SARS-CoV-2 and influenza virus co-infection

Since December, 2019, coronavirus disease 2019 (COVID-19) has been an international public health emergency.1, 2, 3 Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mimics the influenza virus regarding clinical presentation, transmission mechanism, and seasonal coincidence.³ Thus, co-infection by both viruses is feasible. To the best of our knowledge, only one case of co-infection is known, although the diagnosis was sequential.⁴ Here, we present four cases of SARS-CoV-2 and influenza co-infection, diagnosed simultaneously.

Patients 1–3 were men aged 53, 78, and 56 years, respectively, and patient 4 was a woman aged 81 years (table ). All four patients had a medical history of hypertension. Patients 1 and 4 had a history of end-stage kidney disease on haemodialysis, and patients 2 and 4 had type 2 diabetes. All four patients attended the emergency department because of non-productive cough, fever, and dyspnoea for 3 days.

Table.

Analytical findings of four patients with severe acute respiratory syndrome coronavirus 2 and influenza virus co-infection

	CRP (mg/dL [<1 mg/dL])			LDH (U/L [<234 U/L])			Ferritin (ng/mL [20–400])			D-dimer (ng/mL [<500])			Lymphocyte count (×109 cells per L [0·9–4·5])			Platelets count (×109 cells per L [130–400])			Ultrasensitive troponin I (ng/L [<45·2])
	0 h	24 h	72 h	0 h	24 h	72 h	0 h	24 h	72 h	0 h	24 h	72 h	0 h	24 h	72 h	0 h	24 h	72 h	0 h	24 h	72 h
Patient 1 (man, 53 years)	4·3	10	10	NA	191	209	NA	905	1203	NA	700	1300	0·6	0·4	0·3	125	101	86	191	168	300
Patient 2 (man, 78 years)	14·0	15·0	3·6	314	340	283	NA	162	235	NA	NA	2100	0·3	0·3	0·5	60	60	81	NA	NA	NA
Patient 3 (man, 56 years)	2·1	3·18	NA	NA	NA	NA	280	305	NA	200	200	NA	1·2	1·8	NA	199	205	NA	2·8	2·9	NA
Patient 4 (woman, 81 years)	1·3	6·1	9·7	247	231	250	NA	NA	NA	200	NA	NA	0·5	0·5	0·7	99	78	78	1748	648	836

Numbers in square brackets correspond to the normal laboratory values. CRP=C-reactive protein. LDH=Lactate dehydrogenase. NA=not available.

Physical examination revealed tachypnoea and bronchospasm with low oxygen saturation for all patients except for patient 3, whose values were normal. Chest radiography at admission was pathological in two patients: patient 2 had bilateral infiltrates, and patient 4 had a right bilobar pneumonia. The analytical findings are summarised in the table.

Rapid nucleic acid amplification test for influenza A was positive in patients 1 and 2. Patient 3 tested positive for both influenza A and B, and patient 4 tested positive for influenza B. Following the local diagnosis protocol for SARS-CoV-2, simultaneous RT-PCR was done and was positive for all four patients. Patient 3 was discharged after 48 h without treatment or complications. However, rapid respiratory deterioration, orotracheal intubation, and mechanical ventilation were required for patients 1, 2, and 4.

We initiated treatment with lopinavir–ritonavir 400/100 mg twice a day, oral hydroxychloroquine 200 mg twice a day (in haemodialysis patients, 100 mg twice a day), and oral oseltamivir 150 mg twice a day (in haemodialysis patients, 30 mg every 48 h). Subcutaneous interferon β-1b 8MU was added every 48 h in patients 2 and 4. Patient 1 showed clinical improvement and 72 h after admission he remained stable with minimal oxygen requirements. Patients 1 and 4 remained under mechanical ventilation 72 h after admission.

Here we highlight four cases of SARS-CoV-2 and influenza co-infection and show the implications that such a co-infection can have. The clinical and analytical courses in these patients did not differ from those previously reported for COVID-19.⁵ However, more studies are needed to assess the effect of the SARS-CoV-2 and influenza co-infection in clinical outcomes. We call on the medical community to be aware and take COVID-19 into account as a potential diagnosis even in patients with other viral causes, especially in epidemic areas.