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MMI 445 > Lecture 20- Toxoplasma gondii > Flashcards

Lecture 20- Toxoplasma gondii Flashcards

1
Q

Toxoplasma gondi was first seen by who?

A

Nicolle and Manceaux in 1908

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2
Q

When was the first human case diagnosed?

A

1923

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3
Q

When was the first disseminated case?

A

1940

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4
Q

What are the three main lineages with increasing virulence?

A

Lineage I, II, III

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5
Q

What are the three life stages?

A
  1. Tachyzoites
  2. Bradyzoites (in tissue cysts)
  3. Oocysts
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6
Q

What are the asexual stages?

A
  1. Tachyzoites
  2. Bradyzoites
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7
Q

What is the sexual stage?

A

Oocysts

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8
Q

Where does the asexual and sexual stages occur?

A
  • Asexual = intermediate and definitive host
  • Sexual = definitive host
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9
Q

____ are dead end hosts

A

Humans

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10
Q

What are the key elements in the lifecycle?

A

Cats

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11
Q

Who is the definitive hosts?

A

Cats

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12
Q

Oocysts can exist in the soil for a long time because?

A

They have a resilient shell arounf the mechanisms inside

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13
Q

Descrie horizontal transmission

A
  • Intermediate host = ingests sporulated oocysts from contaminanted food or water and maintains the asexual reproductive cycle
  • Oocysts can remain active in the soil up to one year
  • Cat ingests tissue cysts, oocysts form in cat intestines, sporozoites develop in oocytes which are deposited in feces
  • These sporozoites become infectious for 1-5 days after deposition
  • Tachyzoites are rapidly dividing in macrophages
  • Origin = tissue cysts or oocysts
  • Dissemination in macrophages until adaptive immune response stops it and tissue cysts form (persistent form in tissues)
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14
Q

Describe verticle transmission

A
  • Mother to fetus via placental transfer of tachyzoites
  • Leads to congenital toxoplasmosis
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15
Q

How do humans get infected?

A
  • Ingestion of tissue cysts with bradyzoites in undercooked or raw meat
  • Infective oocysts can be ingested (fecal oral), releasing sporozoites that penetrate the gut wall and disseminate
  • Blood transfusion/organ transplants
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16
Q

Worldwide distribution, incidences vary depending on ?

A

Cultural and social issues

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17
Q

There is a high prevalence where related to undercooked meat?

A

Northern Canada, Europe

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18
Q

What are the three categories of risk factors?

A
  1. Sociodemographic
  2. Biological
  3. Lifestyle
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19
Q

What are sociodemographic risk factors?

A

Increased age, increased warm climate

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20
Q

What are biological risk factors?

A
  • Genetic predisposition (HLA DQ3)
  • Immunodeficiency (common oppertunistic infection)
  • Strain risk factors
21
Q

What are Lifestyle risk factors?

A
  • Contaminated food (raw meat with cysts are major source of human infection)
  • Lamb and sheep > pork > beef
  • Drinking untreated water
  • Food habits (vegans and vegetarians less exposure)
  • Exposure to cats (the feces)
22
Q

T. gondii is a _____

A

Obligate intracellular protozoan

23
Q

Can infect what as intermediate host?

A

Can infect all mammals

24
Q

What does T. gondii infection and Toxoplasmosis mean?

A
  • T. gondii infection = means both asymptomatic and symptomatic infections
  • Toxoplasmosis = means symptomatic infection
25
Q

____ of infections are asymptomatic in immunocompetent hosts

A

90%

26
Q

What are symptomatic infections?

A
  • Mononucleosis like disease
  • Low grade fever
  • Malaise
  • Headache
  • Cervical lymphadenopathy
27
Q

What are some complications of T. gondii?

A
  • Encephalitis
  • Myocarditis
  • Hepatitis
  • Pneumonia
28
Q

Describe the pathogenesis of T. gondii

A
  • No host specificity, able to invade all cell types
  • Ability to form tissue cysts that protect it from immune system
  • Invasive at any stage of cell cycle
  • Outcome of cell invasion dependent on type of cell
  • Macrophages phagocytose into a phagosome which fuses with lysosomes and kills parasite
  • Other cells = parasite enters a vacuole formed by plasma membrane invagination (PV), PV does not sude with lysosomes and does not acidify
  • Toxoplasma cells do not have flagella but glide along host cell surfaces
  • Relocation of surface bound molecules on Toxo (micronemes) = association with the cellular sub membranous actomyosin complex
  • Attach then enter by apical complex into a PV
  • Parasite causes formation of pores in PV
  • Host cells infected with parasite undergo changes (changes caused by the parasite and by the immune response)
29
Q

What are some alterations that occur in the host cells?

A
  • Facilitate parasite nutrient acquisition
  • Enhance host cell survival
  • Avoidance of strong immune response allowing infection to continue
  • Tissue cysts are likely a mechanism by which the parasite avoids interference from the immune system
30
Q

What are the three special structures found in Apicomplexa?

A
  1. Micronemes
  2. Rhoptries
  3. Dense granules
31
Q

What do micronemes do?

A

They function in cell-cell adhesion, motility, etc

32
Q

What do Rhoptries do?

A

Modification of host cell and parasite, secretion only occurs during host cell invasion

33
Q

Describe infection in immunocompetent individuals

A

Symptoms vary from short, self-limiting unspecific illness to severe symptoms with prolonged fever, fatigue and retinochoroiditis (predominant symptoms is cervical lymphadenopathy)

34
Q

Describe infections in immunocompromised patients

A
  • HIV infected patients = increased toxo encephalitis, often result of reactivation of latent infections after rupture of tissue cysts in the CNS
  • SOT = increase CNS or pulmonary toxo, usually result of reactivation, usually within 3 months of transplantation
35
Q

Is it easy or difficult to diagnose pregnant women?

A

Difficult because need seroconversion

36
Q

What is congenital toxo?

A

Acute maternal infection where the tachyzoites transfer from blood to fetus

37
Q

Risk of congenital toxo increased with?

A

Gestation time

38
Q

More severe effects to fetus when infections are?

A

In early gestation (< week 26)

39
Q

Describe early gestation infections

A

Severe disseminated infection with cerebral calcifications, cerebral abscess, retinochoroiditis, hydrocephalus or microcephalus and ascites, may lead to death in utero

40
Q

Describe late gestation infections

A
  • Baby is usually subclinical (not detectable)
  • Neurological and intellectual sequelae can occur after birth in babies who were infected late in gestation
41
Q

How to manage congenital toxo?

A
  • Prenatal screening can be done to determine if the mother is already infected
  • Repeated testing if mother not infected
  • Testing of fetus (amniotic fluid), PCR, imaging if mother is symptomatic
  • Prenatal treatment if infection found with spiramycin (parasitostatic) and/or pyrimethamine-sulfonamide (parasitocidal)
  • Need for long term follow up of children when mother has had toxo = late effects can show up after years
42
Q

What are some lab diagnostics available?

A
  • Detection of tachyzoites or tissue cysts om body fluids or tissue
  • EIA for toxoplasma antibodies
  • Detection of parasite DNA (PCR) in body fluids or tissue samples
  • PCR is very sensitive and specific
  • Acute infection IgM positive or serial specimens (seroconversion)
  • EIA sensitive and specific
43
Q

What is the gold standard for diagnostic?

A

PCR

44
Q

Is there a vaccine available?

A
  • Animal vaccinations do exist (for sheep and goats)
  • Human vaccination do not exist
45
Q

What are some behavioural changes seen in rodents?

A
  • Impaired motor performance
  • Decreased reaction time
  • Increased levels of dopamine
46
Q

What is the manipulation hypothesis?

A

Parasite changes the organisms behaviour to benefit further survival and transmission of the parasite (increases chances for entering a feline)

47
Q

Describe the host-parasite interaction

A
  • Neutrophils have an early role in killing parasite
  • Inactive macrophages to prevent killing
  • Infected host cells resist apoptosis
  • Needs glucose, iron, arginine, ornithine, cholesterol, calcium
  • Toxoplasma can take up lysosomes and sequester them = this may be where they acquire iron and cholesterol
  • Calcium is taken up from host cell cytosol
  • Host cells have their ways of dealing with infection
  • Toxoplasma growth is dependent on tryptophan. Depletion of arginine arrests parasite replication and induces the conversion from tachyzoites to bradyzoites
  • Antibody production
  • MHC I and MHC II presentation important for the adaptive immune response, especially MHC I
  • Effective CD4 and CD8 cell activity important for controlling acute infections
  • Toxoplasma rapidly overcomes hosts with impaired T cell function (AIDS)
  • Interferon gamma produced by T cells (induced by IL-2 from CD4) important for limiting infection
  • Infants have lower MHC I expression, dendritic cells are more immature, produce lower amounts of cytokines
48
Q

Describe intestinal immunity

A
  • Important = route of transmission is through the gut
  • Cysts and oocysts susceptible to pepsin and release bradyzoites or sporozoites which are pepsin resistant
  • Invasion of the gut epithelial cells, dissemination to lymph and blood

MMI 445 (26 decks)

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