A recent article detailing the sad situation of a transplant patient contracting AIDS from the kidney of a living donor, despite negative tests 11 weeks prior to the surgery, had me thinking about transfusions, the blood supply and the spread of infectious disease (a). Unsavory musings, yes, but there’s one particularly exotic disease and a rather sensitive public health situation that I was thinking about that I wanted to explore in this post.
Chagas disease (Trypanosoma cruzi), otherwise known as American trypanosomiasis, is a protozoan parasite endemic to Central and South America. The CDC estimates that a staggering 16-18 million people are infected with T. cruzi in Latin America, mostly in rural locales, with another 25,000 to 100,000 infected immigrants in the United States (b). Typically, the disease is transmitted by triatomine insects that blood-feed on a humans. Their infective feces often enter the bite wound, oral or nasal mucosa, or conjunctivas and transmit the flagellate parasite.
An example of a triatomine specimen capable of transmitting Chagas disease. Image: CDC Public Health Image Library.
The disease has two specific phases. The acute phase is usually a mild febrile infection lasting anywhere from weeks to months. Following this acute phase, researchers believe there is life-long infection with the parasites hiding in the blood and organs of the infected person. Years or decades later, 10 to 30% of those cases can progress to chronic Chagas disease.
The clinical manifestations of chronic Chagas disease are ugly business, characterized by enlargement of the heart and digestive tract, “megaesophagus” and “megacolon” being two common presentations of digestive tract pathologies. Electrocardiographic abnormalities, myocardial lesions, constipation and dysphagia (difficult or painful swallowing) are just a few of the symptoms resulting from infection (c)(d). There is no vaccine for primary infection and no effective drug therapy available for the chronic stages.
The disease may also be spread by congenital infection, oral infection through contaminated fruit, and, as you can guess, by blood transfusion and organ transplantation. Platelet transfusions and renal transplants in particular seem to be problematic, suggesting an as yet unknown immunological component of T. cruzi infection; the liver, pancreas and heart have also been implicated in so-called “allographic transmission” resulting from organ transplantation (b)(h)(i).
Prior to the successful Southern Cone Initiative that tackled both the eradication of the triatomine bug as well as initiating large-scale blood-screening efforts in Latin America in 1991, blood transfusion-transmitted Chagas was a critical public health problem with infectivity rates ranging from 13 to 49% (f). As the issue started drawing attention in public health sectors in the United States, the American Red Cross (ARC) conducted a study and observed evidence of increasing prevalence of the disease in blood donors in Southern California throughout the early 1990s (g). This increase was attributed not only to changes in donor and population demographics but also as a result of recruitment efforts directed towards minority donors in Los Angeles at the time (h).
As late as the year 2007, no policies were in place for compulsory blood-bank screening for Chagas in the United States (b). Upon the release of the first F.D.A. licensed serological test using a parasite lysate ELISA for T. cruzi blood screening in January of 2007, the ARC and Blood Systems Laboratories conducted a study using the test on 14 million blood donors over 16 months. They detected over 500 confirmed Chagas-infected donations (28% of the sample), with the majority of those cases from California and Florida (g).
In terms of actual transmission events in North America, the only reliable numbers I was able to hunt down in the literature were five blood transfusion-transmission and five organ transplant-transmission cases since 1993, an extraordinarily low number (g). Indeed, researchers believe that number to be too low to serve as any true indication of this phenomenon in the US (g)(d).
Megacolon as seen in a deceased patient. Image: Abdul Ghaffar. Click for source.
Of course, this Chagas story has traces of the HIV-infected blood transfusion panic in the late 1980s. Regrettably, there’s even a minority group entangled in the plot-line; evidence strongly suggests that Chagas-infected blood and organs originate from seropositive immigrants from T. cruzi endemic Latin American countries. Luckily, research has consistently indicated that blood donor recipients from seropositive donors are rarely infected with Chagas disease (f)(g)(h). Compared to the 93% of recipients that contract HIV after an infected blood donation, only 13% of recipients become infected after blood transfusion owing to factors such as parasite strain and levels of donor parasitemia (g). Recipients of platelets appear to be most at risk, most likely due to their immunocompromised state (f). The risk for allographic transmission seems to be much greater, determined to be as high as 35% for recipients of infected kidneys (i).
The past several decades have seen the proliferation of blood-bank screening for blood-borne diseases such as HIV-1 and HIV-2, hepatitis B and C, HTLV-I and -II and the etiological agent of syphilis, Treponema pallidum. The HIV epidemic really dragged this issue kicking and screaming to the forefront and since then there have been fantastic strides in implementing screening efforts as well as increasing public awareness of these issues. Chagas disease is the latest infectious disease agent to enter the equation and public health officials have put several tests in place to screen both blood and organ donors for antibodies to previous or ongoing Chagas infection. Of course, blood transfusions and organ transplants are never risk-free but knowing what blood-borne pathogens are lurking out there is the biggest part of the battle.
References
(a) “Transplant patient got AIDS from new kidney; living donor was infected” Arizona Daily Star. 17 Mar. 2011. Web: 20 Mar. 2011 (b) Centers for Disease Control and Prevention (CDC) (2002) Chagas disease after organ transplantation - United States, 2001. MMWR Morb Mortal Wkly Rep.15:51(10):210-2 (c) Despommier, D, Gwadz RW, Hotez PJ & Knirsch CA. Parasitic Diseases. 5th ed. New York: Apple Trees Production, LLC. 2006 (d) Dias E, Laranja FS, Miranda A & Nobrega G. (1956) Chagas' Disease: A Clinical, Epidemiologic, and Pathologic Study. Circulation. 14(6):1035-60 (e) Busch MP, Kleinman SH & Nemo GJ. (2003) Current and Emerging Infectious Risks of Blood Transfusions JAMA. 289(8):959-62. (f) Leiby DA, Read EJ, Lenes BA, Yund AJ, Stumpf RJ, Kirchhoff LV & Dodd RY. (1997) Seroepidemiology of Trypanosoma cruzi, Etiologic Agent of Chagas' Disease, in US Blood Donors. J Infect Dis. 176(4):1047-52. (g) Bern C, Montgomery SP, Katz L, Caglioti S & Stramer SL. (2008) Chagas disease and the US blood supply. Curr Opin Infect Dis.21(5):476-82. (h) Leiby DA, Herron RM Jr, Read EJ, Lenes BA & Stumpf RJ. (2002) Trypanosoma cruzi in Los Angeles and Miami blood donors: impact of evolving donor demographics on seroprevalence and implications for transfusion transmission. Transfusion. 42(5):549-55. (i )Kun H, Moore A, Mascola L, Steurer F, Lawrence G, Kubak B, Radhakrishna S, Leiby D, Herron R, Mone T, Hunter R, Kuehnert M; Chagas Disease in Transplant Recipients Investigation Team (2009) Transmission of Trypanosoma cruzi by heart transplantation. Clin Infect Dis.48(11):1534-40
Centers for Disease Control and Prevention (CDC) (2002). Chagas disease after organ transplantation--United States, 2001. MMWR. Morbidity and mortality weekly report, 51 (10), 210-2 PMID: 11922190
