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__NOTOC__
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Congenital Toxoplasmosis
{{Roseola}}
{{CMG}}:{{AE}}{{DAMI}}


==Overview==


==Historical Perspective==
==[[Roseola overview|Overview]]==
*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>
*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==
==Pathophysiology==
===Infective stages of the Parasite===
The three infective stages of T. gondii include:
*Tachyzoite: It is the rapidly dividing and invasive form, can invade any vertebrate cell type
*Bradyzoite: These result from the conversion from tachyzoites, they are slowly diving form, and are present in the tissue cysts which can remain in the host throughout the lifetime
*Sporozoite: It is the environmental form present in the oocyts


===Mechanism of cell Invasion===
==[[Roseola historical perspective|Historical Perspective]]==
*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, also enhance the growth and virulence of the parasite.
*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===
*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 harbor tissue cysts
*Once the patient has a primary infection with tachyzoites in the blood stream during pregnancy a possible transplacental infection can take place
*The tachyzoites colonize in the placenta and can cross the barrier to reach the fetus in 30% of cases leading to the disease
*The frequency of tachyzoites transfer to the fetus is related to the gestational age with lowest risk in the first trimester and highest in the third trimester
*The factors influencing the transfer of tachyzoites to the fetus is not well understood


==Causes==
==[[Roseola classification|Classification]]==


==Differentiating Toxoplasmosis from other Diseases==
==[[Roseola pathophysiology|Pathophysiology]]==
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 causes|Causes]]==
!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 differential diagnosis|Differentiating Any Disease from other Diseases]]==


==Epidemiology, Demographics==
==[[Roseola epidemiology and demographics|Epidemiology and Demographics]]==
===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 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===
*Toxoplasmosis affects 500 to 5000 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 22.5% of the population above the of 12 is estimated to be infected by Toxoplasma and 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==
==[[Roseola risk factors|Risk Factors]]==  
The main 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 the pregnant women for primary infection include:
*Consumption of raw oyesters 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 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-GangneuxDarde20124">{{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-GangneuxDarde20122">{{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-GangneuxDarde20123">{{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==
==[[Roseola screening|Screening]]==  


==Natural History, Complications, Prognosis==
==[[Roseola natural history, complications and prognosis|Natural History, Complications and Prognosis]]==


==Diagnosis==
==Diagnosis==
 
[[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===
 
===Physical Examination===
 
===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.
*The most commonly used diagnostic test is the PCR of the amniotic fluid and a positive test is diagnostic of congenital Toxoplasmosis.
 
====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 would be present in the baby.
*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 the diagnosis is the the absence of Toxoplasma IgG at 12months of age in the absence of treatment.
 
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
|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>
 
==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}}
 
==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}}


==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==
 
[[Roseola case study one|Case #1]]
===Surgical Therapy===
 
==Prevention==
 
===Primary Prevention===
 
===Secondary Prevention===
 
==References==
{{reflist|2}}
 
{{WH}}
{{WS}}

Latest revision as of 19:04, 22 May 2017


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]:Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]


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Case #1

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