Viral and Invasive Fungal Infection After Liver Transplant — Cause and Effect on Graft Dysfunction | LTSICON Pune 2026

Dr. Chetan Kalal has been invited as Faculty to the LTSICON 2026 Midterm Conference in Pune, where he will lead a Case-Based Panel Discussion on Viral and Invasive Fungal Infection: Cause and Effect Relationship with Graft Dysfunction — one of the most complex and clinically consequential topics in post-liver transplant medicine.

LTSICON (Liver Transplant Society of India Conference) is India’s premier liver transplantation conference, convening the country’s leading transplant surgeons, hepatologists, intensivists, and allied specialists. Invitation as faculty to a case-based panel discussion represents the highest tier of participation — it is a recognition of subspecialty depth, not just attendance.

About LTSICON 2026 — Midterm, Pune

The Liver Transplant Society of India (LTSI) organises both an annual conference and a midterm conference, with rotating national venues. The midterm format typically focuses on intensive clinical learning — case-based discussions, controversial topics, and subspecialty deep-dives that the larger annual meeting cannot accommodate in the same depth.

The case-based panel discussion format places real, de-identified transplant cases before a panel of experts who debate diagnosis, management decisions, and outcomes in real time — the most intellectually demanding and educationally effective format in post-graduate medical education.

Dr. Kalal’s invitation to faculty this session reflects his standing as one of India’s authoritative voices on post-transplant infectious complications and graft dysfunction — a domain that sits at the intersection of transplant hepatology, infectious disease, and critical care.

The clinical topic: Viral and Invasive Fungal Infection — Cause and Effect with Graft Dysfunction

Post-liver transplant infections are the leading cause of morbidity and mortality in the first year after transplantation. The relationship between infection and graft dysfunction is bidirectional and frequently misunderstood in non-specialist settings: infections cause graft dysfunction, and graft dysfunction predisposes to infections. Untangling this relationship determines whether a deteriorating graft is rejected, infected, or both — and the treatment is fundamentally different for each.

Viral infections and graft dysfunction — the CMV problem

Cytomegalovirus (CMV) is the most clinically significant viral pathogen after liver transplantation. It causes two distinct problems:

• Direct CMV disease: CMV hepatitis (the graft itself is the target — rising LFTs, histology showing cytomegalic inclusions), CMV colitis, CMV pneumonitis. In the graft, CMV hepatitis causes a pattern of liver dysfunction that mimics rejection on biochemistry — the distinction requires liver biopsy with immunohistochemistry.
• Indirect CMV effects: CMV is immunomodulatory — it broadly suppresses immune function, increasing susceptibility to other opportunistic infections (bacterial, fungal, other viral). CMV-seropositive recipients receiving organs from CMV-seropositive donors (D+/R+) are at highest risk of clinically significant disease.

Standard prophylaxis: valganciclovir for 3–6 months post-transplant in high-risk patients. Breakthrough CMV despite prophylaxis, or CMV disease in a patient on prophylaxis, requires intravenous ganciclovir and resistance testing. Ganciclovir-resistant CMV (UL97 and UL54 mutations) is an emerging problem requiring foscarnet — a nephrotoxic agent — creating a management dilemma in patients already receiving calcineurin inhibitors.

Epstein-Barr Virus (EBV) and PTLD

EBV causes post-transplant lymphoproliferative disorder (PTLD) — a spectrum from infectious mononucleosis-like illness to aggressive B-cell lymphoma. PTLD is the most feared late viral complication of immunosuppression. EBV viral load monitoring (quantitative PCR) is mandatory in EBV-seronegative recipients (R-) receiving organs from EBV-positive donors (D+) — the highest-risk combination, common in paediatric transplantation.

Graft dysfunction in PTLD can occur via hepatic PTLD (infiltration of the liver graft by lymphoproliferative cells) or via systemic disease with secondary hepatic involvement. The key clinical challenge is distinguishing PTLD from rejection on liver biopsy — both can cause portal inflammation and bile duct injury.

Other viral pathogens

• Hepatitis B recurrence: HBV recurrence in the graft after liver transplantation for HBV-related cirrhosis — prevented with lifelong antiviral therapy (tenofovir or entecavir) plus hepatitis B immunoglobulin (HBIG) in the perioperative period. Fibrosing cholestatic hepatitis B (FCH-B) is a devastating form of graft HBV recurrence with rapid progression to graft failure.
• HCV recurrence: Now effectively treated with direct-acting antivirals (DAAs) post-transplant; fibrosing cholestatic hepatitis C (FCH-C) is rare with current prophylaxis and early treatment.
• Adenovirus, HHV-6, parvovirus B19: Less common but clinically significant in immunosuppressed recipients; may cause hepatitis, bone marrow suppression, or encephalitis depending on the pathogen.

Invasive fungal infections — the underestimated threat

Invasive fungal infections (IFIs) after liver transplantation carry mortality rates of 50–90% for invasive aspergillosis and 30–50% for invasive candidiasis, even with optimal antifungal therapy. They occur predominantly in the first 30–90 days post-transplant, when immunosuppression is most intense and surgical trauma to the biliary tree and vasculature creates entry points.

Invasive candidiasis (Candida albicans, Candida glabrata, Candida krusei) is the most common IFI in liver transplant recipients. Risk factors: prolonged surgery, Roux-en-Y biliary reconstruction, renal replacement therapy, re-transplantation, high intraoperative transfusion requirements. Treatment: echinocandins (caspofungin, micafungin) first-line; azoles for step-down. Candida glabrata and krusei have intrinsic azole resistance — species identification and sensitivity testing are essential.

Invasive aspergillosis (Aspergillus fumigatus predominantly) — the most lethal IFI post-transplant. Pulmonary aspergillosis presenting as cavitating lung lesions in a recipient on high-dose steroids (e.g., post-rejection treatment) is classic. CT chest showing “halo sign” — a nodule surrounded by ground-glass opacity — is the hallmark finding. Treatment: voriconazole first-line; isavuconazole as alternative. Critical interaction: voriconazole is a potent CYP3A4 inhibitor that dramatically increases tacrolimus levels — dose reduction of tacrolimus by 50–75% required immediately on initiation, with twice-weekly tacrolimus monitoring until stable.

Mucormycosis — rare but increasingly reported post-transplant, particularly in diabetic recipients or those receiving high steroid doses. Angio-invasive, rapidly fatal without surgical debridement plus liposomal amphotericin B. COVID-19-associated mucormycosis (CAM) was disproportionately reported in India in 2021 in immunosuppressed patients, including transplant recipients.

Pneumocystis jirovecii pneumonia (PJP) — prevented with trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis for the first 6–12 months post-transplant. Breakthrough PJP in a recipient on prophylaxis suggests compliance failure, drug interaction, or unusually intense immunosuppression.

The cause-and-effect relationship with graft dysfunction

This is the crux of Dr. Kalal’s panel discussion — and the area where clinical errors most commonly occur:

• Infection causing graft dysfunction: CMV hepatitis raises LFTs and bilirubin, mimicking rejection. Fungal cholangitis (Candida in the biliary tree post-Roux-en-Y reconstruction) causes cholestatic LFT pattern. Viral hepatitis (HBV/HCV recurrence, adenovirus) causes hepatocellular injury pattern. All of these can present identically to acute cellular rejection on biochemistry — only liver biopsy differentiates them definitively.
• Graft dysfunction causing infection susceptibility: A dysfunctional graft impairs Kupffer cell function (resident hepatic macrophages), reducing bacterial clearance from portal blood. Reduced synthetic function (low albumin, impaired complement production) reduces opsonisation and immune defence. High bilirubin creates an environment conducive to fungal overgrowth in the biliary system.
• Treatment of one worsening the other: Treating presumed rejection with high-dose steroids (methylprednisolone 1g IV) in a patient who actually has CMV hepatitis will dramatically worsen CMV disease, potentially causing fatal dissemination. Conversely, withholding immunosuppression in a patient with true rejection because of concurrent infection can lead to graft loss. This diagnostic dilemma — infection vs. rejection — is where experienced subspecialty hepatology judgment is most critical.

The single most important principle in managing graft dysfunction with concurrent infection: do not treat rejection empirically without a biopsy. High-dose steroid pulse therapy in undiagnosed CMV hepatitis, invasive aspergillosis, or disseminated candidiasis can be fatal. Liver biopsy with appropriate staining — including immunohistochemistry for CMV, PAS/GMS for fungi, and C4d for antibody-mediated rejection — is the diagnostic gold standard.

Why case-based panel discussion is the right format for this topic

Infection-related graft dysfunction does not follow algorithmic pathways. The interactions between immunosuppression intensity, infecting organism, graft function, and comorbidities are too complex for protocol-based management. Case-based panel discussion — presenting real clinical scenarios to a panel of experts who reason through the diagnosis and management in real time — teaches the pattern recognition and clinical judgment that guidelines alone cannot convey.

Dr. Kalal’s participation as faculty in this format reflects direct inpatient experience managing these exact scenarios at a high-volume liver transplant centre, combined with the academic depth to contextualise each case within current evidence and international guidelines.

Dr. Chetan Kalal — Faculty Profile

Dr. Chetan Kalal is Associate Director, Hepatology & Transplant Medicine, at Gleneagles Hospital Mumbai. He holds DM (Hepatology), MD (Medicine), and MRCP (UK), and is the first DM-qualified Hepatologist in Maharashtra. He is an APASL-AARC consortium member with 26+ PubMed-indexed publications, has received the AASLD Foundation Award, and is regularly invited as faculty to national and international hepatology and liver transplant conferences.

His LTSICON 2026 faculty invitation follows his recent participation as Invited Faculty at DRILLS 7th Edition (June 2026, Pullman Aerocity, New Delhi, ILBS), further establishing his position as one of India’s leading voices in transplant hepatology and post-transplant infectious disease management.

Post-Transplant Care at Gleneagles Hospital Mumbai

Dr. Kalal provides comprehensive post-liver transplant follow-up care at Gleneagles Hospital Mumbai, including:

• Immunosuppression management (tacrolimus, cyclosporin, mycophenolate, steroids) with therapeutic drug monitoring
• CMV and EBV surveillance — quantitative PCR monitoring and pre-emptive therapy
• Antifungal prophylaxis protocols and management of breakthrough IFIs
• Liver biopsy interpretation for rejection vs. infection differentiation
• Long-term graft health monitoring — metabolic complications, de novo malignancy surveillance, bone health

For post-transplant patients outside India — in the UK, USA, UAE, Singapore, Australia, Canada — structured virtual follow-up consultations are available, coordinated with local treating physicians.

Frequently Asked Questions

What is LTSICON?

LTSICON is the Liver Transplant Society of India Conference — India’s principal national conference for liver transplantation, bringing together transplant surgeons, hepatologists, intensivists, and allied specialists. It is held annually with a midterm conference at a rotating venue. Invited faculty status at LTSICON represents national recognition of subspecialty expertise.

What is the most common infection after liver transplant?

Bacterial infections are most common overall (predominantly in the first 30 days, related to surgical site and biliary complications). Among viral infections, CMV is the most clinically significant. Among fungal infections, invasive candidiasis is most common; invasive aspergillosis carries the highest mortality.

How is CMV treated after liver transplant?

CMV prophylaxis: oral valganciclovir for 3–6 months in high-risk recipients. CMV disease treatment: intravenous ganciclovir for 2–3 weeks minimum, with monitoring of CMV viral load to confirm response. Ganciclovir-resistant CMV requires foscarnet. Reduction in immunosuppression, where clinically safe, is an important adjunct to antiviral therapy.

Can voriconazole be used with tacrolimus after liver transplant?

Yes, but with mandatory dose adjustment. Voriconazole potently inhibits CYP3A4, the primary metabolic pathway for tacrolimus. Co-administration without dose reduction causes tacrolimus toxicity (nephrotoxicity, neurotoxicity). Standard practice: reduce tacrolimus dose by 50–75% on starting voriconazole, with twice-weekly tacrolimus level monitoring until a new steady state is reached.

How do you distinguish rejection from infection in a liver transplant recipient?

Clinically, biochemical LFT patterns overlap significantly. The definitive answer requires liver biopsy with H&E, immunohistochemistry for CMV (pp65 antigen), PAS/GMS staining for fungi, and C4d staining for antibody-mediated rejection. Concurrent CMV PCR, fungal cultures, and beta-D-glucan/galactomannan serology complement the histological assessment. Empirical high-dose steroid treatment without biopsy confirmation is hazardous when infection has not been excluded.

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For post-liver transplant follow-up in Mumbai or via virtual consultation internationally, book at drchetankalal.com/book. For international patients: drchetankalal.com/virtual-consult.