Lecture 71 - Leishmaniasis, Toxoplasmosis, and Trypanosomiasis Flashcards

1
Q

toxoplasma Gondii
- what kind of parasite is it?
- what is the definitive host?
-

A

Single celled protozoa

Cats are the definitive host

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2
Q

what are the forms of the Toxoplamsma Gondii?

  • which are infective?
  • which are diagnositic?
  • describe the transmission?
A

Oocysts — infective form which is excreted in feces; fecal oral transmission; contaminated soil, vegetables, water, cat litter

Tissue Cysts – infective form which forms intracellularly in muscle and brain. Can be acquired from eating undercooked pork, lamb

Tachyzoites – the diagnostic stage–localized in brain and muscle tissue. Develop into tissue cyst bradyzoites. Can be transmitted transplacentally, blood tranfusions

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3
Q

What are the different disease forms of Toxoplasmosis

A

Acute Acquired Toxoplasmosis (tachyzoites)

chronic toxoplasmosis – (Bradyzoites)

Reactivated infections

Congenital Toxoplasmosis

Ocular Toxoplasmosis

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4
Q

Compare acute vs chronic toxoplasmosis

A

Acute – Tachyzoites infection
Usually subclinical – asymptomatic
may present with LAD, myalgias
Symptoms more common in immunocompromised
Disease is contained by Th1 response; leads to chronic cystic state

Chronic state – Bradyzoites:
Asymptomatic, lifelong infection
Cysts form in brain and neural tissue
source of reactivation

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5
Q

Congential Toxoplasmosis

    • when would a child become infected?
  • -what are the outcomes of severe infection?
  • -outcomes for most infants?
A

Child infected if the mother becomes infected during gestation

Severe infection – miscarriage, neurological disease, ocular disease, generalized illness (HSM, LAD, Fever)

most – asymptomatic at birth but can have manifestations of occular or cerebral disease later in life

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6
Q

Occular Toxoplasmosis

  • peak age of incidence
  • symptoms and manifesations
A

Peak age of incidce – 20s, 30s from post acute or reactivated disease

Focal necrotizing retinitis; granulomatous inflammation, blurred vision.
Focal scarring can lead to permanent vision loss

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7
Q

Other manifestations of toxoplasmosis, for example in the immunocompromised

A

The disease can remain latent.
Tropism for brain and muscle tissue

Can manifest as cerebral disease, such as encephalaitis

Some association with schizophrenia

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8
Q

Diagnosis of Toxoplasmosis:

  • Serologic: acute, chronic inactive, immunodeficient active
  • what do you do for cerebral toxoplasmosis?
A

Serologic Profiles;
Acute – IgM + rising IgG
Chronic inactive – no IgM, + IgG
immunodef active – no IgM, +IgG

Other: Cerebral toxoplasmosis
- Imaging, brain bx

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9
Q

Treatment of Toxoplasmosis:

what is the treatment regimen for toxo during pregnancy

A

Regimen: Pyrimethamine + Sulfadiazine
(Leukovorin is always given with pyrimethamine)

Pregnancy:
Spiramycine

If Fetus infected:
terminate pregnancy or treat with Pyrimethamine + Sulfadiazine + leucovorin

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10
Q

Prevention of toxoplasmosis

A

Focus on women of child-bearing age and immunocompromised persons

Proper handling of cat liter

Wash hands when handling meat

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11
Q
Chagas Disease -- 
what is the bug?
what is the vector?
what is the technical term for the infection?
Where does it most commonly occur?
A

Bug: Trypanosoma Cruzi

Vector: Triatomine bugs

Name: American Trypanosomiasis

Epi: Mostly in Latin America. Major cause of cardiac disease and mortality
Most cases in the US are from infected immigrant populations

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12
Q

Describe the lifecycle of the Trypanosoma cruiz? How does it infected humans ?

A

The parasite resides in the Gut of the Triatomine vector

Bug takes a blood meal, and defecates out Trypomastigotes on human hosts

Auto-innoculation; rub the feces in eye or wound. Trypomastigoes enters muscle, cardiac or smooth muscle

Differentiates into Amastigotes

Replication leading to rupture of the cell and differentiates back to trypomastigoes

Spreads throughout the blood stream.
Taken up in another blood meal

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13
Q

How is trypanosoma transmitted ?

A

Vector Born –
Trans placental
Ingestion – rare (eg bugs on fruit)

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14
Q

Describe the acute vs chronic phases of trypanosomiasis?

  • symptoms and manifestations
A

Acute: 1-2 months following transmission
Fever, mononucleosis
High levels of parasitemia

Symptomatic < 1%
May lead to acute myocarditis; meningoencephalalitis

Chronic –
Few parasites in the blood
descrtruction of cardiac myocytes; replaced by fibrotic tissue; leading to CHF, arrythmias, complete heart block and thrombo-embolism

the disease is life long and may reactive when immunosuppressed

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15
Q

What are the manifestations of trypanosomiasis?

  • cardiac
  • Gi
A

acute myocarditis
CHF, arrhythmias, complete heart block, thromboembolism

Gi - mega colon, mega esophagus

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16
Q

Diagnosis of Trypanosomiasis

acute vs chronic

A

Acute –
Mircosopy – visualization of purple crescent parasites in the blood
Serology – IgMs

Chronic –
Serology – IgGs
ELISA, IFA
EKG changes, CXR

17
Q

Treatment of Trypanosomiasis

acute, congenital and reactive vs chronic

A

Treatment for acute, congenital, reactivated infection: Nifurtimox Benznidazole

Chronic: Symptomatic treatment, pacemakers, cardiac therapy; Transplant; surgery for GI disease

18
Q

Leishmaniasis –
what causes the disease?
what is the vector?
what are three categories of disease?

A

Protozoan Parasite —
Genus – Leishmania
Many different species

Vector: Sandfly

Disease:
Cutanenous – skin

Mucosal – skin and nasopharynx

Visceral – Entire Reticuloendothelial system

19
Q

Describe the life-cycle of Leishmania

A

Sandfly takes blood meal and injects promastigotes

Promastigotes phagocytized by macrophages

Transform to amastigotes and begin to replicate

Rupture of macrophage and mastigotes begin to spread
and infect other macrophages

Sandfly takes another blood meal ingesting a macrophage infected with amastigoes

differentiate back into promastigotes

20
Q

How is the disease controlled in most immuno competent persons?

what are the immunity profiles for persons with mucosal vs cutaneous vs visceral disease?

A

Control:
Cellular response is necessary for control of disease:

  • Activated macrophages, IFN gamma, IL-12, TNF Alpha

Viseral Disease: lack cellular response

21
Q

Visceral Leishmanisasis:
- what tissues/cells are infected?

  • what is full blown disease called?
  • ## what are the manifestations?
A

Tissues: Reticulo endotheial system (macrophages) of the skin, liver, spleen and bone marrow

Kala-azar

Signs and symptoms: Hepatosplenomegaly, fatigue, fever, anemia

Can lead to bleeding, CHF
Persons die of infections

22
Q
  • What species cause the Visceral leishmaniasis disease ?

- risk factors for the disease?

A

zoonotic Species:
L chagasi
L Infantum

Anthroponotic:
L. donovani

Risk factors:
Poverty, malnutrition, HIV co-infection
Refugee populations

23
Q

Cutaneous Leishmaniasis:

what are the old world parasites:
what are the new world parasites:
what is the manifestation?

A

Old world: Zoonotic and Anthroponotic
L. Tropica, major, infantum

New world: 
L brazileinses (same as mucosal) 

Manifest: single cutaneous lesion
painless unless infected with bacteria

contracted by many soldiers in Operation Desert Storm (L. tropica)

24
Q

Mucosal Leishamaniasis

  • what is the causative species?
  • what is the reason for the disease?

Manifestations?
late manifestations?

A

Disease of hyper-reactivity of the immune system (DTH)

Over-reactive response that doesn’t kill the parasites

Nearly all. L braziliensis
Treatment is difficult

Cutaneous ulcer
lesions of nasopharynx
can lead to gross mutilation of the nose and palate

25
Q

Disseminated cutaneous leishmaniasis disease:

What bugs?
why not localized disease?

A

L amazoenensis
L mexicana

Failure of cell mediated immunity results in lepromatous like nodular lesions over body and face; very chronic; resistant to treatment.

26
Q

Methods for Diagnosis of leishmaniasis

What are the tests and results for cutaneous vs visceral disease ?

A

Methods:
Giemsa smear and Stain

Leishmania Skin Test (similar to PPD, looking for DTH)

Serology

ELISA and PCR for species identification

Cutaneous disease:
Serology Negative
Skin test positive

Visceral –
Skin test negative with active infection
Test positive after treatment
Serology – postive with active disease

27
Q

Treatment of Leishmaniasis:

cutaneous vs visceral
Side effects

alternatives?

Prevention?

A

Cutaneous:
Pentavalent antimonials
Side effects: myalgias, N, V, D, abd
Rare – pancreatitis

Visceral: Lipo AmphoB

alternative –
Paramomycin

Prevention: bug spray; long sleeve shirts and pants