Type A fulminant Clostridium perfringens sepsis indicated RBC/Hb discrepancy; a case report

Clostridium perfringens is one of the most common causes of food poisoning, but can sometimes be curable if treated within a few days. C. perfringens septicemia is a rare, but rapidly fatal disease with a reported mortality rate of at least 60% [1].

C. perfringens type A produces an α-toxin that induces hemolysis by destroying red blood cells, resulting in a failure to supply oxygen to tissues [2, 3]. Hemolysis with signs of septic shock due to C. perfringens infection has been reported as invariably fatal in several reports [1, 4, 5]. We report herein a case of fulminant C. perfringens septicemia with massive acute hemolysis and liver abscess. Despite rapid initiation of antibiotic therapy, the patient died within 3 h of admission to the emergency department (ED).

A previously healthy 76-year-old man presented to the ED 8 h after onset of acute abdominal pain and diarrhea. He had eaten no perishable foods, and no family members had shown any symptoms. His medical history only included endoscopic submucosal dissection for early gastric cancer 6 years prior to the presentation. No family history of note was elicited.

On arrival, the patient looked unwell and flushed. Vital signs were: temperature, 38.6 °C; heart rate, 117 beats/min; blood pressure, 176/93 mmHg; and respiratory rate, 26 breaths/min. Peripheral oxygen saturation was 95% on room air. Abdominal examination revealed mild tenderness in the periumbilical region. The neck was supple. Heart sounds were normal, the lungs were clear to auscultation, and results of neurological and skin examinations were unremarkable. Arterial blood gas analysis revealed metabolic acidosis and compensatory respiratory alkalosis (pH, 7.486; partial pressure of arterial carbon dioxide, 16.1 mmHg; partial pressure of arterial oxygen, 66.1 mmHg; lactate, 86.4 mg/dL; base excess, − 9.2 mmol/L). The blood sample showed hemolysis, which was initially ascribed to an error during collection. Laboratory examination revealed a discrepancy between the red blood cell count (RBC) of 1.91 × 10⁶/mm³ and the hemoglobin (Hb) level of 10.3 g/dL. Other data were as follows: white blood cell count, 20,900/mm³ with 85.6% neutrophils; C-reactive protein, 4.70 mg/dL; procalcitonin, 28.82 ng/mL; platelet count, 545,000/μL; blood urea nitrogen, 27 mg/dL; creatinine, 2.42 mg/dL; serum aspartate aminotransferase, 874 IU/ L; serum alanine aminotransferase, 299 IU/L; and lactate dehydrogenase, 7605 IU/L; Na, 124 mEq/L; Cl, 92 mEq/L; K, 5.8 mEq/L.

Computed tomography performed 45 min after arrival in the ED revealed abscesses with gas in the right posterior lobes of the liver (Fig. 1). In light of this imaging result, he was treated empirically for suspected septicemia from liver abscesses with 1 g of meropenem after blood cultures were obtained.

Multiplex polymerase chain reaction only identified expression of the α toxin gene, and the pathogen isolated from the present patient was shown to be C. perfringens type A (Table 1).

C. perfringens septicemia is rare and typically proves rapidly fatal, with a reported mortality rate of at least 60% [1]. This expeditious lethality is due to a combination of the 7-min doubling time of the organism and the production of a multitude of virulent toxins. C. perfringens is classified into 5 types (types A–E) based on the production of different major lethal toxins [6]. All types of C. perfringens produce α toxin [3], which has been reported to hydrolyze phospholipids in red blood cell membranes, leading to massive hemolysis and severe tissue hypoxia due to the failure of oxygen transport functions [2, 5]. This may cause RBC/Hb discrepancy. The complete blood cell count machine can measure hemoglobin despite the hemolysis, however, it cannot measure the lysed red blood cells.

C. perfringens is an anaerobic Gram-positive bacillus usually found in the human gastrointestinal tract, and is most well-known as the cause of gas gangrene [1]. Several reports have described fatal C. perfringens septicemia associated with liver abscess [1, 7, 8]. Although the exact mechanisms of entry into the blood stream remain unknown, bacterial translocation may occur via portal veins in proximity to abscesses in the liver [9].

The key treatments for this rapidly lethal infection include immediate administration of antibiotics and surgical intervention. In the present case, the patient deteriorated rapidly and died despite administration of a broad-spectrum antibiotic soon after arrival. The ED clinical course was catastrophic and he was not a candidate for surgical intervention. Nishikido and Hashiba have also reported rapidly fatal ED cases despite early antibiotic administrations [1, 5].