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Table of Contents
REVIEW ARTICLE
Year : 2022  |  Volume : 16  |  Issue : 5  |  Page : 57-62

Endemic parasitic disease - Expert group opinion for South Asia for solid-organ transplantation − Leishmaniasis, malaria, toxoplasmosis, filariasis, and strongyloidiasis


1 Institute of Infectious Diseases, Apollo Hospital, Chennai, Tamil Nadu, India
2 Department of Infectious Diseases, Rajiv Gandhi Cancer Hospital, New Delhi, India
3 Department of Nephrology, Madras Medical College, Chennai, Tamil Nadu, India
4 Department of Infectious Diseases, Apollo Hospital, Chennai, Tamil Nadu, India
5 Department of Nephrology, Popular Medical College, Dhaka, Bangladesh

Date of Submission12-Nov-2021
Date of Acceptance18-Mar-2022
Date of Web Publication18-Oct-2022

Correspondence Address:
Dr. Venkatasubramanian Ramasubramanian
Apollo Hospitals, Adjunct Prof Infectious Diseases - Sri Ramachandra Institute of Higher Education and Research, Chennai, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijot.ijot_117_21

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  Abstract 


Although parasitic infections including malaria, leishmania, and toxoplasmosis contribute to a significant burden of the morbidity and mortality of global populations, they remain woefully understudied in solid-organ transplantation with recommendations mainly based on expert opinions. This paradox is due to the fact that the geographic prevalence of most of these infections is restricted to the developing world where priorities of care are different due to economic constraints. Limited availability of transplant programs where parasitic infections are endemic, challenges in diagnosis, re-activation or recrudescence of latent infections which may present at a later date, the lesser impact of these infections in the immune-suppressed host and limited availability of drugs used in the treatment of some of these infections may influence therapeutic interventions. In the Indian sub-continent, malaria, visceral leishmaniasis (VL), filariasis, strongyloidiasis, and toxoplasmosis are endemic. India contributes to 4% of the total global burden of cases of malaria and has the highest number of cases among the South Asian countries. VL is restricted to Bihar and West Bengal in India and liposomal amphotericin, the drug of choice is still prohibitively expensive. The impact of toxoplasmosis, filariasis, and strongyloidiasis in solid-organ transplant is still limited compared to other infections. Challenges are mainly related to donor screening and exclusion as applying western recommendations to these endemic infections may not be practical. Early diagnosis and appropriate therapy improve outcomes.

Keywords: Filariasis, leishmaniasis, malaria, parasite, solid-organ transplant, South Asia, strongyloides, toxoplasmosis


How to cite this article:
Ramasubramanian V, Surendran R, Bansal N, Sridharan S, Gopalakrishnan N, Prasad SG, Rahman M, Bansal SB. Endemic parasitic disease - Expert group opinion for South Asia for solid-organ transplantation − Leishmaniasis, malaria, toxoplasmosis, filariasis, and strongyloidiasis. Indian J Transplant 2022;16, Suppl S1:57-62

How to cite this URL:
Ramasubramanian V, Surendran R, Bansal N, Sridharan S, Gopalakrishnan N, Prasad SG, Rahman M, Bansal SB. Endemic parasitic disease - Expert group opinion for South Asia for solid-organ transplantation − Leishmaniasis, malaria, toxoplasmosis, filariasis, and strongyloidiasis. Indian J Transplant [serial online] 2022 [cited 2022 Dec 9];16, Suppl S1:57-62. Available from: https://www.ijtonline.in/text.asp?2022/16/5/57/358658




  Introduction Top


We live in the age of rapid globalization due to increased and rapid travel. Travel for tourism (including medical), occupation, and visiting family have brought diseases once exotic within everyone's reach. Immigration has also brought geographically restricted diseases to the forefront. Immunesuppression related to transplantation can contribute to opportunistic parasitic diseases with aggressive presentation and poor clinical response. Manifestations of parasitic infections in solid-organ transplant (SOT) can be due to reactivation of latent infections following immune suppression, de novo infections or infections in the recipient through the transplanted organ. The challenges in the management of parasitic infections can be due to the lack of history of earlier exposures, diagnostic challenges, or availability of appropriate drugs in the treatment. The development of drug resistance, especially in falciparum malaria and visceral leishmaniasis (VL) can also impact outcomes. In the Indian sub-continent, malaria contributes to a significant burden in SOT, although VL can occur in certain pockets. Toxoplasmosis is under-recognized and filariasis and strongyloidiasis are seen to a limited extent.


  Leishmaniasis Top


Epidemiology

VL is caused by the protozoan Leishmania donovani (LD) and Leishmania infantum and is transmitted by sandfly.[1] India and Bangladesh contribute significantly to the global burden of VL. VL is the predominant form described in recipients of SOT recipients. Endemic states in India include Bihar, Jharkhand, West Bengal, and Uttar Pradesh.[2]

Clinical features and diagnosis

VL presents as fever with weight loss along with pancytopenia and splenomegaly. Atypical features such as mucosal and cutaneous lesions may be seen as organ recipients are immunosuppressed.[1]

Demonstration of LD bodies in the bone marrow and splenic aspirate remains the gold standard to establish the diagnosis. Serological tests like an antibody to recombinant K-39 antigen may not have good sensitivity due to underlying immunosuppressed state and it can be positive in past infections. Polymerase chain reaction (PCR), if available can be done in marrow aspirate or even in blood.[1]

Pretransplant screening

Routine serologic screening of organ donors from leishmaniasis-endemic areas is not recommended. If an available donor has a record with positive serology, but no clinical evidence of active infection, the organ can be transplanted and the recipient should be monitored in the posttransplant period.[3] For recipients, history and records should be reviewed in endemic states for evidence of the previous leishmaniasis.

Acceptance criteria

Donors with active disease should not be taken and the disease should be fully treated before organ donation is done. Positive serology that may suggest previous exposure, without evidence of active infection, is not a contraindication to donation. In case VL is diagnosed after cadaveric organ transplantation has been performed, recipients should be observed for signs and symptoms of VL. Sequential PCR may be useful but, no specific data exists as donor-derived VL has not been reported so far. There is no role of primary prophylaxis in such cases.[1]

Management

Asymptomatically infected SOT recipients and those with a history of VL, preemptive and primary prophylaxis is not recommended and they should be monitored clinically.

The recommended therapy for VL in transplanted patients is the same as that for immunocompetent individuals: a total dose of 21 mg/kg of liposomal amphotericin B given over 7 doses (1–5 days and on 14th day and 21st day).[4] The role of miltefosine has not been studied in organ transplant recipients with VL. Secondary prophylaxis is not usually required.

Most relapses are reported to occur in the first 2 years posttreatment and the lifetime risk of relapse is 30%. Hence, close clinical monitoring for signs and symptoms is recommended in the 1st year posttreatment and preferably lifelong.[5] For patients who present with relapse, it may be reasonable to extend therapy or maintain the patient on secondary prophylaxis for 3–6 months.[5]


  Prevention Top


Leishmaniasis is acquired by the bite of sandflies. When visiting endemic areas, transplant candidates, recipients or living potential donors should minimize outdoor activities, especially during dusk hours, when sand flies generally are the most active. These individuals should also wear protective clothing, apply insect repellent (i.e., DEET) to exposed skin, use pyrethroid-treated bed nets, and spray dwellings with residual-action insecticides.[1]


  Malaria Top


Malaria is a female anopheles mosquito-borne parasitic tropical disease caused by Plasmodium vivax, falciparum, ovale, malariae, and knowlesi. The incubation period ranges from 2 to 3 weeks for P. vivax and P. ovale, 10–14 days for P. falciparum or P. knowlesi, and 18 days or longer for P. malariae; but, that might vary from 3 to 6 months for some species of P. vivax. Infection with vivax and ovale can cause relapse after months or years after initial infection due to activation of the dormant hypnozoites in the liver.[6] Antimalarial prophylaxis can prolong the incubation period from several weeks to months in a traveller from an endemic area.[7]


  Epidemiology Top


The overall reduction in the burden of malaria has faced a stall in recent years as evidenced by an estimated 219 million cases of malaria in 2017 of which the maximum burden is contributed to by the African region (92%), followed by (SEAR) South-East Asian region (5%). P. vivax has been attributed to causing 37.2% of the infection and Plasmodium falciparum contributes to 62.8% in SEAR. India contributes to 4% of the total global burden of cases which makes it no. 1 among the South Asian countries.[8] Highly endemic states in India include West Bengal, Jharkhand, Chhattisgarh, and Madhya Pradesh [Figure 1].[9]
Figure 1: Malaria endemicity in India

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Clinical features and diagnosis

Malaria typically presents with high-grade fever and chills. Patients may present with complications of malaria-like encephalopathy or renal failure. The severity of malaria depends upon the infecting species (P. falciparum and P. knowlesi are prone to cause severe disease), level of parasitemia, organ transplanted, level of immune suppression, and delays in diagnosis and treatment.

Giemsa-stained thick smear is the gold standard for diagnosis, with a limit of detection from 50 to 500 parasites per microliter. Performed by well-trained personnel, it can even detect lower levels of parasitemia. Rapid diagnostic techniques based on parasite antigens (P. falciparum histidine-rich protein, pan-plasmodium lactate dehydrogenase, pan-aldolase) have varied sensitivity and specificity based upon the commercial product with an average level of detection of 200 parasites/μL. Molecular diagnostics such as real-time PCR have a much higher sensitivity (detecting 0.35 parasites/μL) and can be used to detect asymptomatic parasitemia missed by smear examination to prevent donor-derived infections, although it may prove to be expensive in resource-limited settings such as India.[10] Serological tests are not suitable for diagnosis and rather reflect past exposure to malaria.

Modes of acquiring malaria for organ transplant recipients

Posttransplant infection may occur from the parasitized red blood cells in the donor organ, reactivation of hypnozoites from the donor's liver, reactivation from hypnozoites in the recipient (relapse in case of P. vivax and P. ovale) and recrudescence (from persistent parasite in the blood due to prior infection) and through blood-transfusions during the transplant It may not always be possible to identify the exact mode of transmission in posttransplant infections.[11]

Donor screening

A detailed history of exposure, previous infections, and travel must be obtained from donors and recipients. The cost-benefit ratio of routine screening of donors and recipients is unknown. However, screening is advisable in patients from highly endemic areas and where microscopy or rapid diagnostic tests are easily accessible.

If the screening for a living donor is positive treatment is recommended.[12] The period of deferral for organ donation posttreatment is uncertain and most guidelines extrapolate from local advisory for blood donors.[10] The guidelines for the donation of blood products advise deferral for 6 months (in highly endemic countries like India) to 3 years in regions with low endemicity.[13],[14] In the case of deceased donors, the organ may be used except in cases where the death occurred due to malaria.[15] In all such cases, the recipients will receive treatment. Permanent donor deferral in case of P. malariae infections is advised in some countries such as Brazil.[10]

Posttransplant monitoring

Periodic clinical and laboratory monitoring to be done (with thick and thin smear microscopy, rapid diagnostic tests or PCR) prospectively for 2 months posttransplant.[10] Preemptive therapy is not recommended.

Prevention

Recipients travelling to malaria-endemic regions for transplantation should consult an expert before travel and should take the following measures: prevention of mosquito bite by using insect repellents and using long-sleeved clothing, avoiding outdoor activities, sleeping in a well-screened room and preferably in an air-conditioned room and using the chemoprophylaxis recommended for the general population. The interaction of immunosuppressive agents with the prophylaxis of malaria should be kept in mind [Table 1].
Table 1: Potential interaction between immunosuppressants and anti-infective agents

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  Toxoplasmosis Top


Toxoplasma, a protozoan parasite infects at least 10%–80% of the general population worldwide. Studies show a prevalence of 4.7%–37.3% in India's general population. The infection is generally benign without symptoms or with mild symptoms in immune-competent individuals. It is an opportunistic infection in immunocompromised individuals including patients with HIV, lymphoma, hematological malignancies, and patients on cytotoxic drugs, corticosteroids, and postorgan transplantation.[16] Toxoplasmosis occurring in the first 3 months posttransplant is well recognized and is mostly donor derived. Infections occurring >3–6 months is mainly due to reactivation of latent disease or de novo infection due to immunosuppressive drugs.[11] The prevalence depends upon the seropositive status of the donor and recipient and the use of chemoprophylaxis. In the donor + ve, the recipient –ve (D+/R-) situation, transmission is the highest with the heart (50%–75%) without prophylaxis.

Epidemiology

In a review of toxoplasmosis in the past two decades, it was found, surprisingly, that the incidence of toxoplasma after renal transplant was higher (46.3%) than the heart (34%) and liver (11.7%), while previous studies show very low incidence (<1% in renal and liver transplants). For seropositive recipients (D-/R+), the risk of reactivation is rare and less severe compared to donor-derived infection. Different studies show varying results for the prevalence of the disease ranging from 9% to 56% depending upon the seroprevalence, chemoprophylaxis, and several other factors.[11],[16],[17],[18]

Clinical features and diagnosis

Presentation in posttransplant patients can vary from cerebral abscesses, encephalitis, myocarditis, pneumonitis, chorioretinitis, multiorgan involvement, and disseminated disease. It can mimic organ rejection in cardiac transplant recipients.

PCR-based tests in body fluids in the appropriate clinical setting are the best diagnostic strategy due to the poor sensitivity of serology in immunocompromised patients. In addition, serology may be used to identify new acquisition (seroconversion to positive IgM and IgG) and reactivation (highly avid IgG in the absence of IgM). Demonstration of tachyzoites in tissue and body fluids confirms the diagnosis of toxoplasmosis, as in from an endomyocardial biopsy from a cardiac transplant recipient with myocarditis.[19],[20]

Donor and recipient screening

Pretransplant screening of both the donor and the recipient is important, particularly in cases undergoing heart transplants. Testing for acute infection using IgM or PCR is indicated only if active infection is clinically suspected.[20],[21]

Donor acceptance criteria

The organ need not be rejected if the donor is seropositive. However, the recipient must receive prophylaxis.[20],[21]

Management

Treatment of active disease is the same as that in a nontransplant setting, including pyrimethamine, sulfadiazine, and folinic acid. Alternative drugs include clindamycin, atovaquone, and azithromycin.


  Prophylaxis Top


In the case where the donor is seropositive and the recipient is seronegative, especially in cardiac transplantation, primary chemoprophylaxis with TMP-SMX (160–800 mg) daily or thrice weekly has proven to be effective. Alternatives include primaquine, dapsone, and atovaquone.[20] For cases where recipients have a positive serology, secondary prophylaxis is currently recommended in a setting of hematopoietic stem cell transplant but may also be considered particularly in cases of cardiac transplantation.[16] The regimen for secondary prophylaxis is similar to primary prophylaxis. Duration of the treatment is not well defined, but it is ideal to give prophylaxis for 6 months posttransplant.[11]

Recipient travelling to an endemic area

Travellers should be advised to avoid undercooked meat (may contain toxoplasma cysts), unwashed fruits and vegetables which may be contaminated with cat faeces containing oocysts of toxoplasma.[20]


  Filariasis Top


Filariae are a group of tissue-based nematodes that can grow in the subcutaneous tissue and lymphatic vessels. Four (Wuchereria bancrofti, Brugia malayi, Onchocerca volvulus, and Loa loa) of the eight species that are known to infect humans, cause the most severe infections.[22]

Epidemiology

Transmission of W. bancrofti through the placenta and through infected blood transfusions has been previously described.[23] India harbors nearly 40% of 120 million cases of infection with LF in the world. The states with high endemicity in India are Uttar Pradesh, Bihar, Jharkhand, Orissa, Kerala, and Gujarat. Approximately 389 million are at risk for exposure to filariasis in India.[24]

Clinical features and diagnosis

The disease spectrum can range from asymptomatic patients to episodes of lymphangitis, orchitis, funiculitis, or epididymitis. Long-standing obstruction of lymphatic vessels may lead to hydrocele, chyluria, or lymphatic varices.

Peripheral blood eosinophilia is common but nonspecific. Definitive diagnosis is established by the detection of circulating filarial antigen (for W. bancrofti infection only), demonstration of microfilariae or filarial DNA in the blood, or adult worms in the lymphatics. Rarely, microfilariae and/or adult worms are identified incidentally in tissue biopsies or cytological specimens.[25]

Donor screening

If the index of suspicion is high clinically, peripheral blood smear examinations from the donor could be screened. Donors can be treated if found to be positive before transplant.[25]

Acceptance criteria

Donors with the active disease must be treated fully before organ donation. There is only one documented case of possible transmission of microfilariae of W. bancrofti via a living-donor renal transplant where both donor and recipient were from an area of endemicity. The perioperative biopsy revealed microfilariae and eosinophils in the glomerular and peritubular capillaries.[24]

Management

An anecdotal case report added anti-filarial treatment to the immunosuppressive regimen for 3 weeks with a favorable outcome.

Recipients who travel to an endemic region

Recipients travelling to filarial endemic regions should use individual protection measures against mosquito bites such as the use of insecticide-treated bednets such as those impregnated with DEET.


  Strongyloidiasis Top


Strongyloides stercoralis has the unique ability to complete its life cycle in the environment as well as human beings. Chronic asymptomatic infection can be present for decades and clinical manifestations can occur ever after decades of initial infection.

Epidemiology

This nematode is endemic in tropical and subtropical areas. The global prevalence exceeds 100 million.[19] Strongyloides infection can also occur sporadically in temperate regions. In India, it has been reported to be endemic in at least 10 states (Delhi, Assam, Maharashtra, Tamil Nadu, and Karnataka reporting the maximum number of cases).[26]

Clinical features and diagnosis

The spectrum of infection includes acute or chronic (autoinfection) forms that can manifest as a hyper-infection syndrome and disseminated disease. Strongyloides in the transplant recipients has been described as either reactivation of latent infection or donor-transmitted infection. Clinical manifestations may vary from pulmonary involvement, septic meningitis with gram-negative bacteria that are a part of bowel flora to gastrointestinal hemorrhage or ileus. The above manifestations are more frequent when immunosuppression is significant.

Eosinophilia occurs in the acute phase. However, the absence of the same does not rule out strongyloides infection. Recognition of larvae in specimens such as stools or duodenal aspirates is the golden standard for the diagnosis and sensitivities for a single stool specimen range from 15% to 30%.[20] Larvae may be encountered in pulmonary secretions, cerebrospinal fluid, peritoneal fluid, urine, pleural effusion and blood samples in disseminated disease. Enzyme-linked immunosorbent assay (ELISA) has sensitivities of 70%–90% and specificity of 87%−100% and can be valuable in ruling out the infection.

Pretransplant screening

All living donors from endemic regions must undergo screening either by stool examination for direct microscopy or ELISA assays, where available, and receive therapy before donation. Since the infection cannot be completely eradicated in donors and the adverse effect of therapy is minimal, recipients may be offered preemptive therapy.[27]

Management

Ivermectin (200 mcg/kg oral single dose) is the treatment of choice. It is effective in eradicating adult and larval forms. Few studies suggest that two doses of ivermectin on consecutive days are more efficacious.[28] The course is repeated after 2 weeks. Albendazole (400 mg orally twice a day) for 2–7 days is an alternative choice. In hyper-infection syndrome, ivermectin is given daily until negative stool examination and in a few cases for 2 weeks thereafter.

Recipients travelling to endemic areas

No vaccines or drugs to prevent infection are available. Using shoes and barriers while sitting on the ground can prevent infection with strongyloides while travelling to endemic areas.[29]

Drug interactions between immunosuppressants and anti-infective used for prophylaxis

Infections are common complications in a host undergoing SOT and it is important to be cognizant of the drug interactions between the immunosuppressants and the antimicrobials being used.[30] [Table 1] summarizes the common agents used in the treatment and prophylaxis of parasitic infections in a transplant host and their interactions with chemotherapeutic drugs.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Abstract
Introduction
Leishmaniasis
Prevention
Malaria
Epidemiology
Toxoplasmosis
Prophylaxis
Filariasis
Strongyloidiasis
References
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