Uploaded by Dr. Sujeet K. Mritunjay

42 TOXOPLASMOSIS

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TOXOPLASMOSIS
Outli
nes
 Objective
 TOXOPLASMOSIS
 Epidemiology
 Life Cycle and Diagnosis,
 Prevention and Control
 Exercise on Topic
 Learning Outcomes
 References
TOXOPLASMOSIS
Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii. Toxoplasmosis is usually spread
by eating poorly cooked food that contains cysts, exposure to infected cat feces, and from an infected
mother to her baby during pregnancy. Rarely, the disease may be spread by blood transfusion. It can
be found in cat feces and undercooked meat, especially venison, lamb, and pork. It can also be
transmitted through contaminated water. Toxoplasmosis can be deadly or cause serious birth defects
for a fetus if the mother becomes infected.
The only known definitive hosts
for Toxoplasma gondii are members of
family Felidae (domestic cats and their
relatives). Unsporulated oocysts are
shed in the cat’s feces
SYMPTOMS
Most people who have toxoplasmosis never have any symptoms at all. People who
develop symptoms may experience:a) a fever
b) swollen lymph nodes, especially in the neck
c) a headache
d) muscle aches and pains
e) sore throat
These symptoms can last for a month or more and usually resolve on their own. Toxoplasmosis is
especially serious for people who have weakened immune systems. For these people, they’re at risk
of developing:a) Brain inflammation, causing headaches, seizures, confusion and coma.
b) a lung infection, causing cough, fever, and shortness of breath
c) An eye infection, causing blurry vision and eye pain.
TRANSMISSIONS:-
a) Drinking contaminated water.
b) In rare cases, toxoplasmosis may be transmitted through a blood transfusion or a transplanted organ.
c) Congenital transmittance from mother to fetus can also occur.
d) Transmission may also occur during the solid organ transplant processor hematogenous stem cell
transplants.
e) Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing Toxoplasma
cysts: Infection prevalence in countries where undercooked meat is traditionally eaten has been
related to this transmission method. Tissue cysts may also be ingested during hand-to-mouth contact
after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by
raw meat.
f) Ingestion of unwashed fruit or vegetables that have been in contact with contaminated soil
containing infected cat feces.
g) Ingestion of cat feces containing oocysts: This can occur through hand-to-mouth contact
following gardening, cleaning a cat's litter box, contact with children's sandpits; the parasite can
survive in the environment for months.
h) Ingestion of untreated, unfiltered water through direct consumption or utilization of water for
food preparation.
i) Ingestion of unpasteurized milk and milk products, particularly goat's milk.
j) Ingestion of raw seafood.
k) Exposure to infected cat feces
PATHOGENESIS: - Most cases of toxoplasmosis in humans are probably acquired by the ingestion
of either tissue cysts in infected meat or oocysts in food contaminated with cat feces. Bradyzoites
from the tissue cysts or sporozoites released from oocysts penetrate the intestinal epithelial cells and
multiply in the intestine. Toxoplasma gondii may spread both locally to mesenteric lymph nodes and
to distant organs by invading the lymphatics and blood. Necrosis in intestinal and mesenteric lymph
nodes may occur before other organs become severely damaged. Focal areas of necrosis may
develop in many organs. The clinical picture is determined by the extent of injury to these organs,
especially to vital and vulnerable organs such as the eye, heart, and adrenals. Toxoplasma
gondii does not produce a toxin; necrosis is caused by intracellular multiplication of tachyzoites.
Control/ Prophylaxis/treatment: - Sulfonamides and pyrimethamine (Daraprim) are two
drugs widely used to treat toxoplasmosis in humans. They act synergistically by blocking
the metabolic pathway involving p-aminobenzoic acid and the folic-folinic acid cycle,
respectively. These two drugs usually are well tolerated by the patient, but sometimes
thrombocytopenia, leukopenia, or both may develop. These effects can be overcome
without interrupting treatment by administering folinic acid because the vertebrate host
can utilize presynthesized folinic acid, whereas T gondii cannot.
The commonly used sulfonamides, sulfadiazine, sulfamethazine, and sulfamerazine, are all
effective against toxoplasmosis. Generally, any sulfonamide that diffuses across the host cell
membrane is useful in antitoxoplasmid therapy. Although these drugs are helpful when given
in the acute stage of the disease, usually they will not eradicate infection when active
multiplication of the parasite occurs. Because sulfa compounds are excreted within a few
hours of administration, they must be administered in daily divided doses. Spiramycin, a
drug used in France to treat pregnant women to minimize the effects of congenital
toxoplasmosis, is not approved for toxoplasmosis in the United States.
As yet, there are no effective drugs to kill tissue cysts. No killed vaccine is currently
available to reduce or prevent congenital infections in humans and animals, but a live
vaccine using a nonpersistent T gondii strain is available in Europe and New Zealand to
reduce abortion in sheep. To prevent T gondii infection, several precautions should be taken.
Meat should be cooked to 66°C throughout before eating. Hands should be washed with
soap and water after handling meat. Raw meat should never be fed to cats; only dry or
canned food or cooked meat should be fed. Cats should be kept indoors and litter boxes
changed daily. Cat feces should be flushed down the toilet or burned. Litter pans should be
cleaned by immersing them in boiling water. Gloves should be used while working in the
garden. Children's sandboxes should be covered when not in use
References
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 Campbell JB, Charlton KM (eds): Rabies. Kluwer Acad Publ, Boston, 1988 .
 Centers
for
Disease
Control:
Rabies
prevention
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United
States,
1991.
Recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR
40 (RR-3): 1, 1991 . [PubMed]
 Centers for Disease Control: Compendium of animal rabies control, 1995. MMWR 44
(RR-2): 1, 1995 . [PubMed]
 Dietzschold B, Kao M, Zheng YM. et al. Delineation of putative mechanisms involved in
antibody-mediated clearance of rabies virus from the central nervous system. Proc Natl
Acad Sci USA. 1992;89:7252. [PMC free article] [PubMed]
 Krebs JW, Strine TW, Smith JS. et al. Rabies surveillance in the United States during
1993. J Am Vet Med Assoc. 1994;205:1695. [PubMed]
 Rupprecht CE, Smith JS. Raccoon rabies: the re-emergence of an epizootic in a densely
populated area. Sem Virol. 1994;5:155.
 Smith JS, Orciari LA, Yager PA. et al. Epidemiologic and historical relationships among 87
rabies virus isolates as
determined
by
limited
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analysis.
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Dis. 1992;166:296. [PubMed]
 Winkler WG, Bogel K. Control of rabies in wildlife. Sci Am. 1992;266:86. [PubMed]
 World Health Organization Expert Committee on Rabies: 8th Report. WHO Technical
Report Series no. 824.
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