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The coexistence of acute rheumatic fever (ARF) with malarial infection is uncommon, its pathogenesis remains unexplained and may related to altered immune status, a unique dual challenge in immunology. Both malaria and ARF can present with high fevers, joint pain (arthralgia), making the clinical diagnosis in endemic areas very difficult. Fever pattern is helpful to diagnose the associated infection with ARF and malaria produces a relapsing fever at 48 hrs interval in plasmodium vivax infection. In ARF, virulence factors, infectious burden and genetic susceptibility play a role. The concept of ‘rheumatogenic’ strains is inadequate and the infectious burden of Strep A (streptococcus A) that “primes” the immune system for dysregulation and self-reactivity during the window period between the onset of Strep A infections and the development of ARF, potentially exacerbating the systemic inflammation and autoimmune responses. The circulating antistreptococcal cross-reactive antibodies and malaria-induced immune complexes aggravate the inflammation of carditis and valvulitis in ARF.
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Ramachandran Muthiah (2026) studied this question.
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