Effect of Immunosuppressive Diseases and Rituximab Infusions on Allowing COVID-19 Infection to Relapse



 

Rohan M Prasad, DO1; Shaurya Srivastava, DO1; Enhua Wang, MD1; Jason Z Liu, DO1; Rakesh Gami, MD1; Ayat Abdelgadir, MD1; Akhil Sharma, DO1; Sumugdha Rayamajhi, MD1; Richa Tikaria, MD1

Perm J 2021;25:21.035

https://doi.org/10.7812/TPP/21.035
E-pub: 10/29/2021

ABSTRACT

Introduction: Relapsing COVID-19 infections have been reported, but their etiology and severity are still unknown. In addition, there have been no cases in the literature that associate relapsing infection with immunosuppression, either from a disease course or medications.

Case Presentation: This case series illustrates two patients who developed a relapsed infection, likely from recent rituximab infusions. In addition, both cases depicted a severe form of infection than the initial one. Laboratory investigations revealed these patients were unable to produce COVID-19 antibodies, even though one of the patients received convalescent plasma.

Conclusion: Clinicians should be aware of the possibility of relapsing COVID-19, especially in immunosuppressed patients. Because rituximab induces B-cell depletion, it can also decrease the effectiveness of the COVID-19 vaccine. Therefore, these patients should receive the vaccine before their scheduled rituximab infusion.

INTRODUCTION

On January 30, 2020, the World Health Organization declared a global public health emergency involving COVID-19 that was causing a disease named severe acute respiratory syndrome coronavirus 2.1 This virus is classified under the β subdivision of the family of coronaviruses.2 Relapses of COVID-19 infections have been demonstrated; however, its effect and severity in patients with immunosuppressive disorders and medications is unclear. This case series was prepared following the CARE guidelines.3

CASE PRESENTATION

The following cases illustrate two patients who developed severe, relapsing COVID-19 infections in the setting of recent rituximab infusions and chronic immunocompromised states. In both patients, the relapsing infection was more severe than the initial infection, and antibodies were not detected. This was seen even though 1 of the patients received convalescent plasma.

The first patient, KT, is a 73-year-old woman with a history of hypothyroidism, diabetes, and mantle cell lymphoma who presented for worsening shortness of breath, productive cough, and recurrent fevers for 1 week in January 2021. The patient stated that her last dose of rituximab for the lymphoma was in November 2020. She was initially diagnosed with COVID-19 in December 2020 via 2 positive polymerase chain reaction (PCR) nasal swabs. KT was treated with 10 days of Decadron and 5 days of remdesivir, ceftriaxone, and azithromycin. Initially, she required 2 L of oxygen, but was eventually weaned down to room air. On discharge, her D-dimer level was only mildly elevated; thus, she was not started on anticoagulation. She tested negative on 2 consecutive days from the COVID-19 PCR swabs 7 days after her initial positive test. In addition, on day 12 of that hospital stay she was negative for COVID-19 immunoglobulin G (IgG) antibodies.

In January 2021, KT was found to be COVID-19 positive, 38 days after the initial positive test, and her D-dimer level was greatly elevated (Table 1). Chest x-ray showed bilateral infiltrates (Figure 1). In addition, chest computed tomographic angiography demonstrated pulmonary emboli and bilateral ground-glass infiltrates (Figure 2). COVID-19 IgG antibodies were negative on days 1 and 9 of this hospital course (Table 1). Therefore, KT received cefepime for 7 days and convalescent plasma on days 1 and 12. Eventually, she developed a spontaneous right-side pneumothorax on day 5 (Figure 3) and bilateral pneumothoraces on day 9 (Figure 4). She initially tolerated bilevel positive airway pressure, but required intubation and an intensive care unit transfer. She also received a therapeutic dose of enoxaparin, and placement of bilateral chest tubes, which exhibited slow improvement in her respiratory status. However, KT continued to require maximum levels of ventilation and did not tolerate weaning trials. As a result, on day 20, a tracheostomy tube was placed after 2 preprocedural COVID-19 PCR swabs had a negative result. She patient was eventually discharged to a facility for long-term weaning after 2 negative COVID-19 PCR swab results. A poor prognosis was delivered to the family on the possibility of the patient surviving this disease course. Since discharge from the hospital, KT has tolerated weaning from the vent and is now using a speaking valve. With this progress, she was discharged from long-term rehab and now resides at home with her family. A timeline of KT’s pertinent history and hospital course is depicted in Figure 5.

Table 1. Timeline of care for patient 1, a 73-year-old woman with a history of hypothyroidism, diabetes, and mantle cell lymphoma on rituximab who presented for worsening shortness of breath, productive cough, and recurrent fevers for 1 week

Date

Subjective and objective

Diagnostic testing

Interventions

1/18/21

The patient reports 1 wk of shortness of breath, productive cough, and recurrent fevers.

White blood cells 12 ´ 103 cells/mL

Neutrophils, 94.4%

C-reactive protein, 8.9 mg/dL

Lactic, 1.9 mmol/L

Procalcitonin, 0.16 ng/mL

Ferritin, 1078 ng/mL

Lactate dehydrogenase, 553 U/L

D-dimer, 20.26 mg {FEU}/mL

COVID-19 PCR, positive ´ 2

COVID-19 antibodies, < 3.8

Urine analysis

Blood culture, no growth ´ 2

Chlamydia pneumonia PCR, negative

Mycoplasma pneumonia PCR, negative

Legionella pneumonia PCR, negative

Streptococcus pneumonia urine antigen, negative

Legionella urine antigen, negative

Methicillin-resistant Staphylococcus aureus PCR, negative

Influenza A and B direct antigens, negative

Adenovirus PCR, negative

Parainfluenza 1–4 PCR, negative

Metapneumovirus PCR, negative

Respiratory syncytial virus PCR, negative

Chest x-ray, bilateral pulmonary infiltrates

Computed tomographic angiography of the chest, acute pulmonary emboli and bilateral ground-glass infiltrates

Convalescent plasma was given.

Started heparin drip,

Started cefepime for 7 d.

Infectious disease was consulted.

1/20/21

The patient reports shortness of breath with any movement.

None

Oxygen requirements are increasing.

Consulted pulmonology.

Stopped heparin drip and started daily therapeutic enoxaparin.

1/23/21

The patient has one episode of bloody sputum.

Chest x-ray, right-side pneumothorax and mild vascular congestion

Right chest tube placed.

1/27/21

None

Chest x-ray, new left-side pneumothorax and increasing bilateral infiltrates

COVID-19 antibodies, < 3.8

Transferred to the intensive care unit.

The patient was intubated.

Sedated on fentanyl drip.

Started on norepinephrine and vasopressin drips.

Convalescent plasma was given.

Left chest tube placed.

2/1/21

The patient is agitated and dyssynchronous with the vent.

None

Started cisatracurium drip.

Vasopressors stopped.

2/4/21

Code blue is called for cardiac arrest.

Pulseless electrical activity

Post-code chest x-ray, no new or worsening pneumothoraces

Received 2 rounds of cardiopulmonary resuscitation.

Received 2wo doses of epinephrine, 1 of bicarbonate, and 1 g of calcium chloride.

Return of spontaneous circulation achieved after 6 min.

2/7/21

The patient is not passing spontaneous breathing trials and persistently requires maximum levels of ventilator support.

COVID-19 PCR, negative ´ 2

Tracheostomy performed.

FEU 5 Fibrinogen equivalent units; PCR5 polymerase chain reaction.

tpj21035f1

Figure 1. Admission chest x-ray for KT showing bilateral pulmonary infiltrates.

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Figure 2. Admission computed tomography angiography of the chest for KT. (A) Pulmonary emboli in the left lower branches of the left pulmonary artery. (B) Bilateral ground-glass infiltrates.

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Figure 3. Chest x-ray on day 5 for KT showing right-side apical pneumothorax and mild vascular congestion.

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Figure 4. Chest x-ray on day 9 for KT showing new, left-side, large apical pneumothorax and bilateral infiltrates, which have increased from those seen earlier.

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Figure 5. Timeline of events for KT depicting the pertinent history, admission date, and treatment course.

Our second patient, JP, is a 45-year-old man with a history of secondary progressive multiple sclerosis, a chronic Foley for neurogenic bladder, and recurrent urinary tract infections. He presented in January 2021 with 2 days of difficulty breathing, fever, and sepsis. The patient was treated with multiple regimens for multiple sclerosis, including rituximab infusions starting in June 2015. His most recent rituximab infusion was in September 2020. In October 2020, JP was found to be COVID-19 positive via PCR from a urology preprocedural screening evaluation. His only symptom at that time was a mild cough. Twelve days after his initial positive test, JP retested negative for COVID-19 via PCR.

On admission in January 2021, JP had two COVID-19 PCR results that were positive, which occurred 55 days after his initial positive test. In addition, a urine analysis was consistent with a urinary tract infection (Table 2). The chest x-ray on admission showed mild, right-side hilar infiltrates (Figure 6). JP was treated with guideline-based dexamethasone and intravenous remdesivir along with urine culture sensitivity-directed antibiotics. His fevers and oxygen requirements improved until day 13, when he developed fevers, difficulty breathing, and declining mentation. Repeat imaging later that day revealed progressive bilateral and multifocal airspace opacities (Figures 7 and 8). His COVID-19 IgG antibodies were negative on days 5 and 13 of the hospital course. Convalescent plasma was not given to JP per his and his family’s wishes. Ultimately, he required intubation, continuous renal replacement therapy, and an intensive care unit transfer. COVID-19 PCR on day 28 was once again positive. Unfortunately, as a result of a prolonged intensive care unit course with no improvement in multiorgan failure despite medical treatment, JP’s family decided to pursue comfort care measures on day 30 of his hospital stay. JP’s pertinent history and hospital course are illustrated in Figure 9.

Table 2. Timeline of care for patient 2, a 45-year-old man with a history of secondary progressive multiple sclerosis on rituximab, a chronic Foley for a neurogenic bladder, and recurrent urinary tract infections

Date Subjective and objective Diagnostic testing Interventions
1/7/21 The patient reports 2 d of difficulty breathing, fever, and chills.

White blood cells, 7.5 ´ 103 cells/mL

Neutrophils, 80.7%

C-reactive protein, 12.4 mg/dL

Lactic, 1.4 mmol/L

Procalcitonin, 0.28 ng/mL

Ferritin, 1434 ng/mL

Lactate dehydrogenase, 751 U/L

D-dimer, 15.81 mg {FEU}/mL

COVID-19 PCR, positive ´ 2

Blood culture, no growth ´ 2

Chlamydia pneumonia PCR, negative

Mycoplasma pneumonia PCR, negative

Legionella pneumonia PCR, negative

Streptococcus pneumonia urine antigen, negative

Legionella urine antigen, negative

Methicillin-resistant Staphylococcus aureus PCR, negative

Influenza A and B direct antigens, negative

Adenovirus PCR, negative

Parainfluenza 1–4 PCR, negative

Metapneumovirus PCR, negative

Respiratory syncytial virus PCR, negative

Chest x-ray, mild right-sided hilar infiltrates

Started dexamethasone for 10 d.

Started remdesivir for 5 d.

Started cefepime.

1/12/21 The patient reports symptomatic improvement, including fevers. Oxygen requirements are also decreasing.

Urine culture, Proteus mirabilis (>100,00 CFU/mL), Pseudomonas aeruginosa (50,000–75,000 CFU/mL), sensitive to meropenem

COVID-19 antibodies, 7

Stopped cefepime and started meropenem for 14 d.

Patient declined convalescent plasma.

1/20/21 The patient develops new-onset fevers, shortness of breath, and altered mentation.

Chest x-ray, progressive bilateral and multifocal airspace opacities

COVID-19 antibodies, 5.6

Transferred to the intensive care unit.

Infectious disease was consulted.

Family still declined convalescent plasma.

1/28/21 The patient still has fevers as well as progression of drowsiness and lethargy. None Started bilevel positive airway pressure.
1/30/21 The patient becomes dyspneic, tachycardic, and somnolent despite bilevel positive airway pressure. None

The patient was intubated.

Sedated on fentanyl and propofol drips.

Central venous catheter was placed.

Started norepinephrine drip.

2/3/21 The patient is unresponsive during spontaneous awakening trials. COVID-19 PCR, positive ´ 2

Still hypotensive; added vasopressin drip.

Nephrology was consulted.

Started continuous renal replacement therapy.

30 The patient remains unresponsive. None The family decided to pursue comfort measures.

FEU 5 Fibrinogen equivalent units; PCR5 polymerase chain reaction.

tpj21035f6

Figure 6. Admission chest x-ray for JP showing mild, right-side hilar infiltrates.

tpj21035f7

Figure 7. Chest x-ray on day 13 for JP showing progressive bilateral and multifocal airspace opacities and low lung volumes.

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Figure 8. Computed tomography angiography of the chest on day 13 for JP showing bilateral and multifocal patchy opacities.

tpj21035f9

Figure 9. Timeline of events for JP depicting the pertinent history, admission date, and treatment course.

DISCUSSION

According to the Centers for Disease Control and Prevention, a relapse or reactivation of COVID-19 is when a repeat PCR test is positive during a 90-day window, which indicates prolonged viral shedding. However, it is currently unknown whether these patients require droplet isolation precautions. In comparison, COVID-19 reinfection is 2 positive PCR tests conducted at least 90 days after the initial 2 positive PCR tests, regardless of symptoms, or a repeat positive PCR within 45 to 89 days in a patient with symptoms consistent with COVID-19, other explainable cause for the symptoms, or no recent COVID-19 exposure.4 However, this timeline requires further delineation in immunocompromised individuals. For example, an 89-year-old woman developed a fatal case of COVID-19 reinfection 2 days after starting chemotherapy for Waldenström macroglobulinemia, which correlated with an onset of 59 days after her initial exposure.5 Another differential diagnosis is prolonged shedding of the virus, but these patients are typically asymptomatic.6 Both of the patients in our case series developed symptomatic relapsed COVID-19 infection and more severe forms of the disease than the initial infection. Antibodies were tested multiple times and neither patient was able to produce an adequate response. Moreover, the second patient’s IgG antibody level had decreased despite developing and recovering from COVID-19 (Table 2). Because of the perceived likelihood of infectivity, isolation droplet precautions were initiated in these patients. However, further studies should evaluate the true viral infectivity in relapsed patients to determine the necessity of isolation. In addition, a viral load from the initial infection should be greater than 35 cycle threshold values, and 1 or 2 negative PCR results between the 2 episodes is required.6 Unfortunately, viral loads were not obtained; but, because of the temporal relationship of the symptoms and positive COVID-19 tests, a presumptive assumption was made.

Usually, the first infection of the virus activates B-cell maturation and a primed immune system that acts as a robust and rapid response to protect the host from subsequent infections.7 These antibodies can be detected within 10 to 14 days from the onset of symptoms, but those with a mild form of COVID-19 may have low or undetectable titers.8 Nonhuman primates with a robust humoral immunity consisting of antireceptor-binding domain antibodies were shown to be protected from reinfection. The effectiveness of these neutralizing antibodies can predict disease severity, mortality rate, and reinfection rate.9 The primed immune responses could possibly have a similar effectiveness in preventing the onset of both reinfections and relapses. However, some reports have indicated that patients with antibodies can still develop COVID-19 reinfection.10 Theories and pathogenesis are unclear on the severity of the COVID-19 relapse symptoms and disease course in comparison to the initial infection. Mild reinfections have been explained by the priming of the immune system with a robust and rapid B-cell maturation.6,7 On the other hand, a severe disease course may develop through antibody-dependent enhancement, which is when a virus–antibody immunocomplex binds to cells with a complement or Fc receptor that activates viral cell uptake.2

In the literature, there are previous cases indicating COVID-19 relapses and reinfections with negative PCR results after the initial infection. However, none of these patients had a history of immunosuppression along with negative COVID-19 antibodies.11 Furthermore, 1 case illustrated a patient with mantle cell lymphoma who received rituximab and then had a prolonged course of COVID-19 with persistently positive PCR results.12 Our case series is different; both patients had negative COVID-19 PCR results between the 2 periods of infections. In addition, COVID-19 antibodies were measured at a substantially low level, which indicated a negative immune response. Our 2 cases share similarities; they both have a chronic disease process (mantle cell lymphoma and multiple sclerosis) and recently received rituximab infusions 1 month prior to the initial COVID-19 infection. It is important to note that the first patient received convalescent plasma, which is used to instigate the formation of COVID-19 antibodies.13 However, 2 doses of this treatment method did not result in a detectable amount of antibodies.

Rituximab, a chimeric murine/human anti-CD20 monoclonal antibody that remains in the blood for months after administration, is a likely link between these 2 patients not being able to produce an immune response against COVID-19. The proposed pathogenesis of rituximab eliminating B cells includes complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and stimulation of the apoptotic pathway.14 Therefore, rituximab alters the function of circulating antibodies and memory B lymphocytes.15 The effect of immunosuppression has been proposed to be a risk factor for reinfection, relapse, and a prolonged disease course of COVID-19. However, it also may be protective against severe disease by stunting an overstimulated immune system.2,16 A study on Syrian hamsters showed that the absence of functional B and T cells led to an exaggerated early disease course, decreased viral clearance, and more severe outcomes.17

Because our patients did not receive rituximab directly before their relapse, it must be considered whether the underlying immune process is truly the common factor. Genome sequencing was unable to be done in these patients; thus, we cannot indicate definitively whether these are relapsing or reinfections of COVID-19. Current studies are being conducted to determine an effective treatment regimen for COVID-19 patients. Remdesivir has been shown to decrease viral RNA proliferation; thus, it also shortens the needed recovery time, but it was only evaluated in immunocompetent patients.16 Convalescent plasma may be beneficial in patients who cannot produce antibodies on their own.13,16 In addition, the rituximab-induced B-cell depletion may decrease the effectiveness of the vaccine. Therefore, the vaccine’s initial dosages and boosters should be given before receiving rituximab infusions to allow for a successful B-cell response.18 The current data indicate that antibodies persist for 6 months after being vaccinated, and 8 months after developing a COVID-19 infection.19–22 However, as previously illustrated, immunocompromised patients are at risk for not developing a robust immune response to COVID-19 infections; thus, it must be evaluated whether they are capable of developing an adequate response to the vaccine. Further randomized controlled trials should be conducted to recommend a specific treatment regimen in immunosuppressed patients with an underlying disease or with conditions for which they are taking medication.

CONCLUSION

Relapsing COVID-19 infections are rare, but could be more likely in immunosuppressed patients and more severe than the initial infection. Our case series, in which both patients had immunosuppressive diseases and medications, indicates that further studies should be performed to determine the pathogenesis behind this disease course. Moreover, these patients should receive the vaccine before their scheduled rituximab infusion. In this way, they can mount an appropriate antibody response to the vaccine as well as receive treatment to keep their immunosuppressive disease in control. v

Disclosure Statement

The author(s) have no conflicts of interest to disclose.

Financial Support

No funding support was received.

Author Affiliations

1Department of Internal Medicine, Michigan State University, Sparrow Hospital, Lansing, MI

Corresponding Author

Rohan Prasad, DO (rohanmaprasad@gmail.com)

Author Contributions

Rohan M Prasad, DO, wrote the Discussion, conducted the literature review, edited the final draft, and worked on reviewer comments. Shaurya Srivastava, DO, wrote case narrative 1, conducted the literature review, edited the final draft, worked on reviewer comments, and made the timeline figures. Enhua Wang, MD, wrote case narrative 2, conducted the literature review, edited the final draft, and worked on reviewer comments. Jason Z Liu, DO, conducted the literature review, obtained figures, and helped with writing all sections of the manuscript. Rakesh Gami, MD, conducted the literature review, wrote the Introduction, and helped with writing all sections of the manuscript. Ayat Abdelgadir, MD, wrote the abstract, constructed Table 1, and edited final draft. Akhil Sharma, OD, wrote the Conclusion, constructed Table 2, and edited the final draft. Sumugdha Rayamajhi, MD, and Richa Tikaria, MD, assisted in constructing the final draft.

References

1. World Health Organization. Rolling updates on coronavirus disease (COVID-19). 2020. Accessed February 16, 2021 https://www.who.int/emergencies/diseases/novel-coronavirus-2019/events-as-they-happen. Accessed February 16, 2021.

2. Moore JL, Ganapathiraju PV, Kurtz CP, Wainscoat B. A 63-year-old woman with a history of non-Hodgkin lymphoma with persistent SARS-CoV-2 infection who was seronegative and treated with convalescent plasma. Am J Case Rep 2020 Oct;21:e927812:1–5. DOI: https://doi.org/10.12659/AJCR.927812

3. Riley DS, Barber MS, Kienle GS, et al. CARE 2013 explanation and elaborations: Reporting guidelines for case reports. JClinEpi 2017 Sep;89:218–35. DOI: 10.1016/jclinepi.2017.04.026

4. Tomassini S, Kotecha D, Bird PW, Folwell A, Biju S, Tang JW. Setting the criteria for SARS-CoV-2 reinfection: Six possible cases. J Infect 2021 Feb;82(2):282–327. DOI: https://doi.org/10.1016/j.jinf.2020.08.011

5. Mulder M, van der Vegt DSJM, Oude Munnink BB, et al. Reinfection of SARS-CoV-2 in an immunocompromised patient: A case report. Clin Infect Dis 2020 Oct;ciaa1538:1–2. DOI: https://doi.org/10.1093/cid/ciaa1538

6. Yahav D, Yelin D, Eckerle I, et al. Definitions for coronavirus 2019 reinfection, relapse and PCR re-positivity. Clin Microbiol Infect 2021;27(3):315–318. DOI: https://doi.org/10.1016/j.cmi.2020.11.028

7. To KKW, Hung IFN, Chan KH, et al. Serum antibody profile with COVID-19 reinfection. Clin Infect Dis 2021;72(10):e659–e662. DOI: https://doi.org/10.1093/cid/ciaa1368

8. Zhao J, Yuan Q, Wang H, et al. Antibody responses to SARS- CoV-2 in patients of novel coronavirus disease 2019. Clin Infect Dis 2020 Nov;71(16):2027–34. DOI: https://doi.org/10.1093/cid/ciaa344

9. Garcia-Beltran WF, Lam EC, Astudillo MG, et al. COVID-19-neutralizing antibodies predict disease severity and survival. Cell 2021 Jan;184(2):476–488.e11. DOI: https://doi.org/10.1016/j.cell.2020.12.015

10. Iwasaki A. What reinfections mean for COVID-19. Lancet Infect Dis 2021 Jan;21(1):3–5. DOI: https://doi.org/10.1016/S1473-3099(20)30783-0

11. Osman AA, Al Daajani MM, Alsahafi AJ. Re-positive coronavirus disease 2019 PCR test: Could it be a reinfection? New Microbes New Infect 2020 Sep;37:100748:1–6. DOI: https://doi.org/10.1016/j.nmni.2020.100748

12. Baang JH, Smith C, Mirabelli C, et al. Prolonged SARS-CoV-2 replication in an immunocompromised patient. J Infect Dis 2021 223(1):23–7. DOI: https://doi.org/10.1093/infdis/jiaa666

13. Donato ML, Park S, Baker M, et al. Clinical and laboratory evaluation of patients with SARS-CoV-2 pneumonia treated with high-titer convalescent plasma. JCI Insight 2021 Mar;6(6):143196:1–12. DOI: https://doi.org/10.1172/jci.insight.143196

14. Pescovitz MD. Rituximab, an anti-CD20 monoclonal antibody: History and mechanism of action. Am J Transplant 2006 May;6(5):859–66. DOI: https://doi.org/10.1111/j.1600-6143.2006.01288.x

15. Daniel P, Raad M, Waked R, Choucair J, Riachy M, Haddad F. COVID-19 in a patient treated for granulomatosis with polyangiitis: Persistent viral shedding with no cytokine storm. Eur J Case Rep Intern Med 2020 Sep;7(10):001922:1–4. DOI: https://doi.org/10.12890/2020_001922

16. Malsy J, Veletzky L, Heide J, et al. Sustained response after remdesivir and convalescent plasma therapy in a B-cell depleted patient with protracted COVID-19. Clin Infect Dis 2020 Oct:ciaa1637:1–5. DOI: https://doi.org/10.1093/cid/ciaa1637.

17. Brocato RL, Principe LM, Kim RK, et al. Disruption of adaptive immunity enhances disease in SARS-CoV-2-infected Syrian hamsters. J Virol 2020 Oct;94(22):e01683–20. DOI: https://doi.org/10.1128/JVI.01683-20

18. Guilpain P, Bihan CL, Foulongne V, et al. Rituximab for granulomatosis with polyangiitis in the pandemic of COVID-19: Lessons from a case with severe pneumonia. Ann Rheum Dis 2020 80(1):1–2. DOI: https://doi.org/10.1136/annrheumdis-2020-217549

19. Gaebler C, Wang Z, Lorenzi JCC, et al. Evolution of antibody immunity to SARS-CoV-2. Nature 2021 Mar;591(7851):639–44. DOI: https://doi.org/10.1038/s41586-021-03207-w

20. Dan JM, Mateus J, Kato Y, et al. Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection. Science 2021 Feb;371(6529):eabf4063:1–13. DOI: https://doi.org/10.1126/science.abf4063

21. Choe PG, Kim KH, Kang CK, et al. Antibody responses 8 months after asymptomatic or mild SARS-CoV-2 infection. Emerg Infect Dis 2021 Mar;27(3):928–31. DOI: https://doi.org/10.3201/eid2703.204543

22. Doria-Rose N, Suthar MS, Makowski M, et al. Antibody persistence through 6 months after the second dose of mRNA-1273 vaccine for COVID-19. N Engl J Med 2021 Jun;384(23):2259–61. DOI: https://doi.org/10.1056/NEJMc2103916

Keywords: COVID-19, mantle cell lymphoma, multiple sclerosis, rituximab, antibodies

Date

Subjective and objective

Diagnostic testing

Interventions

1/18/21

The patient reports 1 wk of shortness of breath, productive cough, and recurrent fevers.

White blood cells 12 ´ 103 cells/mL

Neutrophils, 94.4%

C-reactive protein, 8.9 mg/dL

Lactic, 1.9 mmol/L

Procalcitonin, 0.16 ng/mL

Ferritin, 1078 ng/mL

Lactate dehydrogenase, 553 U/L

D-dimer, 20.26 mg {FEU}/mL

COVID-19 PCR, positive ´ 2

COVID-19 antibodies, < 3.8

Urine analysis

Blood culture, no growth ´ 2

Chlamydia pneumonia PCR, negative

Mycoplasma pneumonia PCR, negative

Legionella pneumonia PCR, negative

Streptococcus pneumonia urine antigen, negative

Legionella urine antigen, negative

Methicillin-resistant Staphylococcus aureus PCR, negative

Influenza A and B direct antigens, negative

Adenovirus PCR, negative

Parainfluenza 1–4 PCR, negative

Metapneumovirus PCR, negative

Respiratory syncytial virus PCR, negative

Chest x-ray, bilateral pulmonary infiltrates

Computed tomographic angiography of the chest, acute pulmonary emboli and bilateral ground-glass infiltrates

Convalescent plasma was given.

Started heparin drip,

Started cefepime for 7 d.

Infectious disease was consulted.

1/20/21

The patient reports shortness of breath with any movement.

None

Oxygen requirements are increasing.

Consulted pulmonology.

Stopped heparin drip and started daily therapeutic enoxaparin.

1/23/21

The patient has one episode of bloody sputum.

Chest x-ray, right-side pneumothorax and mild vascular congestion

Right chest tube placed.

1/27/21

None

Chest x-ray, new left-side pneumothorax and increasing bilateral infiltrates

COVID-19 antibodies, < 3.8

Transferred to the intensive care unit.

The patient was intubated.

Sedated on fentanyl drip.

Started on norepinephrine and vasopressin drips.

Convalescent plasma was given.

Left chest tube placed.

2/1/21

The patient is agitated and dyssynchronous with the vent.

None

Started cisatracurium drip.

Vasopressors stopped.

2/4/21

Code blue is called for cardiac arrest.

Pulseless electrical activity

Post-code chest x-ray, no new or worsening pneumothoraces

Received 2 rounds of cardiopulmonary resuscitation.

Received 2wo doses of epinephrine, 1 of bicarbonate, and 1 g of calcium chloride.

Return of spontaneous circulation achieved after 6 min.

2/7/21

The patient is not passing spontaneous breathing trials and persistently requires maximum levels of ventilator support.

COVID-19 PCR, negative ´ 2

Tracheostomy performed.

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