Toxoplasmosis
• •A systemic coccidian protozoan disease. Common parasitic infectionof humans and animals. Infection are frequently asymptomatic, or present as
acute disease with lymphadenopathy or resemble infectious mononucliosis.
• Agent: Toxoplasma gondii an intracellular coccidian protozoan that
complete its sexual life cycle phase in the cat.
Characteristics of organism:
l lThree infective stages:
l lTachyzoites – rapid growth
l Bradyzoites – tissue cyst form, slow growth
l Sphorozoites – oocysts
l lUnsporulated
l Sporulated
l lCapable of growth and replication in a variety of host cells
l lIn macrophages – capable of evading immune mechanisms
l Ability to survive (evading digestion by macrophage) may be due to preventionof lysomal fusion with phagocytic vacuole
l lReproduction (sexual) occurs only in cats - multiplication by cell division;
occurs in most host cell types
• •Epidemiology
l lOccurrence: ubiquitous worldwide
l lHumans
l lSeroprevalence in humans estimated to be ~500,000,000
l Congenital infection: <0.1%
l lAnimals
l lWidespread infection due to prolific oocyst shedding
l lAt any given time, small numbers (~1%) of cats (primarily domestic) may be
shedding oocysts
l lReservoir:
l lThe definitive hosts for T. gondii are cats and other felines which aquire
the infection mainly from eating infected mammals esp. rodents or birds and
propably from oocysts in soil contaminated with cat feces . Felines alone
harbors parasites in int. tract where the sexual stage of the protozoan life
cycle occurs resulting in excretion of oocyst in the feaces for 10-20 days and
rarely longer .
l lThe intermediate hosts: sheep,goats,rodents,swine cattle chickens and other
birds all may carry the infective stage of T. gondii encysted in the tissue (
muscle and brain)
Tissue cyst remain viable for long period perhaps lifelong.
Transmission (to humans):
l lTransplacental – tachyzooites
l Orally – oocysts by hand to mouth, undercooked meat with tissue cysts;
contaminated food or water. Consumption of raw gout milk
l Inhalation –( sporilated oocysts ) rare associated with one outbreak
l lInfected tissue (blood, transplantation)from infected donor.
l lLife cycle:
l lCats acquire infection by eating any of three infective stages in infected
prey (rodents or birds)
l lIntraintestinal cycle – occurs only in cats
l lMultiply in wall of small intestine, produce oocysts
l Oocysts shed in great numbers for 2-3 days
l Oocysts sporulate within 5 days
l Sporulated oocyts highly resistant
l lHealthy cats shed during acute stage, but not after (at least in sufficient
numbers to be infective)
l Congenital infections may occur in sheep and goats (and humans), but uncommon
in cats
l lLife cycle:
l lExtraintestinal cycle – occurs in cats and intermediate hosts (including
humans)
l lcyst from intraintestinal cycle penetrate deep into intestinal wall
l multiply as tachyzoites, spread to other body sites
l lImmune system finally restrains infection, leading to dormant stage (cyst) in
muscle or brain
• •Clinical features
l lCats
l lusually asymptomatic
l Occasionally younger animals or immunocompromised animals show non-specific
signs (fever, lethargy) followed by:
l lpneumonia (mainfested by respiratory distress with gradual increasing
severity)
l Hepatitis - jaundice, vomiting, diarrhea
l CNS – seizures, hyperesthesia, ocular inflammation leading to blindness
l lHumans:
l lNormal hosts:
l lIncubation period: 10-23 days
l ~80% asymptomatic
l Localized infection manifested as lymphadenopathy resolving spontaneously (wks
to months)
l Some may experience fever, myalgia, headache
l Rash, hepatitis - rare
l lHumans:
l lImmunocompromised host (reactivation disease):l lEncephalitis most common manifestation
l lPresent with sever headache, altered mental status, seizure, neurological
deficits, pneumonia, and myocarditis
l Estimated up to 40,000 cases in AIDS patients in US in 1981
l Most common cause of AIDS encephalitis in US
Humans:
l lCongenital infection:
l lOccurs when women becomes infected during pregnancy or with reactivation (if
immunocompromised)
l Most severe when occurs in first trimester
l Varying signs
l lOcular – impaired vision to blindness due to chorioretinitis,
microophthalmia
l lCNS – hydrocephalus, seizures, microencephaly
• •Prevention and control
l lThorough washing of hands after handling meat
l Wear protective gloves when handling litter, gardening, childrens sand boxes
l Testing pregnant women for antibodies (?)
Treatment:
• •Not routinely indicated for a healthy immunocompetent host except
for confirmed initial infection durig pregnancy or presence of active
chorioretinitis, myocarditis or other organ involvement.
l lMulti-drug therapy: pyrimethamine plus trisulfapyrimidines (or sulfadiazine)
and folinic acid ( for patients with sever symptomatic disease. For 4 weeks
l Clindamycin + these agents to treat ocular toxo.
l lSystemic corticosteroids are indicated with irreversible loss of vision.
Infants whose mothers had primary infection or HIV positive during pregnancy
should be treated with pyrimethamine- sulfadiazine- folinic acid during first
year of life.
l lTreatment in pregnancy is problematic. Spiramycin is used to prevent
placental infection
l Spiramycin – used in Europe; safe and effective in pregnancy