Difference between revisions of "South American Trypanosomiasis"

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==Acceptability at Recruitment==
 
NOT ACCEPTABLE
 
 
==Acceptability at CT / Work-Up==
 
NOT ACCEPTABLE
 
 
 
==Individual at Risk==
 
==Individual at Risk==
 
Recipient
 
Recipient
  
 
==Explanation of Condition==
 
==Explanation of Condition==
Infection caused by the parasite trypanasoma cruzi, and spread by the triatomine bug. Also known as Chagas disease, it is endemic to many parts of South and Central America. May be fatal if untreated, and may be transferred via blood or bone marrow.
+
 
 +
Infection caused by the parasite trypanasoma cruzi, and spread by the triatomine bug. Also known as Chagas disease, it is endemic to many parts of South and Central America.  
 +
 
 +
Chagas disease progresses through acute and chronic phases. During the acute phase, infected individuals may exhibit symptoms such as fever, localised swelling, or redness at the site of parasite entry. However, many cases remain asymptomatic, complicating early detection. Following the acute phase, the parasite can persist in a dormant state for decades. In approximately 30-40% of those infected, chronic manifestations emerge 20-30 years later, potentially leading to severe and life-threatening complications, particularly involving the heart (e.g., cardiomyopathy) and the digestive system (e.g., megacolon and megaoesophagus).
 +
 
 +
Moreover, T. cruzi transmission has been documented in cord blood transplants, peripheral stem cell transplants, and bone marrow transplants, underscoring the importance of screening in these contexts.
  
 
See also [http://en.wikipedia.org/wiki/Chagas_disease Chagas Disease]
 
See also [http://en.wikipedia.org/wiki/Chagas_disease Chagas Disease]
  
==Guidance==
+
==At RECRUITMENT==  
====Donor infected or previously infected====
+
 
May cause chronic infection. Not acceptable.
+
A past history of Chagas’ disease should trigger permanent exclusion.
 +
 
 +
A history of being transfused in a Chagas endemic area should trigger serological testing to quantify risk.
 +
 
 +
A history of being born or donor's mother being born in a Chagas endemic area should trigger serological testing to quantify risk.
 +
 
 +
Risks associated with travel history do not need to be considered at recruitment.
 +
 
 +
==At CT/WORK-UP==
 +
 
 +
=== Criteria unrelated to travel history ===
 +
A past history of Chagas’ disease should trigger permanent exclusion.
 +
 
 +
A history of being transfused in a Chagas endemic area should trigger serological testing to quantify risk.
 +
 
 +
A history of being born or donor's mother being born in a Chagas endemic area should trigger serological testing to quantify risk.
 +
 
 +
=== Criteria related to travel history ===
 +
 
 +
A comprehensive lifetime travel history should be assessed, with particular attention to any travel to Chagas-endemic regions in South and Central America:
 +
 
 +
A history of sleeping in dwellings with mud-lined walls, adobe housing, or dwellings with thatched roofs in a rural area should trigger serological testing to quantify risk.
 +
 
 +
=== T. cruzi antibody testing ===
 +
 
 +
Seroconversion for Trypanosoma cruzi antibodies can take up to four months to occur. Therefore, antibody testing is considered reliable only after this period. If travel, and thus potential exposure, occurred less than four months prior to the date of antibody testing, this should be discussed with the medical officer and transplant centre for risk assessment (via concessionary release).
 +
 
 +
==Justification for guidance==
 +
 
 +
The causative organism of Chagas’ disease is the protozoan Trypanosoma cruzi. The infection is a zoonosis that is transmitted to humans by bloodsucking insects of the Reduviidae family (kissing bugs), triatomine subfamily. The animal reservoir includes over 150 species of both wild and domestic mammals. Infection is life-long, but approximately 70% of infected individuals will remain asymptomatic. Furthermore, parasitaemia occurs not only during the acute phase of infection, but also during asymptomatic chronic phases (albeit intermittently and at low levels).
 +
 
 +
Accordingly, Chagas’ is well-known to be transfusion-transmissible and asymptomatic parasitaemia has been detected in blood donors. Cases of transmission via solid organ transplantation and stem cell transplantation have been reported. Though platelet concentrates are the most frequently reported means of transmission, T. cruzi is able to survive refrigeration, freezing and thawing.
 +
 
 +
Chagas’ is endemic to mainland South and Central America. The people most at risk are those who spend early childhood in an endemic area in certain types of dwelling, those who receive blood transfusions in endemic areas, and children whose mothers grew up at risk of Chagas’ disease. Most of this risk can be captured by asking donors their country of birth and whether they have ever received a blood transfusion in a Chagas’-endemic country. The former can be definitively captured at recruitment, while the latter could occur at any time up to work-up.
 +
 
 +
Although the risk of Trypanosoma cruzi infection to travellers is considered very low, a confirmed case in 2024 involving a donor who had recently returned from a short holiday to South America has prompted a revision of guidelines. These updated guidelines recommend screening travellers who may have been exposed to the parasite, namely those who have stayed in rural areas or in high-risk housing conditions (mud-lined huts, adobe housing, structures with thatched rooves).
 +
 
 +
The detection of antibodies to T. cruzi is an established strategy to prevent transmission of infection through blood transfusion. Where available, this strategy can be adapted to assess the risk of prospective HPC donors with identified risk factors for chronic, asymptomatic Chagas’ disease. Because the prevalence of Chagas’ disease varies widely within the populations of endemic areas, it is likely that most donors with identified risk factors – especially those residing in non-endemic countries – will test negative for T. cruzi antibodies.
 +
 
 +
The most commonly used format for serological assays is the enzyme-linked immunosorbent assay (ELISA). A number of commercially available ELISAs are available and two have been licensed by the Food and Drug Administration (FDA) in the US. Other serological assay formats include particle agglutination (PA) and indirect haemagglutination assay (IHA). The Abbott Diagnostics ESA Chagas, an enzyme strip assay, is the only confirmatory assay to be approved by the FDA.
  
====Donor has lived in, or visited, endemic area====
+
==References==
Donors who have ever visited, or lived in, South America should be tested for T.cruzi antibodies at work-up, and only if the donor is at least six months from last date of potential exposure. Those with a positive antibody assay must not donate.
 
  
If the exposure was less than six months ago, then antibodies should be checked and, if negative, donation may proceed at the discretion of the transplant centre.
+
1 Kirchhoff LV. Trypanosoma Species (American Trypanosomiasis, Chagas’ Disease): Biology of Trypanosomes. In Mandell GL, Bennett JE and Dolin R, editors. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 6th ed, 2005:2622-2630.
  
==Pseudonyms or Related Conditions==
+
2 Moncayo A and Silveira AC. Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy. Mem Inst Oswaldo Cruz 2009; 104 (Suppl. 1):17-30.
Chagas Disease
 
  
Trypanasoma cruzi
+
3 Teixeira AR, Hecht MM, Guimaro MC, Sousa AO, Nitz N. Pathogenesis of Chagas’ disease: parasite persistence and autoimmunity. Clin Microbiol Revs 2011; 24: 592-630.
 +
 
 +
4 Oliveira I, Torrico F, Munoz J and Gascon J. Congenital transmission of Chagas disease: a clinical approach. Expert Rev Anti Infect Ther 2010; 8:945-956.
 +
 
 +
5 Stramer SL, Hollinger, FB, Katz, LM, Kleinman, S, Metzel PS, Gregory KR, Dodd, R. Emerging infectious disease agents and their potential threat to transfusion safety. Transfusion. 49. August 2009. Supplement.
 +
 
 +
6 Schmunis GA. Epidemiology of Chagas disease in non-endemic countries: the role of international migration. Mem Inst Oswaldo Cruz 2007; 102 (Suppl.I):75-85.
 +
 
 +
7 Albajar-Vinas P. The hidden Chagas disease burden in Europe. Euro Surveill.2011;16(38):pii=19975.
 +
 
 +
8 Castro E. Chagas’ disease: lessons from routine donation testing. Transfusion Med 2009; 19:16-23.
 +
 
 +
9 Leiby DA, Herron RM Jr, Garratty G and Herwaldt BL. Trypanosoma cruzi parasitaemia in US blood donors with serologic evidence of infection. J Infect Dis 2008; 198:609-613.
 +
 
 +
10 CDC. Chagas disease after organ transplantation – Los Angeles, California, 2006. MMWR 2006; 55:798-800.
 +
 
 +
11 Bern C, Montgomery SP, Katz L, Caglioti S and Stramer SL. Chagas disease and the US blood supply. Curr Opin Infect Dis 2008; 21:476-482.
 +
 
 +
12 Primavera KS, Umezawa ES, Peres BA, Camargo ME, Hoshino-Shimizu S. Chagas'disease: IgA, IgM and IgG antibodies to T. cruzi amastigote, trypomastigote and epimastigote antigens in acute and in different chronic forms of the disease. Rev Inst Med Trop Sao Paulo. 1990 May-Jun;32(3):172-80.
 +
 
 +
13 Young C, Losikoff P, Chawla A, Glasser L and Forman E. Transfusion-acquired Trypanosoma cruzi infection. Transfusion 2007; 47:540-544.
 +
 
 +
14 Jarque I, Salavert M, Peman J. Parasitic Infections in Hematopoietic Stem Cell Transplantation
 +
 
 +
15 https://www.transfusionguidelines.org/dsg/bm/guidelines/so003-south-american-trypanosomiasis-risk
  
 
==Version==
 
==Version==
Version 1, Edition 1
 
  
====Date of Last Update====
+
Version 3
15th June 2012
+
 
 +
12th September 2024

Latest revision as of 13:44, 13 February 2025

Individual at Risk

Recipient

Explanation of Condition

Infection caused by the parasite trypanasoma cruzi, and spread by the triatomine bug. Also known as Chagas disease, it is endemic to many parts of South and Central America.

Chagas disease progresses through acute and chronic phases. During the acute phase, infected individuals may exhibit symptoms such as fever, localised swelling, or redness at the site of parasite entry. However, many cases remain asymptomatic, complicating early detection. Following the acute phase, the parasite can persist in a dormant state for decades. In approximately 30-40% of those infected, chronic manifestations emerge 20-30 years later, potentially leading to severe and life-threatening complications, particularly involving the heart (e.g., cardiomyopathy) and the digestive system (e.g., megacolon and megaoesophagus).

Moreover, T. cruzi transmission has been documented in cord blood transplants, peripheral stem cell transplants, and bone marrow transplants, underscoring the importance of screening in these contexts.

See also Chagas Disease

At RECRUITMENT

A past history of Chagas’ disease should trigger permanent exclusion.

A history of being transfused in a Chagas endemic area should trigger serological testing to quantify risk.

A history of being born or donor's mother being born in a Chagas endemic area should trigger serological testing to quantify risk.

Risks associated with travel history do not need to be considered at recruitment.

At CT/WORK-UP

Criteria unrelated to travel history

A past history of Chagas’ disease should trigger permanent exclusion.

A history of being transfused in a Chagas endemic area should trigger serological testing to quantify risk.

A history of being born or donor's mother being born in a Chagas endemic area should trigger serological testing to quantify risk.

Criteria related to travel history

A comprehensive lifetime travel history should be assessed, with particular attention to any travel to Chagas-endemic regions in South and Central America:

A history of sleeping in dwellings with mud-lined walls, adobe housing, or dwellings with thatched roofs in a rural area should trigger serological testing to quantify risk.

T. cruzi antibody testing

Seroconversion for Trypanosoma cruzi antibodies can take up to four months to occur. Therefore, antibody testing is considered reliable only after this period. If travel, and thus potential exposure, occurred less than four months prior to the date of antibody testing, this should be discussed with the medical officer and transplant centre for risk assessment (via concessionary release).

Justification for guidance

The causative organism of Chagas’ disease is the protozoan Trypanosoma cruzi. The infection is a zoonosis that is transmitted to humans by bloodsucking insects of the Reduviidae family (kissing bugs), triatomine subfamily. The animal reservoir includes over 150 species of both wild and domestic mammals. Infection is life-long, but approximately 70% of infected individuals will remain asymptomatic. Furthermore, parasitaemia occurs not only during the acute phase of infection, but also during asymptomatic chronic phases (albeit intermittently and at low levels).

Accordingly, Chagas’ is well-known to be transfusion-transmissible and asymptomatic parasitaemia has been detected in blood donors. Cases of transmission via solid organ transplantation and stem cell transplantation have been reported. Though platelet concentrates are the most frequently reported means of transmission, T. cruzi is able to survive refrigeration, freezing and thawing.

Chagas’ is endemic to mainland South and Central America. The people most at risk are those who spend early childhood in an endemic area in certain types of dwelling, those who receive blood transfusions in endemic areas, and children whose mothers grew up at risk of Chagas’ disease. Most of this risk can be captured by asking donors their country of birth and whether they have ever received a blood transfusion in a Chagas’-endemic country. The former can be definitively captured at recruitment, while the latter could occur at any time up to work-up.

Although the risk of Trypanosoma cruzi infection to travellers is considered very low, a confirmed case in 2024 involving a donor who had recently returned from a short holiday to South America has prompted a revision of guidelines. These updated guidelines recommend screening travellers who may have been exposed to the parasite, namely those who have stayed in rural areas or in high-risk housing conditions (mud-lined huts, adobe housing, structures with thatched rooves).

The detection of antibodies to T. cruzi is an established strategy to prevent transmission of infection through blood transfusion. Where available, this strategy can be adapted to assess the risk of prospective HPC donors with identified risk factors for chronic, asymptomatic Chagas’ disease. Because the prevalence of Chagas’ disease varies widely within the populations of endemic areas, it is likely that most donors with identified risk factors – especially those residing in non-endemic countries – will test negative for T. cruzi antibodies.

The most commonly used format for serological assays is the enzyme-linked immunosorbent assay (ELISA). A number of commercially available ELISAs are available and two have been licensed by the Food and Drug Administration (FDA) in the US. Other serological assay formats include particle agglutination (PA) and indirect haemagglutination assay (IHA). The Abbott Diagnostics ESA Chagas, an enzyme strip assay, is the only confirmatory assay to be approved by the FDA.

References

1 Kirchhoff LV. Trypanosoma Species (American Trypanosomiasis, Chagas’ Disease): Biology of Trypanosomes. In Mandell GL, Bennett JE and Dolin R, editors. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 6th ed, 2005:2622-2630.

2 Moncayo A and Silveira AC. Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy. Mem Inst Oswaldo Cruz 2009; 104 (Suppl. 1):17-30.

3 Teixeira AR, Hecht MM, Guimaro MC, Sousa AO, Nitz N. Pathogenesis of Chagas’ disease: parasite persistence and autoimmunity. Clin Microbiol Revs 2011; 24: 592-630.

4 Oliveira I, Torrico F, Munoz J and Gascon J. Congenital transmission of Chagas disease: a clinical approach. Expert Rev Anti Infect Ther 2010; 8:945-956.

5 Stramer SL, Hollinger, FB, Katz, LM, Kleinman, S, Metzel PS, Gregory KR, Dodd, R. Emerging infectious disease agents and their potential threat to transfusion safety. Transfusion. 49. August 2009. Supplement.

6 Schmunis GA. Epidemiology of Chagas disease in non-endemic countries: the role of international migration. Mem Inst Oswaldo Cruz 2007; 102 (Suppl.I):75-85.

7 Albajar-Vinas P. The hidden Chagas disease burden in Europe. Euro Surveill.2011;16(38):pii=19975.

8 Castro E. Chagas’ disease: lessons from routine donation testing. Transfusion Med 2009; 19:16-23.

9 Leiby DA, Herron RM Jr, Garratty G and Herwaldt BL. Trypanosoma cruzi parasitaemia in US blood donors with serologic evidence of infection. J Infect Dis 2008; 198:609-613.

10 CDC. Chagas disease after organ transplantation – Los Angeles, California, 2006. MMWR 2006; 55:798-800.

11 Bern C, Montgomery SP, Katz L, Caglioti S and Stramer SL. Chagas disease and the US blood supply. Curr Opin Infect Dis 2008; 21:476-482.

12 Primavera KS, Umezawa ES, Peres BA, Camargo ME, Hoshino-Shimizu S. Chagas'disease: IgA, IgM and IgG antibodies to T. cruzi amastigote, trypomastigote and epimastigote antigens in acute and in different chronic forms of the disease. Rev Inst Med Trop Sao Paulo. 1990 May-Jun;32(3):172-80.

13 Young C, Losikoff P, Chawla A, Glasser L and Forman E. Transfusion-acquired Trypanosoma cruzi infection. Transfusion 2007; 47:540-544.

14 Jarque I, Salavert M, Peman J. Parasitic Infections in Hematopoietic Stem Cell Transplantation

15 https://www.transfusionguidelines.org/dsg/bm/guidelines/so003-south-american-trypanosomiasis-risk

Version

Version 3

12th September 2024