Protozoa II Flashcards
Toxoplasma gondii infectious cycle
- definitive host: domestic cats and relatives
- unsporulated oocysts are shed in cat’s feces
- Ooocysts take 1-5 days to sporulate in the environment and become infective
- Intermediate hosts (birds, rodents) become infected after ingesting soil, water, plant material
- Oocysts transform into tachyzoites shortly after ingestion
- Tachyzoites localize in neural and muscle tissue and develop into cyst bradzoites
- Cats infected after consuming intermediate hosts harboring tissue cysts
- Cats may also become infected directly by ingestion of sporulated oocysts
- Humans become infected by:
1. eating undercooked meat of animals w/ cysts
2. consuming food or water contaminated with cat feces or by contaminated environmental samples (fecal in soil or changing cat’s litter box)
3. blood tranfusion, organ tranplant
4. transplacentally from mom to fetus - in human, parasites form tissue cysts (skel muscle, myocardium, brain, eyes)
- Cysts may remain in human for life
Ingestion of a single cyst can cause infection
T. gondii diagnosis
- (apicomplexan parasite)
- most common protozoa infection in humans
- dx acute infection in immunocompetent with IgM and IgG antibodies against the organism are present in serum; also IgA
- can also see tachyzoites in lymph nodes (acute infec)
Prior infection established by bradyzoites in tissue
PCR
When is risk of SEVERE disease from T. gondii greatest for a fetus?
If primary infection of mother occurs during the first trimester
Intrauterine infections can result in:
chorioretinitis
malformations
neurological sequelae
Mother and newborn can be asymptomatic
What disease is often seen in immunocompromised infected with T. gondii?
In pts with AIDS or Hodgkin’s disease, often see toxoplasma encephalitis
What cell does T. gondii infect?
Macrophages, then replicates in endosomes.
If immunocompetent, macrophages can eventually kill the parasites
How to reduce risk of infection with T. gondii
- thoroughly cook meat
- avoid exposure to cat feces
- prophylactic therapy in immunocompromised with evidence of prior infection (Ab)
General overview of T. gondii
- widespread infection causing flu-like sx and then typically becomes dormant
- reactivates in immunocompromised
- transplacental transmission
- INTRACELLULAR parasite that can infect ANY cell
- higher prevalence in countries that eat raw meat or have many stray cats
- Transmission: oocysts (cats), improperly cooked meat, congenital
Clinical syndromes of T. gondii
-acute acquired toxoplasmosis
-ocular toxoplasmosis
-cerebral toxoplasmosis (AIDS)
-congenital toxoplasmosis (If woman infected before pregnancy, child likely unaffected; if maternal infection occurs less than 6 mo b/f conception, the risk of fetal infection increases; if infected during first tri: fetal incidence at 15% but can cause:
miscarriage
stillbirth
chorioretinitis, hydrocephalus, intracranial calcifications, hepatosplenomegaly, jaundice, fever, anemia, pneumonia
-if maternal infection in 3rd trimester, 65% of fetuses are infected. Neonate usually asx @ birth, but have long term learning disabilities and neurological sequelae
Incidence of T. gondii in US
More than 60 mill chronically infected
over 1 mill new infections/yr
Trypanosomai cruzi (Chagas’ disease) infectious cycle
- an infected triatomine insect vector (“kissing bug”) takes blood meal and releases trypomastigotes in its feces near site
- Trypomastigotes enter the host through the wound or through intact mucosal membranes
- Trypomastigotes invade cells near site of inoculation and differentiate into intracellular amastigotes
- Amastigotes multiply by binary fission, differentiate into trypomastigotes which infect cells and transform to amastigotes
- Bloodstream trypomastigotes do not replicate (resumes when enter cell or ingested by vector)
- When consumed by a new vector (like kissing bug), transform into epimastigotes in vector’s midgut and then into trypomastigotes in hindgut
Transmission can occur in organ transplants, blood transfusions, lab accidents
What causes Chagas’ disease? Sx?
- T. cruzi (S. and Central America)
- transmitted to humans by triatomine insects (reduviid bugs)
-indurated inflammatory lesion @ bite site
-acute sx in about 2 weeks
-fever, enlargement of lymph glands, liver and spleen, and damage to the heart.
- Painless edema
of the eyelids and periorbital tissues (Romana’s sign) may occur when the conjunctiva is the portal of
entry.
-Children are especially susceptible, and mortality rates may reach 10%.
- In the chronic disease, the heart and the intestinal tract are the most common target organs. Symptoms are often caused by dilated
cardiomyopathy, thromboembolism and abnormalities of cardiac conduction
Prevention of Chagas’ disease
bug control, construction and treatment of homes to prevent nesting of bugs, and routine screening of blood for transfusions
Phases of infection
Blood form: extracellular, acute (mild sx @ site of inoculation)
tissue form (intracellular, chronic)
Both stages can be asymptomatic, but 20-30% develop heart abnormalities and dilated esophagus or colon in chronic phase
Can reactivate in immunocompromised hosts
Dx of Trypanosoma infection
-Clinical signs and travel history
- Trypomastigotes in circulating blood or CSF in acute phase
- During the chronic stage, trypomastigotes are usually not found circulating in blood and serologic testing is recommended (biopsy can ID tissue forms)
-Molecular diagnosis (PCR) of Chagas disease is performed when cases of transfusion or transplant
transmission are suspected and for congenital Chagas
Leishmania spp. infectious cycle
- Sandfly takes a blood meal and injects promastigote stage into skin
- Promastigotes are phagocytized by macrophages
- Promastigotes transform into amastigotes inside macrophages
- Amastigotes multiply in cells (including mac) of various tissues
- Sandfly takes a blood meal and ingests macrophages infected with amastigotes
- Amastigotes transform into promastigote stage in midgut
- Divide in midgut and migrate to proboscis
About 20 different species cause infection in humans
Causes of visceral leishmaniasis (kala-azar)
-members of L. donavani complex (L. donovani, L. infantum)
Other forms:
Cutaneous leishmaniasis
Mucosal leishmaniasis
Diagnosis of Leishmaniasis
Lymph node aspirates
and scrapings or biopsies from the edge of lesions are used to diagnose cutaneous forms
specimens of blood, bone marrow, nodes, liver and spleen are used to diagnose visceral leishmaniasis.
The parasites are detected by microscopic examination or by culture of the specimens.
Individual species distinguished using isoenzyme analysis of cultured promastigotes
Serologic methods to test for Ab
Amastigote vs promastigote (leishmaniasis)
Amastigote is only form found in humans
Promastigote only in insect vector
Clinical feature of leishmaniasis
-localized skin ulcers (cutaneous or dermal leishmaniasis)– L. tropica, L. mexicana
- Primary infections in skin that metastasize to mucosal tissues in nose, pharynx where they produce more destructive lesions (mucosal leishmaniasis)–L. braziliensis
- hard palate, nasal septum, larynx erosion may render victim speechless
-Members of L. donavani complex cause disseminated visceral lesions (visceral leishmaniasis or “kala-azar”, ie black disease); can be highly lethal
-Macrophages of the liver, spleen, bone
marrow, lymph nodes and intestine are infected.
-Symptoms take from 3-12 months to appear, and
include fever, diarrhea and malabsorption, hepatosplenomegaly, ascites and lymphadenopathy.
-White victims may have darkened skin, giving the disease its alternate name.
-In patients who are co-infected with HIV, Leishmania species that usually cause cutaneous leishmaniasis may produce disseminated
disease or other atypical presentations.
Prevention of Leishmaniasis
-controlling the vector, preventing insect bites, promptly treating human cases, and eliminating animal reservoirs.
use of insecticide-treated bednets reduces risk.
African Sleeping Sickness (African Trypanosomiasis) infectious cycle
- Tsetse fly takes a blood meal an injects metacyclic trypomastigotes
- metacyclic trypomastigotes transform into bloodstream trypomastigotes, carried to other sites
- multiply by binary fission in body fluids (blood, lymph, spinal fluid)
- trypomastigotes in blood
- Tsetse fly takes blood meal
- Bloodstream trypomastigotes transform into procyclic trypomastigotes in tsetse fly’s midgut
- Multiply by binary fission
- Procyclic trypomastigotes exit midgut, transform into epimastigotes
- Multiply in salivary gland and transorm into metacyclic trypomastigotes
Species that infect humans and cause African sleeping sickness
T. brucei rhodesiense (E. africa)
T. brucei gambiense (w. africa)
Diagnosis of African trypanosomiasis
parasite in body fluid or tissue by microscopy (blood, lymph node aspirates or spinal
fluid)
-IgM in spinal fluid is diagnostic for encephalitic phase of illness
-cannot culture
-mouse inoculation
Clinical features of African trypanosome infection
-trypanosomal chancre at site of bite after 2-3 d
-spreads to bloodstream via lymphatic channels after 2-3 w
-low-grade parasitemia
accompanied by recurrent fever, prominent lymphadenopathy, rash, headache and confusion (Stage I disease)
-Predominatly IgM production reduces parasitemia
-But it can evade immune response by antigenic variation
-Destruction of parasites leads to the formation of circulating immune complexes that are the
probable cause of the anemia and vasculitis seen in the disease
-East African/Rhodesian form: has a primary reservoir in antelope and cattle, the early symptoms and signs are followed by CNS
involvement (Stage II disease) with convulsions, coma and death in 5–9 months.
-West African/Gambian
sleeping sickness, for which humans are the primary reservoir, progresses more slowly.
Lymphadenopathy is more prominent, and bouts of fever may persist for years before the CNS
involvement (Stage II disease) leads to coma and death