Background <p>Brucellosis is a zoonosis caused by <i>Brucella spp.</i>, with <i>B. melitensis</i> the most virulent in humans. Although typically presenting with non-specific systemic symptoms, rare but severe complications—disseminated intravascular coagulation (DIC) and acute liver injury—pose diagnostic and therapeutic challenges. Reports of concurrent DIC and liver injury remain scarce, particularly in China, where molecular epidemiology has revealed genetically diverse <i>B. melitensis</i> lineages.</p> Case presentation <p>A 54-year-old woman from Guilin, Guangxi, presented with a 20-day history of anorexia and fatigue, chills and sweating, and recent ingestion of undercooked mutton. She had hypertension but no hepatic disease. On admission, temperature was 39.7&#xa0;°C with thrombocytopenia (41 × 10<sup>^9</sup>/L) and elevated aminotransferases (ALT 130.7 U/L; AST 178.1 U/L). Empirical ceftriaxone was initiated and later escalated to doxycycline and meropenem during diagnostic uncertainty. By day 5, thrombocytopenia had worsened with hypofibrinogenemia and markedly elevated D-dimer. Blood cultures grew <i>Brucella spp.</i> (subsequently identified as <i>B. melitensis</i>), serum agglutination titer was 1:800, and next-generation sequencing detected 1,216 <i>Brucella</i> reads. DIC was diagnosed (International Society on Thrombosis and Haemostasis score = 6) with acute liver injury. Given a prothrombotic DIC phenotype, therapeutic anticoagulation with nadroparin calcium was started; rifampin was added on day 8. The patient recovered without blood-product transfusion and was discharged on day 11.</p> Conclusions <p>This rare Chinese case illustrates three practice points: (1) maintain a high index of suspicion for brucellosis when unexplained DIC and hepatic injury co-occur in endemic or emerging-endemic settings; (2) use complementary diagnostics—culture, serology, and next-generation sequencing (NGS)—to accelerate confirmation and support lineage-aware public-health interpretation; and (3) pair stepwise, stewardship-concordant antimicrobials with phenotype-guided anticoagulation, which may obviate transfusions and improve outcomes.</p>

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Brucellosis complicated by disseminated intravascular coagulation and liver injury: a case report and review of the literature

  • Weiwei Zhang,
  • Feiyi Xu,
  • Qinghua Zheng,
  • Xiaomin Dong

摘要

Background

Brucellosis is a zoonosis caused by Brucella spp., with B. melitensis the most virulent in humans. Although typically presenting with non-specific systemic symptoms, rare but severe complications—disseminated intravascular coagulation (DIC) and acute liver injury—pose diagnostic and therapeutic challenges. Reports of concurrent DIC and liver injury remain scarce, particularly in China, where molecular epidemiology has revealed genetically diverse B. melitensis lineages.

Case presentation

A 54-year-old woman from Guilin, Guangxi, presented with a 20-day history of anorexia and fatigue, chills and sweating, and recent ingestion of undercooked mutton. She had hypertension but no hepatic disease. On admission, temperature was 39.7 °C with thrombocytopenia (41 × 10^9/L) and elevated aminotransferases (ALT 130.7 U/L; AST 178.1 U/L). Empirical ceftriaxone was initiated and later escalated to doxycycline and meropenem during diagnostic uncertainty. By day 5, thrombocytopenia had worsened with hypofibrinogenemia and markedly elevated D-dimer. Blood cultures grew Brucella spp. (subsequently identified as B. melitensis), serum agglutination titer was 1:800, and next-generation sequencing detected 1,216 Brucella reads. DIC was diagnosed (International Society on Thrombosis and Haemostasis score = 6) with acute liver injury. Given a prothrombotic DIC phenotype, therapeutic anticoagulation with nadroparin calcium was started; rifampin was added on day 8. The patient recovered without blood-product transfusion and was discharged on day 11.

Conclusions

This rare Chinese case illustrates three practice points: (1) maintain a high index of suspicion for brucellosis when unexplained DIC and hepatic injury co-occur in endemic or emerging-endemic settings; (2) use complementary diagnostics—culture, serology, and next-generation sequencing (NGS)—to accelerate confirmation and support lineage-aware public-health interpretation; and (3) pair stepwise, stewardship-concordant antimicrobials with phenotype-guided anticoagulation, which may obviate transfusions and improve outcomes.