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PubMed2025

Clinical and Microbiological Insights into Caseous Lymphadenitis in Sheep and Goats in Khorasan Razavi, Iran.

INTRODUCTION: Caseous lymphadenitis (CLA), a chronic bacterial disease caused by Corynebacterium pseudotuberculosis, significantly impacts small-ruminant health and productivity worldwide, causing economic losses through reduced wool and milk yields, reproductive issues, and carcass condemnation. Despite its importance, CLA prevalence and microbial dynamics remain under explored in Iran, where small ruminants are vital to rural economies. This study assessed the prevalence, clinical manifestations, and bacteriological profile of CLA in Khorasan Razavi Province, northeast Iran, to inform regional control strategies and address potential zoonotic risks. MATERIALS & METHODS: We examined 15 flocks totaling 4,733 animals (4,640 sheep, 93 goats) through clinical inspections and microbiological analysis of pus samples from affected lymph nodes. RESULTS: The results revealed a lymphadenitis prevalence of 11.59% (95% CI, 10.58%, 12.66%), with 8.62% of sheep (400/4640) and 8.60% of goats (8/93) affected, varying across flocks from 0% to 28.57%. Submandibular lymph nodes were most commonly affected (51.35%), followed by retropharyngeal (18.02%) and parotid (15.32%) nodes, with peak incidence in the 2-3-year age group (38.24%), likely linked to shearing practices. Bacteriological analysis of 102 pus samples identified C. pseudotuberculosis in 19.6% (20/102) of cases, characterized by small, dry, white colonies with β-hemolysis on Columbia blood agar. A diverse microbial profile included Actinobacillus spp. (7.8%), Trueperella pyogenes (3.9%), and novel isolates like Acinetobacter spp. and Yersinia spp. (1.0% each), with 43.14% of samples sterile, suggesting chronicity or sampling challenges. CONCLUSION: These findings indicate CLA etiology is complex, extending beyond a single pathogen and influenced by local husbandry practices. The study underscores CLA's economic burden and zoonotic potential, given rare but documented human cases. Integrated control measures-enhanced molecular diagnostics, recombinant phospholipase D (PLD) vaccine trials, and improved biosecurity-are urgently needed. Future research should prioritize genomic strain typing and environmental reservoir analysis to refine CLA management in Northeast Iran, offering insights applicable to similar agroecosystems globally.

Animals↗
PubMed2026

X-linked hyper-IgM syndrome presenting as severe Pneumocystis pneumonia in a 6-month-old infant: a case report.

BACKGROUND: X-linked hyper-immunoglobulin M (XHIGM) syndrome is a rare primary immunodeficiency caused by mutations in the CD40 ligand gene (CD40LG), characterized by defective T-cell-dependent B-cell class-switch recombination. Patients typically present with recurrent infections in early childhood, but diagnosis is often delayed due to heterogeneous clinical manifestations and the fact that serum IgM levels may remain within the normal range in a significant proportion of patients. Here we report a case of XHIGM in an infant whose diagnostic journey began with recurrent lymphadenitis and culminated in life-threatening Pneumocystis jirovecii pneumonia (PJP). CASE PRESENTATION: A 6-month-old male infant was admitted with severe respiratory distress and hypoxemia. He had recurrent axillary lymphadenitis at 1 and 2 months of age and significant failure to thrive. Chest CT showed bilateral consolidative and interstitial opacities. Immunological evaluation revealed markedly decreased IgA, normal IgM and IgG, and profound T-cell lymphopenia. Sputum metagenomic sequencing identified Pneumocystis jirovecii. Whole-genome sequencing identified a hemizygous likely pathogenic CD40LG mutation (NM_000074.3:c.520C>T, p.Q174*); his mother was a carrier. He was treated with mechanical ventilation, trimethoprim-sulfamethoxazole (TMP-SMX), micafungin, corticosteroids, and intravenous immunoglobulin (IVIG), and was discharged after 36 days. CONCLUSIONS: In infants with recurrent or opportunistic infections, persistently low IgA and declining T-cell counts-even when initial screening appears normal-should raise suspicion for underlying immunodeficiency and prompt genetic evaluation. Early aggressive management and evaluation for hematopoietic stem cell transplantation are essential to improve outcomes.Serial immunological evaluation is essential in infants with recurrent or opportunistic infections, as persistently low IgA and declining T-cell counts-even when initial screening appears normal-should prompt genetic evaluation for underlying immunodeficiency. Early aggressive management and evaluation for hematopoietic stem cell transplantation are essential to improve outcomes.

Humans↗
PubMed2026

Human GPR174 deficiency drives polyclonal lymphoproliferative disease via defects in T cell function.

The X-linked G-protein coupled receptor GPR174 is highly expressed in T and B lymphocytes and has immunoregulatory roles in mice, but its function in humans is unknown. We describe a cohort of six individuals who have function-disrupting variants in GPR174 and a clinical phenotype of lymphadenopathy and autoimmunity. Histological analysis of two patient lymph nodes revealed necrotizing lymphadenitis and lymphoproliferation resembling Kikuchi-Fujimoto disease. In-depth analysis of three patients and related carriers revealed overaccumulation of CD8 terminally differentiated effector memory cells re-expressing CD45RA (TEMRA). Patient cells and GPR174-deficient CD8 T cells generated from controls showed less repression of proliferation by the GPR174 ligand lysophosphatidylserine (lysoPS) and an effector-biased gene expression program. GPR174-deficient CD4 T cells were resistant to lysoPS-mediated suppression of IL2 production. In mice, chronic viral infection led to over-accumulation of GPR174-deficient effector CD8 T cells. We describe an inborn error of immunity associated with dysregulated lymphocyte responses that we propose predisposes to exaggerated lymphoproliferation and autoimmunity following viral infection.

Journal Article↗