

Novy-McNeal-Nicolle medium

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23
Q

Key histologic findings in leishmaniasis?

A

Amastigotes w/ kinetoplasts are arrayed around periphery of parasitized histocyte cytoplasm forming the marquee sign organisms are best seen on Giemsa

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24
Q

What are some important characteristics of the Montenegro delayed-skin reaction test?

A

It is positive in most cutaneous leishmaniasis, remains + after cure and is importantly falsely negative in the first (febrile) phase of visceral leishmanisis

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25
Q

What is the prognosis of leischmaniasis?

A

Old World cutaneous: self resolves in 15 months

New World cutaneous: If L. mexicana self-resolves in 75% ; mucocutaneous lishmanisis form L. braziliensis and L. panamensis does not self-resolve and requires treatment

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26
Q

What is the treatment for leishmaniasis and when should it be given?

A

Treat severe/widespread, mucocutaneous or to decrease scarring

  • Tx with pentavalent antimony or amphotericin B for visceral leishmaniasis
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27
Q

What organisms cause the African trypanosomiasis and what is the vector?

A

T. brucei gambiense (west Africa)/ T. Brucei rhodesiense (East Africa)

Vector is Tsetse fly (glossina)

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28
Q

What is the earliest cutaneous sign of African trypanosomiasis?

A

local pruritic inflammatory reaction at site of inoculation, then in 48 hrs you get local lymphadenopathy and ulceration which then forms the eschar

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29
Q

What is the clinical presentation of African trypanosomiasis?

A

fever, headache, and joint pain at irregular intervals

  • Winterbottom’s sign is important: posterior cervical LAD which in 2-3 weeks turns to trypanids (erythematous urticarial or macular diffuse eruptions [6-8 weeks] then later you get the neurologic changes and Kerandel’s deep delayed hyperesthesia, daytime sleepiness (late-stage)
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30
Q

What are the timecourses of the two types of African trypanosomiasis?

A

East African type: progressive over weeks to months

  • West African type: progressive over months to years
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31
Q

Treatment for African Trypanosomiasis?

A

Suramin or pentamidine if early, melarsoprol or eflornithine if there is CNS involvement

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32
Q

What organism causes the American trypanosomiasis (Chagas disease)?

A

T. Cruzi

33
Q

What is the vector of the T. cruzi organism?

A

Triatomine bug (Reduviidae) in central and south America

34
Q

What is the clinical presentation of the American trypanosomiasis?

A

Key is a local inflammatory lesion that is often on the face which represents the entry site (Chagas). This can lead to Romanña’s sign which is unilateral eyelid edema and conjunctivitis at the site of inoculation. This gives sway to unilateral painless palpebral edema

later you can get heart, esophagus, and intestinal enlargement

35
Q

What is the treatment for American Trypanosomiasis?

A

Benznidazole and nifurtimox

36
Q

What organism causes toxoplasmosis?

A

Toxoplasma gondii

37
Q

What is the vector for toxoplasmosis?

A

Intestinal parasite of cats, but also infects dogs and rabbits

38
Q

What is the cutaneous presentation of toxoplasmosis?

A

Hemorrhagic or necrotic papules

  • Acquired dz can occur in pregnant patients and immunocompromised
  • Congenital dz is one of the TORCH organisms
39
Q

What is the treatment for toxoplasmosis?

A

Sulfadiazine and pyrimethamine

40
Q

What is the most common organism that causes cutaneous larva migrans?

A

Ancylostoma brasiliense, also less commonly anyclostoma caninum

41
Q

What is the clinical presentation of cutaneous larva migrans?

A

Erythematous serpiginous cutaneous eruption (usually on feet) as a result of larva penetrating intact epidermis

42
Q

Can cutaneous larva migrans cause systemic disease?

A

No! organisms penetrate into the epidermis but are unable to penetrate human basement membrane zone (therefore unable to cause systemic dz)

43
Q

How quickly does cutaneous larva migrans move?

A

1-2cm/day

44
Q

What is the treatment for cutaneous larva migrans?

A

Albendazole, ivermectin, topical/oral thiabendazole and liquid nitrogen

45
Q

What is larva currens and how is it different from cutaneous larva migrans?

A

Caused by Strongyloides stercoralis

  • It moves faster than cutaneous larva migrans (5-10cm/hr)
  • It is often on different places: indurated serpiginous papule on buttocks/groin
  • Unlike cutaneous larva migrans, larva currens can go systemic. In this cause, patients can get periumbilical (thumbprint) purpura and petechiae on trunk/proximal extremities
46
Q

What is Loeffler’s syndrome?

A

Chronic strongyloidiasis (affects lungs and GI tract; eosinophilia)

47
Q

How can one get larva currens?

A

Contact w/ affect soil (sitting on beach, etc)

48
Q

How do you treat larva currens?

A

Ivermectin or thiabendazole

49
Q

What organism causes onchocerciasis (River Blindness)?

A

Onchocerca volvulus

50
Q

What ist the vector for onchocerciasis and what else does it cause?

A

The Simulium fly (black fly)

It also is the vector for tularemia and has been implicated in causing fogo selvagem.

  • It is present near fast-flowing rivers
51
Q

What places are associated with having the Simulium fly (Black fly) and the associated diseases?

A

Sub-Saharan Africa, South America, and Yemen

52
Q

What is the clinical presentation of onchocerciasis?

A

Pruritic papules (these can be acute, chronic or lichenified) and then this evolves into leopard skin which is depigmentation and atrophy); nodules (onchocercomas over boney prominences, may develop Mazzotti reaction if given diethylcarbamazine

53
Q

What is the mazzotti reaction?

A

Can be life-threatening, characterized by fever, urticaria, swollen and tender lymph nodes, tachycardia, hypotension, arthralgias, edema and abdominal pain that occurs within a week of treatment

54
Q

What is the treatment for onchocerciasis?

A

Ivermectin (treatment of choice), trials underway for doxycycline as it can kill the symbiotic Wolbachia bacteria that come with the organism. Other choice can be surgical excision

55
Q

What is the organism that causes Loiasis?

A

Loa Loa

56
Q

What is the vector for Loa Loa?

A

Chrysops (mango/deer flies; also transit tularemia)

57
Q

Where does loiasis occur?

A

West and central Africa

58
Q

Clinical presentation of Loiasis?

A

Calabar swellings (recurrent migratory focal angioedema on limbs); visible migration of adult worm across eye

59
Q

What is the treatment for loiasis?

A

diethylcarbamazine

60
Q

What are the organisms that cause filariasis?

A

Brugia malayi/timori and Wuchereria bancrofti

61
Q

What are the vectors for filariasis?

A

Mosquito species Culex (also does West Nile virus), Aedes (also vector for chikungunya and dengue and yellow fever) and Anopheles (malaria and yellow fever)

62
Q

What are the clinical presentations of filariasis?

A

Acute: lymphangitis

Chronic: granulomatous reaction in lymphatics leads to lymphedema

63
Q

What is the treatment for filariasis?

A

Diethylcarbamazine

64
Q

What is the difference between swimmers itch and seabather’s eruption?

A

Swimmer’s itch: From freshwater, caused by Schistosoma during the cercarial stage and the lesions occur on uncovered skin in 10-15 hrs after exposure

  • Sea bather’s eruption: Saltwater, causes from Edwarsiella lineata (sea anemone) and lunhce unguiculata (thimble jellyfish) during the larval stage. Occurs in the southern US and Caribbean saltwater and lesions occur on covered areas (bathing suit areas)
65
Q

What organism causes trichinosis?

A

Trichinella spiralis

66
Q

What are the vectors of trichinosis?

A

Pigs, which are then eaten undercooked (undercooked bears is a less common cause)

67
Q

What is the pathogenesis of trichinosis?

A

Humans eat animal meat (muscle) that has larval cysts, then these encyst in the Gi tract and mature into adult organisms, then reproduction occurs and the larvae are produced and these migrate from the GI tract and ecycyst in skeletal muscle

68
Q

Clinical presentation of trichinosis?

A

Primary cutaneous manifestation is bilateral periorbital edema from the type I allergic reaction and petechiae during parasite migration (especially splinter hemorrhages

69
Q

How is the diagnosis of trichinosis made?

A

Elevated IgE can be a clue, a muscle biopsy is diagnostic.

Note: the IgE can be elevated for yrs after treatment

70
Q

What is the treatment for trichinosis?

A

Mebendazole or albendazole and you can use systemic steroids for moderate to severe hypersensitivityreactions

71
Q

What organism causes dracunculiasis?

A

Dranunculus medinensis

72
Q

What is the vector for dracunculiasis?

A

Cyclops water flea at copepod stage

73
Q

What is the clinical presentation of dracunculiasis?

A

Nodules and ulcers on the lower extremity

  • After ingesting the infected cyclops, the organism travels from intestines to subcutaneous tissue and then the adult worms emerge from lesion when reexposed to water
74
Q

Treatment for dracunculiasis?

A

Removal of the worm, wound care, and metronidazole

75
Q

What are the 4 main amoebas causing disease?

A

Acanthamoeba, Balamuthia, Naegleria and entamoeba histolytic

76
Q

What skin conditions can occur as a result of acanthamoeba?

A

Subacute granulomatous amebic encephalitis –> chronic ulcers

77
Q

What is the clinical presentation of Balamuthia disease?

A

Painless, red and granulomatous plaque on central face over trunk or extremities which precedes the CNS involvement

78
Q

What cutaneous findings can be seen in entamoeba histolytica?

A

Cutaneous lesions in the perianal region form GI involvement. Can also be sexually transmitted with a painful ulcerating erythematous plaque

usual involvement in amebic colitis and/or liver/lung involvement

DERM (11) Infections, Infestations, and Bites (13 decks)

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