Leishmaniasis / Toxoplasmosis / Trypanosomiasis Flashcards Preview

Parasitology/Virology > Leishmaniasis / Toxoplasmosis / Trypanosomiasis > Flashcards

Flashcards in Leishmaniasis / Toxoplasmosis / Trypanosomiasis Deck (34)
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1
Q

What is the definitive host of Toxoplasma gondii?

A

Cats

2
Q

How long is someone infected with Toxoplasma gondii?

A

Lifelong

3
Q

Who will present with Toxoplasma gondii infection?

A

Most people are asymptomatic

Disease manifests in immunocompromised or neonates infected in utero

4
Q

What are the 3 stages of the life cycle of Toxoplasma gondii?

A

Oocysts - excreted in feces of cats (definitive host)
Tissue cysts - intracellularly in muscle of intermediate hosts
Tachyzoites - replicate within cells

5
Q

What are modes of transmission of toxoplasmosis?

A

Oocysts - soil, cat litter
Tissue cysts - undercooked meat (espec pork and lamb)
Tachyzoites - transplacentally, transplant, transfusion

6
Q

In what environment is toxoplasmosis common?

A

Places where meat is undercooked (steak tartar, pork)

7
Q

How does toxoplasmosis present in healthy host?

A

Acute infection - tachyzoites
- Usually asymptomatic, occasionally lymphadenopathy

Chronic infection - tissue cysts
- Asymptomatic, lifelong

8
Q

How does toxoplasmosis present in immunocompromised host?

A
Usually reactivated infection
Cerebral infection (lesions) more common than cardiac or pulmonary
9
Q

How does toxoplasmosis present in pregnancy?

A

Maternal infection early in pregnancy can cause miscarriage, abortion, severe neurological or ocular disease, generalized illness

Most congenitally infected infants are asymptomatic at birth but high risk for sequelae later in life

10
Q

What is the presentation of ocular toxoplasmosis?

A

Common sequela of congenital toxoplasmosis

Focal necrotizing retinitis
Granulomatous inflammation of choroid
Blurred vision, pain
Focal scars with permanent loss of vision

11
Q

How is toxoplasmosis diagnosed?

A

Serology
Appearance of lesions on MRI or CT
Atypical: brain biopsy

12
Q

What is the treatment of choice for toxoplasmosis?

A

Pyrimethamine + sulfadiazine

13
Q

How can toxoplasmosis be managed in pregnancy?

A

Spiramycin

14
Q

How can toxoplasmosis be prevented?

A

Get rid of cat or change litter better

For HIV-infected <200 CD4 - TMP-SMX preventive therapy

15
Q

What is the agent of Chagas disease?

A

Trypanosoma cruzi

16
Q

What is the vector of Chagas disease?

A

Riduviid bugs

17
Q

How is Chagas disease transmitted?

A

Vector borne - riduviid bug takes blood meal and defecates, rub feces into bite wound
Transplacental, transfusion, transplantation
Oral (unusual)

18
Q

What is the life cycle of Trypanosoma cruzi?

A

Riduviid bug takes blood meal and defecates
Rub bite and innoculate parasite into wound
Goes through circulation to muscle, tryptomastigotes invade cells
Differentiates into amastigote and replicates
Amastigotes become trypomastigotes and rupture cell, enter blood stream

19
Q

What is the clinical presentation of acute T. cruzi infection (acute Chagas disease)?

A

Usually asymptomatic
Mononucleosis-like febrile illness
Rarely - acute myocarditis (see amastigotes in cardiac myocytes), meningoencephalitis

20
Q

What is the clinical presentation of chronic T. cruzi infection (chronic Chagas disease)?

A

Usually asymptomatic
Cardiomyopathy (destruction of cardiomyocytes and replaced with fibrotic tissue) - can get arrhythmias and complete heart block
GI disease - megaesophagus, megacolon

21
Q

How is Chagas disease diagnosed?

A

Direct visualization of parasites in blood

Serology (IgG for chronic/past infection, IgM suggests acute)

22
Q

What is the treatment for Chagas disease?

A

Nifurtimox

Benznidazole

23
Q

What is the vector for Leishmania?

A

Sand fly

24
Q

What is the life cycle of Leishmania?

A

Sand fly takes blood meal, innoculates parasite into skin
Promastigote stage ingested by macrophage
Multiplies and transforms into amastigotes inside macrophages
Sand fly takes another blood meal and ingests macrophages containing amastigotes

25
Q

What immune response is required to control Leishmaniasis?

A

Cellular

26
Q

What immune response dominates in visceral leishmaniasis?

A

Only humoral, no cellular (cannot control parasite well with just antibodies)

27
Q

What immune response dominates in treated visceral, cutaneous, or mucosal leishmaniasis?

A

Cellular

28
Q

What is the clinical presentation of visceral leishmaniasis (kala-azar)?

A

Hepatosplenomegaly (parasites in macrophages, macrophages building up)
Spiking fevers

29
Q

What is the clinical presentation of mucosal leishmaniasis?

A

Almost all Leishmaniasis braziliensis
Lesions on nose
Immunological hyperreactivity but failure to clear parasites

30
Q

What is the clinical presentation of disseminated leishmaniasis?

A

Lack of immunological reactivity

Get lesions filled with parasites

31
Q

What is the clinical presentation of cutaneous leishmaniasis?

A

Small lesions on skin

See cells filled with amastigotes on histology

32
Q

How is the diagnosis for visceral Leishmaniasis made?

A

Smears, cultures, PCR
Serological tests
Leshmanin skin test negative

33
Q

How is the diagnosis for cutaneous Leishmaniasis made?

A

Smears, cultures, PCR
Sological tests
Leishmanin skin test positive

34
Q

What is the treatment for Leishmaniasis?

A

Pentavalent antimony - Sodium stibogluconate (but very toxic)
Liposomal ampho B (treatment of choice in US)
Miltefosine (recently approved)