Recurrence or Relapse of COVID-19 in Older Patients: A Description of Three Cases

Ludovic Lafaie, MD; Thomas Célarier, MD, MS; Luc Goethals, MsD; Bruno Pozzetto, MD, PhD; Sylvain Grange, MD; Etienne Ojardias, MD; Cédric Annweiler, MD, PhD; Elisabeth Botelho-Nevers, MD, PhD


J Am Geriatr Soc. 2020;68(10):2179-2183. 

In This Article

Abstract and Introduction


Background: COVID-19 has infected millions of people worldwide, particularly in older adults. The first cases of possible reinfection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were reported in April 2020 among older adults.

Design/Setting: In this brief report, we present three geriatric cases with two episodes of SARS-CoV-2 infection separated by a symptom-free interval.

Participants: The participants of this brief report are three cases of hospitalized geriatric women.

Measurements/Results: We note clinical and biological worsening during the second episode of COVID-19 for all three patients. Also, there is a radiological aggravation. The second episode of COVID-19 was fatal in all three cases.

Conclusion: This series of three geriatric cases with COVID-19 diagnosed two times apart for several weeks questions the possibility of reinfection with SARS-CoV-2. It raises questions in clinical practice about the value of testing for SARS-CoV-2 infection again in the event of symptomatic reoccurrence.


Since December 2019, the COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected more than 6 millions people worldwide[1] and is responsible for a large number of deaths, particularly among older adults.[2–5] Isolation and containment are the main measures to break chain contamination in primary prevention in this population;[6] the tertiary prevention is based on the assumption of effective immunization of infected individuals to prevent recurrence of the infection.[5] However, the first cases of possible reinfection by SARS-CoV-2 were reported in April 2020 among adults.[7] Here, we report a recurrence of the SARS-CoV-2 infection in a series of older patients in Saint-Etienne, France.

The clinical and laboratory data of cases are summarized in Table 1.

Patient 1 was an 84-year-old woman with medical history of high blood pressure, beta-lactam allergy, heart failure, atrial fibrillation treated by rivaroxaban, diabetes mellitus, type II, treated with insulin, chronic renal failure, and chronic respiratory failure under long-term oxygen (1 L/15 h a day). The patient exhibited specific symptoms of COVID-19, with cough, fever, and respiratory signs with oxygen desaturation at 79%. The COVID-19 diagnosis was made on the typical computed tomographic (CT) scan appearance on March 24, 2020, with bilateral ground glass lesions predominating on the right lung (Figure 1-A1), confirmed by a positive SARS-CoV-2 reverse transcription–polymerase chain reaction (RT-PCR) performed on nasopharyngeal sample on March 26 (cycle threshold (Ct) of 31.4). She was hospitalized in an acute-care unit dedicated to COVID-19 on the same day. The patient received levofloxacin for 7 days and a short course of corticosteroids by methylprednisolone, which resulted in clinical and biological improvements, allowing the patient to be referred to a COVID-19 rehabilitation care unit on April 7. During her stay in this unit, C-reactive protein (CRP) and lymphocyte rate were normalized. On May 4, more than 1 month after the first episode, the patient presented with hyperthermia and respiratory signs. She was readmitted into an acute-care unit dedicated to COVID-19, and SARS-CoV-2 RT-PCR tests were performed on May 8, in nasopharyngeal swab and sputum, and were positive (Ct of 17.5 and 18.1, respectively). Viral cultures of sputum and nasopharyngeal secretions performed on Vero cells showed cytopathic effect in plaque assay. Virological sequencing has been performed and belongs to the B1 (European) lineage, according to the Pangolin classification.[8] Chest CT scan was compatible with COVID-19 acute infection and revealed bilateral moderate lung lesions (10%–25%), which were greater than previously (Figure 1-A2). The biological inflammatory syndrome was marked, with CRP at 304.5 mg/L and a deep lymphopenia at 0.47 Giga/L and interleukin (IL)-6 = 235 ng/L. Neutralizing antibodies to SARS-CoV-2 were negative on May 8 and faintly positive (rate of 1:10) on May 15. The patient was treated symptomatically with oxygen therapy and noninvasive ventilation due to respiratory acidosis from May 12. She received levofloxacin from May 5 and aztreonam from May 8, although no superinfection was documented. Methylprednisolone, 60 mg/d, was added on May 10. Immunotherapy by tocilizumab (8 mg/kg) was administered on May 12. The patient finally died on May 17 due to respiratory and heart failure despite high-dose furosemide.

Figure 1.

Chest computed tomography scans.

Patient 2 was a 90-year-old dependent woman living in a nursing home and exhibiting diabetes mellitus, type II, hypertension, hypothyroidism, and major neurodegenerative pathology (Alzheimer's disease). Diagnosis of COVID-19 was suspected in early April 2020 based on a clinical picture of cardiorespiratory decompensation with atrial fibrillation with fever and was confirmed on April 5 with SARS-CoV-2 RT-PCR positive test on a nasopharyngeal specimen (Ct of 21). She was hospitalized in a COVID-19 acute-care unit. The chest CT scan revealed signs of pleural effusions bilaterally, with no sign typical of pulmonary SARS-CoV-2 infection (Figure 1-B1). The patient received various treatments with preventive anticoagulation (the risk-benefit ratio was not in favor of curative anticoagulation), diuretics, and antibiotics by ofloxacin and 5 days of prednisolone, 40 mg/d. Clinical improvement was noted, and the patient was transferred to a COVID-19 rehabilitation care unit on April 21, before she was able to return to her nursing home on May 7. The patient kept an inflammatory syndrome with a CRP stable at 55 in the context of chronic pressures sores. Her second hospitalization, in a COVID-19 acute-care unit, on May 11, was motivated by the onset of major dehydration with hypernatremia measured at 166 mmol/L, oxygen saturation at 93% under 4 L of oxygen, melena, and marked deterioration of her general condition. Biology reported a marked lymphopenia at 0.18 Giga/L and CRP at 181 mg/L. The SARS-CoV-2 RT-PCR test was positive on a nasopharyngeal swab (Ct at 18.8) on May 6. On May 14, following respiratory degradation, a chest CT scan showed pulmonary condensation and bilateral diffuse crazy paving affecting approximately 25% to 50% of the lung parenchyma, with bilateral proximal lobar pulmonary embolism (Figure 1-B2). No serological test was performed. Palliative care was decided after discussion with the family and multidisciplinary validation. The patient finally died on May 19.

Patient 3 was an 84-year-old woman with medical history of rhythmic heart disease treated with a pacemaker, pulmonary embolism treated with rivaroxaban, arterial hypertension, and rheumatoid arthritis treated with methotrexate, 15 mg/wk, and corticosteroids (prednisone, 13 mg/d). She exhibited symptoms of COVID-19, combining fever, asthenia, ageusia, and respiratory signs with dry cough, polypnea (breathing rate = 32/min), oxygen desaturation with 93% under 3 L of oxygen. She was hospitalized in an acute-care unit dedicated to COVID-19 on April 16, 2020, with a positive diagnosis of COVID-19 based on a typical chest CT scan showing lung lesions, such as crazy paving and ground glass opacity greater than 50% bilaterally (Figure 1-C1). The SARS-CoV-2 RT-PCR test performed on nasopharyngeal sample was negative twice. These were probably false negatives due to inadequate sampling. Patient has typical COVID-19 symptoms, and no other infectious cause was found. Sputum could not be collected. The CRP was measured at 160 mg/L and lymphocytes at 0.13 Giga/L. The patient received ceftriaxone for 7 days, rovamycine for 5 days, and discontinuation of methotrexate treatment replaced by an increase in corticosteroids (prednisone = 60 mg/d) and oxygen therapy until 4 L. There was a clinical-biological improvement, with oxygen withdrawal and normalization of the inflammatory syndrome that allowed the patient to be referred to a rehabilitation care unit dedicated to COVID-19 on April 27 under prednisone, 30 mg/d. Sudden respiratory deterioration occurred on May 6, with 80% desaturation requiring oxygen therapy, dry cough, and fever. Nasopharyngeal samples for SARS-Cov-2 RT-PCR test were found positive (Ct at 16.9 and 14.7 on May 8 and 11, respectively). Viral culture was performed on Vero cells and found positive. Virological sequencing has been performed and belongs to the B1 (European) lineage, according to the Pangolin classification.[8] CT scan revealed a severe bilateral pneumonia (Figure 1-C2). At readmission, biology reported marked lymphopenia at 0.23 Giga/L, CRP at 146 mg/L, and IL-6 at 201 ng/L. A rise of neutralizing antibodies against SARS-CoV-2 was observed from May 8 to May 15 (titers from <10 to 40). She received ceftriaxone and methylprednisolone, 60 mg/d, from May 8 and high-flow oxygen. Cotrimoxazole was adjuncted on May 19 to exclude plausible pneumocystosis superinfection. After validation in a multidisciplinary meeting, the patient received convalescent COVID-19 plasma transfusion on May 16. However, the respiratory status deteriorated, with major desaturation despite 20 L of oxygen and she finally died on May 23.