Toxoplasmosis of animals and humans Flashcards
(13 cards)
Toxoplasma gondii FH
cat
Toxoplasma gondii IH
Wide range of mammals and birds
Toxoplasma gondii location
FH: GIT
IH: tissue cysts
Toxoplasma gondii clinical signs
Dogs (IH):
Acute - fever, lymph node enlargement, nose and eye discharge, tonsilitis, dyspnoea, diarrhoea, progressive weight loss, pneumonia
Chronic - hepatitis, myocarditis, pneumonia, nerve symptoms (apathy, tremors, ataxia, hemiparesis, paresis, paralysis)
Other animals (IH): abortions, CNS disorders, pigs have same as dogs, asymptomatic (horses, race game, poultry).
Cats: fever, reduced appetite, lethargy, diarrhoa, asymptomatic. Eye form causes retinitis with retinal inflammation, uveitis, chorioretinitis. Lethal in cats with impaired immune system.
Toxoplasma gondii life cycle
PP:
* 20-24 days with oocysts
* 7-10 days when consuming tachyzoites
* 3-5 days when eating bradyzoites
Life cycle
Intermediate hosts - Infection occur via:
- Ingestion of sporulated oocysts (containing sporozoites) from contaminated food, water or soil.
- Ingestion of tissue cysts (containing bradyzoites) from undercooked or raw meat.
- Tachyzoites via organ transplantation or blood transfusion.
- Transplacental transmission of tachyzoites can also occur during acute infection in pregnancy
Intestine – sporozoite
- In intestinal lumen, sporozoites are released from sporulated oocysts (excystation), and invade intestinal epithelium (enterocytes), where they starts multiplying in various cell types (macrophages, fibroblasts and neurons).
- Sporozoites differentiate into tachyzoites, which disseminate through the bloodstream and lymphatics, invading various cell types (macrophages, fibroblasts and neurons, and muscle cells) and penetrates other tissue (lymph, liver, lungs, brain).
- Endodyogeny (internal budding): tachyzoites multiply asexually.
- Tachyzoites invade into mesenteric lymph node (spread to the LNs) and then can go to various parts (extraintestinal organs) of the body: brain, muscle, eye, fetus.
- Tachyzoites convert into bradyzoites under immune pressure. During transition, they can temporarily for pseudocysts, which are clusters of tachyzoites enclosed within a host cell, but not yet surrounded by a true cyst wall. Eventually, true tissue cysts (with bradyzoites) are formed, particularly in immune-privileged sites (muscle, brain).
Intestine – bradyzoite
- Bradyzoites are released from tissue cysts, and invade enterocytes.
- Later they invade other tissues.
- Bradyzoites disseminate and replicate as tachyzoites, continuing extraintestinal cycle.
Final host (felids) - Ingestion of IH
- Cats consume IH harboring tissue cysts with bradyzoites.
- Bradyzoites are released in intestine and invade enterocytes.
- Schizogony (asexual): occur in enterocytes, producing merozoites, which invade neighboring cells.
- Gametogony (sexual): Merozoites differentiate into sexual stages; macrogametocytes (female) and microgametocytes (male), which then develop into macro- and microgametes.
- Fusion of macro and microgamete form a zygote, which develop into unsporulated oocyst.
- Unsporulated oocysts are shed in cat feces and sporulate in environment within 1-5 days, becoming infective.
Ingestion of sporulated oocyst
1. Oocysts releases sporozoites
2. Tachyzoites invade tissue (schizogony) or differentiates into gametocytes to form new oocysts (gametogony).
Toxoplasma gondii pathogenesis
During proliferation in tissues, tachyzoites inside host cells causes cell lysis, inflammation and tissue necrosis.
Bradyzoites in tissue cysts can remain dormant and cause autoinfection.
Congenital toxoplasmosis: tachyzoites can cross placenta and infect fetal brain and retina (inflammation, necrosis) –> hydrocephalus, chorioretinitis and intracranial calcifications.
Ocular toxoplasmosis: congenital or postnatal. Results from RE-ACTIVATION of bradyzoites in retinal tissue.
Loss of functional immune system: immunosuppression leads to reactivation of latent bradyzoites. Tachyzoites then divide rapidly, esp. CNS and lungs. Leads to severe toxoplasmic encephalitis, pneumonitis, myocarditis, or multisystem involvement.
Toxoplasma gondii diagnosis
- Detection of oocyst: difficult since shedding happens before clinical signs
- Dif.dig: Hammondia hammondi
- Serology: IgG, IgM - higher titers
- Seropositive cats are epidemiologically safe, only in immunosuppressed cats can secondary infection and oocyst production occur!
Toxoplasma gondii treatment
- Toltrazuril
- Clindamycin + trimetoprim
- Sulfanomides + trimetoprim
Toxoplasma gondii control
- Avoid raw and undercooked meat.
- Wash raw fruit.
- Clean cat litter box regularly (remove feces).
Humans can have VERTICAL transmission.
Toxoplasma gondii egg size
10-12um
What is the pathogenesis of Toxoplasmosis in humans?
Tachyzoites directly destroy host cells, especially parenchymal and reticuloendothelial cells
CS of toxoplasmossi in human
Prenatal (congenital) toxoplasmosis
- stillbirths, chorioretinitis, intracerebral calcification, hydrocephalus, neurological damage, learning difficulties
Postnatal toxoplasmosis - ln enlargement, local hypersensitivity, bv blockage, cell death near cyst, lymphadenopathy without fever
1-2 weeks incubation
Toxoplasma gondii diagnosis of human
Detection of antibodies in serum
High titers of IgM, IgA
Low IgG initially
