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 Table of Contents  
Year : 2019  |  Volume : 19  |  Issue : 2  |  Page : 31-61

Parasitic infestation in organ transplant recipients: a comprehensive review in the absence of robust evidence

1 Nephrology Department, Jaber El Ahmed Military Hospital, Safat, Kuwait and Ahmed Maher teaching hospital, Cairo; School of Medicine, Institute of Learning and Teaching, Faculty of Health and Science, University of Liverpool
2 School of Medicine, Institute of Learning and Teaching, Faculty of Health and Science, University of Liverpool; Paediatric Nephrology Department, Nottingham Children Hospital, Nottingham
3 School of Medicine, Institute of Learning and Teaching, Faculty of Health and Science, University of Liverpool; Paediatric Nephrology Department, Royal Hospital for Children, Glasgow
4 School of Medicine, Institute of Learning and Teaching, Faculty of Health and Science, University of Liverpool; Renal Transplant Department, Royal Liverpool University Hospitals, Liverpool
5 School of Medicine, Institute of Learning and Teaching, Faculty of Health and Science, University of Liverpool; Sheffield Kidney Institute, Sheffield Teaching Hospitals, University of Sheffield, Sheffield, UK

Date of Submission31-Mar-2019
Date of Acceptance31-Mar-2019
Date of Web Publication12-Jun-2019

Correspondence Address:
Ahmed Halawa
Sheffield Teaching Hospital, Herries Road, Sheffield S5 7AU
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jesnt.jesnt_15_19

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The real effect of parasitic infection on transplant recipients is not known. Interestingly, only 5% of human parasitic infections can affect functioning of transplanted organs. Parasitic infections manifest in two different ways: first, systemic illness, including anemia and constitutional symptoms, and second, local syndromes, which are usually confined to the lower gastrointestinal tract. Examples for pathogens causing systemic disease are Plasmodium malaria, Leishmania, Trypanosoma, and Toxoplasma. On the contrary, protozoal infection with Cryptosporidium and microsporidia, or the nematodes such as Strongyloides, may manifest with the local syndromes. Management of these infections in transplant recipients entails the following: prevention, timely diagnosis, cultures, specific serological tests, and PCR testing. Once the diagnosis is established, prompt medical/surgical interventions should be instituted to save these patients from developing hyperinfection or disseminated parasitic syndromes, involving, for example, the lungs or the central nervous system.

Keywords: parasitic infections, prevention and treatment, solid organ transplant, chloroquine plus primaquine

How to cite this article:
Abbas F, El Kossi M, Kim JJ, Shaheen IS, Sharma A, Pararajasingam R, Halawa A. Parasitic infestation in organ transplant recipients: a comprehensive review in the absence of robust evidence. J Egypt Soc Nephrol Transplant 2019;19:31-61

How to cite this URL:
Abbas F, El Kossi M, Kim JJ, Shaheen IS, Sharma A, Pararajasingam R, Halawa A. Parasitic infestation in organ transplant recipients: a comprehensive review in the absence of robust evidence. J Egypt Soc Nephrol Transplant [serial online] 2019 [cited 2023 Jan 28];19:31-61. Available from: http://www.jesnt.eg.net/text.asp?2019/19/2/31/260214

  Introduction Top

In 2012, an ambitious international campaign ‘London Declaration on Neglected Tropical Diseases’ professed to achieve control and eradication of 10 of the neglected tropical diseases by 2020. The pool of organ transplant recipients (TRs) continues to expand. Increased rates of migration and travel to endemic zones with high rate of parasitic infections have exposed immunosuppressed patients to these life-threating conditions. Malaria, leishmaniasis, strongyloidiasis, and schistosomiasis are the most devastating infections, and they are relatively common. If timely diagnosis and prompt treatment is not instituted, the natural course of these diseases may end in fatality. In Europe, toxoplasmosis poses risk to heart and bone marrow TRs, manifesting as myocarditis, encephalitis, or disseminated disease. One of the most common manifestations of parasitic disease is diarrheal illness. In Europe, the most prevalent protozoa infections related to diarrhea are Giardia duodenalis and Cryptosporidium [1].

Regrettably, parasitic diseases in organ TR are the least studied types of infection. There are paucity of published data concerned with this type of infection with few prospective trials and a complete lack of randomized trials. However, guidelines from several centers have addressed specific recommendations for Trypanosoma cruzi infection control in this cohort of patients. New therapeutic options for treatment of Strongyloides infection have been recently published. Furthermore, new diagnostic techniques are currently provided for faster and more reliable diagnosis. In this review, we aim to discuss prevention and management of parasitic infections in patients with a life-long immunosuppression [2].

Why parasitic infestation in solid organ transplant recipients are a serious issue?

Parasitic infections in TR can occur de novo or owing to recrudescence of a latent infection. De novo infections can occur through natural means or through transmission through the transplant organ. In view of rise in global travel all over the world, the incidence of parasitic infections among TR in solid organ transplant (SOT) is expected to expand. The following explanations have been addressed:
  1. Spread of transplant facilities in endemic zones.
  2. Referral of donors/recipients carrying latent or asymptomatic infection to developed countries.
  3. Organ donation offered by immigrants coming from endemic areas.
  4. Travel to endemic areas for leisure tourism.
  5. Increasing popularity of ‘transplant tourism’ where donors are available on ‘sale’.
  6. Loss of the ‘potential’ antiparasitic effect of cyclosporine A (CyA) with the advent of the new immunosuppressive regimens devoid of CyA [2].

  Epidemiology Top

Of 342 documented parasites affecting humans, 20 can affect human kidney [3]. However, the majority of these infections are subclinical or self-limited [4]. Four parasitic infections pose epidemiologic and clinical risks of significant extent: schistosomiasis, malaria, filariasis, and leishmaniasis ([Figure 1] and [Table 1]) [1]. Although rare, the parasitic infections in the developed world are increasingly been reported. There are two possible reasons why this issue has not been given the due importance: (a) much lesser incidence of transplants performed in the developing countries (15% of the global transplant numbers) [5] and (b) the attitudes and professional behavior of physicians in developing countries regarding reporting and publishing [2]. Data from the United States Registry Renal Data System (USRDS) indicate that infection is generally responsible for 20% of overall post-transplant mortality [6]. However, in contrary to viral and bacterial infections, parasitic infections are not classified separately; therefore, their contribution to mortality figures cannot be determined with precision. Although parasitic infections are well-recognized post-transplant sequelae, yet their diagnosis can be easily missed.
Figure 1 Global distribution of the major parasitic infestations in solid organ transplant recipients.

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Table 1 The most important parasitic infections after transplantation in Europe

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The exact incidence of post-transplant parasitic infections is not known; however, their prevalence is much less reported as compared with bacterial and viral infections. Of all varieties, only 5% of human pathogenic parasites have been noted to cause significant illness in TR [7]. Post-transplant parasitic diseases can be grouped into two clinical profiles: first, an acute systemic illness in the form of anemia, constitutional symptoms, and multiorgan dysfunction, as well as acute allograft dysfunction that can be frequently confused with acute rejection, for example, malaria, leishmaniasis, trypanosomiasis, and toxoplasmosis, and second, a localized form of presentation, which includes lower gastrointestinal tract (GIT) manifestations that can be seen with either protozoa (Cryptosporidium and microsporidia) or nematodes (Strongyloides).

The dissemination of a localized infection, however, can induce a devastating systemic response ([Figure 2]). Low threshold of suspicion is necessary to establish the diagnosis. Definitive diagnosis can be then established by parasite detection in tissues biopsy or body fluids through histological examination or culture, or via PCR testing. Serology testing for antibody detection is feasible in certain parasitic diseases but not widely available for other infection. Furthermore, specific lesions may show a characteristic imaging appearance particularly in the cerebral parasitic syndromes [7].
Figure 2 Mortality rates in parasitic infections in solid organ transplant [1]. KTx: kidney transplantation; LTx: liver transplantation.

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How could a transplant recipient acquire parasitic infection?

TRs may acquire parasitic infections in three different modes [7]:
  1. Transmission via the transplant organ, carrying parasite within the transplanted organ, or has been developing in intravascular phase, for example, Plasmodium [8], Leishmania [9], Trypanosoma [10], and Toxoplasma [11].
  2. Recrudescence of a latent infection: in immunocompetent host, parasites can survive for many years without overt clinical manifestations. If the host immunity has been blunted by immunosuppression, this latent infection can be reactivated. The reactivation process can be observed with leishmaniasis [9], malaria [12],[13], strongyloidiasis [14], and American trypanosomiasis [10].
  3. Conventionally acquired new infection: a primary parasitic disease can be acquired through either (a) oral-route infections, for example, cryptosporidiosis [15], and transfusion-acquired disease, for example, babesiosis [16] or (b) re-infection, for example, schistosomiasis [17] and malaria [18].

  Immunopathogenesis Top

Significant advances have been made in understanding the pathophysiology of parasitic diseases, as immunopathology of host in response to parasitic infections became clearer after World War II [19]. There is general agreement that ‘innate response’ is responsible for thwarting most of the parasitic burden. This is followed by an ‘adaptive immune response’, which involves helper T cell types 1 (TH1) and 2 (TH2). With certain types of parasitic infections, a ‘state of tolerance’ evolves, that is compatible with persistent and recalcitrant inhabitance of parasite as in case of schistosomiasis [20]. Clinical manifestations, including effect on renal function, are known to be related to the immunological reactions of these parasitic infestations [21]. It is established that ‘acute’ phases of parasitic infection are primarily accompanied with a TH1 response, whereas the late and ‘chronic’ complications are a result of TH2 response. Although most of the glomerulopathies can be primarily attributed to immune complex deposition including the circulating parasitic antigens and host immunoglobulins, the cell-mediated response, on the contrary, leads to chronic indolent response, such as schistosomal granuloma. Early glomerular deposits, however, contain complement as well as IgM, whereas IgG antibodies are predominant in the late immune complex deposits [22]. Progressive glomerular lesions can be also owing to IgA deposits [23].

Parasitic antigens may trigger the following responses leading to further insult to the host:
  1. autoimmunity [24],
  2. coinfection [25], and
  3. disrupted macrophage function [26].

Disruption of the macrophage integrity, on the contrary, has been also implicated in two pathological processes:
  1. predisposition to amyloidosis [27] and
  2. progression of glomerular lesions in schistosomiasis [28].

In TR, parasites trigger cellular immune response to the allograft as well. TH1 cells are the early responders of parasitic infections, which is followed by TH2 dominated phase in late phase of acute infection (e.g. malaria) [29], and persistently in its chronic phase (e.g. schistosomiasis) [30]. CD4 and CD25, in addition to regulatory T cells, have been implicated in optimizing the immunological balance between the parasite and its host [31],[32]. Not surprising, a similar immunological cascade can be observed in the setting of organ transplant. The fundamental role exerted by TH1 cells in the development of allograft rejection made it a logical target of various immunosuppressive protocols. However, the role of regulatory T cells in expanding allograft longevity and development of tolerance is well recognized [33]. Although the ‘CD8+ lymphocytes’ are the fundamental killer cells in organ transplant, macrophages and eosinophils, on the contrary, are the two major effector responders to parasitic infection [34],[35]. In TR with stable function, however, there is accommodation (or a tolerance of varying degree) and truce in the host immune response (similar to antiparasitic immunity), as antigen-processing cells from the donor are harbored in recipient’s lymphatic system. Similarly, some parasites are encased with recipient’s chronic reaction, thereby, limiting elimination of parasite. Macrophages and eosinophils are rather resistant to immunosuppressive medications [7].

Clinical features of parasitic diseases

The absence of any overt clinical manifestations in chronically infected patients is common. TR with reduced immune-competence can experience an overt disease. Patients with uncontrolled parasite replication may develop local tissue invasion or a disseminated disease. The characteristic acute presentation is the result of TH1 proinflammatory profile. Parasites implicated in systemic diseases include protozoal infections, for example, malaria, babesiosis, toxoplasmosis, trypanosomiasis, leishmaniasis, as well as disseminated acanthamebiasis and microsporidiosis. Fever and anemia are the most commonly encountered symptoms at presentation. Other findings include lymphoid hyperplasia and cardiac, pulmonary, neurological, and cutaneous manifestations according to the infested location [7]. Acute kidney injury can be due to associated interstitial nephritis (e.g. leishmaniasis) or hemodynamic disturbance (e.g. malaria), which can be misinterpreted as acute allograft rejection. On the contrary, local syndromes are primarily intestinal, in the form of colicky abdominal pain and diarrhea. Best example for this class is the alimentary protozoa Cryptosporidium, Acanthamoeba, and Microsporidia, as well as the nematodes such as Strongyloides and Trichuris ([Figure 3]). Hepatobiliary involvement usually complicates such types of protozoal diseases. Moreover, bronchopulmonary involvement can be induced by the migrating Strongyloides, whereas biliary obstruction can be developed by the migrating Ascaris worms [7].
Figure 3 Diagnostic flow chart for parasitic infestation in solid organs transplant recipient.

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  Tissue and blood protozoal infections Top


Epidemiology and risk factors

Toxoplasmosis is a zoonotic disease that is developed as a result of infection with the protozoa Toxoplasma gondii. TR can get infected via contaminated food or water, transmission through infested graft, or it can be a recrudescence of a dormant infection. Organ transplantation from Toxoplasma seropositive to seronegative cardiac TR poses 57–75% chance of manifesting the disease at 3 months after transplant, in the absence of effective prophylaxis. The most commonly encountered means of donor transmission is the activation of latent infection present within the donor’s cardiac allograft. Transmission with noncardiac allograft, however, has been also reported [36],[37]. In countries such as France, Latin America, and sub-Saharan Africa, where toxoplasmosis is endemic, prevalence may exceed 90%. Prevalence of T. gondii seropositivity in the ultrasound (US) ranges from 10 to 40% [38]. Primary infection can be acquired through the following risk factors: ingested cysts with undercooked meat or contaminated soil, contamination with oocysts present in feline feces, maternal–fetal transmission, through blood transfusion, or through SOT [39]. Water-borne infection is uncommonly reported [40]. In one series in a single center, 22 of 15 800 SOT recipients were reported to have toxoplasma infection. Although 90% of TR were seronegative at the time of transplantation, mortality rate was 13.6% [36].


Salient features of toxoplasma infection include pyrexia, myocarditis, hepatosplenomegaly, meningitis, brain abscess, chorioretinitis, pulmonary involvement, hepatitis, pancytopenia, or disseminated infection. Manifestations can appear 3 months after transplantation; however, late presentations may be seen, particularly after withdrawal of the chemoprophylaxis [36],[37],[41].

Direct detection

Diagnosis of this disease can be accomplished via T. gondii recognition in blood, body fluids, or tissue samples. T. gondii can be isolated from blood through either inoculation of human cell clinical sample or mouse inoculation. The latter usually necessitates prolonged time to elucidate a conclusion and is likely more costly. Utilizing the amniotic fluid may be helpful in congenital disease diagnosis [42].

Indirect detection

Indirect detection is indicated for two types of patients:
  1. pregnant women and
  2. immunocompromised patients.

Detection of IgG is possible via enzyme-linked immunosorbent assay (ELISA) testing, IgG avidity test, and the agglutination and differential agglutination tests. An immunocompromised patient may not have a strong antibody response to the T. gondii infection − their IgM and IgG levels may be lower than expected even though they have an active case of toxoplasmosis. The following diagnostic techniques can be also admitted:
  1. Brain biopsy.
  2. Lymph node biopsy.
  3. Bronchoalveolar lavage.
  4. Amniocentesis: at 20–24 weeks’ gestation with suspicion of congenital disease.
  5. Lumbar puncture: used to recognize an evidence of increased intracranial tension.

‘Tachyzoites’ may be identified in tissues/smears provided by biopsy. Moreover, they can be demonstrated in cerebral spinal fluid (CSF). The latter may show mononuclear pleocytosis with increased protein level. Tachyzoites indicates ‘acute infection’; on the contrary, tissue cysts and bradyzoites can be seen with chronic/latent infection as well as in acute infection/reactivation (https://emedicine.medscape.com/article/229969-workup).

Final diagnosis

It can be accomplished through the following:
  1. evidence of seroconversion.
  2. tachyzoites recognition in tissue biopsy ([Figure 4]), or
  3. detection of toxoplasma DNA via PCR testing of the infected tissues [43].
    Figure 4 Toxoplasmosis. (a) Oocysts in the excreta of cats. (b) Free, rapidly multiplying tachyzoites released from ruptured tissue macrophages. (c) Zoitocyst in muscle tissue, filled with slowly multiplying bradyzoites. Adapted with permission from Barsoum RS [7].

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Molecular diagnosis and PCR

Molecular diagnostic techniques for toxoplasmosis include conventional PCR, nested PCR, and real-time PCR for recognition of T. gondii DNA in clinically provided samples. Basic protocol for molecular recognition of T. gondii has been through applying the conventional PCR-targeted B1 gene. However, repetitive element of 529 bp in length has recently shown a sensitivity of 10 times than that of the sensitivity with B1 gene. Real-time PCR detecting T. gondii DNA based on 529 bp repetitive element is the most frequently applied molecular diagnostic test for toxoplasma diagnosis. PCR examinations utilizing body fluids, for example, CSF, amniotic fluid, bronchoalveolar lavage, and blood, are all valid to establish an efficacious in diagnosis. Unfortunately, PCR testing can detect T. gondii DNA in only one-third of the recipients with ocular toxoplasmosis [42].

Central nervous system toxoplasmosis

It is identified as multiple ring-enhancing lesions within the basal ganglia or cerebrum on central nervous system (CNS) radiological examination, particularly if there is associated antitoxoplasma IgG seropositivity. Pre-emptive therapy, however, should be instituted immediately without any delay.

Stem cell transplant recipient

Lesion enhancement is inversely correlated with the intensity of immunosuppression, and there are not enough data regarding radiographic views in patients with SOT [44].

Brain biopsy

It may be resorted to in resistant cases. CSF examination may show mild mononuclear pleocytosis and/or an increased protein content. Recognition of this parasite’s DNA via PCR testing utilizing the CSF of HIV/AIDS patients has been reported with better specificity (96–100%); however, its sensitivity is much lower (52–98%) [45]. Tachyzoites may be rarely observed in a centrifuged CSF sample [42].

Heart failure may represent an underlying myocarditis; diagnosis can be made by identification of tachyzoites on cardiac muscle biopsy. Chorioretinitis may be presented as scotomata, blurring of vision, or as a photophobic sight. Fundoscopy may demonstrate yellowish-white, cotton-like elevated lesions that arrange in a nonvascular pattern (different from the perivascular pattern in retinopathy seen in patients with cytomegalovirus); viral inflammation may also be seen. Pulmonary involvement can be observed as fever, shortness of breath, nonproductive coughing, and reticulonodular infiltrations in chest radiography. This pathological paradigm may simulate Pneumocystis jiroveci pneumonic pattern; however, toxoplasma tachyzoites can be recognized in the bronchoalveolar lavage aspirates. Skin lesions, on the contrary, may be rarely seen after hematopoietic stem cell transplant [46].

Chagas disease (American trypanosomiasis)


The inciting vector is the protozoan parasite Trypansoma cruzi. Disease transmission to humans can occur via the contaminated feces of the ‘triatomine insect’ vector [47]. Other modes of T. cruzi transmission include blood transfusion, mother to fetus transmission, oral ingestion as well as donor organ transmission. Eight to nine million subjects are currently living with Chagas infection in the endemic areas in most Latin America, and 2–5 million of them have Chagas cardiomyopathy. Ever increasing human migration has resulted in 0.3–1 million subjects at risk of being positive for T. cruzi infection in the US [48],[49]. T. cruzi prevalent disease may involve 100 mammalian species or more in many areas worldwide including the southern and southwestern US. Mammals have been affected in sylvatic modes of infection, including raccoons, monkeys, forest rats, etc.

In 2016, the WHO estimation denoted that almost 6–8 million individuals may express T. cruzi infection, and mostly 12 000 yearly mortalities can be related to the effect of this disease [50]. Furthermore, immigrant carriers of the parasite from the endemic zones may currently distribute the infection through many individuals in the industrialized world [51]. Clinically, human involvement has two separate presentations: acute event and chronic disease. In immunocompetent individuals, spontaneous resolution of infection can occur even if untreated, but in the absence of specific therapy, infection can persist despite intact immunity and the patient may become chronically infested [47]. Surprisingly, the indeterminate phase (clinically latent) may exist for 10–30 years and could be lifelong. Approximately one-third of patients with chronic infection may proceed to an irreversible involvement of the heart (27%), esophagus and colon (6%), and peripheral nervous system (3%) [52].

Modes of transmission of T. cruzi to humans

In the past, T. cruzi can be easily transmitted through the contaminated skin abrasions, conjunctival lesions, and other amenable surfaces with fecal matter of the infested victors. This mode of transmission has been greatly diminished. On the contrary, infection transmission through blood/blood products has been discarded after the advent of the advanced techniques of serological screening and the mandated screening of every blood donor [53].

Pregnant and lactating recipients

In the contrary to T. gondii, T. cruzi vertical transmission is possible with frequent pregnancies. Transmission of T. cruzi through breast milk feeding is entirely rare, and breastfeeding is not contraindicated with chronic T. cruzi infection. Transmission of T. cruzi through ingested food/drink contaminated with feces of infected hosts has been documented [54]. Finally, a rare accidental transmission via the produced infective pathogen of T. cruzi in the laboratory has been also reported [55]. In the transplant community, three different scenarios may be observed:
  1. Heart TR with chronic T. cruzi infection at risk of reactivation.
  2. Noncardiac TR with chronic T. cruzi infection at risk of reactivation.
  3. Uninfected organ TR receiving organs/blood from T. cruzi-infected donors.

Chagas cardiomyopathy

Chagas cardiomyopathy has been estimated to be the third leading cause for cardiac transplantation in Brazil (∼22% of the performed cardiac transplantation) [56]. Compared with other causes, the outcomes of post-heart transplant cardiomyopathy owing to T. cruzi do not differ significantly [56],[57]. The reported incidence of post-transplant reactivation may approach 27% [56] up to 43% [58] in TR. Risk factors include acute rejection, mycophenolate mofetil therapy, and neoplastic transformation [56]; however, others may disagree with these figures [58]. Clinical manifestations include fever, cutaneous manifestations, and myocarditis (clinically and histologically may simulate rejection) [59]; however, asymptomatic parasitemia may supervene. Cutaneous manifestations may include rash that simulates ‘panniculitis’, and a skin biopsy can explore Trypanosoma pathogens. Prompt and timely diagnosis, careful monitoring, in addition to a better response to therapy can only result in a favorable outcome [58].

Chronic T. cruzi among nonheart allograft transplant recipient

In nonheart TR, experience is limited to kidney transplantation [10]. Infection/reactivation has been observed primarily within the first year after transplant. Reactivation features including fever, panniculitis, myocarditis, encephalitis, as well as asymptomatic parasitemia have been mostly observed [10],[59],[60].

Uninfected organ transplant recipient receiving organs or blood from T. cruzi-infected donors

Acute T. cruzi infection can be observed in T. cruzi seronegative recipients of seropositive donors after transplantation [61]. The reported transmission rates from seropositive donors to seronegative TR may approach 20% for kidney TR [62] and 22–29% of liver transplant [62],[63]. Considering the robust avidity of T. cruzi for heart tissues, a higher rate of infection transmission in cardiac transplantation will be expected [61]. Clinically, there is pyrexia, weight loss, anorexia, hepatosplenomegaly, and acute myocarditis. Symptomatic presentation can be observed as long as an average of 112 days (range: 23–240) after transplantation [61],[64].


Acute cases of Chagas disease can be seen as an inflammatory sign called ‘chagoma’ owing to T. cruzi infection. It can be clearly observed at the location of the vector inlet. Histopathologic criteria may include interstitial edema, lymphocytic invasion, as well as reactive hyperplasia of the draining lymph nodes. With disruption of the infested host cells, trypomastigotes will be freed, so that they can be microscopically recognized. Once the parasite has been disseminated, muscles, including myocardial muscles, will be infested. Acute myocarditis, in the form of patchy necrosis and infected myocardial cells, may develop. Pseudocysts may be seen as intracellular aggregations of amastigotes [65].

In chronic Chagas disease, the heart is the most commonly involved organ. In autopsy of patients who died of Chagas heart failure, bilateral ventricular enlargement is markedly observed, which is more obvious in the right side. Thinning of the ventricular walls with mural thrombi and apical aneurysmal dilatation may be seen. Furthermore, global interstitial fibrosis, ubiquitous lymphocytic infiltration, and atrophied myocardial cells may all be observed [65]. T. cruzi parasites are rarely seen in microscopic studies of stained myocardial sections; however, T. cruzi specific PCR testing has recognized parasites in the focal inflammatory areas. Pathologic alterations involving the cardiac conducting system of chronically chagasic hearts can be also observed with its ultimate effect in dysrhythmia evolution. The bundle of hyperinfection syndrome (HIS) can be disrupted by the intense fibrous chronic lesions. Chronic GIT Chagas disease may encompass dilatation with hypertrophied lesions of various digestive system [65]. The devastating effect of chronic cardiac parasitism, however, can be expressed in three ways:
  1. cardiac arrhythmias,
  2. congestive heart failure, and
  3. thrombo-embolic sequelae of the intracardiac clots to systemic organs [66].

Diagnosis of chronic T. cruzi infection in organ transplant recipient and donors

The diagnosis can be made by detecting antibodies to T. cruzi antigens, which is frequently performed by enzyme immunoassay or immunofluorescence assay techniques. A variety of approved assays are available in many countries. Unfortunately, there is no one single test that is reliable enough to arrive at a prompt clinical diagnosis. Consequently, the advent of two different serologic techniques that rely on several antigens and/or methodologies is better applied to ensure validity of the diagnostic results [56]. A third test, however, may be added in case of contradictory results. Serological tests are of limited value in organ TR with acute and chronic T. cruzi infection.

Direct parasitological testing techniques for diagnosis include the following:

(a) Microscopic examination of fresh buffy coat preparations, (b) peripheral blood smears with Giemsa-stain ([Figure 5]a), and (c) PCR whole blood or tissue biopsy ([Figure 5]). Of note, PCR testing [available at Center for Disease Control and Prevention (CDC)] can provide the best sensitive results and can be definitely positive up to several weeks before the infested trypomastigotes could be detected by microscopic detection in the peripheral blood or via a prepared buffy coat [67]. Positivity of PCR is not reliable in the absence of clear evidence of disease reactivation with chronic T. cruzi infection.
Figure 5 Chagas disease. (a) Trypomastigotes of Trypanosoma cruzi (usually observed in abundance in blood smears from infected immunocompromised patients). (b) Amastigotes of T. cruzi in cardiac muscle. With permission from Barsoum RS [7].

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Blood culture is of limited benefit as prolonged time is usually warranted (2–8 weeks). TR receiving organ from a seropositive donor to a seronegative TR as well as recipients with chronic T. cruzi disease should be thoroughly monitored, so that prompt therapy can be early instituted before the disease clinically manifests.

Transplanted organs from seropositive donors to seronegative recipients

Donor-derived T. cruzi disease has been reported; the actual rate of transmission is not known [62]. Kidney and liver allografts from infected donors may be permitted with close post-transplant surveillance. However, considering the high avidity of T. cruzi organisms to the cardiac tissues, receiving hearts from infected donors is currently prohibited [2]. No available data are concerned with other organs.

PCR assays

The advent of PCR testing to recognize T. cruzi has been thoroughly evaluated through the past 25 years. Methodology for the best mode for PCR testing for T. cruzi has been published, but the concerned kits are not for commercial use. PCR testing for T. cruzi pathogen has currently many clinical implications. By far, the first one is that used in patients with chronic infection on benznidazole or nifurtimox therapy, where PCR positivity indicates failure of therapy, but considering variation in sensitivity intense, PCR negativity, on the contrary, will not be beneficial. Second, PCR testing for this pathogen may have its effect on recognition of acute Chagas infection, especially in congenitally acquired T. cruzi disease, as its sensitivity has been shown to be higher as compared with microscopic techniques. Finally, PCR assays are the preferred technique to detect T. cruzi infection in insect vectors and in suspected food of pathogen contamination [68]. Further testing may be required with intense immunosuppression load such as follows:
  1. pyrexia of unknown origin or
  2. suspected allograft rejection [62].



Through the bite of the female sandfly, leishmaniasis infection is transmitted to humans. Leishmaniasis can be originated from a heterogeneous family of protozoal infection that belongs to the genus Leishmania. Several clinical syndromes can be presented by this parasite. Approximately 350 million people are vulnerable for acquired infection. Another 12 million may harbor the parasite. Leishmaniasis is prevalent in the tropical/subtropical countries, and it is endemic in European Mediterranean zones. Of note, 90% of the global disease loads of visceral leishmaniasis have been reported from India, Bangladesh, Nepal, Sudan, and Brazil [69]. Clinically, disease presentation can be delayed as late as 30 years after the infectious event; consequently, distant exposure to the parasite should be considered in differential diagnosis.

Data from the WHO reported leishmania endemicity in 98 countries in five continents (Africa, Asia, Europe, North America, and South America). Almost 0.7–1.3 million cases of cutaneous disease and 0.2–0.4 million cases of visceral disease have been documented annually [70]. India may express the largest load of visceral disease, as ∼14 000 newly diagnosed cases have been reported in 2013 [71]. Nearly 90% of mucocutaneous cases are prevalent in Bolivia, Brazil, and Peru [70],[72]. However, aggressive clinical presentation may be observed in organ TR previously lived or visited an endemic zone. Acquisition of infection, however, can be seen in three ways:
  1. post-transplant primary infection,
  2. post-transplant recrudescence of dormant infection, or
  3. donor’s infected graft that is transmitted within transplant procedures [73],[74].

Leishmaniasis in organ TR is mostly reported with kidney transplantation [75], however, it has been observed in liver [75], heart [75], lung [76] and kidney-pancreas transplants [77]. Approximately 18 months after transplant should have been elapsed before the disease can be clinically diagnosed.

Clinical manifestations

Severity of the clinical manifestations relies primarily on the causative pathogen as well as the integrity of the patient’s immune mechanisms. Clinically, presentation simulates that seen with immunocompetent individuals including fever, hepatosplenomegaly, and pancytopenia [78]. One report observed that the average time to disease onset is about 1 month after transplantation; other reports, however, have documented that reactivation was delayed as far as 55 and 96 months after transplantation [79],[80].

Cutaneous/mucocutaneous leishmaniasis, on the contrary, is mostly induced by species of Leishmania mexicana complex and subgenus Viannia in industrialized countries and Leishmania major, Leishmania tropica, and Leishmania aetheopica in the developing countries. Cutaneous/mucocutaneous diseases are less frequently observed in the TR community and need a prolonged time to manifest [81].


Visceral leishmaniasis

Direct recognition of amastigotes via tissue biopsy or in culture demonstrating the promastigotes is the key step in the diagnosis of visceral leishmaniasis through (a) bone marrow aspirate or (b) splenic aspirate ([Figure 6]a). Regarding immunocompetent individuals, splenic biopsy has greater sensitivity as compared with bone marrow aspirate (96 vs. 70%) to establish the diagnosis [82]. On the contrary, in organ TR, bone marrow aspirate has shown a sensitivity rate of 98%. Biopsy of other tissues, however, for example, LN or intestine, can be used as an occasional alternate.
Figure 6 Leishmaniasis. (a) Macrophage filled with amastigotes of Leishmania donovani. (b) Facial ulcerating nodule of cutaneous leishmaniasis. With permission from Barsoum RS [7].

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Serological examination for visceral leishmaniasis is reported to be highly sensitive (92%) in organ TR in one systematic series. However, two remarkable drawbacks of serology have been observed:
  1. It may cross-react with other parasitic species.
  2. It cannot differentiate between previous exposure and a currently active disease.

A high sensitivity rate for visceral leishmaniasis diagnosis has been also reported to the urinary antigen testing as well as the serum PCR [83],[84].

Cutaneous and mucocutaneous leishmaniasis

Tissue biopsy for histopathology and culture studies is mandated for cutaneous or mucosal leishmaniasis. To fulfil the diagnosis, speciation can be accomplished via isoenzyme analysis or species-specific monoclonal antibody. The use of a histopathological specimen for quantitative or semiquantitative PCR testing can result in a high diagnostic utility ([Figure 6]b) [85].



Malaria is one of the most prevalent diseases worldwide. According to Barsoum [86], an Egyptian specialist on parasitic nephropathies, ‘life cycle of this protozoan is ideal for becoming a notorious post-transplant infection’. Fever and anemia are the typical manifestations [87]. More than one million deaths per year in addition to more than 300 million acute cases have been attributed to malaria in developing countries.

Modes of transmission

It is transmitted as follows:
  1. bite of the female Anopheles mosquito.
  2. blood transfusion, and
  3. organ transplant, particularly in areas with a large number of immigrants [87].

Unfortunately, malaria does not offer any postinfectious protective immunity; instead, a certain level of resistance to severe infection may be acquired via frequent exposure to the parasite and its prolonged existence in the liver, microvasculature, and in the circulation. Ineffective immunity may explain the absence of identifiable parasitemia with increased frequency of asymptomatic cases in individuals coming from endemic areas. This observation reflects certain risk of transmission of malaria through blood or organ donation. Transmitted malaria has been reported through the donated organ [88]; however, other cases may be attributed to contaminated blood/blood products [89]. In the developed world, malaria is rarely reported unless the TR has visited an endemic region or has received an organ from a donor coming from an endemic zone. The main plasmodia species are Plasmodium ovale, P. vivax, P. malariae, and P. falciparum; all of them have been reported in TR. Salient features are usually seen early after transplant and can be observed in the kidney, liver, and heart TR [88],[89],[90]. Pyrexia is usually the most common clinical feature, however, it is not necessarily paroxysmal or manifests in a cyclic paradigm [91],[92].


Microscopic identification of the parasite in a thick or a thin blood smear is typical for diagnosis ([Figure 7]a and b). A wide range of rapid diagnostic techniques became available through certain dipsticks that permit the identification of specified plasmodia antigens in a clinically manifest disease [93]. The available alternative techniques include the following:
  1. ELISA testing for P. falciparum antigen.
  2. Immunofluorescence assay for species-specific enzymatic technique.
  3. DNA hybridization and DNA and mRNA amplification via PCR technique.
Figure 7 Giemsa-stained blood films showing red cells infected with malaria and babesiosis. (a) Exflagellated Plasmodium falciparum gametocytes (infective to mosquitoes). (b) Ring form of P. falciparum. (c) Ring forms of Babesia microti. With permission from Barsoum RS [7].

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Post-transplant malaria can usually be diagnosed through detection of the parasite in a blood smear during febrile period particularly with associated thrombocytopenia and unexplained hemolysis [94].


It is a tick-borne, zoonotic protozoal disease that develops owing to infection with the vector Babesia spp. that invades the RBCs causing its lysis ([Figure 7]c). A variety of babesia species can induce human affection. It includes B. microti mainly seen in northeastern US, B. divergens in European countries, and B. duncani in western US. The most virulent one, however, is B. divergens. Ticks of the Ixodes genus is responsible of human transmission. Three reports in the literature have been published about babesiosis in TR, and they were all related to blood transfusion. They include two kidneys and one heart TR [16],[95],[96]. There is no Food and Drug Administration (FDA)-approved Babesia test available for blood product screening.

Risk factors

The risk factors for aggressive disease include asplenia, immunocompromised host, and old aged recipients. Salient features vary from silent cases to a devastating disease. Patient can present early with fever and loss of weight that can be deteriorated to severe hemolytic disease [usually presents as a post-transplant Hepatosplenomegaly (HUS) or hemophagocytosis], ARDS, multiple organ failure syndrome, and may even end fatally. Blood profile usually demonstrates hemolytic anemia, thrombocytopenia, and conjugated hyperbilirubinemia. Severity of the disease, however, correlates well with the magnitude of the parasitemia load.


The diagnosis of babesiosis can be accomplished via either microscopic examination of a peripheral blood smear or through PCR testing of the blood. Of note, misdiagnosis can occur owing to confusion between Plasmodia spp. and Babesia spp. owing to similar morphology on microscopic examination ([Figure 7]b and c), as both species can invade the RBCs. However, DNA testing via PCR as well as the history of geographic epidemiologic exposure can help differentiating between the two diseases. Bone marrow biopsy for babesiosis-infected patients may show hemophagocytosis and histiocytosis [2].


Free-living amoebas

Environmental exposure to this protozoal pathogen may lead to fatal outcome in immunosuppressed individual. Isolation of free-living amebae (FLA) can be easily provided from soil, sand, sea water, swimming pools, and other regional sources [97],[98]. Three clinical modes of presentations have been reported in amoebiasis:
  1. granulomatous amoebic encephalitis (GAE),
  2. disseminated amoebic disease, and
  3. amoebic keratitis. In normal individuals, the disease is confined to the cornea, precisely limited to subjects with contact lenses.

Granulomatous amoebic encephalitis

It is rarely seen but is almost always a devastating fatal disease. Besides Acanthamoeba species, other FLA such as Balamuthia mandrillaris and Sappinia pedata can induce GAE. Early manifestations may include cutaneous or pulmonary affection. Recurrent panniculitis-like lesions, subcutaneous lesions associated with eosinophilia, and chronic rhino-sinusitis have been reported [97],[98]. If the protozoa succeeds to invade the blood–brain barrier, outcome is very poor. Clinically, there is culture-negative pyrexia, cough, nausea, vomiting, headache, dizziness, behavioral alterations, and confusion [97]. GAE was primarily seen after bone marrow transplant but can be also observed after SOT and in HIV/AIDS patients [97].

Risk factors include immunosuppression, past history of nasal drainage, contact with polluted water/garden soil, and traumatic events with cutaneous lacerations [97],[98]. Imaging studies may elucidate subarachnoid hemorrhages, hydrocephalus, ring-enhanced lesions, and cortical and scattered hypodense lesions. Tissue biopsies, CSF studies, serology, and PCR testing may help early diagnosis. Mortality rate may exceed 90% ([Figure 2]) [97],[98].

Protozoan infection-induced diarrhea

Mostly 10–30% of TR may experience diarrheal illness [99], leading to dehydration, malabsorption syndrome, frequent hospitalizations, and non-compliance to medications, associated with low quality of life [99]. Diarrhea is considered one of the most common complaints after transplant. Surprisingly, diarrheal episodes is usually omitted and considered by many physicians as a nonpreventive adverse effect of the immunosuppressive medications. General causes of diarrheal illness in the transplant community may encompass the following:
  1. diabetic neuropathy,
  2. infectious pathogens [100], and
  3. medications (e.g. mycophenolate mofetil, tacrolimus, rapamycin, and antibiotics).

Infectious microorganisms include bacterial infections (Clostridium, Shigella, and Salmonella enteritis), viruses (cytomegalovirus, rotavirus and adenovirus) in addition to the parasitic infection, which is the essential cause for infectious diarrhea [99],[101]. Intestinal parasites-induced diarrhea is commonly seen in some regions, for example, in Iran, 33.3% of kidney TR may express infection with one or more intestinal parasitic agents [102].
  1. Amoebic dysentery: The causative pathogen is Entamoeba histolytica, which is a common cause of bloody diarrhea in endemic areas. Infected individuals may approach 400–500 million; however, only 10% of colonized hosts show symptoms [103],[104]. Classic presentation includes bloody diarrhea accompanied by colicky postprandial abdominal pain [104]. Of note, 50 million cases of invasive E. histolytica disease have been reported annually all over the world, and 100 000 of them may develop grave outcome [42]. Risk factors include steroid therapy [104] that could be complicated by multiple liver abscesses [105] or pulmonary amoebiasis [42]. However, only few cases of amoebic dysentery disease have been observed after SOT and after bone marrow transplant in USA and Japan [103],[104].
  2. Giardiasis: Giardia duodenalis (formerly named G. lamblia) is considered one of the most famous universal intestinal parasitic diseases that can lead to diarrheal illness worldwide ([Figure 8]a) [106]. Clinically, giardiasis can induce nonbloody diarrhea, distension, foul-smelled stool, abdominal cramps, and malaise as well as malabsorption syndrome [107]. Only 3% of traveler’s diarrhea can be attributed to giardiasis. Generally, giardiasis comprises less than 1% of post-transplant parasitic diseases. The observed low incidence of this disease can be explained by the marvelous response to metronidazole therapy. In highly endemic regions, some centers apply routine screening and treatment of giardiasis in pretransplant period [107].
    Figure 8 Intestinal protozoa in transplant recipients. (a) Giardia lamblia. (b) Enterocytozoon bieneusi (causing microsporidiosis). (c) Cryptosporidium. Adapted with permission from Barsoum RS [7].

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  3. Cryptosporidiosis: it is a common cause of traveler’s diarrhea [108]. Infection can be feco-oral transmitted from infected individuals, or from contaminated water/food with Cryptosporidium oocysts [99],[108],[109] ([Figure 8]c). In immunocompetent individuals, diarrhea is usually scanty and self-limited, mostly of 2–26 days duration [108]. In endemic zones, for example, Pakistan, cryptosporidiosis has been observed in 53% of TR with diarrheal illness [108].
  4. Cystoisosporiasis (isosporiasis): This is caused by Cystoisospora belli (previously named Isospora belli), a protozoal pathogen prevalent all over the world, particularly in tropical and subtropical regions [99]. In immunocompetent individuals, C. belli can induce self-limited diarrhea, but life-threatening disease is not common. Infection can occur via ingestion of oocysts present in contaminated food and water [99]. Post-transplant diarrheal illness owing to C. belli has been reported after kidney transplantation in many countries [110].
  5. Microsporidiosis: microsporidia are intracellular spore-forming protozoa. These pathogens are prevalent worldwide and can live in the intestinal lumen of insects, birds as well as in mammals. Two well-recognized species in human intestinal microsporidiosis are (a) Enterocytozoon bieneusi (90%) ([Figure 7]c and [Figure 8]b) and (b) Encephalitozoon intestinalis (10%). Infection can occur after ingestion/inhalation of the resistant microsporidia spores to the environmental factors, person-to-person transmission, or through other mammals or insects. Diarrhea is usually mild, but dissemination of infection in immunocompromised patient can be grave [111]. The reported cases of human microsporidiosis, however, are mainly prevalent in immunosuppressed patients, particularly among HIV/AIDS patients [99]. Post-transplant diarrhea induced by E. bieneusi has been reported in many European countries and in the US [112] ([Figure 9]). Cases with donor-derived CNS microsporidiosis induced by E. cuniculi infection have been reported in 2017 in the US. All three recipients received organs from a single donor [114].
    Figure 9 Tissue specimens from a kidney transplant recipient with concurrent parasitic infections after traveling to the Dominican Republic. (a) Tissue section stained with Gram chromotrope. Note the apical location of a cluster of Enterocytozoon bieneusi spores at arrow and single spore at arrowhead. (b) Tissue section stained with hematoxylin and eosin, demonstrating numerous sites in which Cyclospora spores are in developing stages. (c) Higher power image of Cyclospora spores, showing the developing meronts. (d) IF reactivity (bright green) of the various life cycle stages of Cyclospora with a positive anti-Cyclospora serum sample. (e) Note the bright fluorescence of the various parasite stages just below the apical (luminal) surface of the epithelial cells. Permission is available. Adapted with permission from Visvesvara et al. [113]

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Sushi and sashimi fish-borne parasitic zoonosis

Sushi and sashimi are well-known traditional Japanese dishes. In Japanese restaurants and sushi bars, they are primarily prepared from relatively expensive marine fish, for example, tuna, yellow tail, red snapper, salmon, and flatfish. Exclusively, salmon is an important intermediate host for the fish tapeworm Diphyllobothrium latum. Despite the widespread prevalence of Anisakis larvae in marine fish, fish that are preferentially served in Japanese restaurants and sushi bars are less contaminated or could be free of Anisakis larvae. On the contrary, other popular/cheap marine fish, for example, cod, mackerel, and squid seem to be highly infested with Anisakis larvae and are primarily consumed at home or at public restaurants. Except for Anisakis and D. latum, marine fish usually only serve few transmittable parasite species to humans [115].


Although diphyllobothriasis can be diagnosed by detection of ova or proglottids in the feces, Anisakiasis can be diagnosed through antigen-capture ELISA that has 100% sensitivity and specificity [115].

  Intestinal nematodes Top

Strongyloides stercoralis


Mostly 100 million subjects worldwide have been infected with S. stercoralis [116]. This intestinal nematode is endemic in tropic and sub-tropic countries; moreover, it has been reported in temperate zones [116]. S. stercoralis has the ability to develop its life cycle in the environment as well as in humans. Consequently, it has a unique ‘auto-infective’ cycle that results in a prolonged and persistent type of infection.

Reproduction of the adult females can occur both sexually and asexually (parthenogenesis). The laying of eggs can present in two forms: (a) rhabditiform larvae that is usually defecated with stools to start a new life cycle, and, (b) filariform larvae that may disseminate the infection through penetrating the intestinal mucosa. Under the effect of the immunosuppression burden, transformation of rhabditiform larvae into filariform larvae could be intensified, leading to a massive larval infestation, occupying the intestinal lumen or the perianal area to auto-reinfect the host. Consequently, a huge number of adult worms may infest the intestinal lumen that may result in lung involvement and dissemination of the pathogen to other organs.

Clinical syndromes include acute and chronic/auto-infections: hyperinfection syndrome (HIS) and disseminated disease (DD). Criteria of the HIS include acceleration of larvae reproduction, migration and increased parasitic load with manifest clinical disease; the larvae, however, are usually confined to the lungs as well as the GIT systems ([Figure 10]). DD, on the contrary, includes the components of HIS in addition to larvae distribution to systemic organs. Risk of HIS and DD evolution has been attributed to alterations in host immune integrity that is primarily related to the immunosuppressive burden. Moreover, HTLV-I coinfection can add more to the risk of HIS/DD progression. Strongyloidiasis has been reported in organ TR in two forms: (a) reactivation of latent infection and (b) donor-transmitted infection [117],[118]. Strongyloidiasis is a serious infection in TR, with mortality rates exceeding 50% in HIS and 70% in DD [118].
Figure 10 Strongyloidiasis. (a) Strongyloides pneumonitis associated with hyperinfection in a kidney transplant recipient. (b) Migrating larvae in subcutaneous lymphatics (arrows). (c) Hatching eggs in human intestine. Adapted with permission from Barsoum RS [7]

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Clinical presentations are variable and may include pulmonary involvement, septic sequelae or Gram-negative rods-induced meningitis, which occur with intestinal flora contaminating the parasite while in migration. GIT manifestations include bloody diarrhea, adynamic ileus, as well as gastrointestinal hemorrhage. The latter can be induced via larval penetration through the gut wall. However, severity of these manifestations is maximized early when the immunosuppression burden in its maximal intensity. Comorbid conditions, on the contrary, present with SOT (e.g. lymphoma, hypogammaglobulinemia and malnutrition) and may trigger earlier progression to HIS/DD syndromes [119].


In the acute phase, eosinophilia can be found in infected recipients. In chronic infection, HIS/DD, and immunocompromised hosts, there may be a lack of elevation in eosinophilic count. However, absence of eosinophilia does not exclude the diagnosis [120],[121]. Recognition of larvae in collected specimens, particularly in stools (typical finding only in HIS/DD as they show persistent larval existence) as well as in duodenal aspirates ([Figure 11]) [122],[123], is the golden standard for diagnosis. However, when DD syndrome supervenes, larvae may be encountered in pulmonary secretions, CSF, peritoneal fluid, urine, pleural effusion, and blood samples. With mild/moderate disease, the density of the stool larvae is declined with intermittent discharge. For duodenal fluid aspiration, despite more sensitive as compared with direct stool testing, it shows only 76% sensitivity and encompasses an invasive intervention procedure.
Figure 11 Histology of the duodenal biopsy taken during the first esophagogastroduodenoscopy (hematoxylin and eosin): (a) multiple Strongyloides stercoralis larvae in the duodenum mucosa (arrows); (b) magnified image showing transverse sections of the larvae. Adapted from Galiano et al. [122], Open access.

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Serological testing is usually more sensitive, despite inability to distinguish active from previous infection; moreover, it may not be available worldwide. ELISA is very sensitive (80–95%) and more specified (90%) in normal individuals [124]. On the contrary, immunocompromised hosts may show reduced sensitivity up to 68%, with specificity at 89% [125]. Applying combined techniques in immunocompromised patients may augment the sensitivity up to 90% [126]. Presence of other helminthic diseases, however, may result in false-positive results; consequently, local epidemiological survey is essential to establish a positive predictive value. A gelatin particle indirect agglutination has a sensitivity rate of 98.2% and specificity rate of 100% [121].

  Trematoda Top



Of all parasitic infections, schistosomiasis is considered the second most common tropical disease [127]. Schistosomal disease is predominantly prevalent in warmer climates; species vary according to the geographic distribution with distinct clinical syndromes that are species related. Schistosomiasis is a fresh-water-borne disease that is mainly endemic in rural areas. Although Schistosoma mansoni and Schistosoma Japonicum can result in intestinal and hepatic disease, S. hematobium, on the contrary, is mainly confined to the kidney and urinary tract. Less commonly reported, Schistosoma mekongi and S. intercalatum that can be complicated by intestinal and/or liver disease.

Schistosomiasis is a disease caused by flat worms, which are usually harbored in either the portal or perivesical venous plexus in humans as well as many other mammals. It is the only reported trematode that has been related to SOT parasitic infection. They lay their eggs that find an exit via the rectal or bladder wall. Once these eggs get in contact with fresh water, they hatch releasing many miracidia that infect specific snails, therein mature into cercariae, the cycle phase responsible for human infection [7]. After penetrating the skin/mucous membrane of the infected host, cercariae develop into schistosoma, the latter migrate through lymphatics to blood stream where they finally settle in the hepatic sinusoids and can mature into adult worms.

In theory, transmission of infection can occur via blood transfusion or through an infected donated organ that is possible only during the short stage of parasite migration. Of note, this mode of infection transmission has not been reported. However, TR are vulnerable for new infection or may be re-infected if no alteration in their habits is made regarding the contact with the infested sources. This scenario has been observed in Egyptian TR [17], where 23% of high-risk TR were currently re-infected. Clinical presentation in these patients, however, is not different from that observed in naturally infected immunocompetent hosts. Recurrence of schistosomal glomerulopathy in endemic zones has been also observed. Furthermore, MPGN with schistosomal antigen deposition has been observed in a KTR who had primarily infested with S. mansoni. Recrudescence of a case of liver schistosomiasis has also been observed in a hepatic TR who was previously harboring the same species [128]. Considering the chronic nature of schistosomal infection, where these worms can live for many years, prophylactic therapy has been suggested for previously infected patients before transplant [7].

Salient features

Heavy S. mansoni infection can result in pipe stem fibrosis that occur around the hepatic portal veins, as a result of huge number of schistosomal eggs in hepatic tissues with evolution of portal hypertension. Intestinal manifestations usually include abdominal pain, anorexia, and diarrhea. Urinary disease can be clinically manifest as hematuria, dysuria and urine frequency. On the long run, infection chronicity can induce fibrous tissue formation and urinary tract calcification that may be complicated by obstructive uropathy and end-stage renal disease. Schistosomal nephropathy can also result in end-stage renal disease. On the contrary, Mahmoud and his associates reported that treated schistosomiasis has no significant effect on patient/graft outcomes, with no evidence of re-infection. An increased rate of acute and chronic CyA nephrotoxicity in addition to increased incidence of UTI and urological sequelae has also been observed. The effect of immunosuppression on the clinical course of the disease is not exactly clear. Moreover, schistosomal re-infection after hepatic transplantation is rarely reported possibly developed owing to reactivation of latent infection due to the immunosuppressive load [128]. Schistosomal disease can be theoretically transmitted to TR; however, adult worms cannot replicate within the host, and they are only transmitted as nonreplicating adult worms. Acute Schistosoma infection is usually asymptomatic. Almost 60% of the infected cases are seen in chronic status, despite advanced hepatic deterioration only observed in 4–8% of patients [126]. Both donors and TR may deny any past history of infection. Several cases of successful schistosomal infected organ donation have been reported [129]. It is not known whether TR with donor-related disease are vulnerable for the systemic hypersensitivity reaction that is seen in primary infection (Katayama fever). Post-transplant immunosuppressive therapy, however, may alter disease presentation. Clinical symptoms could be also misinterpreted as acute allograft rejection.


Ectopic Schistosomal ova may find their way to the CNS via the anastomosis between lumbar veins (inferior vena cava tributaries) and the internal vertebral venous vasculature. Through deposition in the adjacent spinal cord, granuloma may supervene [130], or they may transmit vertically during coughing or straining to be barged into brain substance. However, the small size of S. japonicum eggs as compared with other species facilitates their way into the brain, hence the avidity of this species to cerebral Schistosomiasis, including cortex, subcortical white matter, basal ganglia, as well as the internal capsule. On the contrary, lumbosacral myelopathy is more commonly encountered with S. mansoni and S. hematobium [131]. Neuro-schistosomiasis is the most devastating complication associated with Schistosomal disease. It can be clinically presented as a manifestation of elevated intracranial tension, myelopathy, and radiculopathy. Untreated patients may develop irreversible glial scars. Complications of neuro-schistosomiasis may include encephalopathy with headache, seizures, motor deficit, and ataxia. Spinal manifestations may encompass lumbar and radicular pain, muscle weakness, sensory losses, as well as bladder malfunction.

Definite diagnosis

Schistosomiasis can be finally diagnosed via the following:
  1. Tissue biopsy (rectal snip) ([Figure 12] and [Figure 13]) [132].
    Figure 12 Calcified Schistosomal ova in a rectal biopsy. Normal mucosa overlying submucosal layer containing numerous calcified Schistosoma japonicum eggs. Adapted from Barsoum et al. [132], 2013, Open access.

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    Figure 13 Histopathological lesions in schistosomiasis. (a) Active Schistosoma mansoni granuloma. Note the central deformed ovum with a lateral spike and the surrounding mononuclear and few polymorphonuclear cells. (b) Sheet of live Schistosoma hematobium cells. (c) Multiple granulomata around S. hematobium worms and egg debris. Note the intact female worm and a coronal section in a male worm in a bladder venule, and the surrounding mononuclear cellular reaction and fibrotic granulomata. Granulomata coalesce to form tubercles, nodules or masses. The submucosa and muscle layers are also involved in the inflammatory process. Adapted from Barsoum et al. [132], Open access.

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  2. Serology (serum or CSF): a list of serologic tests rely primarily on S. mansoni antigens and can cross-react with antigens of other parasitic pathogens. Of note, the antibody level cannot be correlated with the severity of infection, so we cannot rely on serology in monitoring therapeutic response. In TR, seroconversion may be delayed in primarily infected recipients.
  3. Stool/urine examination:
    1. PCR assay: using patient’s urine, PCR testing has a 94.4% sensitivity and 99.9% specificity for schistosomal diagnosis. PCR has the ability to detect/quantify schistosomal DNA in stool or urine (https://emedicine.medscape.com/article/228392-medication#2).
    2. Urinary and fecal microbiology ([Figure 14]): urine microbiology is fundamental with suspected vesicular involvement owing to S. hematobium infection. Gross and microscopic hematuria are frequent. Fecal microbiologic studies performed on a thick smear are vital in primary bowel schistosomiasis. Gross or occult blood in stool may be positive. An experienced lab technician may explore morphologic details with staining to recognize a single and mixed schistosomal infestation (https://emedicine.medscape.com/article/228392-medication#2) [133].
      Figure 14 Schistosoma mansoni. Male (larger worm) and female adults. Permission from Dr. Barsoum RS. Adapted with permission from Barsoum et al. [132]

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  Cestodes Top

Echinococcosis (hydatid-alveolar cyst disease)


Echinococcosis is a parasitic disease originating from consumption of eggs of either (a) Echinococcus granulosus or (b) E. multilocularis. Although the former usually harbors in domestic dogs, which results in hydatid disease, the latter is usually found in wild canines causing alveolar cystic disease. Humans are considered the intermediate hosts. Clinically, hydatid cysts are mostly symptomless. If developed, however, clinical manifestations are usually related to the mass effect of the continuously growing cysts, cyst leakage, rupture, or secondarily infected. Continuous hydatid cyst growth, however, can result in end-stage liver cell failure, which can also result from therapy-related adverse effects. Hepatic transplant has been performed in end-stage liver cell failure owing to hydatid invasion. These liver TR did not receive anti-parasitic medications and did not develop recurrence or death related to hydatid disease [134]. Interestingly, in a heart TR, the growth rate of the hydatid liver cysts was not exaggerated upon the immunosuppressive load that suggests the possibility of liver transplant with presence of hydatid cysts [135]. In E. multilocularis disease, larvae are continuously proliferating with alveolar cyst formation and indefinite cystic growth. As they resemble slowly growing metastatic lesions, they ultimately warrant surgical eradication. Clinically, alveolar echinococcosis may simulate hepatobiliary malignancy. However, it is a potentially lethal disease within 10 years, if not surgically resected [136].


Hydatid cysts are frequently incidentally discovered on routine radiological examination. History of epidemiological exposure can help in a presumptive diagnosis. Serology can also be used to confirm the presumptive diagnosis. Serologic testing may provide potential sensitivity of 60–95%. E. multilocularis-related disease should be distinguished from a possible hepatic carcinoma. Liver biopsy, however, is of limited use owing to the high risk of hydatid spread. Consequently, diagnosis is best confirmed by imaging in addition to antibody detection via recombinant antigens. ELISA measuring the anti-E. granulosus IgG titers can be used to estimate the magnitude of a possible recurrence [136].

  Insects (ectoparasites) Top

An ectoparasitic infestation is a parasitic disease caused by an organism that lives mainly on the surface of the host, for example, scabies crab louse (pubic lice), pediculosis (head lice), and Lernaeocera branchialis (cod worm). It is a rare disease in Europe. A serious type of Sarcoptes scabiei infestation called ‘Norwegian scabies’ (crusted scabies) has been reported after kidney transplant. Secondary bacterial infection may ensue with multiple brain abscesses particularly in severely immunocompromised recipients [137].

  Prevention of parasitic infection in solid organ transplant Top

Tissue and blood protozoa

Prevention of toxoplasmosis

Screening for previous infection is only recommended before heart transplant, but less advised with other organ transplant. Current reports suggested routine screening only in areas with high toxoplasma seroprevalence, but not in areas with low prevalence, particularly so, in the era of routine trimethoprim/sulfamethoxazole (TMP/SMX) prophylaxis [138],[139].

Primary prophylaxis

The routine administration of TMP/SMX for TR protection after SOT [2],[140],[141] is currently the most widely used agents for toxoplasma prophylaxis. The effective TMP/SMX dose supported by many studies (160 mg of TMP, 800 mg of SMX) three times weekly for ∼3 months up to lifelong. Alternative therapy to TMP-SMX which has been thoroughly tried in HIV/AIDS is dapsone plus pyrimethamine, plus leucovorin. Some experts have suggested the use of pyrimethamine with or without sulfadiazine for high-risk cardiac TR [141]. To avoid primary infection, TR are advised to avoid direct contamination with undercooked meat, soil materials, or animal fecal matter that may harbor toxoplasma cysts. Toxoplasma seropositive heart TR as well as seronegative heart TR receiving organs from seropositive donors are advised to commence prophylactic therapy against toxoplasma disease with TMP/SMX. Prophylactic therapy duration after transplantation is not clear, but many experts advise lifelong prophylaxis with either double-strength TMP/SMX (160 mg of TMP, 800 mg of SMX) one tablet three times per week or single strength TMP/SMX (80 mg of TMP, 400 mg of SMX) one tablet daily.

Chagas disease (American trypanosomiasis)

Prevention of Chagas disease

In endemic areas in Latin America, screening for T. cruzi infection in donors and TR is recommended. Regarding areas of low prevalence (e.g. US), public screening of at-risk cohorts should be arranged according to local epidemiological situations, and ‘targeted screening’ for all communities is advised [62]. The later is particularly essential for those of Latin American origin. Almost 19% of the US organ procurement organizations have commenced either public or targeted screening for T. cruzi parasitism [142].

Routine post-transplant prophylactic anti-T. Cruzi is currently not recommended in TR receiving organs from seropositive source or have a past history of previous infection amenable for reactivation. Alternatively, a pre-emptive strict monitoring plan is advised with institution of therapy once activity of infection has been observed. Screening for active disease, through serum PCR and peripheral blood examination, to detect parasitemia is currently recommended for TR with acute T. cruzi infection as well as those with evidence of chronic infection at risk of reactivation.

Most of the endemic countries have addressed legitimate and mandatory regulations to examine the donated blood for evidence of parasitemia. Mexico is the most recently applied example [143]. Given the recent great advancement accomplished in the management of Chagas disease obviously indicates that the major hurdle impeding the complete eradication of T. cruzi disease is mainly financial reasons. Consequently, no further major advances, regarding expanding the scope of Chagas disease pathogenesis, genetic screening, novel diagnostic techniques, or a breakthrough vaccine innovation [144], are currently warranted for disease eradication. Other authors, however, disagree with the application of such high-technology techniques in dealing with Chagas disease [145].

Prevention of leishmaniasis

There are not enough data suggesting that screening potential TR for visceral leishmaniasis will be beneficial. However, seropositive recipients at the time of transplant should be clinically observed for manifestations of reactivation. In view of the limited data about potential donor-transmitted disease, screening of donors cannot be recommended [146].

Prevention of malaria

Meticulous screening of donors with recent visit or residence (previous 3 years) in malaria-endemic zones is currently advised. The available techniques include thick/thin blood smear staining with Geimsa and other stains, which are of limited value in asymptomatic patients.

Moreover, the rapid diagnostic techniques capable of detecting HRP2 antigen may be considered if an expert reviewer of the thick and thin blood smears is not available. For TR traveling to malaria-endemic regions, proper chemoprophylaxis should be considered to protect them during their travel. Special attention should be paid regarding the use of chloroquine prophylaxis, as it can potentiate CyA blood levels thereby requiring dose adjustment. TR traveling to endemic areas should be given a robust chemoprophylaxis and educated regarding risk-reducing measures to prevent infection. Medical expert consultation is advised before international travel to limit the risk of infection [2].

In August 2018, ‘tafenoquine’ attained an additional indication for adults of 18 years age or above as a valid prophylactic agent in case of traveling to endemic malaria zones. A 100-mg tablet (Arakoda) is provided as a loading dose (before traveling), another maintenance dose while being in endemic zone, and lastly then a final prophylactic dose upon leaving that zone [147].

Prevention of babesiosis

Contaminated food and water are the main sources for intestinal protozoal infection. TR should not drink untreated well or lake water; instead, they should better drink treated domestic water or bottled water. There are no available data supporting consumption of bottled water over other sources. Person-to-person as well as zoonotic transmissions have been observed. TR should be thoroughly educated about these potential risks.

Prevention of Cryptosporidium

TR must be advised against utilizing untreated well/lake water and should avoid occasional water swallowing during swimming in public water pools. Of note, chlorination cannot disinfect this parasite, adding to the difficulties of infection control. With evidence of ongoing Cryptosporidium exposure, installation, with prompt maintenance, of special household water filters helps the limitation of infection transmission [2].

Prevention of Entamoeba histolytica

Contaminated food and water are considered the primary source of infection. TR should be advised to avoid untreated well/lake water; instead, they should better drink treated domestic water or bottled water. Sexually transmitted disease has been reported. TR should be educated about the potential risk of this mode of infection. TR should be advised to avoid potential sources of contaminated food/water [2].

Prevention of giardiasis

It includes proper hygiene with avoidance of exposure to contaminated water/food [107].

Prevention of sushi and sashimi-associated infestations

The FDA recommends preservation of fish used for raw consumption by storing at less than −35°C for 15 h. or at less than −20°C for 7 days. Furthermore, the European Union-Hazard Analysis and Critical Control Points recommends that marine fish used for raw consumption must be frozen at less than −20°C for more than 24 h. However, these precautions are less strictly applied in countries where such legal regulations have not been implemented. Risk of infection by eating sushi and sashimi will be consequently higher. Both travelers and physicians in developed world should be aware about the potential risks and possible symptomatology of such diseases caused by consumption of these ethnic dishes. Particular attention should be directed to the local ethnic dishes that depend on the local freshwater or brackish-water fish and wild animal meat that is dealt as sashimi and believed that its consumption may induce mysterious tonic results. They behave as intermediate or reservoir hosts for many zoonotic parasites, which are not prevalent in developed countries [115].

Intestinal nematodes

Prevention of strongyloidiasis

To control the rate of primary infection, TR are advised to be aware of the modes of parasitic transmission and to wear suitable closed footwear in endemic regions through scheduled educational programs. To limit the possibility of disease dissemination in subclinical or in pauci-symptomatic hosts, a full detailed history, extended screening programs, parasitological workup activities, and serologic facilities are warranted before institution of transplantation [148].

A thorough questionnaire should be administered about international travels, job description, volunteer missions, or military service abroad, which many subjects deny considering it a ‘travel.’ Empiric therapy, however, should be instituted in the following situations:
  1. Unexplained eosinophilia.
  2. Past history of parasitic disease.
  3. Prolonged residence in or travelling to endemic regions including the remote history [149].

Considering the possibility of graft transmission, donor’s epidemiologic information may invite the need for additional serologic monitoring, or instituting pre-emptive therapy before transplant [122],[125],[150]. Living donors with evidence of infection should be promptly managed before donation. TR of infected donors, however, must commence empirical therapy immediately after transplant with thorough monitoring of disease relapse.


Prevention of schistosomiasis

Advice against the exposure to fresh water in endemic areas is a fundamental step to prevent primary infection. Donor-derived infection as well as relapsed cases can be managed through screening of both donors and TR coming from endemic zones, with prompt management of any positive cases.


Prevention of echinococcosis

Primary prevention mandates avoidance of contaminated dog fecal matter that could be the natural primary source of echinococcal eggs. A particular attention should be directed to sheep-caring dogs, or dogs fed with sheep residue, those are at highest risk of contamination with E. granulosus. To limit the risk of exposure, perfect hand hygiene after dealing with these animals is also advised. Considering that wild animals are the definitive hosts for E. multilocularis, direct contact and transmission of this infection is rarely seen. Avoidance of contaminated sheep dog fecal material will limit the risk of echinococcal infection transmission. An extended period of therapy post-transplant or percutaneous therapy is widely applied in TR vulnerable for high risk of relapse.

Tissue and blood protozoa

Treatment of toxoplasmosis

In view of absence of general agreement for optimal therapy for post-SOT toxoplasmosis, the availability of extensive studies regarding therapy for HIV/AIDS patients can serve as a guide for therapy in the transplant community.

Currently recommended medications in toxoplasmosis therapy are mainly directed against tachyzoite form of T. gondii; however, the encysted form (bradyzoite) will not be eliminated. Of note, pyrimethamine is the most effective drug and is mostly included in various therapeutic protocols ([Table 2]). Leucovorin (i.e. folinic acid) must be concomitantly provided to protect against bone marrow depression. Another drug (e.g. sulfadiazine and clindamycin) should be added, unless there is clear contraindication [155]. By far, the most effective and reliable therapeutic combination is pyrimethamine plus sulfadiazine or trisulfapyrimidines (sulfamerazine+sulfamethazine+sulfapyrazine combination). These medications are active against tachyzoites and can induce synergistic effect if used in combination. Careful monitoring of the dosage regimens is mandated as they differ according to patient variables (e.g. immune status and pregnancy) (https://emedicine.medscape.com/article/229969-workup). According to its response, ‘induction therapy’ (6 weeks) is composed of pyrimethamine (plus leucovorin) and sulfadiazine to combat tachyzoites; this is usually followed by chronic suppressive therapy (secondary prophylaxis) to hamper recrudescence of infection [156]. Considering the chronic immunosuppressed status of the TR, medications of low toxicity, for example, TMP/SMX, are currently recommended for chronic suppression of parasite [151].
Table 2 Treatment of parasitic infection in organ transplant recipients

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Treatment of Chagas disease (American trypanosomiasis)

The presence of acute infection following transplantation or recrudescence of latent infection mandates therapy of this parasite. Available medications for Chagas disease include nifurtimox and benznidazole [157]. Significant untoward effects for benznidazole include rash and a dose-dependent peripheral neuritis. Nifurtimox, on the contrary, is associated with gastrointestinal adverse effects, for example, anorexia, nausea, and weight loss. CNS manifestations can also manifest, for example, irritability, insomnia, and tremors. Compared with nifurtimox, benznidazole is better tolerated among TR with less drug interactions; consequently, benznidazole is selected to be the first therapeutic line. Therapy of patients with T. cruzi infection is aimed at eradicating the parasites with specific drug therapy and to control disease manifestations related to its irreversible lesions.

In 2017, benznidazole was approved by the FDA for Chagas disease therapy for children of 2–12 years old. Both benznidazole and nifurtimox therapies are confined to their capability of parasitological cure, particularly in patients with chronic T. cruzi infection. Furthermore, there is a lack of randomized controlled trials documenting that therapy of chronically infected subjects with either benznidazole or nifurtimox may improve their outcomes. Consequently, utilizing these medications in such patient’s cohort is still controversial. Safety and efficacy of benznidazole have been instituted in two placebo-controlled clinical trials in children of 6–12 years old. The results of antibody testing have been shifted from positive to negative in 55–60% of children on benznidazole therapy, compared with 5–14% who received placebo. Safety and pharmacokinetics of benznidazole therapy and the necessary information for drug dosage in children as young as 2 years of age have been provided in another series [158]. Of note, the CDC recommends instituting the anti-parasitic therapy for all cases of acute (i.e. congenital) or reactivated dormant Chagas disease and chronic T. cruzi infection in children as old as 18 years. Moreover, the current CDC guidelines indicate robust recommendations to treat chronically infected adults of 50 years old or younger with no evidence of advanced Chagas cardiomyopathy [159].


Management of visceral leishmaniasis

Goals of therapy include the following: (a) elimination of Leishmania infection, (b) limitation of morbidity, and (c) prevention of complications, recurrence, and evolution of mucocutaneous lesions. Clinicians should be vigilant for the sequelae of reticuloendothelial system compromise. Patients may develop hemorrhage or neutropenia with subsequent infectious complications, for example, pneumonia or diarrhea. Severe anemia or profound bleeding may necessitate blood transfusion. Broad-spectrum antibiotics are usually advised to manage intercurrent infection.

Anti-parasitic pentavalent antimonial agents

The pentavalent antimonials, for example, sodium stibogluconate (Pentostam) or meglumine antimonate, are considered the cornerstone of the therapeutic regimens for all forms of leishmaniasis. Sodium stibogluconate was the agent of choice in many countries and the only recommended therapy in the US, but unfortunately, resistance has been evolving. The following regimens are recommended on the Indian subcontinent:
  1. Liposomal amphotericin B alone (single dose, the drug of choice for Kala-Azar eradication).
  2. Liposomal amphotericin B in a single dose plus 7 days of oral miltefosine or 10 days of paromomycin.
  3. Miltefosine plus paromomycin for 10 days.
  4. Amphotericin B deoxycholate: 0.75–1 mg/kg/day via infusion, daily or on alternate days for 15–20 doses.
  5. Miltefosine orally for 28 days or paromomycin intramuscular (IM) for 28 days.
  6. Pentavalent antimonials: 20 mg Sb5+/kg/day IM or intravenous (IV) for 30 days in areas with effective response, for example, India (


Potency of amphotericin B in immunocompromised patients appears to be similar to that observed in immunocompetent subjects. However, the rate of relapse may approach 24% of cases in solid organ TR as early as 1 month and as late as 5 years. Intermittent doses of amphotericin can be effective to prevent relapse of the disease, that is, secondary prophylaxis, which is supported by randomized controlled trials involving patients with both HIV/AIDS and visceral leishmaniasis.

Resistant visceral leishmaniasis

The evolution of drug resistance can be attributed to primary or secondary causes including the following:
  1. Late diagnosis.
  2. Immunologic bankrupt.
  3. Coinfection with HIV/AIDS disease.
  4. Development of resistant strains of the pathogen.
  5. Non-compliance to medication protocol with dose interruption or under-dosing.

Stibogluconate-resistant disease should be replaced by alternate agents, for example, liposomal amphotericin (0.5–3 mg/kg), on alternate days until a dose of 20 mg/kg (https://emedicine.medscape.com/article/220298-treatment#showall).

Oral miltefosine

Miltefosine is considered the sole oral therapy with proved efficacy in leishmania management. It has been developed primarily as an antineoplastic drug, but later on, antiproliferative properties against leishmaniasis have been observed with this agent, in addition to its anti-Trypanosoma parasitism. Its efficacy has mostly addressed in areas, for example, India, with a well-known drug resistance toward conventional therapy. In August 2013, the CDC addressed an investigational new drug protocol for miltefosine against FLA therapy in the US. In March 2014, the CDC approved miltefosine for mucocutaneous as well as visceral leishmaniasis in adults/adolescents (12 years or older), weighing at least 66 lb, and neither pregnant nor breastfeeding (https://emedicine.medscape.com/article/220298-treatment#showall). First-line therapy for visceral leishmaniasis is the liposomal amphotericin B. To protect against possible relapse, secondary prophylaxis could be beneficial in selected patients. On the contrary, the pentavalent antimony compounds are advised as a first line therapy for severe cases of cutaneous or mucocutaneous type.

Treatment of malaria

Therapy of malaria depends mainly on antiplasmodium medications. Enough data should be provided regarding plasmodia species, geographical spread, and their sensitivity patterns. P. vivax, P. malariae, P. ovale, and uncomplicated P. falciparum in chloroquine-responsive protocol are amenable for chloroquine therapy. Unfortunately, chloroquine-resistant P. vivax has been observed in Oceania. For uncomplicated P. falciparum cases acquired from chloroquine-resistant regimen, they can be managed with artemisinin combination therapy, quinine-based regimen, or mefloquine. However, in advanced P. falciparum, IV artesunate should be instituted, followed by doxycycline or mefloquine. Primaquine should be administrated to abort the relapse of P. vivax and P. ovale (G6PD deficiency should be excluded). Of note, malaria is a potentially lethal disease in solid-organ TR. However, early recognition with institution of the specific therapy can achieve perfect and safe recovery. P. falciparum, drug intoxication as well as other superadded coinfection may result in a detrimental outcome. If quinine is included in a therapeutic regimen, it may interfere with CyA metabolism, leading to lower therapeutic level [92].

Summary of recommendations

  1. P. falciparum: quinine-based regimen: quinine (or quinidine) sulfate plus doxycycline or clindamycin or pyrimethamine-sulfadoxine; alternate regimen: artemether-lumefantrine, atovaquone-proguanil, or mefloquine.
  2. P. falciparum susceptible to chloroquine (a few regions in Central America and Middle East): chloroquine.
  3. P. vivax and P. ovale: chloroquine plus primaquine.
  4. P. malariae: chloroquine
  5. P. knowlesi: similar to P. falciparum [152].

In July 2018, the FDA approved ‘tafenoquine’, an anti-plasmodia 8-aminoquinoline derivative, for eradication (hindering relapse) of P. vivax in patients of 16 years age or older and received the proper antimalarial treatment for acute P. vivax infection. This agent is active against ALL stages of P. vivax. Tafenoquine is provided as a single oral dose on the first or second day of the suitable antimalarial therapy (e.g. chloroquine) for acute P. vivax infection. As tafenoquine increases the liability of hemolytic anemia in G6PD deficiency, patients must be examined before institution of this agent. However, ‘tafenoquine’ is contraindicated in the following situations:
  1. Known hypersensitivity.
  2. G6PD deficiency (or unknown).
  3. Breastfeeding an infant with G6PD deficiency (or unknown) [160].

Treatment of babesiosis

Immediate and prompt therapy should be initiated for this devastating disease, particularly with severe immunosuppressive burden. There are no available studies addressing the treatment of babesiosis in TR. ‘Exchange transfusion’, however, is indicated with (a) parasitemia more than 10%, (b) extensive hemolysis, and (c) advanced renal and/or hepatic and/or pulmonary deterioration [153].

Reduction of the immunosuppressive load should be early instituted. For patients capable of taking oral medications, atovaquone plus azithromycin is a good option. Alternatively, clindamycin plus quinine can be administrated. One prospective, nonblinded, randomized trial, (atovaquone plus azithromycin) was proved to be as effective as clindamycin plus quinine, but with less untoward effects (15 vs. 72%). The most common adverse effects with atovaquone plus azithromycin were diarrhea and rash (8% each); on the contrary, clindamycin plus quinine showed more tinnitus (39%), diarrhea (33%) as well as impaired hearing acuity (28%).

Azithromycin, however, may increase serum level of tacrolimus (Tac), and TR must be observed for Tac toxicity. Sirolimus and Tac metabolism, on the contrary, may be hampered by the CYP3A4 inhibitor quinidine ([Table 3]).
Table 3 Drug interaction between antiparasitic drugs and immunosuppressive agents (https://www.uptodate.com/drug-interactions/?source=responsive_home#di-document)

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Optimal regimen of therapy of this disease among TR is not completely understood; persistent relapse has been observed in other immunocompromised patients. In one report, 14 immunocompromised patients who mostly had B-cell lymphoma and were asplenic or had treated with rituximab, antibabesial therapy was mandated to be maintained for at least 6 weeks, so that complete cure could be optimally achieved. After established negative blood smear results, recovery from the active disease occurs in 11 patients when antimicrobials were maintained for at least 2 weeks [161]. Three of them (21%) have died, which sheds light on the aggressiveness of this disease in this cohort of patients and the need to extend the duration of therapy with meticulous monitoring, as compared with normal subjects. Resistance − despite rare − to (atovaquone/azithromycin) regimen is more likely in immunocompromised subjects [162]. Blood smear is a feasible technique to evaluate therapeutic response and for early detection of disease relapse; if PCR is available, it can be added instead. First line of therapy, however, is the conventional therapy. Relapse rate of infection could be high; consequently, repetition of high doses with alternative therapeutic protocols may be urgently warranted.

Entamoeba histolytica

Treatment of amoebiasis

Metronidazole or tinidazole can be administrated for the active trophozoite stage (tissue amebicide). This should be followed by paromomycin to eradicate cystic forms. Interestingly, one case of hepatic amoebiasis has been successfully managed with metronidazole in a liver TR [109]. Luminal agent alone can be administered for asymptomatic infection with E. histolytica to guard against transmission and invasive complications. Nitazoxanide is reported to achieve a cure rate of more than 90% in some series [163]. For complete eradication of the organism, it is mandatory to utilize a tissue amoebicide (e.g. metronidazole) combined with a luminal agent (paromomycin), unless the patient was an asymptomatic carrier. On the contrary, more prolonged therapeutic courses is ultimately warranted for hepatic amoebiasis.

Treatment of microsporidia (Enterocytozoon bieneusi and Cyclospora cayetanensis)

Although patient with E. bieneusi infection can be treated by albendazole, patients with C. cayetanensis infection can be managed with TMP/SMX. Reduction of the immunosuppression burden is advised. Clearance of diarrheal episodes can be expected after 1 week [118].

Treatment of diphyllobothriasis and anisakiasis infestation

Fish-borne parasitic infestation may have an appropriate management via anthelmintic medications after proper and early diagnosis. Although diphyllobothriasis can be treated by a single dose of praziquantel (10–20 mg/kg), anisakiasis infestation on the contrary can be managed by albendazole (400–800 mg for 6–21 days) [115].

Intestinal nematodes

Treatment of strongyloidiasis

Ivermectin is proved to be the treatment of choice [154], and it is also effective in eradicating both adult parasites and larvae from the intestinal lumen in healthy subjects [160],[164]. Repeating the therapeutic course after 2 weeks is advised to control primary forms in life cycle before they mature to advanced stage. Untoward effects are mild and usually uncommon.

Albendazole, on the contrary, is the second-line of therapy, as it has a cure rate of only 45–75% [154],[164]. The medication with most clinical experience is thiabendazole; however, it is the least satisfactory medication owing to its frequent relapses and untoward effects [123]. The role of ivermectin in control of hyperinfection or disseminated disease in TR is very limited, with clinical failure frequently reported [165].

The heavy burden of Strongyloides infection requires daily doses, with additional booster doses for a couple of weeks to abort the risk of relapse. Combination or sequential ivermectin and albendazole is advised by some experts. The presence of malabsorption constitutes a vital challenge impeding oral therapy; rectal ivermectin, however, can be used alternatively [166].

The parenteral veterinary formula of ivermectin, on the contrary, has been used subcutaneously with variable success [125],[167]. This formulation is not approved by the FDA. S. stercoralis and HTLV-1 coinfection typically mandates prolonged therapeutic courses as no medication reliably can completely cure this parasite. It is typically recommended that daily ivermectin should be administrated until visible pathogens are entirely cleared; within additional 1–2 weeks thereafter, course repetition is usually advised with significant clinical manifestations or with relapse of eosinophilia [168].


Treatment of schistosomiasis

Praziquantel: Praziquantel is the standard therapy for this serious parasite. A good response/outcome has been reported in several TR who have been treated with praziquantel as shown in case reports [128] (https://emedicine.medscape.com/article/228392-medication#2). Higher doses, however, are mandated for S. Japonicum and S. mekongi therapy. There are no available data about change in potency or toxicity with the use of praziquantel in TR. CyA may alter praziquantel metabolism leading to higher drug levels with more liability for toxic drawbacks; no available data, however, about interactions with other immunosuppressive medications. CyA, on the contrary, showed anti-schistosomal properties particularly with S. mansoni as per in vitro and in animal trials. This beneficial effect of CyA, however, has not been confirmed in humans.

Mechanism of action: Praziquantel is a well-tolerated agent. It can be used for individuals as well as for mass therapeutic programs. Mechanism of action is multifactorial; this agent can induce ultrastructural alterations leading to increased permeability to calcium ions and its accumulation within the parasite cytosol leading to muscle contractions and finally worm paralysis. The worm ‘tegument membrane’ (natural covering) will be seriously disrupted, making the worm vulnerable for patient’s immune defense mechanisms with ultimately worm death. Cure rate with praziquantel may exceed 85%. Even with absence of complete cure, egg loading rate will be largely declined (https://emedicine.medscape.com/article/228392-medication#2).

Oxamniquine (Vansil): Oxamniquine has the ability disrupt the tegument of the male schistosomal worm, so that the parasite can be destroyed by the patient’s immune defense mechanisms. Moreover, oxamniquine can hinder female worms from egg production. This medication is only directed against S. mansoni, and its cure rate may approach 60–90% (https://emedicine.medscape.com/article/228392-medication#2) [133].

Treatment of schistosomal neurologic disease: in neurologic schistosomal disease, praziquantel combined with glucocorticoids should be administered. Steroids are beneficial to limit the inflammation and edema formed around eggs. With the presence of seizures, anticonvulsant therapy should be instituted (https://emedicine.medscape.com/article/228392-medication#2).


Treatment of echinococcosis

Two arms of management have been recommended for TR proved to harbor hydatid disease: (a) surgical removal of the hydatid cysts, and (b) medical therapy with albendazole before transplant [169]. Presurgical umbrella of ‘albendazole’ for 7–10 days is advised to protect against intraoperative secondary seeding. If intraoperative spillage occurs, an additional course of ‘praziquantel’ is better advised. Donors from endemic zones may harbor undiagnosed hydatid cysts that may be occasionally discovered during organ procurement. In the light of shortage of organs for transplantation, some experts have suggested that livers contaminated with hydatid cysts can be utilized for transplantation in condition that the cyst is solitary and calcified [170]. Moreover, this cyst should not be communicating with biliary tree and is amenable for closed surgical resection with no harm to the main vascular and biliary trees [171]. Albendazole therapy should be continued for at least 2 years after transplant (even with successful curative surgery) [172]. Application of the PAIR (percutaneous puncture, aspiration, injection, and re-aspiration) technique has been reported to occlude some cysts before surgical eradication, but it would pose significant risk of type 1 anaphylaxis, which is potentially life threatening. On the contrary, radical surgical excision is mandated to control E. multilocularis infection, however, recent recommendations addressed an evidence that prolonged therapy with benzimidazole can slow down the progression of this type of infection.


A prompt surgical resection of an echinococcal cyst, followed by a prolonged course of albendazole is advised in case of infected candidate for transplant. Preoperative course of albendazole may limit the risk of secondary seeding in case of intraoperative cyst content spillage or with PAIR. Patients with echinococcosis are candidate for early ‘liver transplantation’ in the following situations:
  1. Recurrent biliary infections.
  2. Presence of ‘hilar’ involvement.
  3. Variceal bleeding owing to portal hypertension.
  4. Secondary biliary cirrhosis with associated ascites.
  5. Presence of lesions invading the hepatic veins and the inferior vena cava.

Pretransplant evaluation should include investigating extrahepatic involvement, to exclude disease extension to the lung and the brain. The only exclusion criterion for liver transplantation is CNS involvement [172]. The main indications for transplant, however, in one report involving 16 European transplant centers were (a) huge parasitic cyst [172] and (b) biliary disease with hilar parasitic involvement.

The rate of survival with no recurrence may approach 77% after 1 year and 45% after 10 years. Five patients have been transplanted for liver alveolar echinococcosis in China in spite of noticeable technical difficulties [173]. Timing of interference is fundamental, with best results achieved if transplantation proceeded before the vascular tree has been compromised [174]. Immunosuppression may trigger parasitic growth with increased risk of recurrence; consequently, immunosuppressive agents should be reduced to the minimal accepted level.

  Conclusion Top

In a TR, post-transplant parasitic infections pose a unique set of challenges. An awareness of sequelae of parasitic infections is crucial, as organ donation by donors from endemic areas has been on the rise. Furthermore, TRs may harbor parasitic pathogens after visit to endemic zone owing to work or for leisure. Transplant clinicians can identify parasitic infection early by lowering their threshold of suspicion. Timely diagnosis through appropriate sampling and using correct laboratory techniques would enable pre-emptive therapeutic intervention to control parasitic infections, particularly with the presence of hyperinfection syndromes.


Authors would like to acknowledge the precious permission offered by Professor R. Barsoum as well as Dr GS Visvesvara for allowing us to use the figures and diagrams included in their valuable articles.

Dr Abbas designed the study, did data collection, and wrote the manuscript. Mohsen El Kossi, Jon Jin Kim, Ihab Shaheen, Ajay Sharma, and Ravi Pararajasingam reviewed and edited the manuscript. Ahmed Halawa played a role in conceptualization, designing the study, supervising the data collection, and reviewing and editing the manuscript.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14]

  [Table 1], [Table 2], [Table 3]

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