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| __NOTOC__ | | __NOTOC__ |
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| Congenital Toxoplasmosis
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| | {{CMG}}:{{AE}}{{DAMI}} |
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| ==Overview==
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| ==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>
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| *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>
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| *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>
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| *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>
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| *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>
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| *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>
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| *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>
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| *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>
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| ==Causes== | | ==[[Roseola historical perspective|Historical Perspective]]== |
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| ==Risk Factors== | | ==[[Roseola classification|Classification]]== |
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| ==Screening== | | ==[[Roseola pathophysiology|Pathophysiology]]== |
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| ==Epidemiology, Demographics== | | ==[[Roseola causes|Causes]]== |
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| ==Natural History, Complications, Prognosis== | | ==[[Roseola differential diagnosis|Differentiating Any Disease from other Diseases]]== |
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| ==Diagnosis== | | ==[[Roseola epidemiology and demographics|Epidemiology and Demographics]]== |
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| ===History and Symptoms=== | | ==[[Roseola risk factors|Risk Factors]]== |
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| ===Physical Examination=== | | ==[[Roseola screening|Screening]]== |
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| ===Laboratory Findings=== | | ==[[Roseola natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| Principles and methods used for the diagnosis of congenital toxoplasmosis:
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| {| class="wikitable"
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| !Principle
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| !Detection
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| !Method
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| !Findings supporting the diagnosis of
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| Toxoplasmosis
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| |-
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| |Toxoplasma specific
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| humoral responses
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| |IgG, IgM, IgA | |
| |Dye test, ELISA, and ELISA-like assays,
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| ISAGA, immunofluorescence,
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| agglutination
| | ==Diagnosis== |
| |Positive IgM after 5 days of life and in the absence | | [[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]] |
| of blood transfusions. Positive IgA after 10 days
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| of life. Persistence of Toxoplasma IgG beyond 1 year of age
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| |-
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| |IgG, IgM, and IgA to specific | |
| Toxoplasma antigen
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| |Western blot | |
| |Presence of specific bands only seen in the
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| newborn or bands with higher intensity than
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| maternal ones for IgG and/or IgM and/or IgA
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| in a reference laboratory
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| |- | |
| |Toxoplasma | |
| nucleic acid
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| amplification
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| |DNA | |
| |PCR | |
| |Positive result in any body fluid (e.g., amniotic | |
| fluid, cerebrospinal fluid, peripheral blood, urine
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| |- | |
| |Immunohistochemistry of | |
| Toxoplasma specific antigens in tissue
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| |Antigens | |
| |Immunoperoxidase | |
| |Positive result in any tissue (e.g., brain or other | |
| fetal tissue
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| |Visualization by microscopy
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| |Visual identification of tachyzoites
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| and/or cysts
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| |Stains such as hematoxylin/eosin,
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| Giemsa
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| |Positive identification in a reference laboratory
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| |-
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| |Isolation of Toxoplasma
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| |Whole live parasite | |
| |Inoculation in peritoneal cavity of
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| mice
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| |Detection of live cysts from any body fluid or
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| tissue that has been inoculated in mice in a
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| reference laboratory
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| |Brain imaging
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| |Brain calcifications, hydrocephaly,
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| microcephaly
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| |Ultrasound, computed tomography,
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| brain magnetic resonance imaging
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| |Findings can be suggestive but are not diagnostic | |
| of CT since other etiologies may result in
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| similar findings
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| |Retinal exam | |
| |Inflammation in choroidal and
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| retinal layers
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| |Ophthalmological exam
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| |Retinochoroidal lesions can be highly suggestive
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| or, at times, diagnostic of congenital Toxoplasmosis
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| |} | |
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| ==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]] |
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| ===Medical Therapy=== | | ==Case Studies== |
| | | [[Roseola case study one|Case #1]] |
| ===Surgical Therapy===
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| ==Prevention==
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| ===Primary Prevention===
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| ===Secondary Prevention===
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| ==References==
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| {{reflist|2}}
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| {{WH}}
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| {{WS}}
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