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__NOTOC__
__NOTOC__
{{SI}}
==Overview==
Toxoplasmosis is a part of TORCH group of infections which includes Rubella, Cytomegalovirus, Herpes virus. These pathogens can be transmitted from the mother to the fetus during pregnancy and cause congenital infections leading to permanent disability in the fetus and fetus loss in severe cases. The causative pathogen for Toxoplasmosis is a protozoan parasite, Toxoplasma gondii.It is estimated that 25 to 30% of the world's population is infected with Toxoplasma.<ref name="pmid15194258">{{cite journal| author=Montoya JG, Liesenfeld O| title=Toxoplasmosis. | journal=Lancet | year= 2004 | volume= 363 | issue= 9425 | pages= 1965-76 | pmid=15194258 | doi=10.1016/S0140-6736(04)16412-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15194258  }} </ref> In United States 89% of women in the childbearing age are susceptible to have an acute infection and at risk for transmitting the parasite to the baby if the primary infection occurs during the gestational period.<ref name="pmid18624630">{{cite journal| author=Montoya JG, Remington JS| title=Management of Toxoplasma gondii infection during pregnancy. | journal=Clin Infect Dis | year= 2008 | volume= 47 | issue= 4 | pages= 554-66 | pmid=18624630 | doi=10.1086/590149 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18624630  }} </ref>


==Historical Perspective==
{{Roseola}}
*In 1908, Nicolle and Manceaux described the parasite in the blood, spleen and liver of a North African rodent–gundi (Ctenodactylus gundi), due to its similar appearance as leishmania they named it Leishmania gondii.<ref name="pmid19217908">{{cite journal| author=Weiss LM, Dubey JP| title=Toxoplasmosis: A history of clinical observations. | journal=Int J Parasitol | year= 2009 | volume= 39 | issue= 8 | pages= 895-901 | pmid=19217908 | doi=10.1016/j.ijpara.2009.02.004 | pmc=2704023 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19217908  }}</ref>
{{CMG}}:{{AE}}{{DAMI}}
*In 1909, Nicolle and Manceaux renamed the parasite as T. gondii.<ref name="pmid192179082">{{cite journal| author=Weiss LM, Dubey JP| title=Toxoplasmosis: A history of clinical observations. | journal=Int J Parasitol | year= 2009 | volume= 39 | issue= 8 | pages= 895-901 | pmid=19217908 | doi=10.1016/j.ijpara.2009.02.004 | pmc=2704023 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19217908  }}</ref>
*In 1937, Sabin & Olitsky described that Toxoplasma was an obligate intracellular parasite and could be passed onto laboratory animals by intracranial,  subcutaneous, intraperitoneal inoculation of brain homogenates (The slurry of tissues and cells which results when cell structure has been mechanically disrupted). They have also suggested that ingestion of Toxoplasma contaminated tissue can result in Toxoplasmosis.<ref name="Heath1945">{{cite journal|last1=Heath|first1=Parker|title=TOXOPLASMOSIS|journal=Archives of Ophthalmology|volume=33|issue=3|year=1945|pages=184|issn=0093-0326|doi=10.1001/archopht.1945.00890150028003}}</ref>
*In 1937 to 1940, Wolf and Cowen have described necrotic and granulomatous lesions on autopsy of a 3 day old infant's brain infected with Toxoplasma. They have also reported that the mothers were asymptomatic but carried antibodies against Toxoplasma and the possibility of congenital transmission was expressed.<ref name="Paige1942">{{cite journal|last1=Paige|first1=Beryl H.|title=TOXOPLASMIC ENCEPHALOMYELITIS|journal=American Journal of Diseases of Children|volume=63|issue=3|year=1942|pages=474|issn=0096-8994|doi=10.1001/archpedi.1942.02010030044004}}</ref><ref name="pmid19870956">{{cite journal| author=Wolf A, Cowen D, Paige BH| title=TOXOPLASMIC ENCEPHALOMYELITIS : IV. EXPERIMENTAL TRANSMISSION OF THE INFECTION TO ANIMALS FROM A HUMAN INFANT. | journal=J Exp Med | year= 1940 | volume= 71 | issue= 2 | pages= 187-214 | pmid=19870956 | doi= | pmc=2135077 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19870956  }}</ref>
*In 1940, Pinkerton and Weinman reported the first fatal case of Toxoplasmosis in an adult.<ref name="pmid192179083">{{cite journal| author=Weiss LM, Dubey JP| title=Toxoplasmosis: A history of clinical observations. | journal=Int J Parasitol | year= 2009 | volume= 39 | issue= 8 | pages= 895-901 | pmid=19217908 | doi=10.1016/j.ijpara.2009.02.004 | pmc=2704023 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19217908  }}</ref>
*In 1948, Sabin and Feldman developed a serological test to identify infected individuals by using antibodies specific to Toxoplasma, called the Sabin Feldman Dye test. The serological test when used in large population studies showed a high proportion of humans and domestic animals carried antibodies against Toxoplasma.<ref name="pmid17744024">{{cite journal| author=Sabin AB, Feldman HA| title=Dyes as Microchemical Indicators of a New Immunity Phenomenon Affecting a Protozoon Parasite (Toxoplasma). | journal=Science | year= 1948 | volume= 108 | issue= 2815 | pages= 660-3 | pmid=17744024 | doi=10.1126/science.108.2815.660 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17744024  }} </ref>
*In 1965, Desmonts described that ingestion of under-cooked and uncooked meat plays a role in the pathogenesis of Toxoplasmosis.<ref name="pmid5853186">{{cite journal |vauthors=Desmonts G, Couvreur J, Alison F, Baudelot J, Gerbeaux J, Lelong M |title=[Epidemiological study on toxoplasmosis: the influence of cooking slaughter-animal meat on the incidence of human infection] |language=French |journal=Rev Fr Etud Clin Biol |volume=10 |issue=9 |pages=952–8 |year=1965 |pmid=5853186 |doi= |url=}}</ref>
*In 1970, Dubley described the life cycle of the parasite and established that the cats are the definitive hosts and any warm blooded animal can be an intermediate host.<ref name="pmid5467864">{{cite journal| author=Dubey JP, Miller NL, Frenkel JK| title=Characterization of the new fecal form of Toxoplasma gondii. | journal=J Parasitol | year= 1970 | volume= 56 | issue= 3 | pages= 447-56 | pmid=5467864 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5467864  }} </ref><ref name="pmid4927658">{{cite journal| author=Dubey JP, Miller NL, Frenkel JK| title=The Toxoplasma gondii oocyst from cat feces. | journal=J Exp Med | year= 1970 | volume= 132 | issue= 4 | pages= 636-62 | pmid=4927658 | doi= | pmc=2138867 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4927658  }} </ref><ref name="pmid5359949">{{cite journal| author=Hutchison WM, Dunachie JF, Siim JC, Work K| title=Life cycle of toxoplasma gondii. | journal=Br Med J | year= 1969 | volume= 4 | issue= 5686 | pages= 806 | pmid=5359949 | doi= | pmc=1630290 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5359949  }} </ref>
==Classification==
There is no classification for congenital Toxoplasmosis.


==Pathophysiology==
===Pathogenesis===
====Infective stages of the Parasite====
The three infective stages of T. gondii include:<ref name="pmid19430635">{{cite journal| author=Ferguson DJ| title=Toxoplasma gondii: 1908-2008, homage to Nicolle, Manceaux and Splendore. | journal=Mem Inst Oswaldo Cruz | year= 2009 | volume= 104 | issue= 2 | pages= 133-48 | pmid=19430635 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19430635  }}</ref>
*Tachyzoite: It is the rapidly dividing and invasive form, can invade any vertebrate cell type
*Bradyzoite: These are the result of conversion from tachyzoites, they are slowly diving form and are present as tissue cysts, which can remain in the host throughout the lifetime in the muscles.
*Sporozoite: It is the environmental form present in the oocyts


====Mechanism of cell Invasion====
==[[Roseola overview|Overview]]==
*The initial step of invasion is attachment of the tachyzoite to the host cell membrane. A set of protiens help in the adherence and penetration of the host cell membrane, these proteins also enhance the growth and virulence of the parasite.<ref name="pmid194306352">{{cite journal| author=Ferguson DJ| title=Toxoplasma gondii: 1908-2008, homage to Nicolle, Manceaux and Splendore. | journal=Mem Inst Oswaldo Cruz | year= 2009 | volume= 104 | issue= 2 | pages= 133-48 | pmid=19430635 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19430635  }}</ref>
*In the host cell the parasite forms a vacuole where it divides for 6 to 9 cycles after which the parasites are released into the circulation.  It is an active process which is dependent on the increase in intracellular calcium stores.


====Pathogenesis of Vertical Transmission====
==[[Roseola historical perspective|Historical Perspective]]==
*Different modes of transmission of T.gondii to have a primary infection in a healthy mother include:
**Ingestion of tissue cysts from raw meat and uncooked meat.
**Ingestion of food, fruits, vegetables or water contaminated by oocysts in the cat feces.
**Infection after a solid organ transplant, heart transplant patients are at the highest risk as it can contain tissue cysts.
*Once the patient has a primary infection with tachyzoites in the blood stream during pregnancy a possible transplacental infection can take place.<ref name="pmid103594072">{{cite journal| author=Dunn D, Wallon M, Peyron F, Petersen E, Peckham C, Gilbert R| title=Mother-to-child transmission of toxoplasmosis: risk estimates for clinical counselling. | journal=Lancet | year= 1999 | volume= 353 | issue= 9167 | pages= 1829-33 | pmid=10359407 | doi=10.1016/S0140-6736(98)08220-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10359407  }}</ref>
*The tachyzoites colonize in the placenta and can cross the barrier to reach the fetus in 30% of cases leading to the disease.<ref name="pmid22079164">{{cite journal| author=Robert-Gangneux F, Murat JB, Fricker-Hidalgo H, Brenier-Pinchart MP, Gangneux JP, Pelloux H| title=The placenta: a main role in congenital toxoplasmosis? | journal=Trends Parasitol | year= 2011 | volume= 27 | issue= 12 | pages= 530-6 | pmid=22079164 | doi=10.1016/j.pt.2011.09.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22079164  }} </ref>
*The frequency of transmission of the tachyzoites to the fetus is related to the gestational age, with low transmission rates in the first trimester (10-15%) and highest transmission rates in the third trimester(60-90%). However the disease is more severe if the infection is acquired early in the pregnancy.<ref name="pmid10359407">{{cite journal| author=Dunn D, Wallon M, Peyron F, Petersen E, Peckham C, Gilbert R| title=Mother-to-child transmission of toxoplasmosis: risk estimates for clinical counselling. | journal=Lancet | year= 1999 | volume= 353 | issue= 9167 | pages= 1829-33 | pmid=10359407 | doi=10.1016/S0140-6736(98)08220-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10359407  }} </ref>
*The factors influencing the transfer of tachyzoites to the fetus is not well understood.


===Gross Pathology===
==[[Roseola classification|Classification]]==
*T.gondii has tropism for central nervous system and mosty affects the brain and eye. Areas of necrosis in the brain can be demonstrated on autopsy.


===Microscopic Pathology===
==[[Roseola pathophysiology|Pathophysiology]]==
*Brain autopsy in patients with congenital diagnosis demonstrates periaqueductal and periventricular vasculitis with necrosis.<ref name="pmid18128617">{{cite journal| author=FRENKEL JK| title=Pathogenesis, diagnosis and treatment of human toxoplasmosis. | journal=J Am Med Assoc | year= 1949 | volume= 140 | issue= 4 | pages= 369-77 | pmid=18128617 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18128617  }} </ref><ref name="pmid4592096">{{cite journal| author=Frenkel JK| title=Pathology and pathogenesis of congenital toxoplasmosis. | journal=Bull N Y Acad Med | year= 1974 | volume= 50 | issue= 2 | pages= 182-91 | pmid=4592096 | doi= | pmc=1749352 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4592096  }} </ref>
*Fetal tissue and placenta can demonstrate  T. gondii cysts with the Wright-Giemsa stain and also immunoperoxidase staining using T. gondii–specific antibodies.<ref name="pmid7026410">{{cite journal| author=Conley FK, Jenkins KA, Remington JS| title=Toxoplasma gondii infection of the central nervous system. Use of the peroxidase-antiperoxidase method to demonstrate toxoplasma in formalin fixed, paraffin embedded tissue sections. | journal=Hum Pathol | year= 1981 | volume= 12 | issue= 8 | pages= 690-8 | pmid=7026410 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7026410  }} </ref>


==Causes==
==[[Roseola causes|Causes]]==
Congenital Toxoplasmosis is caused by a coccidian parasite Toxoplasma gondii. The infective tachyzoites reach the fetus by transplacental route.


==Differentiating Toxoplasmosis from other Diseases==
==[[Roseola differential diagnosis|Differentiating Any Disease from other Diseases]]==
The most important congenital infections, which can be transmitted vertically from mother to fetus are the [[TORCH infections]]. These infections have overlapping features and hence, must be differentiated from Toxoplasmosis  :<ref name="pmid25677998">{{cite journal |vauthors=Neu N, Duchon J, Zachariah P |title=TORCH infections |journal=Clin Perinatol |volume=42 |issue=1 |pages=77–103, viii |year=2015 |pmid=25677998 |doi=10.1016/j.clp.2014.11.001 |url=}}</ref><ref name="pmid25654000">{{cite journal |vauthors=Ajij M, Nangia S, Dubey BS |title=Congenital rubella syndrome with blueberry muffin lesions and extensive metaphysitis |journal=J Clin Diagn Res |volume=8 |issue=12 |pages=PD03–4 |year=2014 |pmid=25654000 |pmc=4316306 |doi=10.7860/JCDR/2014/10271.5293 |url=}}</ref>
<SMALL>


{| class="wikitable"
==[[Roseola epidemiology and demographics|Epidemiology and Demographics]]==
!Congenital Infection
!Cardiac Findings
!Skin Findings
!Ocular Findings
!Hepatosplenomegaly
!Hydrocephalus
!Microcephaly
!Intracranial Calcifications
!Hearing deficits
|-
!Toxoplasmosis
|
|
* [[Petechiae]]
* [[Purpura]]
* [[Maculopapular rash]]
|
* [[Chorioretinitis]]
|✔
|✔
|✔
|Diffuse intracranial calcifications
|
|-
!Treponema pallidum
|
|
* [[Petechiae]]
* [[Purpura]]
* [[Maculopapular rash]]
|
* [[Chorioretinitis]]
* [[Glaucoma]]
|✔
|
|
|
|
|-
!Rubella
|
* [[Patent ductus arteriosus (PDA)]]
* [[Pulmonary artery stenosis]]
* [[Coarctation of the aorta]]
* [[Myocarditis]]
|
* [[Petechiae]]
* [[Purpura]]
|
* [[Chorioretinitis]]
* [[Cataracts]]
* [[Glaucoma]]
* [[Microphthalmia]]
|✔
|✔
|✔
|
|✔
|-
!Cytomegalovirus (CMV)
|✔
|
* [[Petechiae]]
* [[Purpura]]
|
* [[Chorioretinitis]]
|✔
|
|✔
|Periventricular calcifications
|✔
|-
!Herpes simplex virus (HSV)
|
* [[Myocarditis]]
|
* [[Petechiae]]
* [[Purpura]]
* [[Vesicles]]
|
* [[Chorioretinitis]]
|✔
|✔
|✔
|
|✔
|-
!Parvovirus B19
|
* [[Myocarditis]]
|
* [[Petechiae]]
* [[Subcutaneous]] [[edema]]
|
* [[Chorioretinitis]]
* [[Cataracts]]
|✔
|
|
|
|
|}


</SMALL>
==[[Roseola risk factors|Risk Factors]]==


==Epidemiology, Demographics==
==[[Roseola screening|Screening]]==  
===Prevalence===
*It is estimated that 25 to 30% of the world's population is infected with Toxoplasma.<ref name="pmid15194258">{{cite journal| author=Montoya JG, Liesenfeld O| title=Toxoplasmosis. | journal=Lancet | year= 2004 | volume= 363 | issue= 9425 | pages= 1965-76 | pmid=15194258 | doi=10.1016/S0140-6736(04)16412-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15194258  }} </ref>
*In United States 89% of women in the childbearing age are susceptible to have an acute infection and at risk for transmitting the parasite to the baby if the primary infection occurs during the getational period.<ref name="pmid18624630">{{cite journal| author=Montoya JG, Remington JS| title=Management of Toxoplasma gondii infection during pregnancy. | journal=Clin Infect Dis | year= 2008 | volume= 47 | issue= 4 | pages= 554-66 | pmid=18624630 | doi=10.1086/590149 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18624630  }} </ref>
*In United States the age adjusted seroprevalence rate is 22.5%. There is significant variation in the distribution with highest prevalence reported in the North-eastern states and lowest in the western states.<ref name="pmid11495859">{{cite journal| author=Jones JL, Kruszon-Moran D, Wilson M, McQuillan G, Navin T, McAuley JB| title=Toxoplasma gondii infection in the United States: seroprevalence and risk factors. | journal=Am J Epidemiol | year= 2001 | volume= 154 | issue= 4 | pages= 357-65 | pmid=11495859 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11495859  }} </ref>
*In countries such as North America, Northern Europe and in Sahelian countries of Africa low seroprevalences of 10% to 30% are observed. In countries of Central and Southern Europe, tropical African countries and Latin America the seroprevalence is around 30 to 50%. This shows the variation within the countries and as well as between the countries.<ref name="pmid19433092">{{cite journal| author=Pappas G, Roussos N, Falagas ME| title=Toxoplasmosis snapshots: global status of Toxoplasma gondii seroprevalence and implications for pregnancy and congenital toxoplasmosis. | journal=Int J Parasitol | year= 2009 | volume= 39 | issue= 12 | pages= 1385-94 | pmid=19433092 | doi=10.1016/j.ijpara.2009.04.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19433092  }} </ref>


===Incidence===
==[[Roseola natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
*Toxoplasmosis affects 500 to 4000 new borns every year.<ref name="pmid11740319">{{cite journal| author=Jara M, Hsu HW, Eaton RB, Demaria A| title=Epidemiology of congenital toxoplasmosis identified by population-based newborn screening in Massachusetts. | journal=Pediatr Infect Dis J | year= 2001 | volume= 20 | issue= 12 | pages= 1132-5 | pmid=11740319 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11740319  }} </ref><ref name="pmid15580732">{{cite journal| author=Lopez A, Dietz VJ, Wilson M, Navin TR, Jones JL| title=Preventing congenital toxoplasmosis. | journal=MMWR Recomm Rep | year= 2000 | volume= 49 | issue= RR-2 | pages= 59-68 | pmid=15580732 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15580732  }} </ref>
*In United States, Toxoplasmosis affects 1.1 million people every year.<ref name="urlCDC - Toxoplasmosis - Epidemiology & Risk Factors">{{cite web |url=https://www.cdc.gov/parasites/toxoplasmosis/epi.html |title=CDC - Toxoplasmosis - Epidemiology & Risk Factors |format= |work= |accessdate=}}</ref>
===Race===
*The prevalence of Toxoplasmosis is higher in non-Hispanic black population and Mexican Americans than non-Hispanic white population.<ref name="pmid17827351">{{cite journal| author=Jones JL, Kruszon-Moran D, Sanders-Lewis K, Wilson M| title=Toxoplasma gondii infection in the United States, 1999 2004, decline from the prior decade. | journal=Am J Trop Med Hyg | year= 2007 | volume= 77 | issue= 3 | pages= 405-10 | pmid=17827351 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17827351  }} </ref>
===Age===
*A decreasing trend in prevalence is reported in the population of U.S born persons aged between 12 to 49 years; with 14% between the years 1988 to 1994, and 9% in the years 1999 to 2004. This trend is attributed to the improvement of hygienic conditions, changes in farming systems, the consumption of frozen meat, and the feeding of cats with sterilized food.<ref name="pmid17827351">{{cite journal| author=Jones JL, Kruszon-Moran D, Sanders-Lewis K, Wilson M| title=Toxoplasma gondii infection in the United States, 1999 2004, decline from the prior decade. | journal=Am J Trop Med Hyg | year= 2007 | volume= 77 | issue= 3 | pages= 405-10 | pmid=17827351 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17827351  }} </ref>
*The similar decreasing trend of seroprevalence is been reported in France and Netherlands.<ref name="pmid20587361">{{cite journal| author=Villena I, Ancelle T, Delmas C, Garcia P, Brezin AP, Thulliez P et al.| title=Congenital toxoplasmosis in France in 2007: first results from a national surveillance system. | journal=Euro Surveill | year= 2010 | volume= 15 | issue= 25 | pages=  | pmid=20587361 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20587361  }} </ref><ref name="pmid20492743">{{cite journal| author=Hofhuis A, van Pelt W, van Duynhoven YT, Nijhuis CD, Mollema L, van der Klis FR et al.| title=Decreased prevalence and age-specific risk factors for Toxoplasma gondii IgG antibodies in The Netherlands between 1995/1996 and 2006/2007. | journal=Epidemiol Infect | year= 2011 | volume= 139 | issue= 4 | pages= 530-8 | pmid=20492743 | doi=10.1017/S0950268810001044 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20492743  }} </ref>
===Developing Countries===
*In countries with poor hygienic measures and using unfiltered surface water for consumption reported higher seroprevalence rates. In these countries the childhood population is at a higher risk of acquiring the infection, the mean age is reported to be 15 years.<ref name="pmid19324041">{{cite journal| author=Jones JL, Dubey JP| title=Waterborne toxoplasmosis--recent developments. | journal=Exp Parasitol | year= 2010 | volume= 124 | issue= 1 | pages= 10-25 | pmid=19324041 | doi=10.1016/j.exppara.2009.03.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19324041  }} </ref><ref name="pmid15958156">{{cite journal| author=Ertug S, Okyay P, Turkmen M, Yuksel H| title=Seroprevalence and risk factors for toxoplasma infection among pregnant women in Aydin province, Turkey. | journal=BMC Public Health | year= 2005 | volume= 5 | issue=  | pages= 66 | pmid=15958156 | doi=10.1186/1471-2458-5-66 | pmc=1177966 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15958156  }} </ref><ref name="pmid12533282">{{cite journal| author=Bahia-Oliveira LM, Jones JL, Azevedo-Silva J, Alves CC, Oréfice F, Addiss DG| title=Highly endemic, waterborne toxoplasmosis in north Rio de Janeiro state, Brazil. | journal=Emerg Infect Dis | year= 2003 | volume= 9 | issue= 1 | pages= 55-62 | pmid=12533282 | doi=10.3201/eid0901.020160 | pmc=2873742 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12533282  }} </ref>
 
==Risk Factors==
The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with Toxoplasma oocysts excreted in cat feces.<br>
The risk factors which predispose pregnant women for primary infection include: <ref name="pmid15696004">{{cite journal| author=Boyer KM, Holfels E, Roizen N, Swisher C, Mack D, Remington J et al.| title=Risk factors for Toxoplasma gondii infection in mothers of infants with congenital toxoplasmosis: Implications for prenatal management and screening. | journal=Am J Obstet Gynecol | year= 2005 | volume= 192 | issue= 2 | pages= 564-71 | pmid=15696004 | doi=10.1016/j.ajog.2004.07.031 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15696004  }} </ref>
*Consumption of raw oysters and clams<ref name="pmid15562605">{{cite journal| author=Lindsay DS, Collins MV, Mitchell SM, Wetch CN, Rosypal AC, Flick GJ et al.| title=Survival of Toxoplasma gondii oocysts in Eastern oysters (Crassostrea virginica). | journal=J Parasitol | year= 2004 | volume= 90 | issue= 5 | pages= 1054-7 | pmid=15562605 | doi=10.1645/GE-296R | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15562605  }}</ref>
*Eating undercooked meat which includes pork, beef and lamb<ref name="pmid18508057">{{cite journal| author=Dubey JP, Jones JL| title=Toxoplasma gondii infection in humans and animals in the United States. | journal=Int J Parasitol | year= 2008 | volume= 38 | issue= 11 | pages= 1257-78 | pmid=18508057 | doi=10.1016/j.ijpara.2008.03.007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18508057  }}</ref>
*Drinking unpasteurized goat’s milk<ref name="JonesDargelas2009">{{cite journal|last1=Jones|first1=Jeffrey L.|last2=Dargelas|first2=Valerie|last3=Roberts|first3=Jacquelin|last4=Press|first4=Cindy|last5=Remington|first5=Jack S.|last6=Montoya|first6=Jose G.|title=Risk Factors forToxoplasma gondiiInfection in the United States|journal=Clinical Infectious Diseases|volume=49|issue=6|year=2009|pages=878–884|issn=1058-4838|doi=10.1086/605433}}</ref>
*Exposure to kitten litter
*Working with meat<ref name="Robert-GangneuxDarde2012">{{cite journal|last1=Robert-Gangneux|first1=F.|last2=Darde|first2=M.-L.|title=Epidemiology of and Diagnostic Strategies for Toxoplasmosis|journal=Clinical Microbiology Reviews|volume=25|issue=2|year=2012|pages=264–296|issn=0893-8512|doi=10.1128/CMR.05013-11}}</ref>
*Low socioeconomic status<ref name="Robert-GangneuxDarde2012">{{cite journal|last1=Robert-Gangneux|first1=F.|last2=Darde|first2=M.-L.|title=Epidemiology of and Diagnostic Strategies for Toxoplasmosis|journal=Clinical Microbiology Reviews|volume=25|issue=2|year=2012|pages=264–296|issn=0893-8512|doi=10.1128/CMR.05013-11}}</ref>
*Poor Hygiene<ref name="Robert-GangneuxDarde2012">{{cite journal|last1=Robert-Gangneux|first1=F.|last2=Darde|first2=M.-L.|title=Epidemiology of and Diagnostic Strategies for Toxoplasmosis|journal=Clinical Microbiology Reviews|volume=25|issue=2|year=2012|pages=264–296|issn=0893-8512|doi=10.1128/CMR.05013-11}}</ref>
*Drinking unfiltered water<ref name="Robert-GangneuxDarde2012">{{cite journal|last1=Robert-Gangneux|first1=F.|last2=Darde|first2=M.-L.|title=Epidemiology of and Diagnostic Strategies for Toxoplasmosis|journal=Clinical Microbiology Reviews|volume=25|issue=2|year=2012|pages=264–296|issn=0893-8512|doi=10.1128/CMR.05013-11}}</ref>
*Immunocompromised state
 
==Screening==
*Majority of the countries do not follow standard screening for the detection of Toxoplasma infection during the antenatal period.
*In countries such as France, Austria, Brazil standard screening is followed during the antenatal period for detecton of  toxoplasmosis .<ref name="pmid22639318">{{cite journal| author=Doğan K, Kafkaslı A, Karaman U, Atambay M, Karaoğlu L, Colak C| title=[The rates of seropositivity and seroconversion of toxoplasma infection in pregnant women]. | journal=Mikrobiyol Bul | year= 2012 | volume= 46 | issue= 2 | pages= 290-4 | pmid=22639318 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22639318  }} </ref>
*Women are tested for antibodies aganist Toxoplasma on their first antenatal visit, and if they are seropositive they are followed up periodically in every trimester to examine the trends in IgG tite levels.<ref name="BergholdHerzog2016">{{cite journal|last1=Berghold|first1=Christian|last2=Herzog|first2=Sereina Annik|last3=Jakse|first3=Heidelinde|last4=Berghold|first4=Andrea|title=Prevalence and incidence of toxoplasmosis: a retrospective analysis of mother-child examinations, Styria, Austria, 1995 to 2012|journal=Eurosurveillance|volume=21|issue=33|year=2016|issn=1025-496X|doi=10.2807/1560-7917.ES.2016.21.33.30317}}</ref>
*Women who seroconvert during gestation, fetal testing by amniocentesis and fetal blood sampling is recommended to identify the infection status in the fetus.
 
==Natural History, Complications, Prognosis==
===Natural History===
Congenital Toxoplasmosis is due to transplacental transmission of infective tachyzoites to the developing fetus. The severity of clinical manifestation is dependent on the timing of the infection during gestation. Early gestational infection results in a miscarriage, still birth or a new born with neurological abnormalities. Late gestational infection is asymptomatic in majority of children at birth but they develop neurological abnormalities and vision changes in the 1st or 2nd decade.<ref name="pmid11333376">{{cite journal| author=Jones JL, Lopez A, Wilson M, Schulkin J, Gibbs R| title=Congenital toxoplasmosis: a review. | journal=Obstet Gynecol Surv | year= 2001 | volume= 56 | issue= 5 | pages= 296-305 | pmid=11333376 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11333376  }} </ref>
===Complications===
If left untreated congenital Toxoplasmosis results in mental retardation, seizures, motor difficulties, severe vision loss, hydro or microcephalus and hearing loss.<ref name="WebsterStillwaggon2011">{{cite journal|last1=Webster|first1=Joanne P.|last2=Stillwaggon|first2=Eileen|last3=Carrier|first3=Christopher S.|last4=Sautter|first4=Mari|last5=McLeod|first5=Rima|title=Maternal Serologic Screening to Prevent Congenital Toxoplasmosis: A Decision-Analytic Economic Model|journal=PLoS Neglected Tropical Diseases|volume=5|issue=9|year=2011|pages=e1333|issn=1935-2735|doi=10.1371/journal.pntd.0001333}}</ref>
 
===Prognosis===
Prognosis of congenital Toxoplasmosis is dependent on the severity of the disease. Severe infection causes death at an early age, asymptomatic infection at birth will present in the 1st or 2nd decade with progressive chorioretinitis with poor prognosis.


==Diagnosis==
==Diagnosis==
The presence of intracranial calcifications, hydrocephalus and chorioretinitis is a classic traid of congenital Toxoplasmosis.
[[Roseola history and symptoms|History and Symptoms]] | [[Roseola physical examination|Physical Examination]] | [[Roseola laboratory findings|Laboratory Findings]] | [[Roseola electrocardiogram|Electrocardiogram]] | [[Roseola chest x ray|Chest X Ray]] | [[Roseola CT|CT]] | [[Roseola MRI|MRI]] | [[Roseola echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Roseola other imaging findings|Other Imaging Findings]] | [[Roseola other diagnostic studies|Other Diagnostic Studies]]
===History and Symptoms===
The severity of manifestations in the newborn are dependent on the fetal age when the infection occurred and the trimester of pregnancy the mother gets infected. The disease is severe in mothers who acquire infection in the first trimester.
====Symptoms in the Mother====
*Acute infection of Toxoplasma in an asymptomatic women can be easily missed as they present with flu like symptoms, lymph node swelling in the neck and rarely a skin rash.
*Early gestational infection results in a miscarriage or a still birth.
 
====Symptoms in newborn====
The clinical manifestations in the newborn are dependent on the month of gestation the infection has occurred - earlier the infection more severe the disease.
'''Infection in early pregnancy''' : Neuro-ocular symptoms are typical presenting features in Congenital Toxoplasmosis.
*Involvement of the CNS can present with psycho-motor retardation and seizures.<ref name="pmid14023494">{{cite journal| author=COUVREUR J, DESMONTS G| title=Congenital and maternal toxoplasmosis. A review of 300 congenital cases. | journal=Dev Med Child Neurol | year= 1962 | volume= 4 | issue=  | pages= 519-30 | pmid=14023494 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14023494  }} </ref><ref name="pmid4698952">{{cite journal| author=Saxon SA, Knight W, Reynolds DW, Stagno S, Alford CA| title=Intellectual deficits in children born with subclinical congenital toxoplasmosis: a preliminary report. | journal=J Pediatr | year= 1973 | volume= 82 | issue= 5 | pages= 792-7 | pmid=4698952 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4698952  }} </ref>
*Chorioretinitis presents with impaired vision.
*Obstruction in the ventricles results in accumalation of CSF, causing enlargement of the head and increased intracranial pressure symptoms such as vomiting, headache, confusion and double vision.<ref name="pmid16098868">{{cite journal| author=Chen KT, Eskild A, Bresnahan M, Stray-Pedersen B, Sher A, Jenum PA| title=Previous maternal infection with Toxoplasma gondii and the risk of fetal death. | journal=Am J Obstet Gynecol | year= 2005 | volume= 193 | issue= 2 | pages= 443-9 | pmid=16098868 | doi=10.1016/j.ajog.2004.12.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16098868  }} </ref><ref name="HutsonWheeler2015">{{cite journal|last1=Hutson|first1=Samuel L.|last2=Wheeler|first2=Kelsey M.|last3=McLone|first3=David|last4=Frim|first4=David|last5=Penn|first5=Richard|last6=Swisher|first6=Charles N.|last7=Heydemann|first7=Peter T.|last8=Boyer|first8=Kenneth M.|last9=Noble|first9=A. Gwendolyn|last10=Rabiah|first10=Peter|last11=Withers|first11=Shawn|last12=Montoya|first12=Jose G.|last13=Wroblewski|first13=Kristen|last14=Karrison|first14=Theodore|last15=Grigg|first15=Michael E.|last16=McLeod|first16=Rima|title=Patterns of Hydrocephalus Caused by CongenitalToxoplasma gondiiInfection Associate With Parasite Genetics|journal=Clinical Infectious Diseases|volume=61|issue=12|year=2015|pages=1831–1834|issn=1058-4838|doi=10.1093/cid/civ720}}</ref>
*Jaundice
*Focal neurological deficits and learning disabilities
*Feeding difficulties
*Hearing impairment
*Skin rash
*Fever
'''Infection later in the pregnancy''': Majority of the infected newborns remain asymptomatic at birth.<ref name="pmid14023494">{{cite journal| author=COUVREUR J, DESMONTS G| title=Congenital and maternal toxoplasmosis. A review of 300 congenital cases. | journal=Dev Med Child Neurol | year= 1962 | volume= 4 | issue=  | pages= 519-30 | pmid=14023494 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14023494  }} </ref>
*Children develop psycho-motor retardation and retinochoroiditis later in life.
*Loss of vision is a common symptom and is seen in 95% of infants due to chorioretinitis.
 
===Physical Examination===
Typical examination findings in Toxoplasmosis include chorioretinitis, hydrocephalus and developmental delay. The presence of following physical examination findings are suggestive of congenital Toxoplamosis:<ref name="pmid14023494">{{cite journal| author=COUVREUR J, DESMONTS G| title=Congenital and maternal toxoplasmosis. A review of 300 congenital cases. | journal=Dev Med Child Neurol | year= 1962 | volume= 4 | issue=  | pages= 519-30 | pmid=14023494 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14023494  }} </ref><ref name="pmid12776962">{{cite journal| author=Jones J, Lopez A, Wilson M| title=Congenital toxoplasmosis. | journal=Am Fam Physician | year= 2003 | volume= 67 | issue= 10 | pages= 2131-8 | pmid=12776962 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12776962  }} </ref>
*Low birth weight
*Bulging anterior fontanelle in hydrocephalus
*Microcephaly
*Developmental delay
*Spasticities and paresis
*Ophalmologic examination findings include:
**Macular-pigmented lesions with a central necrotic area on the retina on fundoscopic examination suggest chorioretinitis. "Headlight in the fog" is the characteristic description of ocular Toxoplasmosis.<ref name="ModrzejewskaPatalan2016">{{cite journal|last1=Modrzejewska|first1=Monika|last2=Patalan|first2=Jacek|last3=Kulik|first3=Urszula|last4=Czeszyńska|first4=Maria|title=Ocular manifestation of congenital toxoplasmosis, clinical implication – case report|journal=Polish Gynaecology|volume=87|issue=03|year=2016|pages=226–230|issn=0017-0011|doi=10.17772/gp/61990}}</ref>
**Glaucoma, cataracts, vitreous opacification, retinal hemorrhage or detachment, and optic atrophy can be demonstrated in longstanding infection.
*Sensorineural deafness
*Hepatosplenomegaly
*Maculopapular rash
 
===Laboratory Findings===
====Prenatal Diagnosis====
*During the period of gestation Toxoplasma is diagnosed by the presence of parasite in the amniotic fluid or in the fetal tissue by DNA amplification, microscopy or by isolation of the organism.<ref name="pmid10521739">{{cite journal| author=Foulon W, Pinon JM, Stray-Pedersen B, Pollak A, Lappalainen M, Decoster A et al.| title=Prenatal diagnosis of congenital toxoplasmosis: a multicenter evaluation of different diagnostic parameters. | journal=Am J Obstet Gynecol | year= 1999 | volume= 181 | issue= 4 | pages= 843-7 | pmid=10521739 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10521739  }} </ref>
*The most commonly used diagnostic test is the PCR of the amniotic fluid and a positive test is diagnostic of congenital Toxoplasmosis.<ref name="pmid10521739">{{cite journal| author=Foulon W, Pinon JM, Stray-Pedersen B, Pollak A, Lappalainen M, Decoster A et al.| title=Prenatal diagnosis of congenital toxoplasmosis: a multicenter evaluation of different diagnostic parameters. | journal=Am J Obstet Gynecol | year= 1999 | volume= 181 | issue= 4 | pages= 843-7 | pmid=10521739 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10521739  }} </ref>
 
====Postnatal Diagnosis====
The most commonly used diagnostic investigation for early dectection is the serological detection of antibodies (IgG, IgM and IgG) in the serum of the infant. A combination of all the antibodies is done as the maternal IgG can cross the placenta and give false positive result.
*In the postnatal period the gold standard for diagnosis of Congenital Toxoplasmosis is the persistence of Toxoplasma IgG by 12months of age.
*During the postnatal period the standard to rule out diagnosis is the the absence of Toxoplasma IgG at 12months of age in the absence of treatment.
 
===Imaging Studies===
====Ultrasound====
*In Toxoplasma seropositive pregnant women with negative amniotic PCR and a high degree of suspicion fetal ultrasound is done to rule out hydrocephalus, intracranial calcifications, and intrauterine growth retardation.<ref name="pmid12868082">{{cite journal| author=Gay-Andrieu F, Marty P, Pialat J, Sournies G, Drier de Laforte T, Peyron F| title=Fetal toxoplasmosis and negative amniocentesis: necessity of an ultrasound follow-up. | journal=Prenat Diagn | year= 2003 | volume= 23 | issue= 7 | pages= 558-60 | pmid=12868082 | doi=10.1002/pd.632 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12868082  }} </ref>
====Principles and various methods used for the diagnosis of congenital toxoplasmosis:====
{| class="wikitable"
!Principle
!Detection
!Method
!Findings supporting the diagnosis of Toxoplasmosis
|-
| rowspan="2" |Toxoplasma specific humoral responses<ref name="pmid26141811">{{cite journal| author=Tanimura K, Nishikawa A, Tairaku S, Shinozaki N, Deguchi M, Morizane M et al.| title=The IgG avidity value for the prediction of Toxoplasma gondii infection in the amniotic fluid. | journal=J Infect Chemother | year= 2015 | volume= 21 | issue= 9 | pages= 668-71 | pmid=26141811 | doi=10.1016/j.jiac.2015.05.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26141811  }}</ref>
|IgG, IgM, IgA
|Dye test, ELISA, ELISA-like assays,ISAGA, immunofluorescence, agglutination
|
*Positive IgM after 5 days of life and in the absence of blood transfusions
*Positive IgA after 10 days of life
*Persistence of Toxoplasma IgG beyond 1 year of age
|-
|IgG, IgM, and IgA to specific Toxoplasma antigen
|
Western blot
|
*Presence of specific bands only seen in the newborn or bands with higher intensity than maternal ones for IgG and/or IgM and/or IgA in a reference laboratory
|-
|Toxoplasma nucleic acid amplification
|DNA
|PCR
|
*Positive result in any body fluid (e.g: amniotic fluid, cerebrospinal fluid, peripheral blood, urine)
|-
|Immunohistochemistry of Toxoplasma specific antigens in tissue
|Antigens
|Immunoperoxidase
|
*Positive result in any tissue(e.g., brain or other fetal tissue)
|-
|Visualization by microscopy
|Visual identification of tachyzoites and/or cysts
|Stains such as hematoxylin/eosin, Giemsa
|
*Positive identification in a reference laboratory
|-
|Isolation of Toxoplasma
|Whole live parasite
|Inoculation in peritoneal cavity of mice
|
*Detection of live cysts from any body fluid or tissue that has been inoculated in mice in a reference laboratory
|-
|Brain imaging
|
*Brain calcifications
*Hydrocephaly
*Microcephaly
|
Ultrasound, CT, brain MRI
|
*Findings can be suggestive but are not diagnostic of congenital Toxoplasmosis since other etiologies may result in similar findings
|-
|Retinal exam
|Inflammation in choroidal and retinal layers
|Ophthalmological exam
|
*Retinochoroidal lesions can be highly suggestive or, at times, diagnostic of congenital Toxoplasmosis
|}
<small>Table adopted from Laboratory Diagnosis of Congenital Toxoplasmosis<ref name="PomaresMontoya2016">{{cite journal|last1=Pomares|first1=Christelle|last2=Montoya|first2=Jose G.|last3=Kraft|first3=C. S.|title=Laboratory Diagnosis of Congenital Toxoplasmosis|journal=Journal of Clinical Microbiology|volume=54|issue=10|year=2016|pages=2448–2454|issn=0095-1137|doi=10.1128/JCM.00487-16}}</ref> </small>
 
===Interpretation of Serological Tests===
{{familytree/start}}
{{familytree | | | | | | | A01 | | | | | | | | | | | | | | | | |A01=IgG/IgM(ideally performed in the first trimester}}
{{familytree | | | | | | | |!| | | | | | | | | | | | | | | | | | | | | | }}
{{familytree | |,|-|-|-|v|-|^|-|v|-|-|-|.| | | | | | | | | | | | | | | | }}
{{familytree | |!| | | |!| | | |!| | | |!| | | | | | | | | | | | | | | | }}
{{familytree | B01 | | B02 | | B03 | | B04 | | | | | | | | | | |B01='''Negative IgG and IgM'''|B02='''Positive IgG''' <br>'''Negative IgM'''|B03='''Positive IgM'''<br>'''Negative IgG'''|B04='''Positive IgG and IgM'''}}
{{familytree | |!| | | |!| | | |!| | | |!| | | | | | | | | | | | | | | | }}
{{familytree | |!| | | |!| | | |!| | | |!| | | | | | | | | | | | | | | | }}
{{familytree | C01 | | C02 | | C03 | | C04 | | | | | | | | | | | C01= ❑ No serologic evidence of Toxoplasma infection<br>❑ Risk of congenital Toxoplasmosis only if the woman aquires infection during the pregnancy<br>❑ Counsel about the preventive measures for T.gondii| C02= '''<18 weeks of gestation''' Infection aquired in the past and prior to the pregnancy<br>❑ Risk of infection is zero unless the patient is immunocompromised<br>  '''≥18 weeks of gestation'''<br>❑ It is difficult to establish the timing of infection|C03=Repeat IgG and IgM in 1 to 3weeks|C04=Serum should be sent to reference laboratory for confirmatory testing}}
{{familytree | |!| | | |!| | | |!| | | | | | | | | | | | | | | | | | | | }}
{{familytree | |!| | | |!| | |,|^|-|-|-|-|-|-|-|-|-|-|.| | | | | | | | | }}
{{familytree | |!| | | |!| | |!| | | | | | | | | | | |!| | | | | | | | | }}
{{familytree | D01 | | D02 | |D03| | | | | | | | | | D04 | | | | | | |D01= Follow up testing is indicated during gestation to detect seroconversion|D02= '''≤ 18 weeks of gestation'''<br> ❑  No further action indicated <br> '''>18 weeks of gestation'''<br>❑ Compare to previous serological tests and send samples to a reference laboratory to confirm the timing of infection| D03= ❑ '''Negative IgG''' and '''Positive IgM''' <br>❑ Does not have clinical relevance<ref name="pmid8968902">{{cite journal| author=Liesenfeld O, Press C, Montoya JG, Gill R, Isaac-Renton JL, Hedman K et al.| title=False-positive results in immunoglobulin M (IgM) toxoplasma antibody tests and importance of confirmatory testing: the Platelia Toxo IgM test. | journal=J Clin Microbiol | year= 1997 | volume= 35 | issue= 1 | pages= 174-8 | pmid=8968902 | doi= | pmc=229533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8968902  }} </ref>|D04= ❑ '''Positive IgG and IgM'''<br> ❑ Seroconverted and fetus is at risk<br> ❑ Initiate treatment and consider PCR}}
{{familytree/end}}
<small>Table adopted from Management of Toxoplasma gondii Infection during Pregnancy<ref name="MontoyaRemington2008">{{cite journal|last1=Montoya|first1=Jose G.|last2=Remington|first2=Jack S.|title=Clinical Practice: Management ofToxoplasma gondiiInfection during Pregnancy|journal=Clinical Infectious Diseases|volume=47|issue=4|year=2008|pages=554–566|issn=1058-4838|doi=10.1086/590149}}</ref> </small>
 
==Approach for the management of Congenital Toxoplasmosis==
===Approach during pregnancy with known seropositive status===
Screening programs benefit the clinicians with information regarding maternal serological and amniotic fluid PCR test results, precise gestational age at which the mother was infected, and detailed anti-Toxoplasma treatment history which play a vital role in the management of congenital Toxoplasmosis.
{{familytree/start}}
{{familytree | | | | | | | | | A01 | | | | | |A01=Maternal Infection Status}}
{{familytree | | |,|-|-|-|-|-|-|+|-|-|-|-|-|-|.| }}
{{familytree | | B01 | | | | | B02 | | | | | B03 |B01=❑ No maternal infection acquired during pregnancy and remains seronegative one month after birth '''or'''<br> ❑ Maternal infection acquired prior to pregnancy|B02=❑ Maternal infection acquired during pregnancy '''and'''<br>❑ Positive PCR of amniotic fluid|B03=❑ Maternal infection acquired during the pregnancy and a negative amniotic fluid PCR '''or'''<br> ❑ Amniocentesis was not done}}
{{familytree | | |!| | | | | | |!| | | | | | |!| |}}
{{familytree | | C01 | | | | | C02 | | | | | C03 |C01= No Infant Follow up|C02=Confirmed diagnosis of Congenital Toxoplasmosis|C03=❑ Testing for IgG, IgM, IgA at birth by Western blot or by conventional serologies at ≥ 10 days of life<br>❑ If diagnosis not made at initial testing, follow up testing with IgG, IgM, IgA at 1 month age and every 2 months thereafter is indicated}}
{{familytree | | | | | | | | | |!| | | | | | |!| |}}
{{familytree | | | | | | | | | |!| | | |,|-|-|^|-|-|.| |}}
{{familytree | | | | | | | | | D01 | | D02 | | | | D03 | D01=❑ Initiate Treatment and <br>❑ Order a serological test for IgG, IgM and IgA to further confirm the diagnosis and to rule out a false positive PCR test result|D02=Presence of any one of the below criteria is diagnostic of congenital Toxoplasmosis:<br> ❑ Presence of IgM and/or IgA ≥ 10 days of life and/or during the follow up test samples<br>❑ In new born presence of specific band or bands with higher intensity than maternal ones for IgG/IgM/IgA on Western blot<br> ❑ Persistant increase in IgG titer without treatment ≤ 12months of age|D03=❑ Diagnosis of Toxoplasma is excluded if: <br>❑ The absence of IgG titer without treatment is documented ≤ 12months of age}}
{{familytree | | | | | | | | | | | | | |!| | | | | |!|}}
{{familytree | | | | | | | | | | | | | |!| | | | | |!|}}
{{familytree | | | | | | | | | | | | | |!| | | | | |!|}}
{{familytree | | | | | | | | | | | | | E01| | | | E02|E01=❑ Confirmed diagnosis of Congenital Toxoplasmosis<br>❑ Inititate Treatment|E02=Diagnosis exlcuded}}
{{familytree/end}}
<small>Table adopted from Laboratory Diagnosis of Congenital Toxoplasmosis<ref name="PomaresMontoya2016">{{cite journal|last1=Pomares|first1=Christelle|last2=Montoya|first2=Jose G.|last3=Kraft|first3=C. S.|title=Laboratory Diagnosis of Congenital Toxoplasmosis|journal=Journal of Clinical Microbiology|volume=54|issue=10|year=2016|pages=2448–2454|issn=0095-1137|doi=10.1128/JCM.00487-16}}</ref> </small>
 
==Approach to the patient with unknown Toxoplasma serology status==
{{familytree/start}}
{{familytree | | | | | | | | | A01 | | | | | |A01= ❑ Suspicion of acquired infection and/or <br>❑ Clinical signs at birth <br>❑ As antenatal screening is not performed during gestation, parallel testing of maternal serum with the newborn serum should be done}}
{{familytree | | |,|-|-|-|-|-|-|+|-|-|-|-|-|.| }}
{{familytree | | B01 | | | | | B02 | | | | |B03|B01=❑ Maternal serum is Toxoplasma seronegative at birth and confirmed to remain negative 1 month after birth '''or''' <br>❑ Confirmation of maternal infection acquired prior to gestation|B02= ❑ PCR of CSF, urine, whole blood depending on the clinical signs in the baby|B03= ❑ Testing for IgG, IgM, IgA by conventional serologies ≥10 days of life}}
{{familytree | | |!| | | | | | |!| | | | | | |!|}}
{{familytree | | |!| | | |,|-|-|^|-|-|.| |,|-|^|-|.|}}
{{familytree | | C01 | |C02 | | | C03| |C04| | C05|C01=No infant follow up|C02= Positive|C03= Negative|C04=If diagnosis is not made on the initial testing| C05= Presence of IgG plus IgM and/or IgA}}
{{familytree | | | | | | |!| | | | | |`|-|v|'| | | |!|}}
{{familytree | | | | | | |!| | | | | | | |!| | | | |!|}}
{{familytree | | | | | | |!| | | | | | | |!| | | | |!|}}
{{familytree | | | | | | D01 | | | | | | D02| | | |D03|D01=❑ Confirmed Diagnosis<br>❑ Initiate Treatment|D02= ❑ Follow up testing with IgG, IgM, IgA at 1 month age and every 2 months thereafter is indicated|D03= ❑ Confirmed Diagnosis<br>❑ Initiate Treatment}}
{{familytree | | | | | | | | | | | | | | |!| | | | | | | | |}}
{{familytree | | | | | | | | | | | | | | |!| | | | | | | | |}}
{{Family tree| | | | | | | | | | | |,|-|-|^|-|-|.| | | | | |}}
{{familytree | | | | | | | | | | | |!| | | | | |!| | | | | |}}
{{familytree | | | | | | | | | | | E01|| | | |E02| | E01= Presence of any one of the below criteria is diagnostic of congenital Toxoplasmosis:<br>❑ Presence of IgM and/or IgA >10 days of life and/or during the follow up test samples<br> ❑ Persistant increase in IgG titer without treatment ≤12months of age|E02= ❑ Diagnosis of Toxoplasma is excluded if: <br> ❑ The absence of IgG titer without treatment is documented ≤ 12months of age}}
{{familytree | | | | | | | | | | | |!| | | | | | |!| | | |}}
{{familytree | | | | | | | | | | | |!| | | | | | |!| | | |}}
{{familytree | | | | | | | | | | | F01| | | | | F02| F01=❑ Confirmed Diagnosis of Congenital Toxoplasmosis<br>❑ Initiate Treatment|F02= Diagnosis Excluded}}
{{familytree/end}}
<small>Table adopted from Laboratory Diagnosis of Congenital Toxoplasmosis<ref name="PomaresMontoya2016">{{cite journal|last1=Pomares|first1=Christelle|last2=Montoya|first2=Jose G.|last3=Kraft|first3=C. S.|title=Laboratory Diagnosis of Congenital Toxoplasmosis|journal=Journal of Clinical Microbiology|volume=54|issue=10|year=2016|pages=2448–2454|issn=0095-1137|doi=10.1128/JCM.00487-16}}</ref> </small>


==Treatment==
==Treatment==
[[Roseola medical therapy|Medical Therapy]] | [[Roseola surgery|Surgery]] | [[Roseola primary prevention|Primary Prevention]] | [[Roseola secondary prevention|Secondary Prevention]] | [[Roseola cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Roseola future or investigational therapies|Future or Investigational Therapies]]


===Medical Therapy===
==Case Studies==
The principle for medical therapy of Congenital Toxoplasmosis is based on the timing of diagnosis.
[[Roseola case study one|Case #1]]
*Pregnant women diagnosed with primary Toxoplasma infection: Spiramycin should be initiated and identification of infection status in the fetus by amniocentesis and fetal blood sampling should be done. If fetal infection is ruled out, spiramycin should be continued throughout the pregnancy.<ref name="pmid7982341">{{cite journal| author=Matsui D| title=Prevention, diagnosis, and treatment of fetal toxoplasmosis. | journal=Clin Perinatol | year= 1994 | volume= 21 | issue= 3 | pages= 675-89 | pmid=7982341 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7982341  }} </ref><ref name="pmid20967235">{{cite journal| author=Cortina-Borja M, Tan HK, Wallon M, Paul M, Prusa A, Buffolano W et al.| title=Prenatal treatment for serious neurological sequelae of congenital toxoplasmosis: an observational prospective cohort study. | journal=PLoS Med | year= 2010 | volume= 7 | issue= 10 | pages=  | pmid=20967235 | doi=10.1371/journal.pmed.1000351 | pmc=2953528 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20967235  }}</ref>
**It is administered orally at a dosage of 1.0 g (or 3 million U) every 8 h (total dosage of 3 g or 9 million U per day).
*In patients with established fetal infection: Pyrimethamine, sulfadiazine, and folinic acid should be given throughout the pregnancy and it is shown to decrease infection of the placenta, neurological sequalae and ocular symptoms.<ref name="pmid23343802">{{cite journal| author=Paquet C, Yudin MH, Society of Obstetricians and Gynaecologists of Canada| title=Toxoplasmosis in pregnancy: prevention, screening, and treatment. | journal=J Obstet Gynaecol Can | year= 2013 | volume= 35 | issue= 1 | pages= 78-81 | pmid=23343802 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23343802  }} </ref><ref name="pmid11821337">{{cite journal| author=Thulliez P| title=Commentary: Efficacy of prenatal treatment for toxoplasmosis: a possibility that cannot be ruled out. | journal=Int J Epidemiol | year= 2001 | volume= 30 | issue= 6 | pages= 1315-6 | pmid=11821337 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11821337  }} </ref>However, it does not reduce the rate of transmission and the regimen is contraindicated in the first trimester of pregnancy due to the teratogenic effect.<ref name="pmid9988811">{{cite journal| author=Foulon W, Villena I, Stray-Pedersen B, Decoster A, Lappalainen M, Pinon JM et al.| title=Treatment of toxoplasmosis during pregnancy: a multicenter study of impact on fetal transmission and children's sequelae at age 1 year. | journal=Am J Obstet Gynecol | year= 1999 | volume= 180 | issue= 2 Pt 1 | pages= 410-5 | pmid=9988811 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9988811  }} </ref>
*In infants with established infection, low or high dose pyrimethamine with sulfadiazine throughout the first year of life, showed better outcomes compared to untreated infants. <ref name="pmid8054436">{{cite journal| author=McAuley J, Boyer KM, Patel D, Mets M, Swisher C, Roizen N et al.| title=Early and longitudinal evaluations of treated infants and children and untreated historical patients with congenital toxoplasmosis: the Chicago Collaborative Treatment Trial. | journal=Clin Infect Dis | year= 1994 | volume= 18 | issue= 1 | pages= 38-72 | pmid=8054436 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8054436  }} </ref><ref name="pmid14959784">{{cite journal| author=Binquet C, Wallon M, Quantin C, Kodjikian L, Garweg J, Fleury J et al.| title=Prognostic factors for the long-term development of ocular lesions in 327 children with congenital toxoplasmosis. | journal=Epidemiol Infect | year= 2003 | volume= 131 | issue= 3 | pages= 1157-68 | pmid=14959784 | doi= | pmc=2870066 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14959784  }} </ref>
====Follow Up====
*Infants with congenital Toxoplasmosis should be followed up regularly to examine for presence of motor abnormalities, cognitive outcomes, vision impairment, formation of new eye lesions, and hearing loss.<ref name="pmid16619149">{{cite journal| author=McLeod R, Boyer K, Karrison T, Kasza K, Swisher C, Roizen N et al.| title=Outcome of treatment for congenital toxoplasmosis, 1981-2004: the National Collaborative Chicago-Based, Congenital Toxoplasmosis Study. | journal=Clin Infect Dis | year= 2006 | volume= 42 | issue= 10 | pages= 1383-94 | pmid=16619149 | doi=10.1086/501360 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16619149  }} </ref>
*Systemic corticosteriods are recommended for reducing the inflammation from chorioretinitis.<ref name="pmid:    27723657">{{cite journal| author=Ozgonul C, Besirli CG| title=Recent Developments in the Diagnosis and Treatment of Ocular Toxoplasmosis. | journal=Ophthalmic Res | year= 2017 | volume= 57 | issue= 1 | pages= 1-12 | pmid=:    27723657 | doi=10.1159/000449169 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27723657  }} </ref>
 
===Management of HIV Positive Pregnant Women===
*HIV positive patients are at a higher risk for reactivation of Toxoplasmosis and transmission to fetus.<ref name="MontoyaRemington2008">{{cite journal|last1=Montoya|first1=Jose G.|last2=Remington|first2=Jack S.|title=Clinical Practice: Management ofToxoplasma gondiiInfection during Pregnancy|journal=Clinical Infectious Diseases|volume=47|issue=4|year=2008|pages=554–566|issn=1058-4838|doi=10.1086/590149}}</ref><ref name="Camposde Andrade2014">{{cite journal|last1=Campos|first1=Flávia Alves|last2=de Andrade|first2=Gláucia Manzan Queiroz|last3=de Pádua Santos Lanna|first3=Antônio|last4=Lage|first4=Bruno Freitas|last5=Assumpção|first5=Maria Vitória Mourão|last6=Pinto|first6=Jorge A.|title=Incidence of congenital toxoplasmosis among infants born to HIV-coinfected mothers: case series and literature review|journal=The Brazilian Journal of Infectious Diseases|volume=18|issue=6|year=2014|pages=609–617|issn=14138670|doi=10.1016/j.bjid.2014.05.008}}</ref>
*Data is inconclusive on the effectiveness of the standard treatment regimen.
*In Toxoplasma seropositive pregnant women with CD4 cell count of less than 200 cells/mm ³ should receive trimethoprim-sufamethoxazole(80mg/400mg), one tablet a day as a prophylaxis.<ref name="urlHIV/AIDS Treatment Guidelines | AIDSinfo">{{cite web |url=https://aidsinfo.nih.gov/guidelines |title=HIV/AIDS Treatment Guidelines &#124; AIDSinfo |format= |work= |accessdate=}}</ref>
*In Toxoplasma seropositive pregnant women with CD4 greater than 200cells/mm³ spiramycin is suggested for the duration of pregnancy.
 
===Surgical Therapy===
There are no surgical management measures for the treatment of congenital Toxoplasmosis.
 
==Prevention==
 
===Primary Prevention===
Prevention is the best way to reduce the transmission of disease. The following are recommended by the CDC to reduce the risk of transmission of Toxoplasma from the environment.<ref name="urlCDC - Toxoplasmosis - Prevention & Control">{{cite web |url=https://www.cdc.gov/parasites/toxoplasmosis/prevent.html|title=CDC - Toxoplasmosis - Prevention & Control |format= |work= |accessdate=}}</ref><ref name="pmid11125923">{{cite journal| author=Foulon W, Naessens A, Ho-Yen D| title=Prevention of congenital toxoplasmosis. | journal=J Perinat Med | year= 2000 | volume= 28 | issue= 5 | pages= 337-45 | pmid=11125923 | doi=10.1515/JPM.2000.043 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11125923  }} </ref>
*Avoid drinking untreated drinking water.
*Wear gloves when gardening and during any contact with soil or sand because it might be contaminated with cat feces that contain Toxoplasma.
*Wash hands with soap and warm water after gardening or contact with soil or sand.
*Teach children the importance of washing hands to prevent infection.
*Keep outdoor sandboxes covered.
*Feed cats only canned or dried commercial food or well-cooked table food, not raw or undercooked meats.
*Change the litter box daily if you own a cat. The Toxoplasma parasite does not become infectious until 1 to 5 days after it is shed in a cat's feces.
*If you are pregnant or immunocompromised: Avoid changing cat litter if possible. If no one else can perform the task, wear disposable gloves and wash your hands with soap and warm water afterwards.
*Keep cats indoors.
*Do not adopt or handle stray cats, especially kittens. Do not get a new cat while you are pregnant.
 
===Reducing the risk of transmission from meat===
To prevent risk of toxoplasmosis from food:<ref name="urlCDC - Toxoplasmosis - Prevention & Control2">{{cite web |url=https://www.cdc.gov/parasites/toxoplasmosis/prevent.html |title=CDC - Toxoplasmosis - Prevention & Control |format= |work= |accessdate=}}</ref>
*Cook food to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked.
*For Whole Cuts of Meat (excluding poultry): Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest* for three minutes before carving or consuming.
*For Ground Meat (excluding poultry): Cook to at least 160° F (71° C); ground meats do not require a rest time.
*For All Poultry (whole cuts and ground): Cook to at least 165° F (74° C), and for whole poultry allow the meat to rest for three minutes before carving or consuming.
 
===Secondary Prevention===
*Countries such as France and Austria recommend prenatal screening for Toxoplasma, by antibody measurement in the pregnant mother to establish the status of infection. <ref name="pmid3336419">{{cite journal| author=Daffos F, Forestier F, Capella-Pavlovsky M, Thulliez P, Aufrant C, Valenti D et al.| title=Prenatal management of 746 pregnancies at risk for congenital toxoplasmosis. | journal=N Engl J Med | year= 1988 | volume= 318 | issue= 5 | pages= 271-5 | pmid=3336419 | doi=10.1056/NEJM198802043180502 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3336419  }} </ref>
*Pregnant women with active infection are treated with spiramycin, it is shown to reduce the transplacental transmission by 60%.<ref name="pmid2681638">{{cite journal| author=Hohlfeld P, Daffos F, Thulliez P, Aufrant C, Couvreur J, MacAleese J et al.| title=Fetal toxoplasmosis: outcome of pregnancy and infant follow-up after in utero treatment. | journal=J Pediatr | year= 1989 | volume= 115 | issue= 5 Pt 1 | pages= 765-9 | pmid=2681638 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2681638  }} </ref>
 
==References==
{{reflist|2}}
 
{{WH}}
{{WS}}
<references />

Latest revision as of 19:04, 22 May 2017


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