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Parasitic infection from blood transfusions.

Is your blood bank following traditional and recent recommendations for excluding donors to prevent rare parasitic infections from entering the blood supply?

Parasitic infection is an uncommon complication of blood transfusion therapy in the United States. Roughly five such cases are known to occur annually.[1] These infections are uncommon because a transfusion-transmitted parasitic infection can occur only if three conditions prevail: a parasitemic individual qualifies as a blood donor, parasites survive the processing and storage of donated blood, and infected blood is transfused in a sufficient dose to a susceptible patient. Because current criteria require prospective blood donors to appear healthy and without symptoms of infection, symptomatic parasitemic individuals are normally excluded.

Unfortunately, some parasitemic individuals are asymptomatic and appear healthy, so screening of donors becomes difficult. As a result, four kinds of parasitic infection have been documented to occur in the U.S. following blood donation: malaria, babesiosis, toxoplasmosis, and Chagas disease.[2] African sleeping sickness, microfilariasis, and leishmaniasis also have been transmitted by blood transfusion, but to my knowledge have not been documented to do so within the U.S.

In the discussion that follows, each of the parasitic organisms known to cause transfusion-transmitted parasitic infection in the U.S. and the strategies employed to keep these infections uncommon will be reviewed. In addition, in light of the recent announcement by the Department of Defense and the American Association of Blood Banks regarding the possible risk of transfusion-transmitted leishmaniasis, a few words will also be said about Leishmania tropica. * Malaria. The most common transfusion-transmitted parasitic infection documented in the U.S., malaria causes about three cases per year.[3] The transfusion-acquired infection is transmitted by the asexual intraerythrocytic forms of the parasite. These parasites can survive for more than a week in RBCs stored at 4 [degrees] C, for more than two years in frozen RBCs, and for the shelf life of platelet concentrates.[3] Although cell-free blood components are believed not to transmit malaria, some cases have been reported after transfusion of cryoprecipitated antihemophilic factor (AHF).[4]

Four species of malaria cause transfusion-transmitted infection in humans.[3-5] The infection may become evident from a little over a week to several months after the transfusion of infected blood when the recipient develops fevers, chills, headache, and hemolysis.[3] The incubation period tends to be shortest for Plasmodium falciparum and longest for Plasmodium malariae (Figure 1).

Transfusion-transmitted malaria can be lethal, particularly those cases caused by P. falciparum.[3] The risk of fatal infection is increased when the patient is asplenic.[6] Since there is no exoerythrocytic stage associated with transfusion-transmitted malaria, the disease may be treated with therapy that kills the erythrocytic parasites.[3-6]

The current policy of deferring blood donations for up to three years from individuals who have been present in malaria-endemic areas[7] has helped keep the risk of this complication to its current low level. This deferral policy, however, fails to prevent all transfusion-transmitted infections, since some individuals may be infected with P. vivax or P. ovale for more than three years, and with P. malariae for life.[3] The most common cause of transfusion-transmitted malaria in the U.S. is P. malariae, which accounts for about 40% of cases.[3]

Although transfusion-transmitted malaria is uncommon in the U.S., the risk could increase if more individuals with asymptomatic malarial infection attempted to donate blood. During and immediately after the Vietnam war, the incidence of malaria acquired from transfusion increased substantially as infected but asymptomatic people from the Armed Forces became blood donors after returning home.[8] A similar situation could develop during the 1990s from American troops who served in malaria-endemic areas of the Persian Gulf.

As a discussion later in this article will reveal, the prospect of transfusion-transmitted leishmaniasis from the same returning group led the Department of Defense and the American Association of Blood Banks to announce that military personnel and other individuals returning from the Persian Gulf should be deferred as donors of transfusable blood components until Jan. 1, 1993.[9] * Babesiosis. Babesiosis is caused by Babesia microti, which, like malaria, is an intraerythrocytic parasite.[10] Unlike malaria, however, babesiosis is endemic within the Northeast region of the United States. Because some individuals may be parasitemic yet asymptomatic with B. microti, they qualify occasionally as blood donors.

B. microti can survive for over a month in RBC stored at 4 [degrees] C.[10] It also survives storage in frozen RBC and in platelet concentrates. Babesiosis is documented to complicate transfusions less often than malaria; fewer than 10 cases are on record in the U.S., possibly because of under-reporting.[10]

Transfusion-transmitted babesiosis may become evident through symptoms in four to eight weeks following an infected transfusion. The transfusion recipient may become febrile with chills, headache, and hemolysis.[10] In some cases, especially those affecting immunocompromised or asplenic individuals, fulminant hemolysis, renal failure, and even death may ensue.

In order to prevent transfusion of B. microti-infected blood, the Standards of the American Association of Blood Banks require that individuals with a history of babesiosis be deferred permanently from blood donation.[7] Because transfusion-transmitted babesiosis occurs so uncommonly, the deferral policy is probably sufficient at this time to protect the blood supply from contamination with B. microti. * Toxoplasmosis. Toxoplasmosis is an extraerythrocytic infection caused by the ubiquitous parasite Toxoplasma gondii.[11] The infection is zoonotic; members of the cat family are the definitive host. Humans can be infected with T. gondii through any of five major routes: by accidentally ingesting T. gondii oocysts after handling infected cats, infected cat litter, or infected soil; by eating undercooked infected beef, pork, lamb, or goat; by direct contamination of open wounds; by organ transplantation; and by blood transfusion.[12] infection with T gondii may be lifelong.

Over 50% of the U.S. population may harbor the organism in the tissues in its cyst form.[12] Most infected individuals appear healthy and are asymptomatic. Although many blood donors are probably infected with T gondii, it is likely that blood donors are parasitemic only rarely. If present in blood at the time of donation, T gondii could survive for up to 50 days at 4 [degrees] C in citrated whole blood.[13]

Most T gondii infections probably go unnoticed clinically. They may result in lymphadenopathy, malaise, fever, headache, sore throat, splenomegaly, hepatomegaly, and rash. This illness may mimic infectious mononucleosis. Retinopathy and lethal infections may occur in immunocompromised hosts.[11]

Although the potential for transfusion transmission of T. gondii exists, the only documented cases of transfusion-transmitted toxoplasmosis have occurred following transfusion of leukocyte concentrates that were obtained from individuals with chronic myelogenous leukemia.[14] Current donor eligibility criteria would prohibit the selection of such donors. * Chagas disease. Transfusion-transmitted Chagas disease is caused by the extraerythrocytic parasite Trypanosoma cruzi (Figure 2). Asymptomatic infected individuals may be parasitemic for life.[15] Economic problems and political turmoil in Latin America have increased the migration of T cruzi-infected Central Americans, South Americans, and Mexicans to the United States. It has been estimated that about 100,000 infected individuals now live in the U.S.[16] Should an infected individual donate blood, T cruzi could survive in RBCs stored at 4 [degrees] C for more than two weeks. Platelets and plateletpheresis could also transmit infection.

Acute infection with T cruzi may be asymptomatic. In some cases, however, especially in immunocompromised patients, acute Chagas disease may cause cardiac complications, including arrhythmia, cardiomegaly, congestive heart failure, and meningoencephalitis.[16] Acute infection can be fatal.

Two cases of transfusion-transmitted acute Chagas disease have been documented in the United States: one in Los Angeles and one in New York City.[17,18] A third, unconfirmed case may have occurred in Texas.[19] Because most patients infected Path T cruzi by transfusion are not recognized as having acute Chagas disease, the two cases mentioned above may represent only the tip of an iceberg. This is important because while acute Chagas disease may go unrecognized, chronic Chagas disease may affect 20% to 30% of infected individuals.[15] They may develop cardiomegaly, megaesophagus, or megacolon years to decades after the infected transfusion.

Serologic tests are currently in use in areas where Chagas disease is endemic to detect individuals who might transmit T cruzi by transfusion. Nevertheless, no standardized serologic tests are in routine use in the U.S. to screen blood donors. Rather, the 14th edition of AABB Standards requires permanent deferral of individuals who have a history of Chagas disease.[7]

Some U.S. institutions follow a policy of deferring blood donations from individuals who have a high risk of being infected with T cruzi, even if no history of Chagas disease is elicited during predonation screening.[20] This would include deferral of Latin American immigrants and citizens of nonendemic countries who have had potential exposure to the parasite via vector contact or transfusion.

The decision to follow such a policy should be made locally based upon an analysis of the donor population. For example, in the blood bank at the Los Angeles County + University of Southern California Medical Center, about a third of the individuals in the donor base are born in countries where Chagas disease is endemic.21 Furthermore, 0.1% to 1% of individuals who qualify as blood donors at that institution based upon FDA and AABB donor eligibility criteria show serologic evidence of possible infection math T cruzi.[21] Therefore, in 1989 our blood bank began to ask predonation screening questions to identify individuals at high risk of asymptomatic T cruzi infection.[20] The following description summarizes the policy in effect at LAC + USC to prevent collecting blood from T cruzi-infected blood donors:

Blood donations are deferred whenever the prospective donor has a history of a positive test for T cruzi or a diagnosis of Chagas disease. In addition, donations are deferred if the prospective donor has been present in a country endemic for Chagas disease and if any of the following risk factors exists: * The donor shows symptoms of Chagas disease; * The donor may have had direct contact with the vector of Chagas disease as a result of living in substandard housing; or * The donor previously underwent a blood transfusion while in a Chagas disease-endemic area.

This approach has resulted in the deferral of several individuals who might have transmitted Chagas disease by blood transfusion. * Leishmaniasis. No cases of transfusion-transmitted leishmaniasis have been documented in the U.S., although transfusion-transmitted Leishmania donovani infection (Kala-azar) has occurred elsewhere. On Nov. 12, 1991, however, the Department of Defense informed the public of a newly recognized form of visceral leishmaniasis, caused by the parasite L. tropica, among seven military personnel. All the infected individuals served in the Persian Gulf area during Operation Desert Shield or Desert Storm.[22]

Since L. tropica usually causes only a cutaneous form of leishmaniasis, the finding of a visceral form of this infection was surprising. It was reasoned that if L. donovani, which causes a visceral form of leishmaniasis, can be transmitted by transfusion, perhaps the same is true for L. tropica. Consequently, it has been recommended that individuals who have traveled to or visited Bahrain, Iraq, Kuwait, Oman, Qatar, Saudi Arabia, the United Arab Emirates, or Yemen on or after Aug. 1, 1990, be deferred as donors of transfusable blood components until at least Jan. 1, 1993. Donors of plasma intended for further manufacture need not be similarly deferred. * Keeping rare disease rare. Transfusion-transmitted parasitic infections are uncommon in the United States. Changes in the incidence of parasitic infections here, however, could lead to an increase in the number of cases of post-transfusion parasitic infection. In this author's opinion, the most likely organism to pose an increasing threat to the U.S. blood supply is T cruzi due to the influx of infected people into the U.S. It is anticipated that serologic tests will become available for testing donors for evidence of possible infection with T cruzi - if not on a national level, perhaps on a regional or local one.

Cause of malaria

Plasmodium malariae (x 688) is the most common cause of transfusional parasitic infection. The parasite can survive for more than a week in RBCs stored at 4 [degrees] C, for more than two years in frozen RBCs, and for the shelf life of platelet concentrates.

Cause of Chagas disease

One reason for the growing presence in the United States of Trypanosoma cruzi (x 688), which causes Chagas disease, is increased immigration of refugees from Central America. Asymptomatic infected individuals may be parasitemic for life.

References

[1.] Shulman IA, Appleman MD. An overview of unusual diseases transmitted by blood transfusion within the United States. In: Westphal RG, Carlson KB, Turc JM, eds. Emerging Global Patterns in Transfusion Transmitted Infections. Arlington, Va: American Association of Blood Banks; 1990: 1: 1-29. [2.] Shulman IA Parasitic infections, an uncommon risk of blood transfusion in the United States. Transfusion. 1991; 31: 479480. [3.] Turc JM. Malaria and blood transfusion. In: Westphal RG, Carlson KB, Turc JM, eds. Emerging Global Patterns in Transfusion Transmitted Infections. Arlington, Va: American Association of Blood Banks; 1990: 2: 31-43. [4.] Wells L, Ala FA. Malaria and blood transfusion. Lancet. 1985; 1: 1317-1318. [5.] Shulman IA, Saxena S, Nelson JM, Furmanski M. Neonatal exchange transfusion complicated by transfusion-induced malaria. Pediatrics. 1984; 73: 330-332. [6.] Westphal R. Transfusion-transmitted malarial infections. In: Smith DM, Dodd RY. Transfusion Transmitted Infections. Chicago: ASCP Press; 1991; 10: 167-180. [7.] Widmann FK, ed. Standards for Blood Banks and Transfusion Services. 14th ed. Arlington, Va: American Association of Blood Banks; 1991. [8.] Dover AS, Schultz MG. Transfusion-induced malaria. Transfusion. 197 1; 11: 353-357. [9.] AABB Faxnet #57. Arlington, Va: American Association of Blood Banks; Nov. 12, 1991. [10.] Popovsky MA. Babesiosis and Lyme disease: A transfusion medicine perspective. in: Westphal RG, Carlson KB, Turc JM, eds. Emerging Global Patterns in Transfusion Transmitted Infections. Arlington, Va: American Association of Blood Banks; 1990: 3: 45-64. [11.] Remington JS, McLeod R. Toxoplasmosis. in: Braude Al, ed. Infectious Diseases and Medical Microbiology. 2nd ed. Philadelphia: WB Saunders; 1986. [12.] Krick JA, Remington JS. Toxoplasmosis in the adult - an overview. N Engl J Med. 1978;298:550-553. [13.] Wolfe MS. Parasites, other than malaria, transmissible by blood transfusion. In: Greenwalt TJ, Jamieson GA, eds. Transmissible Disease and Blood Transfusion. New York, NY: Grune & Stratton; 1975:267-277. [14.] Siegel SE, Lunde MN, Gelderman AH, et al. Transmission of toxoplasmosis by leukocyte transfusion. Blood. 1971; 37: 388-394. [15.] Gudino MD, Linares J. Chagas disease and blood transfusion. In: Westphal RG, Carlson KB, Turc JM, eds. Emerging Global Patterns in Transfusion Transmitted Infections. Arlington, Va: American Association of Blood Banks; 1990; 4: 65-86. [16.] Schmunis GA. Trypanosoma cruzi, the etiological agent of Chagas' disease as a contaminant of blood supplies: A problem of endemic and nonendemic countries. Transfusion. 1991; (3): 547-557. [17.] Grant IH, Gold JW, Wittner M, et al. Transfusion associated acute Chagas' disease acquired in the USA. Ann Intern Med. 1989; 111:849-851. [18.] Geiseler PJ, Ito JI, Tegtmeir BR, et al. Fulminant Chagas' disease in bone marrow transplantation. In: Abstracts of the 1987 Interscience Conference on Antimicrobial Agents and Chemotherapy, p. 169. [19.] Skolnick A. Deferral aims to deter Chagas' parasite. JAMA. 1991; 265:173. [20.] Appleman MA, Shulman IA, Saxena S, Kirchhoff LV. Tiypanosoma cruzi infection among blood donors in Los Angeles, California. Proceedings of the Joint Congress of the International Society of Blood Transfusion and the American Association of Blood Banks. Los Angeles, Sept. 10-16, 1990. Abstract S753. [21.] Kerndt P, Waskin H, Shulman IA, et al. Trypanosoma cruzi antibody among blood donors in Los Angeles, California. Transfusion. 1988; 28:31S. [22.] Doddridge IRD. Memorandum to AABB Institutional Members. AABB recommendations regarding reducing the possible risk of transmission of Leishmania tropica by transfusions. Arlington, Va: American Association of Blood Banks; Nov. 12, 1991.

The author is director of transfusion medicine at LAC + USC Medical Center and at the Kenneth Norris Cancer Hospital and Research Institute, and associate professor of pathology at the University of Southern California, Los Angeles.
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Author:Shulman, Ira A.
Publication:Medical Laboratory Observer
Date:Sep 1, 1992
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