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Tissue protozoans (including leish) Flashcards

1
Q

Leish vector: New world v. old world

A

Lutzomyia -new, phlebotomus -old

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2
Q

DCL v. DSL

A

Diffuse (no use) cutaneous leish: L amazonensis, mexicana, aethiopca; massive/abundant in smear, negative skin test, NEVER ulcerates, lepromatous lesions, very chronic, NO mucosal involvement

DSL: DISSEMinated: L braziliensis, L mexicana, Scanty/rare in the smear, strongly positive, frequent ulceration, acneiform, frequent mucosal involvement

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3
Q

Leishmania infective stage

A

promastigote

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4
Q
A

leish, promastigote

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5
Q
A

amastigote of leish (diagnostic stage)

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6
Q

Difference between T Cruzi and T brucei

A
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7
Q

Trypanosoma Cruzi Life cycle

A

Triatomine bug takes a blood meal–>metacyclic trypomastigotes penetrate the various cells at bite wound site and transform to amastigotes–>amastigotes multiply in infected tissues–>transform into trypomastigotes–>triatomine bug takes the blood meal–epimastigotes in the midgut–>multiply in midgut–>metacyclic trypomastigotes in hindgut

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8
Q

Toxoplasma gondii Infective stage, diagnostic stage, modes of transmission

A

Infective: Bradyzoites, mature oocysts with sporozoites, tachyzoites;
Diagnostic stage: tissue cysts with bradyzoites, tachyzoites
Modes of transmission: undercooked meat, contaminated food/water with cat, blood transfusion, organ transplant, transplacenta

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9
Q
A

Toxoplasma gondii tachyzoite

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10
Q
A

toxoplasma gondii bradyzoite (usually spherical in the brain, more elongated in cardiac/skeletal muscles)

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11
Q

Naegleria Fowleri infective and diagnostic stage

A

Infective: trophozoites
Diagnostic: trophozoites

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12
Q

primary amebic meningoencephalitis

A

naegleria fowleri

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13
Q
A

Naegleria Fowleri-large single nucleus with large dense karyosome

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14
Q

Acanthamoeba infective and diagnostic stage

A

I: Trophozoites
D: Trophozoites, cysts

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15
Q

granulomatous amebic encephalitis, keratitis

A

acanthomoeba

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16
Q
A

acanthamoeba trophozoite

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17
Q
A

acanthamoeba cyst

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18
Q

Granulomatous amebic encephalitis

A

Balamuthia Mandrillaris

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19
Q
A

Balamuthia Mandrillaris (pleomorphic, long/slender pseudopodia, large single nucleus)

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20
Q
A

balamuthia mandrillaris cyst

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21
Q

starts as pink colored papule, enlarges and develops into a nodule or plaque with central softening, painless ulceration with indurated border

A

localized cutaneous leishmaniasis

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22
Q
A

leish

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23
Q

Disseminated cutaneous leishmaniasis caused by

A

braziliensis, guyanensis, mexicana-several lesions

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24
Q

diffuse cutaneous leish

A

caused by aethiopica, mexicana, amazonensis; localized lesion, does not ulcerate; they have a low immune response

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25
Q

mucosal leishmaniasis caused by

A

LV Braziliensis, LV Guyanensis, LV Panamensis, LL Amoazonensis

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26
Q

how to diagnose leish

A

immunological test with the skin test; elisa
or direct smear

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27
Q

How to treat LCL

A

Antimony for 20 days, Amph B, Miltefosine

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28
Q

what are the 3 evolutive forms of t cruzi

A

amastigote: ONLY in tissues, Epimastigote: ONLY in intestine of the vector, trypomastigote: posterior intestine of the vector and in the blood of the reservoirs

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29
Q

3 types of vector

A

rhodnius prolixus, triatoma infestans, panstrongylus megistus

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30
Q

how to transmit t cruzi

A

vectors
Blood transfusion, mother to child, oral route (Acai) lab accident

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31
Q

What are the phases of T cruzi infection and how can you measure for it

A

1-2 weeks: Acute phase-romana sign, chagoma: Positive smear, culture, PCR
4-8 weeks: Chronic phase: negative smear but positive PCR/serology
Indeterminate form: asymptomatic–>can progress ot the determinate form over the next several years

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32
Q

RBBB in a person from endemic region of Tcruzi

A

Chagas cardiomyopathy

33
Q

how to treat pregnant women for chagas

A

You don’t-its all about detecting congenital chagas first, then treating baby with beznidazole or nifurtimox

34
Q

in acute chagas, can you breast feed

A

trypomastigotes have been detected in milk in this stage-so recommend against

35
Q

Treatment of chagas

A

Beznidazole and Nifurtimox

36
Q

3 ways to control chagas disease

A

insecticides, housing improvement, sanitary education

37
Q
A

Trypanosoma brucei gambiense
Trypanosoma brucei rhodesiensee

38
Q

Vector of aftrican sleeping sickness

A

glossina spp: tsetse fly

39
Q

What is the life cycle of glossina

A

tsetse flies suck blood q3-4 days; some of hte parasites (1%) transform in procyclic (midgut) and then metacyclic trypomastigotes (salivary gland). TseTse become infectious 2-3 weeks after blood meal

40
Q

TB Gambiense epidemic mostly where

A

Central and West AFrica

41
Q

painful, erysepilas presentation

A

Tb Rhodesiense

42
Q

37year old man with fever, Hepatosplenomegaly and cutaneous foot lesion after a trip to africa

A

T. B. Rhodesiense (trypanosomal chancre)

43
Q

low grade fever, winterbottom sign, edema (face), malnutrition, pruriritis (rash)

A

Tb Gambiense

44
Q

Winterbottom sign

A

posterior cervical LAD-Tb Gambiense

45
Q

Acute high fever, LAD, edema, rash, petechiae, multiorgan failure

A

Tb rhodesiense

46
Q

patient from Africa

A

Winterbottom sign-Tb gambiense

47
Q

What are the late states of African Sleep sickness

A

Both Tb gambiense and Tb rhodesiense can go to meningoencephalitic stage (gambiense is usuallly more frequent)

48
Q

How to diagnose T b gambiense and T b rhodensience

A

LP: Presence of Tryps in CSF AND PResence of 5 leukocytpes

49
Q

what is the big difference between trypanasoma brucei gambiense and trypanosoma brucei rhodesiense

A

TB Grambiense: Slow progressing neurological disease
TB Rhodesiense is mainly an acute systemic febrile illness

50
Q

How to diagnose Tb Gambiense:

A

screening with serology; confirm with parasitological blood smeaer, lymph node aspiration, CSF

51
Q

how to diagnose Tb Rhodesiense

A

blood smear

52
Q

What are the screening tools of gambiense int he field

A

-card agglutination trypanasoma test -CATT
-Lateral flow immunochromatographic assay

53
Q

What is the best diagnostic test of gambiense?

A

Mini-Anion exchange centrifugation-concentration methods (85%)

Microhematocrit centrifugation concentration method (60%)

LN Aspiration (40%)

Blood smeear (25-30%)

54
Q

Who (in non endemic settings) gets Tb Rhodesiense?

A

Almost exclusively toursists-from tanzania, malawi, zambia

55
Q

Who (in non endemic populations) gets tb gambiense

A

mostly migrants (from DRC, Gabon, Angola)

56
Q

What are the available treatments for african sleeping sickness

A

pentamidine, or suramin, or melarsoprol, or eflornithine
+ fexinidazole

57
Q

What can we treat with Pentamidine-what are the side effects

A

Efficacious in Tb Gambiense HAT
No good CNS penetration
SEs: Painful intramuscular administration, hypoglycemia, hypotension, cardiac arrythmia

58
Q

What is NECT

A

nifurtimox-eflornithine combination tehrapy0good for second stage african trypanosoma brucei gambiense

59
Q

WHO guideline to treat patients with first stage gambiense HAT:

A

Fexinidazole

60
Q

Patients with 2nd stage gambiense HAT if CSF <100 WBC

A

fexinidazole

61
Q

Patients with second stage gambiense HAT if CSF >100 WBC

A

Nifurtimox-eflomithine combination therapy

62
Q

What is the follow up for gambiense-HAT

A

Minimal 2 years; LP every 6 months for second stage; cure if WBC<5, Relapse if tryp or WBC>50

63
Q

How to treat rhodesiense first stage HAT treatment? What are the side effects?

A

Suramin-proteinuria, exfoliative dermatitis, mazotti (if onchocerciasis)

64
Q

second stage of rhodesiense treatment? Side effects?

A

suramin + melarsoprol + prednisolone ; very toxic (encephalitis)

65
Q

types of visceral leish

A

L dovanni, L Archibaldi, L Chagasi, L Donovani, L Infantum

66
Q

What is the difference between L infantum/chagasi and L donovani

A

Infantum/chagasi: Animal reservoir (dogs) -latin america, asia, mediterranean
L Donovani: Human reservoir (indian subcontinent, east africa)

67
Q

Clinical manifestations of Visceral Leish

A

Fever, slenomegaly, hepatomegaly, LAD, cachexia, hyperpigmentation

68
Q

Complications of visceral leish

A

malnutrition, symptomatic anemia, superinfections, petechial rash
*if untreated, lethal

69
Q

Description of Post-Kala Azar Dermal Leishmaniasis

A

pale spots, painless nodules on the face, thorax, arms, legs, and then genitals
(very common in Africa, not as much in India)

70
Q

fever >2 weeks, splenomegaly or weight loss with pnacytopenia. What is your clinical suspicion?

A

Visceral Leishmaniasia

71
Q

How to diagnose VL

A

parasitological diagnosis, Serology, Urine antigen, Molecular

72
Q

What ist he highest sensitivity for parasite detection in VL?

A

Spleen
Then bone marrow
Then LN (Low sensitivity)

73
Q

From spleen aspirate

A

extracellular amastigotes

74
Q

what is the specific RDT for visceral leish

A

rK38 RDT (especially in INdia)

75
Q

What is the treatment of VL?

A

Pentavalent antimonials x 30 days
Paromomycin 21 days
Amphotericin B
Miltefosine

76
Q

What is toxicity of pentavalent antimonials

A

cardiac, pancreatitis, liver, renal
*Resistant in India

77
Q

PKDL Treatment

A

Antimonials /liposomal amphotericin in E Africa
Amph B/Miltefosine (India)-same tx but longer

78
Q

how to prevent relapse in VL + HIV patients

A

secondary ppx with pentamidine

Tropical Medicine (19 decks)

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