Anaphylaxis following enteral exposure to Chlorella vulgaris

Background

Anaphylaxis is an acute life-threatening allergic response to an antigen precipitated by the release of inflammatory mediators and cytokines and can often prove fatal if left untreated. Antigens or allergens can comprise of a vast number of substances including common foods and synthetic materials.1 In Australia, food allergy occurs in about 10% of infants, 4%–8% of children and 2% of adults, and the overall cases of food-related anaphylaxis have increased twofold in the last 10 years. According to the Australian Bureau of Statistics, Australia leads globally in deaths from anaphylaxis, with food-related events accounting for approximately 7% of deaths.2

Chlorella vulgaris is a green unicellular microalga that has long been used as a food source containing macronutrients and micronutrients including proteins, omega-3, polyunsaturated fatty acids, polysaccharides, vitamins and minerals.3 C. vulgaris is thought to expedite muscle recovery by improving the regenerative capacity of young and senescent myoblasts and promoting myoblast differentiation.4 While a few studies investigating the allergic and toxic properties of several other Chlorella sp have been documented, no case of C. vulgaris-induced anaphylaxis has been reported. Given the general dearth of scientific literature describing the allergic properties of Chlorella sp, we seek to expand the existing knowledge pool by demonstrating the anaphylactic potential of orally ingested C. vulgaris. Additionally, we highlight the importance of obtaining a thorough history in navigating diagnostic red herrings, and we explore the diagnostic utility of tryptase levels in the evaluation of anaphylaxis.

Case presentation

A 75-year-old man was admitted to the emergency department of a major tertiary hospital with a systolic blood pressure of 50 mmHg, wheeze and a widespread urticarial rash. He was previously well with no history of allergies or anaphylaxis and denied any preceding infective symptoms. His comorbidities included hypertension, hypercholesterolemia and an endovascular aneurysm repair for an abdominal aortic aneurysm. On examination, he appeared very unwell with a mottled abdomen and a widespread urticarial rash, had cool peripheries, and was disorientated to time and place. Apart from severe hypotension, his other vital signs, including temperature, were unremarkable. There were no obvious foci of infection based on preliminary physical examination and investigations apart from a history of self-reported diarrhoea. On admission to the intensive care unit, his blood pressure had already improved to 115/50 mmHg after administration of intramuscular epinephrine and intravenous hydration in the ambulance. He was subsequently given intravenous piperacillin–tazobactam and further intravenous hydration. There were no further requirements for inotropic or vasopressor support.

Initial laboratory findings demonstrated an increased white cell count of 19.5×10⁹/L with elevated neutrophils of 10.8×10⁹/L and lymphocytes of 7.3×10⁹/L. These readings all normalised within 12 hours. The peripheral blood film demonstrated leucocytosis suggestive of a reactive response, despite a normal C reactive protein level. Faecal cultures including Clostridium difficile toxin and Norovirus PCR tests, urine analysis, blood cultures and influenza tests all returned negative. Urea, electrolytes and creatinine levels were also within the normal ranges. A routine chest X-ray demonstrated hyperinflated lungs without any infective features. Given his prior history of an abdominal aorta repair, a CT angiogram was additionally performed to rule out an abdominal aortic aneurysm rupture or an endovascular leak, and it confirmed an absence of these pathologies.

Given the high clinical index of suspicion for anaphylaxis, tryptase levels were obtained on admission within the recommended time frame of 1–6 hours.5 All three blood samples demonstrated elevated levels of tryptase: 52.7 µg/L (on admission), 45.9 µg/L (one hour later) and 17.6 µg/L (six hours later). These tryptase levels subsequently normalised in blood samples obtained 12 hours later, indicative of an acute anaphylactoid reaction.

Given the significant improvement in our patient’s medical condition by the second day of admission, he was transferred to a general medical ward, where our treating team revisited the history of his presenting circumstances. On targeted questioning, he revealed having consumed a powdered C. vulgaris supplement which he normally fed his pigeons to prepare them for ‘pigeon racing’. He claimed to have had two doses of the supplement with each dose amounting to 4g of C. vulgaris. He had consumed the first dose a day before hospitalisation and the second dose several hours prior to his hospital admission. His anaphylactoid symptoms had began approximately three hours after his second dose.

Our patient was eventually discharged before the availability of the serum tryptase results with a planned follow-up at an allergy clinic. Given the clear temporal relationship between the oral ingestion of his C. vulgaris supplement, his anaphylactoid symptoms and elevated tryptase levels, we retrospectively concluded that his hospital presentation was in fact an anaphylactoid reaction to C. vulgaris.

Outcome and follow-up

Our patient failed to attend our six-week follow-up appointment at the general medicine clinic. A phone consultation was organised a week later, where he confirmed there was no recurrence of his anaphylactoid symptoms since avoiding the C. vulgaris supplement. He also failed to attend follow-up appointments at the allergy clinic for further diagnosis. He had made the unilateral decision to forgo the appointments given the complete resolution of his symptoms.