Cryptosporidiosis in a young male with systemic lupus erythematosus: A fatal case report

Introduction

Systemic lupus erythematosus (SLE) is a chronic auto-immune disease with multisystem involvement which requires prolonged immuno-suppression for disease control. While these improve survival, they increase susceptibility to infection, which remains a major cause of morbidity and mortality, especially in resource-limited and tropical settings.

Gastro-intestinal (GI) manifestations are common and may arise from active disease, treatment-related toxicity, or infectious complications. Mycophenolate mofetil (MMF), a cornerstone of lupus nephritis therapy, frequently causes diarrhoea, which can mask other serious aetiology. Opportunistic pathogens, particularly protozoa such as Cryptosporidium, are important differential diagnoses but are often under-recognized.

Cryptosporidium infection is typically self-limited in immuno-competent hosts but can be life-threatening in immuno-suppressed individuals. Although well documented in HIV-infected populations, it has been rarely reported in SLE. Infections may also act as triggers for lupus flares, further complicating clinical management.

We present a fatal case of cryptosporidiosis in a young male with SLE on immuno-suppressive therapy, highlighting the diagnostic challenges and emphasizing the need for early recognition of opportunistic infections in tropical practice.

Case report

A 17-year old male, diagnosed with SLE (lupus nephritis-class IV) in March 2025, had received a treatment regime with intravenous cyclophosphamide. In August, this was changed to MMF 500 mg bd.

Two weeks prior to admission in the last week of August, he developed persistent vomiting and watery diarrhoea (6–7/day) with abdominal pain. Switching to mycophenolate sodium (which is mainly absorbed in small intestine) did not relieve symptoms.

On admission, he was hypotensive (80/50 mmHg), dehydrated, and required inotropic support. There was no evidence of rash or oral ulcers. The joints were non-tender, with no swelling or deformities noted. Cardiovascular examination revealed no pericardial rub nor muffled heart sounds. Abdominal examination showed neither tenderness nor organomegaly.

The initial laboratory evaluation revealed a haemoglobin level of 127 g/L, total leucocyte count of 7.9 × 10⁹/L, and platelet count of 384 × 10⁹/L. Renal parameters were deranged with a serum creatinine of 176.8 µmol/L and urea of 21.3 mmol/L. Electrolyte assessment showed hyponatraemia (sodium 133 mmol/L) and hypokalaemia (potassium 2.3 mmol/L). Serum proteins were reduced, with total protein 59 g/L and albumin 29 g/L. Immunological testing demonstrated a strongly positive ANA (>500 U/mL) and anti-dsDNA antibody (280.28 IU/mL), along with low complement levels (C3 0.53 g/L, C4 0.12 g/L). Liver function tests were within normal limits, with no elevation of bilirubin or hepatic enzymes. Stool examination was negative for ova and cysts, and no motile organisms were seen on hanging drop preparation; however, stool for Cryptosporidium (modified AFB stain) was positive. The procalcitonin level was markedly elevated at 26 µg/L. This suggested an underlying septic process superimposed on a lupus flare, rather than lupus activity alone.

He was started on nitazoxanide 500 mg bd, with immuno-suppressive therapy withheld. He was given one session of haemodialysis in view of oliguria, but despite such treatment and supportive care, he remained in refractory shock and succumbed after four days of admission.

Discussion

Systemic lupus erythematosus (SLE) frequently presents with gastrointestinal symptoms, but the underlying cause may be difficult to determine. Symptoms may result from disease activity, adverse drug effects, or infections, each of which may mimic the other. Although diarrhoea is common with mycophenolate mofetil (MMF), persistence despite dose and therapy adjustment should prompt evaluation for infection or search for lupus enteritis.^1,2

Cryptosporidiosis may cause severe, protracted diarrhoea, malabsorption, dehydration, and death in immuno-suppressed patients.^3,4 Poor outcomes, particularly when recognition is delayed, are to be expected. In tropical regions, where exposure risk is high, early recognition is crucial.

This case illustrates key diagnostic challenges. The initial attribution of diarrhoea to MMF delayed consideration of opportunistic infection. Additionally, whilst lupus enteritis can mimic infection, and serological activity (elevated dsDNA, low complement) may confound interpretation, high levels of inflammatory markers should sound warning bells. Whilst infections are known to trigger lupus flares, distinguishing between flare and infection is critical, as increasing immuno-suppression may worsen infection.^5,6

Despite appropriate antimicrobial therapy with nitazoxanide, our patient succumbed to refractory shock. Mortality in cryptosporidiosis among immuno-suppressed individuals is notorious, but is frequently related to delayed diagnosis, severe electrolyte imbalance, and haemodynamic compromise.^3,4

The value of early stool testing using modified acid-fast staining, an inexpensive and widely available method, is essential. Managing SLE in tropical regions should provoke a high index of suspicion for opportunistic infections when assessing persistent diarrhoea. Persistent diarrhoea in SLE should not be attributed solely to drug toxicity.