Torrey v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS No. 18-807V Filed: August 26, 2026

* * * * * * * * * * * * * * * SUSAN V. TORREY, *

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Petitioner, *

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v. *

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SECRETARY OF HEALTH * AND HUMAN SERVICES, *

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Respondent. *

* * * * * * * * * * * * * * * Nancy R. Meyers, Esq., Turning Point Litigation, Greensboro, N.C., for petitioner. Mallori B. Openchowski, Esq., U.S. Department of Justice, Washington, D.C., for respondent.

DECISION 1 Roth, Special Master:

On June 7, 2018, Susan Torrey (“petitioner”) filed a petition pursuant to the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10 et seq. 2 (“Vaccine Act” or “the Program”). Petitioner alleged that she suffered from Guillain-Barré Syndrome (“GBS”) as the result of the Prevnar 13 pneumonia (“Prevnar” or “Prevnar 13”) vaccine she received on July 20, 2015. Petition, ECF No. 1. Respondent argued that this case is not appropriate for compensation under the terms of the Act. ECF No. 14 at 1.

After carefully analyzing and weighing the evidence presented in accordance with the applicable legal standards, the undersigned finds that petitioner failed to provide preponderant evidence that her Prevnar 13 vaccine played a role in her development of GBS. Thus, petitioner has failed to satisfy her burden of proof under Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1280 (Fed. Cir. 2005).

I. Issues to be Determined

Petitioner’s diagnosis of GBS is undisputed. The issue is whether petitioner provided preponderant evidence to satisfy all three Althen Prongs. Petitioner’s Motion for Ruling on the Record (“Motion”) at 5; Respondent’s Response (“Response”) at 13.

II. Background

A. Procedural History

The petition was filed on June 7, 2018, along with petitioner’s affidavit and medical records. Petitioner’s Exhibits (“Pet. Ex.”) 1-7, ECF No. 1. It was assigned to the undersigned the next day. ECF No. 4.

Respondent filed his Rule 4(c) Report on April 18, 2019, recommending against compensation. ECF No. 14.

Petitioner filed expert reports and medical literature on October 31, 2019, January 31, 2020, June 12, 2020, February 4, 2021, May 7, 2021, July 16, 2021, July 23, 2021, January 31, 2022, and February 2, 2022. Pet. Ex. 8-68, ECF Nos. 20, 24, 27, 36, 39, 44-45, 51-52. Respondent filed his expert reports and medical literature on March 4, 2020, August 14, 2020, April 8, 2021, September 14, 2021, and May 1, 2023. Respondent’s Exhibits (“Resp. Ex.”) A-L, ECF Nos. 25, 28, 38, 49, 65.

An entitlement hearing was initially scheduled for March 7 and 8, 2023 then rescheduled for March 23 and 24, 2023. ECF Nos. 48, 55. During the pre-hearing conference on January 30, 2023, petitioner advised that, given the number of expert reports filed, she preferred to file a Motion for Ruling on the Record and requested that the upcoming hearing be cancelled. ECF No. 62.

Petitioner filed a Motion for Ruling on the Record on August 29, 2023. Motion, ECF No. 67. Respondent filed his Response on February 15, 2024. Response, ECF No. 70. Petitioner filed a Reply on April 10, 2024. Reply, ECF No. 74.

The matter is ripe for adjudication.

B. Medical History Prior to the Prevnar 13 Vaccine

Petitioner has a significant medical history including but not limited to hypertension, gout, hyperlipidemia, chronic obstructive pulmonary disease (“COPD”), and chronic hypoxic respiratory failure. Pet. Ex. 3 at 7, 10.

Petitioner presented to her primary care physician (“PCP”) on July 13, 2015 with complaints of no energy, being tired all the time, waking 3-4 times a night, and her eyes being swollen shut in the morning. Pet. Ex. 2 at 19. Her oxygen saturation level was at 56-62%, breath sounds were down, and respiration was at 110. She was sent to the emergency room (“ER”). Id.

Upon presentation to the ER, petitioner reported 6 months of progressive weakness and shortness of breath. Her shortness of breath had worsened over the past 4-5 days. “She was found to have acute on (sic) chronic respiratory failure from COPD and [congestive heart failure], as well as community acquired pneumonia.” Pet. Ex. 1 at 5. Petitioner was deemed a “critically ill patient” and admitted. Id. at 14. More specifically, her acute respiratory failure was “[l]ikely multifactorial, related to undiagnosed but longstanding COPD with acute exacerbation, possibly pulmonary [hypertension], fluid overload from heart failure, and community acquired pneumonia.” Continuous bipap was required. Id. at 5. She reported increasing fatigue over the past 4 months to the point of having to sleep or lay down most of the day, with overall decreased strength and inability to sustain any energy. Id. at 78-79. The past three days were much worse. She had a daily cough that was sometimes productive, which she attributed to smoking. Her oxygen saturation at her PCP’s visit that morning was 60%, and she was sent to the ER via ambulance. Azithromycin, 3 ceftriaxone, 4 methylprednisone, Lasix, 5 and nebulizer treatments were administered in the ER. Id. at 79. Petitioner’s initial chest x-ray revealed right posterior basilar infiltrate possibly from pneumonia or aspiration. Id. at 30. Continued short-term follow up x-rays with appropriate treatment was recommended to ensure clearing or establish chronicity. Id. CT angiography revealed “[h]eterogeneous density in the right lower lobe consistent with pneumonia. Minimal patchy densities in left lower lobe and in the right middle lobe also concerning for pneumonia. Query potential aspiration as etiology. . . Moderate right pleural effusion. Small left pleural effusion . . . No pulmonary emboli.” Id. at 29.

A follow up chest x-ray on July 15, 2015 revealed slight progression of right lower lobe pneumonia now with blunting of the CP angle consistent with a small pleural effusion. Pet. Ex. 1 at 30-31. Chest x-ray on July 16 revealed hyperinflated lungs, with bibasilar atelectasis 6/infiltrate asymmetrically more pronounced on the right. Id. at 31. Chest x-ray on July 18 was unchanged with both lungs hyperinflated suggestive of emphysema and respiratory bronchiolitis. 7 Pet. Ex. 6 at 23. Chest x-ray on July 19 revealed “[m]ild central bronchitis or reactive airway disease. Small- to-moderate right and trace left pleural effusions with bibasilar compressive and subsegmental atelectasis.” Id. at 22.

Petitioner’s initial blood work when admitted on July 13, 2015 showed a normal white blood cell (“WBC”) count, but then increased to 18.6 [reference range of 4.5-11.0] on July 16, 2015 with “toxic granulation occasional hypersegmented neutrophils occasional.” 8 Pet. Ex. 1 at 51-58, 74, 80. The record included that petitioner was “certainly critically ill even though she does not feel like this.” Id. at 21. CT revealed right and left lower lobe and right middle lobe infiltrates “consistent with probable multilobar pneumonia,” as well as moderate right pleural effusion and small left pleural effusion. Multifocal pneumonia raised concern for “possible endocarditis.” Id. The diagnostic impression included multilobar pneumonia, “community-acquired versus aspiration, acute.” Id. at 22. On July 20, 2015, the hospitalist wrote, “Pneumonia. Completed course w/abx (antibiotics).” Id. at 100. She was given the subject Prevnar 13 vaccination at discharge along with prescriptions for Spiriva and Symbicort. Id. at 7-8. The discharge diagnoses included community-acquired pneumonia and acute and chronic respiratory failure. Id. at 5.

C. Medical History After the Prevnar 13 Vaccine

On August 3, 2015, fourteen days post-vaccination, petitioner presented to the ER with muscle cramping, “rubber legs,” “skin crawling,” and insomnia since her discharge from the hospital. On that day, she also had left lateral chest and right mid back cramping intermittently lasting 5-10 seconds. Pet. Ex. 7 at 70. Her symptoms were suspected to be related to new medications prescribed during her hospitalization. She was discharged home with a prescription for Ativan to help with insomnia. Id. at 72, 75-76.

Petitioner presented to her PCP on August 4, 2015. She reported that she felt okay after being discharged from the hospital, but 6 days ago she began to feel bad, was not sleeping, felt like her skin was crawling, her legs were like rubber, and she had multiple falls. She went to the ER, had multiple tests, and was told it was likely from the Spiriva. She was given Ativan which did not help. Pet. Ex. 2 at 18. She reported that she was not using the Proair because she could not figure out how to use the machine. She was prescribed Valium for sleep and advised to consult a pulmonologist, continue using her walker for fall prevention, and use Spiriva for difficulty breathing. She was also to remain on oxygen. Id.

The PCP added a note to the record on August 5, 2015, that petitioner reported that she did not sleep well with Valium. The nurse practitioner noted that Spiriva has some “funky” side effects, she may need prednisone for her breathing, and she will need physical therapy for her legs if she does not improve. She was to try two Valium that night. Pet. Ex. 2 at 18.

Petitioner presented to the ER on August 7, 2015, reporting chronic diffuse myalgia, bilateral leg swelling that was worsening, dizziness, insomnia, frequent falls, and right knee pain. Onset of leg swelling was noted as “chronic.” Pet. Ex. 7 at 63, 67. Laboratory results were normal. Id. at 65-67. Chest x-ray revealed no acute disease process. She declined admission due to concerns over insurance coverage. She was discharged home with a prescription for Lyrica. Id. at 67.

Petitioner returned to the ER later that day and was admitted with body pain, bilateral leg weakness, and worsening leg symptoms. The record noted that she perceived numbness and tingling as body pain and was using increased doses of narcotics for this. Pet. Ex. 3 at 3, 6. She was noted to be a “confusing historian” but consistently complained of skin crawling and 9/10 aching all over without pain medication. The only thing that helped was a hot bath. Her PCP had recommended Valium for sleep which did not work. She was exhausted. Id. at 6. She believed the inhalers she was prescribed were causing the problem and stopped taking them all. Id. She appeared uncomfortable and confused at times after being given Dilaudid. Id. at 7. The etiology of her complaints was unclear but potentially related to the effects of new medications versus dehydration versus some other neurological or demyelinating process. Id. at 9. All medications were withheld but for Lisinopril. Id. Physical and occupational therapy evaluations were done for fall prevention. Norco and Dilaudid for pain were ordered. Azithromycin was administered in the ER for right lobe chest x-ray findings but discontinued because of low suspicion of pneumonia at that time. She had acute kidney disease and hyponatremia. 9 Id.

A neurological consultation on August 8, 2015 noted her recent hospitalization with acute hypoxic respiratory failure, COPD, and community acquired pneumonia treated with antibiotics and diuretics. She required portable oxygen. Her husband reported that after her discharge she was able to run errands the following days. But at some point in the past few weeks, she had pain in her torso and legs that interfered with her sleep. The leg weakness began sometime last week and progressed. She needed a walker and assistance, then needed to crawl. Now she can’t crawl and has some weakness in her arms. However, petitioner stated that her arm strength was “pretty good.” Pet. Ex. 3 at 10. She reported some “crawling paresthesias” in her fingertips and feet. Touch to her feet and hands induced prickling or a tingling sensation. She had no bladder issues but took medication for constipation. Her history of type 2 diabetes was noted. Id. The impression following history and examination was subacute evolving weakness with pain and less prominent paresthesias in her feet and fingertips consistent with GBS. Id. at 13. Reflexes were absent in her legs, hypoactive in her arms, and absent in the left bicep. There was generalized weakness in all four extremities proximally, worse in her legs than her arms with minimal sensory impairment in her feet. She also had weakness on the left side of her face. Brain MRI and lumbar puncture (“LP”) were ordered. Id. The neurologist noted recent community-acquired pneumonia and chronic respiratory failure likely from chronic obstructive pulmonary disease. Id.

The brain MRI was normal. The LP revealed elevated protein levels consistent with GBS, and a five-day course of IVIG was started. Pet. Ex. 3 at 2-16, 34-36, 54, 63, 69. A chest x-ray showed mild interstitial densities consistent with atelectasis or pneumonitis. 10 Id. at 32. Lab work revealed borderline mycoplasma pneumonia 11 IgG antibodies at 0.316 12 [reference range <0.100] and mycoplasma pneumonia IgM levels at 0.060 [reference range <0.770]. 13 Id. at 54. Lower extremity doppler revealed chronic deep venous thrombosis on the right. Id. at 3, 31. Her symptoms progressed to where she was unable to move her legs but upon discharge could wiggle her toes and flex her ankles. Id. at 3. She had weakness in the upper extremities but could use them. Id. The discharge diagnoses included but were not limited to GBS status post-IVIG, acute chronic pain and anxiety, hypokalemia, acute kidney injury, COPD, chronic respiratory failure, diastolic heart failure, and type 2 diabetes. Id. at 2.

Petitioner was discharged to inpatient rehabilitation from September 11, 2015 through September 24, 2015. She improved significantly and was independent with self-care with the exception of needing standby assistance with showering. She used contact guard assistance and front-wheeled walker for kitchen and laundry activities. She was independent with bed transfers and mobility, was ambulating up to 200 feet with a front wheeled walker and standby assistance, fatigued rapidly and had 4/5 strength in her quadriceps upon discharge. She required assistance with stairs. Pet. Ex. 3 at 70, 72. She continued to need oxygen by nasal canula. Id. at 73. The impression included clinically improved GBS. Id. at 71. She was to continue PT as outpatient. Id. at 70.

Petitioner reported continued improvement at a follow up neurology visit on October 13, 2015, and not needing her walker on some days. Pet. Ex. 4 at 6. She continued to have severe peripheral neuropathic pain. Id. at 8. She was going to physical therapy. Examination revealed ongoing bilateral basilar crackles, so she was sent for chest x-ray to identify whether this was a continuing problem with pneumonia or pleural effusions. No acute disease was demonstrated. Id. at 8, 10. She complained of significant fatigue while taking Gabapentin. The dose was reduced. Id. at 8.

Petitioner presented for recheck on October 27, 2015. She was attending outpatient physical therapy, had improved strength, was using a walker only for long distance mobility in public, and was driving but complained of some knee and calf discomfort. She still required oxygen by nasal cannular. Pet. Ex. 5 at 2.

Petitioner presented to Dr. Jackson, the pulmonologist, on November 18, 2015. She was on full-time oxygen for COPD and was using Spiriva daily but had not needed albuterol. Her oxygen levels at home measured in the 80s while off oxygen. Pet. Ex. 6 at 12. The assessment was severe COPD. Id. at 13. She reported being hesitant about future immunizations after suffering GBS two months after receipt of a standard pneumovax vaccine. Spiriva was to continue. Id. at 14.

Petitioner presented to her PCP on November 30, 2015 without oxygen or her walker. Her gait was “reasonably normal.” She was to be seen by cardiology every three months and the pulmonologist wanted her on round-the-clock oxygen. She did not want to do either. Pet. Ex. 2 at 14.

About four months later, on March 21, 2016, petitioner returned to Dr. Jackson. She was finishing pulmonary rehabilitation later that week but still required oxygen. She reported that either the physical or respiratory therapist told her she never had significant COPD and that her “respiratory troubles” were all GBS-related. Dr. Jackson advised petitioner that her original hospitalization prior to developing GBS was due to respiratory failure from COPD. Pet. Ex. 6 at 9-10.

Petitioner complained to her PCP on April 29, 2016 that she was frustrated claiming that she did not have lung or heart problems prior to suffering GBS and was now impaired. Pet. Ex. 7 at 39.

She presented to the neurologist for follow up on May 3, 2016 with “dramatic improvement in weakness and walking” and was able to function independently. She still had some shortness of breath and fatigability but no longer used a walker. The record included that “[s]he did receive a pneumonia vaccination prior to her discharge in Nampa, which has been attributed to the cause of her GBS although there has been some question of whether the GBS may have started sooner.” 14 Pet. Ex. 4 at 3. The impression was that she was improving with symptoms now isolated to her feet, and she had the potential for continued improvement “as long as 1-1/2 to 2 years after [AIDP] . . . In terms of her lung capacity etc., I am not certain if there will be any further improvement of the deficits related to [AIDP]”. Id. at 4. She was doing water aerobics. Id. at 3. Further improvement in paresthesias in her legs may result in further weaning of gabapentin. Id. at 4.

By June 21, 2016, when petitioner presented for her Medicare wellness examination, she reported improvement in strength and stamina since GBS diagnosis. She was doing water aerobics three times weekly. She required oxygen daily. Pet. Ex. 7 at 28. Her examination was essentially normal. Id. at 31-32. The assessment included chronic conditions of essential hypertension, chronic congestive heart failure, COPD mixed type, and dyslipidemia. Id. at 33. She had no falls in the past year and no problems with walking or balance. Id. The assessment and plan no longer included GBS. Id. at 28-33. Her subsequent visits for her chronic conditions did not include GBS or Gabapentin. Pet. Ex. 6 at 6; Pet. Ex. 7 at 22, 26-27, 16, 19-20, 11, 14.

At an October 16, 2017 visit with Dr. Jackson, she reported doing yard work instead of water aerobics for activity. Her functional status was good with some dyspnea with strenuous exertion but no chest discomfort or leg swelling. She had been clinically stable for the past year. The assessment was chronic respiratory failure with hypoxia and COPD. Pet. Ex. 6 at 4.

She was subsequently noted to have decreased hearing bilaterally and a two-week history of left shoulder pain. Pet. Ex. 7 at 4. She was referred to orthopedics for her shoulder complaints and cardiology for heart failure. Id. at 8-10.

More recent records include monoarticular arthritis since she was 19 years old with progression over the past few years. Pet. Ex. 69 at 5. She had gout, exacerbations of COPD with chronic bronchitis and emphysema, required hospitalizations, had congestive heart failure, hypertension, chronic respiratory failure with hypoxia, pulmonary nodule, chronic kidney disease, daytime sleepiness, dependence on enabling machines and devices, eosinophilia, glucose intolerance, history of nicotine dependence, and pulmonary hypertension. Id. at 7; Pet. Ex. 71 at 8; Pet. Ex. 72 at 11, 15; Pet. Ex. 73 at 8. She also has degenerative osteoarthritis in multiple sites. Pet. Ex. 69 at 12. She had GBS “thought to have been associated with Pneumovax.” Id. at 20.

D. Petitioner’s Affidavit Petitioner’s affidavit was filed along with her petition affirming that her symptoms lasted more than six months and that she had not filed a civil action or received any award or judgment arising from her vaccine related injury. ECF No. 1.

III. Expert Opinions Explanation of certain medical terms is required for better understanding of the experts’ opinions. This case involves that the Prevnar 13 vaccine, which protects against pneumonia and disease caused by Streptococcus pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, and 23F. Pet. Ex. 13.

Streptococcus is a genus of gram-positive, homofermentative lactic acid bacteria of the family Streptococcaceae, consisting of nonmotile, non–spore-forming cocci occurring in pairs or chains. Streptococcus pneumoniae is the species of Streptococcus known as pneumococcus. It is the usual cause of lobar pneumonia, a type of acute bacterial pneumonia with abundant edema usually limited to just one lobe of a lung, which also causes other serious, acute, pyogenic disorders such as meningitis, septicemia, empyema, and peritonitis. Dorland’s at 1448, 1451-52, 1753.

Mycoplasma is a genus of bacteria of the family Mycoplasmataceae, made up of round, highly pleomorphic, gram-negative cells that are bounded by a single triple-layered membrane and lack a true cell wall. Mycoplasma pneumoniae is a species of Mycoplasma that often causes inapparent infections or mild respiratory tract disease but can also cause mycoplasma pneumonia, the most common form of primary atypical pneumonia. Dorland’s at 1199-1200, 1451.

The Prevnar 13 vaccination does not protect against Mycoplasma pneumoniae. Pet. Ex. 13.

A. Petitioner’s Expert, Dr. Steinman 15

Dr. Steinman issued seven expert reports. Pet. Ex. 8; Pet. Ex. 33; Pet. Ex. 38; Pet. Ex. 54; Pet. Ex. 55; Pet. Ex. 59; Pet. Ex. 66. In summarizing petitioner’s medical history, he included type 2 diabetes that was under control, chronic obstructive pulmonary disease, and community acquired pneumonia of unknown etiology prior to receipt of the Prevnar vaccine. Pet. Ex. 8 at 5-6; Pet. Ex. 3 at 7, 10.

He explained that GBS is where the immune system destroys the myelin sheath that surrounds the axons of peripheral nerves or the axons themselves. Pet. Ex. 8 at 6; Pet. Ex. 11.

He included the composition of the Prevnar 13 vaccine which contains antigens of streptococcus pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, and 23F, each linked to a non-toxic diphtheria CRM197 protein. Pet. Ex. 33 at 7-8. He wrote that the “Prevnar 13 vaccine does not resemble pneumococcus” 16 but rather “is a brilliant creation of medical science where 13 pneumococcal sugars are bound to a protein carrier, known as CRM197, [which is] only one amino acid differen[t] from diphtheria toxin. The vaccine is formulated in alum to enhance its immunogenicity.” Pet. Ex. 59 at 2.

i. Prong 1 Dr. Steinman based his theory on molecular mimicry where shared structures on a virus or bacteria or in a vaccine can trigger cross-reaction. Pet. Ex. 8 at 6; Pet. Ex. 33 at 7; Pet. Ex. 12. He identified two molecular mimics relevant to GBS that are present in the Prevnar 13 vaccine. The first is the phospholipid composition of the pneumococcal polysaccharide antigen, specifically phosphoglycerol and phosphocholine molecules. The second is from the CRM protein conjugate. Pet. Ex. 8 at 8, 19; Pet. Ex. 33 at 8, 24; Pet. Ex. 59 at 2.

For the first mimic, Dr. Steinman asserted that peer reviewed literature and his own research indicate that phospholipids make up the majority of the myelin sheath in humans and are targeted by antibodies in neuroinflammation, specifically in GBS. Pet. Ex. 8 at 8; Pet. Ex. 16; Pet. Ex. 18. Ho demonstrated that “phosphoglycerol and phosphocholine are the main targets of the immune attack in individuals with multiple sclerosis” and play a critical role in immunogenicity of the Prevnar 13 vaccine. Pet. Ex. 8 at 8; Pet. Ex. 17; Pet. Ex. 33 at 10; Pet. Ex. 34; Pet. Ex. 36. Chang instructs that a “phospholipid linkage is quite necessary for immunogenicity of [] polysaccharides” in the vaccine, which is how the vaccine induces the desired immune response. Pet. Ex. 33 at 12; Pet. Ex. 35. Gilburd and Nakos found that anti-phospholipid antibodies were present in GBS patients. Pet. Ex. 8 at 8-9; Pet. Ex. 14; Pet. Ex. 15; Pet. Ex. 33 at 14-15; Pet. Ex. 59 at 3. Gilburd studied GBS sera and found 6 out of 16 sera had autoantibodies to one or more of the antibodies studied which included phosphatidyl-ethanolamine, phosphatidyl-choline, and phosphatidyl-serine; 2 of 6 were reactive to phosphatidyl-serine or phosphatidyl-choline. Pet. Ex. 8 at 9; Pet. Ex. 14. Nakos found phospholipid antibodies in patients with GBS. Pet. Ex. 59 at 3-4; Pet. Ex. 15. Barbar and Bryson each showed how the immune system targets phosphoglycerol where X-ray diffraction studies have shown that antibodies can have “exquisite specificity” directed to the polysaccharide component of 23F contained in the Prevnar vaccine that “binds to the phosphate group in the essential phosphoglycerol.” Pet. Ex. 59 at 6-8; Pet. Ex. 60; Pet. Ex. 62. Chuang found that the 19A component of the vaccine contains phosphorylcholine which “plays a key role in the pathophysiology of the pneumonia infection.” Pet. Ex. 8 at 9-10; Pet. Ex. 19; Pet. Ex. 33 at 15. Thus, antibodies to phosphorylcholine produced in response to the Prevnar 13 vaccine could mistakenly target myelin triggering GBS. Pet. Ex. 33 at 15.

Dr. Steinman proposed that the second mimic is CRM197, the protein conjugate in the Prevnar 13 vaccine that mimics contactin-1, a human protein present on the peripheral nerves and “a known target of the immune system in GBS.” Dr. Steinman performed a BLAST search 17 identifying areas of homology between CRM197 and contactin-1. Pet. Ex. 8 at 10, 13-15; Pet. Ex. 33 at 16-23; Pet. Ex. 38 at 7; Pet. Ex. 59 at 9. He then used the Immune Epitope Database (“IEDB”) to evaluate whether the sequences found during the BLAST search have been described in humans. Pet. Ex. 8 at 16-17. Dr. Steinman identified sequences that are “recognized by human immune cells.” Pet. Ex. 38 at 4.

Based on his own experimental encephalomyelitis (“EAE”) studies in mice (Gautam I, Gautam II, and Gautam III), Dr. Steinman maintained that 5 of 12 shared amino acids, even if not consecutive, are sufficient to induce neuroinflammation via molecular mimicry. Pet. Ex. 8 at 11- 13; Pet. Ex. 33 at 16-18; Pet. Ex. 25; Pet. Ex. 26; Pet. Ex. 27; Pet. Ex. 59 at 9; Pet. Ex. 63; Pet. Ex. 66 at 4-5; Pet. Ex. 67. He cited Raju which demonstrated that humans mount T cell responses to sequences contained in the diphtheria molecule, which differs from CRM197 by only one amino acid. Pet. Ex. 59 at 9-10; Pet. Ex. 64. He added that the route of administration of an antigen determines whether it will be immunogenic or therapeutic. Myelin protein used in an adjuvant injected subcutaneously is pathogenic and can cause paralysis, while native myelin peptides administered without an adjuvant systemically suppresses paralysis and brain inflammation. Pet. Ex. 38 at 3, 4-5; Pet. Ex. 39.

Dr. Steinman added that the alum contained in the Prevnar vaccine is a contributor to the development of GBS. Pet. Ex. 38 at 4-5; Pet. Ex. 59 at 11. Eisenbarth showed that alum triggers the production of cytokines IL-1 and IL-18. Pet. Ex. 38 at 5; Pet. Ex. 45; Pet. Ex. 46; Pet. Ex. 47. Studies show that IL-1 and IL-18 serum levels are upregulated during active GBS when compared to controls, implicating these cytokines in the pathogenesis of immune-mediated peripheral nervous system demyelination. Pet. Ex. 38 at 5-7; Pet. Ex. 49; Pet. Ex. 50; Pet. Ex. 51. Yu concluded that IL-18 “plays a critical role in the pathogenesis of autoimmune demyelinating disease of the [peripheral nervous system]”. Pet. Ex. 38 at 6; Pet. Ex. 51. Additionally, alum induces Th2 responses with self-antigens and has been shown to be “exceptionally dangerous.” Pet. Ex. 38 at 4-5.

Dr. Steinman cited to articles as associating GBS with S. Pneumococcus and with pneumococcal vaccine. Pet. Ex. 55 at 5-6; Pet. Ex. 56; Pet. Ex. 57. Ravishankar described GBS as a rapid onset of muscle weakness caused by the immune system attacking the peripheral nerves. While the causes remain “elusive,” studies have linked GBS to influenza vaccine, but the authors noted that the “pneumococcal vaccine remains to be studied.” Pet. Ex. 55 at 6; Pet. Ex. 57. Yuki studied Group A beta-hemolytic streptococcus 18 causes of immune-mediated disorders such as rheumatic fever and acute glomerulonephritis, with one patient presenting with Fisher’s Syndrome (“FS”) variant of GBS, “however, the association of FS with group A streptococcal infection was not shown. Some patients may develop FS with group A streptococcal infection, but the bacterium is not a major antecedent agent in FS.” Pet. Ex. 55 at 6; Pet. Ex. 58.

Dr. Steinman acknowledged that epidemiological studies have not shown an increased risk of GBS with pneumococcal vaccines, which is reassuring for vaccine safety but does not rule out Prevnar 13 vaccine as a cause of GBS in some people. Pet. Ex. 8 at 17; Pet. Ex. 33 at 23; Pet. Ex. 59 at 11. Haber discussed ten reports of GBS following Prevnar 13 vaccine and one report of GBS following receipt of Prevnar 13 and influenza vaccines; only one individual had an upper respiratory infection prior to the onset of GBS. Pet. Ex. 59 at 11; Pet. Ex. 65; Pet. Ex. 66 at 3-4.

At the time he issued his reports in this case, Dr. Steinman asserted that his theories had been accepted in two other vaccine cases where Special Master Gowen and Special Master Horner found the petitioners entitled to compensation. Pet. Ex. 66 at 2.

ii. Prong 2 Dr. Steinman concluded that petitioner’s GBS was the result of the Prevnar 13 vaccination. He acknowledged that petitioner suffered from an acute exacerbation of COPD and community- acquired pneumonia just prior to her receipt of the Prevnar 13 vaccination. He acknowledged the capacity for some infections, specifically C. jejuni, EBV (Epstein Barre Virus), and CMV (cytomegalovirus) to induce GBS but argued that since the microbe of petitioner’s infection was not determined, he could not account for an unknown pathogen causing GBS, making the Prevnar 13 vaccine the most “likely culprit” for her GBS. Pet. Ex. 8 at 18, 19; Pet. Ex. 31; Pet. Ex. 33 at 23-24; Pet. Ex. 38 at 2-3; Pet. Ex. 54 at 1-2; Pet. Ex. 55 at 4-5; Pet. Ex. 66 at 2-3. Additionally, he focused on one note in the record where the consulting doctor wrote pneumonia was not likely because petitioner had a normal white cell count, thereby “lowering the weight of this potential factor” in petitioner’s development of GBS. Pet. Ex. 54 at 1; Pet. Ex. 55 at 4; Pet. Ex. 66 at 3. He concluded that “[t]he Prevnar 13 vaccine far outweighs the unknown and only possible pneumonia.” Pet. Ex. 54 at 2.

iii. Prong 3 Dr. Steinman relied on Schoenberger to support onset 10-14 days after vaccination as reasonable. Pet. Ex. 8 at 17, 19; Pet. Ex. 30; Pet. Ex. 33 at 23, 25.

B. Respondent’s Expert, Dr. Fujinami 19

Dr. Fujinami authored five reports. He concluded that Prevnar 13 vaccine cannot cause immune-mediated GBS. Resp. Ex. C at 1; Resp. Ex. L at 2. Dr. Fujinami asserted that the phospholipids phosphatidylserine and phosphatidylcholine 20 are present in the myelin of both the peripheral and central nervous systems. If Dr. Steinman were correct and the Prevnar 13 vaccine generates antibodies against these phospholipids, then the antibodies would cause both central and peripheral nervous system inflammation. Petitioner here only had neuroinflammation and demyelination in the peripheral nervous system. Resp. Ex. C at 3, 5; Resp. Ex. F at 3; Resp. Ex. L at 1.

i. Prong 1 Dr. Fujinami asserted that Gilburd described one GBS patient who had autoantibodies to phosphatidylcholine and phosphatidylserine in serum. However, the authors believed that the “autoantibodies are probably produced as a result of the myelin damage rather than cause the demyelination.” Resp. Ex. C at 3 (emphasis in original); Pet. Ex. 14. Gilburd also concluded that there was no significant association between the presence of specific antiphospholipid antibodies when compared to controls in the study. Resp. Ex. L at 2; Pet. Ex. 14. Therefore, Gilburd does not support petitioner’s theory that autoantibodies to phospholipids are pathogenic. Resp. Ex. C at 3; Resp. Ex. L at 2. Nakos observed that all 9 GBS patients studied developed antiphospholipid antibodies during the course of their disease while none of the controls did, indicating that antiphospholipid antibodies increase with time in GBS patients. Further, Nakos supported the conclusion in Gilburd that the neuroinflammation triggered the production of antiphospholipid antibodies—not the other way around. Resp. Ex. L at 2-3; Pet. Ex. 14; Pet. Ex. 15. Kanter and Wang also found that antiphospholipid antibodies arose after neuroinflammation. Resp. Ex. L at 3; Pet. Ex. 16; Pet. Ex. 18. Dr. Fujinami argued that Dr. Steinman failed to produce any peer- reviewed published articles that support his opinion that these autoantibodies are pathogenic. Resp. Ex. J at 2; Resp. Ex. L at 4. Further, these autoantibodies may be present in individuals without autoimmune disease. Resp. Ex. J at 2.

Dr. Fujinami discussed the structure of the polysaccharide antigen in the Prevnar 13 vaccine. He argued that if Dr. Steinman were correct that there is a mimic in the vaccine that binds to the phosphate component of phospholipids on peripheral myelin, then the “structure should protect against neuroinflammation rather than potentiate neuroinflammation.” Resp. Ex. C at 3; Resp. Ex. L at 1-2. He noted that Ho, a study Dr. Steinman co-authored, involved an EAE model for multiple sclerosis. The mice were treated with a derivative of oxidized phosphatidylcholine, which “unexpectedly reduced the severity of EAE throughout the disease course” by suppressing autoreactive T cell activation. Resp. Ex. C at 3-4; Pet. Ex. 17. Ho distinguished between reactive and nonreactive lipid structures, listing 4 phospholipids as nonreactive, and concluded that “not all phosphate phospholipids react with the anti-phospholipids antibodies.” Resp. Ex. L at 2; Pet. Ex. 17 at 5. Dr. Fujinami pointed out that there is a conflict between the findings in Ho, that phosphatidylcholine could prevent or treat autoimmune diseases, with Dr. Steinman’s theory that the polysaccharide antigen in the Prevnar 13 vaccine could be harmful. Resp. Ex. C at 4.

Dr. Fujinami addressed Dr. Steinman’s second theory involving a mimic between CRM197 in the vaccine and contactin-1 in humans that can cause GBS. Resp. Ex. C at 4. Dr. Fujinami took issue with Dr. Steinman’s use of BLAST searches and IEDB tools “to infer a more likely than not” occurrence. Resp. Ex. L at 4-5. In his own research on molecular mimicry, computer searches are used to compare microbial sequences with “disease inducing sites” in myelin basic protein. These tools are not useful where the “disease inducing site” in GBS is unknown, and it is unknown whether a “disease inducing site” in contactin-1 even exists. Resp. Ex. L at 5. If Dr. Steinman were correct that CRM197, being only one amino acid different from diphtheria toxin, had molecular mimicry with contactin-1 and was capable of causing GBS, then a multitude of vaccinated individuals as described in Raju should develop GBS. Resp. Ex. J at 2; Resp. Ex. L at 5; Pet. Ex. 64. Chen showed “[t]his is clearly not the case.” Resp. Ex. J at 2; Resp. Ex. E Tab 1.

Finally, Dr. Fujinami pointed out that the Prevnar 13 vaccine contains alum, an aluminum phosphate adjuvant, which “favors an immunoregulatory immune response . . . [and is] not considered conducive for an aggressive acute neuroinflammatory immune response, such as is observed in GBS.” Resp. Ex. C at 4; Resp. Ex. F at 2-3; Pet. Ex. 47; Pet. Ex. 48. An injection of alum induces IL-1b, which modulates an immune response towards Th2 and can modulate the effects of IL-18. Resp. Ex. F at 2-3.

Dr. Fujinami discussed the findings of Sicotte and Wallberg which showed that genetically susceptible animals immunized with whole myelin or myelin derived proteins adsorbed to alum did not develop autoimmune neuroinflammation. Resp. Ex. C at 4; Resp. Ex. C Tab 2; Resp. Ex. C Tab 3; Resp. Ex. F at 1-3. In Wallberg, the mice received myelin oligodendrocyte glycoprotein (“MOG”) adsorbed to alum and were protected from EAE; Sicotte found that the animals that received MOG had better axon repair when the spinal cord was damaged. Resp. Ex. C at 4; Resp. Ex. C Tab 2; Resp. Ex. C Tab 3. Similarly, Kuerten & Lehmann compared complete Freund’s adjuvant 21 (“CFA”) with alum in EAE and found that the use of CFA resulted in neuroinflammation and EAE, while use of alum did not induce EAE. Resp. Ex. F at 2-3; Pet. Ex. 41; Pet. Ex. 67; Resp. Ex. L at 4. Applying those findings to this case, Dr. Fujinami explained that the Prevnar 13 vaccine contains glycoconjugates adsorbed to alum, which may be beneficial against the development of autoimmune neuroinflammatory disease rather than causal of neuroinflammation, as Dr. Steinman suggests. Resp. Ex. C at 4; Resp. Ex. F at 2-3.

Further, Dr. Fujinami distinguished receipt of a Prevnar 13 vaccine from the EAE models and multiple sclerosis studies cited by Dr. Steinman. Resp. Ex. F at 1-2. In Pedotti I, Pedotti II, and Kappos, the subjects were given self-peptides that mimic portions of myelin proteins as therapy but developed the Th2 immune response of anaphylaxis or hypersensitivity. Resp. Ex. F at 1-3; Pet. Ex. 42; Pet. Ex. 43; Pet. Ex. 44; Pet. Ex. 50. The critical difference between petitioner’s receipt of the Prevnar vaccination with these three studies is that the studies involved “treatment therapies for already active autoimmune disease, with no reference to disease initiation.” Resp. Ex. F at 2. Dr. Fujinami asserted that Prevnar 13 was used to prevent disease, not treat it. Id.

Dr. Fujinami concluded that no large-scale epidemiological study has found an increased risk of GBS with pneumococcal vaccines, specifically Prevnar 13 vaccine. Resp. Ex. C at 5; Resp. Ex. C Tab 1; Resp. Ex. H at 1-2; Pet. Ex. 28; Pet. Ex. 29. Dr. Steinman relied on case reports associating pneumococcus with GBS to show an association between the Prevnar 13 vaccine and GBS but conceded that “[t]he Prevnar 13 vaccine does not resemble the pneumococcus.” Resp. Ex. J at 2; Pet. Ex. 59 at 2. Dr. Fujinami further added that no studies demonstrate that infection with pneumococcus or Corynebacterium (the source of CRM197 with a single amino acid change) leads to GBS. Resp. Ex. L at 5.

ii. Prong 2 Dr. Fujinami argued that for molecular mimicry to result in clinical autoimmune disease, an active infection is required, and there is nothing live in the Prevnar 13 vaccine. Resp. Ex. L at 4. Dr. Fujinami agreed there are infections known to cause GBS. Hartung found that about two- thirds of GBS patients reported symptoms of a respiratory or gastrointestinal infection 1-4 weeks prior to the onset of GBS symptoms, with c. jejuni, CMV, EBV, and mycoplasma pneumoniae 22 as known precipitants of GBS. Resp. Ex. H at 1-2; Resp. Ex. J at 1; Pet. Ex. 31. Hao studied fourteen infectious pathogens and found that 53% of GBS patients tested positive for recent infections. Resp. Ex. H at 2; Pet. Ex. 31; Resp. Ex. H Tab 2. According to Dr. Fujinami, petitioner “was not tested for mycoplasma pneumonia which is associated with GBS around 5% of the time.” Resp. Ex. H at 2. Nevertheless, it is not necessary to know a microbe’s identity to consider it a possible factor in the development of GBS. Resp. Ex. H at 1; Resp. Ex. J at 1. Dr. Steinman failed to consider that petitioner had a respiratory infection diagnosed as pneumonia which, like the Prevnar 13 vaccine, was in close temporal proximity to the onset of her GBS symptoms. Resp. Ex. J at 1.

C. Respondent’s Expert, Dr. Jamieson 23

Dr. Jamieson issued five reports. She detailed petitioner’s medical course, including petitioner’s visit with the primary care physician on July 13, 2015, hospital admission that same day for acute exacerbation of COPD and acute community-acquired pneumonia, and her receipt of the Prevnar 13 vaccine upon her discharge home on July 20, 2015. Resp. Ex. A at 2-3. Petitioner was admitted to the hospital again on August 7, 2015 with ascending, progressive pain and weakness, ultimately diagnosed as acute inflammatory demyelinating polyradiculoneuropathy (“AIDP”) or GBS based on CSF findings. Id. at 3-4.

Dr. Jamieson described GBS as an autoimmune disorder that is an acute, monophasic illness that causes weakness due to peripheral nerve injury with most patients having a full recovery over weeks to months following treatment and therapy. AIDP is the most common form of GBS in the United States. Resp. Ex. A at 9.

Dr. Jamieson noted that petitioner’s onset of GBS/AIDP symptoms was about a week after her hospitalization for aggravated COPD and community-acquired pneumonia which infection preceded her receipt of the Prevnar 13 vaccine. She was treated and “had total functional recovery . . . within 6 months from the onset of her neurological symptoms due to GBS. By 6 months after the onset of GBS, she no longer had any motor deficit related to the neurological disorder and her ongoing functional impairment was totally related to her pre-existing, unrelated pulmonary disease.” The sensory symptoms in her feet that persisted beyond 6 months “could be related to her diabetes.” Resp. Ex. A at 8, 11-12; Resp. Ex. K at 2. Dr. Jamieson concluded that petitioner’s “current functional impairment is solely the result of her unrelated pulmonary disease.” Resp. Ex. A at 12.

Dr. Jamieson explained that GBS is thought to be the result of an immune reaction to a trigger, most commonly infection but also surgery, trauma, and some vaccinations. Resp. Ex. A at 9. Roughly two-thirds of GBS patients report respiratory or gastrointestinal symptoms within 4 weeks preceding onset of weakness. Resp. Ex. A at 9; Resp. Ex. A Tab 4; Resp. Ex. A Tab 6; Resp. Ex. E at 2-3; Resp. Ex. E Tab 4; Resp. Ex. E Tab 5. Campylobacter jejuni is the most commonly identified precipitant of GBS, but other pathogens like Mycoplasma pneumoniae have also been associated with GBS. Resp. Ex. A at 9; Resp. Ex. A Tab 8. More recently, there have been several published cases of GBS triggered by SARS-CoV-2; thus, C. jejuni, EBV, or CMV are not the only infections that can cause GBS. Resp. Ex. E at 1-2; Resp. Ex. E Tab 2; Resp. Ex. E Tab 3. Hartung noted that in around 60% of infection-caused GBS, the infectious pathogen is unidentified. Thus, even though a specific pathogen was not identified in petitioner, the known respiratory infection “is a much more relevant causative preceding event as compared to the unknown trigger of a Prevnar 13 pneumonia vaccination.” Resp. Ex. G at 1-2; Resp. Ex. G Tab 1; Resp. Ex. I at 1; Resp. Ex. K at 1-2.

Dr. Jamieson discussed the pneumococcal vaccine noting that it has been studied and determined to have no association with GBS. Resp. Ex. A at 10; Resp. Ex. I at 1. Baxter, a retrospective study which included 415 cases between 1995 and 2006, found no association with any vaccination. Resp. Ex. A at 10; Resp. Ex. A Tab 2. Chen found no increased risk of GBS within 180 days after any vaccination or combination of vaccinations. Resp. Ex. E at 1; Resp. Ex. E Tab 1. Tseng studied the risk of adverse events that required medical attention following Prevnar 13 and Prevnar 23 vaccinations and found only 4 cases of GBS among 313,136 Prevnar 13 doses administered. Resp. Ex. A at 10; Resp. Ex. A Tab 1. Haber concluded that there were no disproportionate reports of GBS after Prevnar 13 vaccination based on data from VAERS reports. Resp. Ex. A at 10; Resp. Ex. A Tab 10; Resp. Ex. I at 2-3; Resp. Ex. K at 2. The patient in Ravishankar, unlike petitioner, did not fit the Brighton Collaboration GBS criteria, making the article uninformative on an association between Prevnar 13 and GBS. Resp. Ex. A at 11; Resp. Ex. A Tab 13; Resp. Ex. A Tab 14.

Dr. Jamieson noted that Dr. Steinman acknowledged the lack of epidemiological evidence showing an increased risk of GBS associated with Prevnar 13. He instead relied on Schoenberger– 45-year-old data involving the viral swine flu vaccine—to show that 10-14 days is reasonable for onset of GBS after the bacterial Prevnar 13 vaccine. Resp. Ex. A at 8; Resp. Ex. A Tab 3. Further, Dr. Steinman acknowledged the association between GBS and infection but dismissed petitioner’s preceding pneumonia because she “did not have an infection with Campylobacter, EBV or CMV.” Resp. Ex. A at 8, 9, 11-12; Resp. Ex. E at 1. Dr. Jamieson added that petitioner’s hospitalization prior to her receipt of the Prevnar vaccine was for respiratory failure with acute respiratory infection that required steroids and antibiotics, opining this infection was the likely trigger of petitioner’s neurological symptoms with onset about a week after discharge and eventually diagnosed as GBS. Resp. Ex. E at 2-3; Resp. Ex. G at 2.

Dr. Jamieson further noted that Dr. Steinman cited materials that included the U.S. Patent for Prevnar 13 but then discussed the structural composition and antigenicity of streptococcus pneumonia, not the Prevnar 13 vaccine. No information was provided that indicated any epidemiological linkage between Prevnar 13 vaccine and GBS. Resp. Ex. A at 8. Dr. Jamieson argued that the evidence supports that multiple viral and bacterial pathogens can trigger GBS but not that the Prevnar 13 vaccine is a trigger. Resp. Ex. I at 3.

IV. Parties’ Arguments

A. Petitioner’s Motion for Ruling on the Record and Reply Petitioner relies on Dr. Steinman’s theory that the components of the Prevnar 13 vaccine can and did initiate an autoimmune reaction where antibodies mistakenly attacked and damaged myelin. Motion at 7-8. Dr. Steinman identified two phospholipids in the Prevnar 13 vaccine, glycerophosphate and glycerocholine, that mimicked the phospholipids in petitioner’s myelin. Id. at 15; Reply at 5. Alternatively, he opined that the CRM197 protein conjugate in the vaccine mimicked contactin-1 in petitioner’s peripheral nerves. Id. Dr. Steinman opined that the immune system mistakenly mounted a response to both nerve proteins and vaccine components, resulting in GBS. Id. He used BLAST searches to identify potential mimics and relied on the theory of molecular mimicry, which has been accepted as reliable in vaccine cases for years. Id. at 8, 16 (citations omitted); Reply at 4. Moreover, Dr. Steinman’s theory for Prevnar 13 and GBS has been accepted by several other special masters. Motion at 9; Reply at 4-6; see Gross v. Sec’y of Health & Human Servs., No. 17-1075V, 2022 WL 9669651, at *35-39 (Fed. Cl. Spec. Mstr. Sept. 22, 2022); Maloney v. Sec’y of Health & Human Servs., No. 19-1713V, 2022 WL 1074087, at *30-32 (Fed. Cl. Spec. Mstr. Mar. 17, 2022); Pierson v. Sec’y of Health & Human Servs., No. 17-1136V, 2022 WL 322836, at *27-31 (Fed. Cl. Spec. Mstr. Jan. 19, 2022); Koller v. Sec’y of Health & Human Servs., No. 16-439V, 2021 WL 5027947, at *16-20 (Fed. Cl. Spec. Mstr. Oct. 8, 2021); see also Tracy v. Sec’y of Health & Human Servs., No. 16-213V, 2022 WL 1125281 (Fed. Cl. Spec. Mstr. Mar. 30, 2022) (finding in favor of the petitioners in a Prevnar 13 / transverse myelitis case).

Petitioner argued that she received the Prevar 13 vaccine, developed symptoms 10 days later, and was admitted to the hospital with a diagnosis of GBS. Motion at 18. She argued that Dr. Steinman’s theory explains how the Prevnar 13 vaccine caused an autoimmune inflammatory reaction that culminated in the development of GBS within a medically appropriate accepted timeframe consistent with the theory of molecular mimicry. Id. at 19, 20. Petitioner asserts that her treaters linked her GBS to the Prevnar 13 vaccine. Id. at 19; Reply at 7. “Given the close temporal relationship between Petitioner’s vaccination and the onset of symptoms, combined with the consistent diagnosis of treating doctors and a medical opinion with a plausible theory explaining how the vaccine caused GBS, Petitioner submits that she has far surpassed the required showing under Althen Prong 2.” Motion at 19.

Further, petitioner argued that respondent failed to exclude the Prevnar 13 vaccine as a substantial factor in petitioner’s development of GBS and therefore failed to satisfy his burden in proving alternative cause. Motion at 21-22. To prove alternative cause, respondent submitted that petitioner had “suspected” pneumonia, but Dr. Steinman explained that “there was never a definitive pneumonia diagnosis.” Petitioner argued that “an unknown antigen that was never diagnosed should not be sufficient ‘proof’ to carry Respondent’s burden.” Id. at 22; Reply at 8.

Finally, she argued that respondent’s position is contradictory, on the one hand arguing that petitioner’s “possible pneumonia” was an alternative cause for her GBS while also arguing against petitioner’s causation theory because wild pneumonia bacteria are not associated with GBS. Reply at 8. Respondent cannot have it both ways. Id.

B. Respondent’s Response Respondent argues that petitioner failed to support a causal relationship between the Prevnar 13 vaccine and petitioner’s development of GBS. Response at 1. Further, petitioner failed to satisfy the six-month severity requirement. Id. at 13-14, 29.

Respondent argues that “s. pneumoniae is not an agent that is associated with GBS,” thus it is illogical to conclude that the vaccine, which contains the same polysaccharide components as the bacterium, could cause GBS. Response at 14. Further, Dr. Steinman’s proffered theory was rejected in Trollinger v. Sec’y of Health & Human Servs., No. 16-473V, 2023 WL 2521912 (Fed. Cl. Spec. Mstr. Feb. 17, 2023) and Deshler v. Sec’y of Health & Human Servs., No. 16-1070V, 2020 WL 4593162 (Fed. Cl. Spec. Mstr. July 1, 2020). Dr. Jamieson’s and Dr. Fujinami’s opinions rebut Dr. Steinman’s theories. Id. at 17-25.

Further, respondent summarized petitioner’s hospitalization prior to her onset and diagnosis of GBS for respiratory failure due to chronic COPD, CHF, pulmonary hypertension, and “possible ‘community acquired pneumonia.’” Response at 26. He noted that a CT angiogram of her chest revealed densities consistent with pneumonia. Id. He argued that Dr. Jamieson and Dr. Fujinami extensively discussed the medical records that clearly indicated that petitioner suffered from an upper respiratory infection, a known trigger of GBS, prior to her onset of GBS. Id. at 27. He then addressed petitioner’s reliance on the temporal relationship between the vaccine and onset of GBS, noting that petitioner’s treaters referring to that relationship carries little weight without any basis for ascribing causation. Id.

V. Standards for Adjudication

A. Severity Requirement The Vaccine Act requires a petitioner show by preponderant evidence that they “suffered the residual effects or complications of such illness, disability, injury, or condition for more than 6 months after the administration of the vaccine.” § 11(c)(1)(D)(i); see Song v. Sec'y of Health & Human Servs., 31 Fed. Cl. 61, 65-66 (1994), aff'd, 41 F.3d 1520 (Fed. Cir. 2014) (noting that a petitioner must demonstrate the six-month severity requirement by a preponderance of the evidence). A petitioner must offer evidence that leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence.” Moberly ex rel. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010) (citations omitted). Finding that a petitioner has met the severity requirement cannot be based on petitioner’s word alone, though a special master need not base their finding on medical records. See § 13(a)(1); see Colon v. Sec’y of Health & Human Servs., 156 Fed. Cl. 534, 541 (2021).

B. Legal Standard Regarding Causation The Vaccine Act provides two avenues for petitioners to establish causation. First, a petitioner may demonstrate a “Table” injury—i.e., an injury listed on the Vaccine Injury Table that occurred within the provided time period. 42 U.S.C. § 300aa-11(c)(1)(C)(i). “In such a case, causation is presumed.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed on the Vaccine Injury Table, a petitioner may demonstrate an “off-Table” injury, which requires that the petitioner “prove by a preponderance of the evidence that the vaccine at issue caused the injury.” Capizzano, 440 F.3d at 1320; see § 11(c)(1)(C)(ii); see also Wright v. Sec’y of Health & Human Servs., 22 F.4th 999, 1006 (Fed. Cir. 2022) (defining the term “residual effects” in the Act, as “detrimental conditions within the patient, such as lingering or recurring signs and symptoms” of the alleged vaccine injury, which are compensable). A petitioner need not show that the vaccination was the sole cause, or even the predominant cause, of the alleged injury; showing that the vaccination was a “substantial factor” and a “but for” cause of the injury is sufficient for recovery. Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006); Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999). Petitioners are not required “to eliminate alternative causes as part of establishing [their] prima facie case.” Doe v. Sec’y of Health & Human Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); see Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1152 (Fed. Cir. 2007) (holding that a “petitioner does not bear the burden of eliminating alternative independent potential causes”). Once a petitioner has proven causation by preponderant evidence, “the burden then shifts to the respondent to show by a preponderance of the evidence that the injury is due to factors unrelated to the administration of the vaccine.” Deribeaux ex rel. Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013) (citing 42 U.S.C. § 300aa-13(a)(1)(B)).

To prove causation in an off-Table case, a petitioner must satisfy the three-pronged test established in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen requires that a petitioner show by preponderant evidence that a vaccination they received caused their injury “by providing: (1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.” Id. at 1278. Together, these prongs must show “that the vaccine was ‘not only a but-for cause of the injury but also a substantial factor in bringing about the injury.’” Stone v. Sec’y of Health & Human Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (quoting Shyface, 165 F.3d at 1352-53). Causation is determined on a case-by-case basis, with “no hard and fast per se scientific or medical rules.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Petitioners are not required to identify “specific biological mechanisms” to establish causation, nor are they required to present “epidemiologic studies, rechallenge, the presence of pathological markers or genetic disposition, or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280). “[C]lose calls regarding causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.

Each Althen prong requires a different showing. Under the first prong, a petitioner must provide a “reputable medical theory” demonstrating that the vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citation omitted). To satisfy this prong, a petitioner’s “theory of causation must be supported by a ‘reputable medical or scientific explanation.’” Andreu, 569 F.3d at 1379 (quoting Althen, 418 F.3d at 1278). This theory need only be “legally probable, not medically or scientifically certain.” Id. at 1380 (emphasis omitted) (quoting Knudsen, 35 F.3d at 548). Nevertheless, “petitioners [must] proffer trustworthy testimony from experts who can find support for their theories in medical literature.” LaLonde, 746 F.3d at 1341.

The second Althen prong requires proof of a “logical sequence of cause and effect.” Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). Even if the vaccination can cause the injury, a petitioner must show “that it did so in [this] particular case.” Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted). “A reputable medical or scientific explanation must support this logical sequence of cause and effect,” Id. at 961 (citation omitted), and “treating physicians are likely to be in the best position to determine whether a logical sequence of cause and effect show[s] that the vaccination was the reason for the injury,” Paluck v. Sec’y of Health & Human Servs., 786 F.3d 1373, 1385 (Fed. Cir. 2015) (quoting Andreu, 569 F.3d at 1375).

The third Althen prong requires that a petitioner establish a “proximate temporal relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This “requires preponderant proof that the onset of symptoms occurred within a timeframe for which, given the medical understanding of the disorder’s etiology, it is medically acceptable to infer causation-in-fact.” De Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due to the fact that onset was too late after the administration of a vaccine for the vaccine to be the cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the temporal relationship is not such that it is medically acceptable to conclude that the vaccination and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Human Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered, logically, the vaccine could not have caused the illness.”).

A. Legal Standard Regarding Fact Finding

The process for making factual determinations in Vaccine Program cases begins with analyzing the medical records, which are required to be filed with the petition. § 11(c)(2). Medical records created contemporaneously with the events they describe are presumed to be accurate and “complete” such that they present all relevant information on a patient’s health problems. Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). In making contemporaneous reports, “accuracy has an extra premium” given that the “proper treatment hang[s] in the balance.” Id. Contemporaneous medical records that are clear, consistent, and complete warrant substantial weight “as trustworthy evidence.” Id. Indeed, “where later testimony conflicts with earlier contemporaneous documents, courts generally give the contemporaneous documentation more weight.” Campbell ex rel. Campbell v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006); see United States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1948). But petitioners can support their claim with oral testimony if it is credible and consistent with the medical records. See, e.g., Stevenson ex rel. Stevenson v. Sec’y of Health & Hum. Servs., No. 90- 2127V, 1994 WL 808592, at *7 (Fed. Cl. Spec. Mstr. June 27, 1994) (crediting the testimony of a fact witness whose “memory was sound” and “recollections were consistent with the other factual evidence”). In short, “the record as a whole” must be considered. § 13(a).

B. Evaluating Expert Testimony

Establishing a sound and reliable medical theory connecting the vaccine to the injury often requires a petitioner to present expert testimony in support of his or her claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). The Supreme Court’s opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), requires that courts determine the reliability of an expert opinion before it may be considered as evidence. “In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’ establishes a standard of evidentiary reliability.” Id. at 590 (citation omitted). Thus, for Vaccine Act claims, a “special master is entitled to require some indicia of reliability to support the assertion of the expert witness.” Moberly ex rel. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1324 (Fed. Cir. 2010). The Daubert factors are used in weighing the reliability of scientific evidence proffered. Davis v. Sec’y of Health & Hum. Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of expert testimony already admitted”). Where both sides offer expert testimony, a special master’s decision may be “based on the credibility of the experts and the relative persuasiveness of their competing theories.” Broekelschen, 618 F.3d at 1347 (citing Lampe, 219 F.3d at 1362). And nothing requires the acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too great an analytical gap between the data and the opinion proffered.” Snyder ex rel. Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)).

C. Consideration of Medical Literature

Finally, although this decision discusses some but not all of the literature in detail, the undersigned reviewed and considered all of the medical records and literature submitted in this matter. See Moriarty ex rel. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record evidence even though [s]he does not explicitly reference such evidence in h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master is ‘not required to discuss every piece of evidence or testimony in her decision.’”) (citation omitted), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

VI. Discussion

A. Severity Requirement As a threshold matter, respondent argued that petitioner had not satisfied the six-month severity requirement of the Act based on Dr. Jamieson’s opinion that petitioner’s GBS symptoms resolved in less than 6 months and her ongoing complaints were associated with her other co- morbidities including diabetes and COPD. Response at 29; Resp. Ex. A at 8, 11-12; Resp. Ex. K at 2. Dr. Steinman did not address this issue.

Regardless, the medical records sufficiently establish that petitioner suffered the residual effects of her GBS beyond 6 months. The record for her May 3, 2016 neurology follow-up includes ongoing complaints, prompting the neurologist to note that she may continue to improve up to 2 years after GBS. Pet. Ex. 4 at 3-4. Furthermore, the PCP record on January 31, 2018, includes that her neuropathy from GBS was well-controlled with gabapentin, and she was to continue taking the medication. Pet. Ex. 7 at 4, 8.

Based on the medical records, petitioner has satisfied the six-month severity requirement by preponderant evidence. § 11(c)(1)(D)(i).

B. The Althen Prongs Because petitioner does not allege an injury listed on the Vaccine Injury Table, the claim is classified as “off-Table.” As noted above, to prevail in an “off-Table” claim, petitioner must prove by preponderant evidence that she suffered an injury and that this injury was caused by the vaccination at issue and manifested within a medically reasonable timeframe. See Capizzano, 440 F.3d at 1320.

Notably, at this juncture, dozens of Prevnar 13 / GBS cases have been decided with different special masters reaching different conclusions based on the evidence before them. The results in any vaccine case depend on the facts presented in that specific case and the weight afforded to the experts’ theories and opinions. A theory in one case may be insufficient because it is not well developed, even if that same theory submitted by the same expert was determined to be sound and reliable in a different case where it was more developed and better articulated. Moreover, a theory may be sound and reliable in one case but unpersuasive in another because the proffered theory was effectively rebutted by other evidence in the record. De Bazan, 539 F.3d at 1353 (“The government, like any defendant, is permitted to offer evidence to demonstrate the inadequacy of the petitioner’s evidence on a requisite element of the petitioner’s casein-chief (sic).”).

The undersigned takes notice of the conclusions reached by the other special masters but is not bound by them. See, e.g., Boatmon v. Sec'y of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); Gamboa-Avila v. Sec’y of Health & Human Servs., 170 Fed. Cl. 441 (2024) (“Dissimilar circumstances justify disparate outcomes.”), aff'd, 166 F.4th 1318 (Fed. Cir. 2026). This matter must be decided on the evidence filed herein and the facts of this particular case–not on the findings or facts from any other Prevnar 13 / GBS case.

All three Althen Prongs are in dispute. Based on the facts and circumstances of this case, specifically that preponderant evidence shows that petitioner suffered from community-acquired pneumonia from which she was “critically ill” two weeks prior to the onset of her GBS and prior to her receipt of the subject vaccination, the analysis turns largely on Prong 2. Because of the combination of weak evidence submitted to satisfy Prong 1 with evidence of a known cause of GBS prior to the onset of petitioner’s symptoms, the undersigned finds that the vaccine was not a more likely than not cause of petitioner’s GBS.

i. Althen Prong 1 The first Althen prong requires petitioner to provide a “reputable medical theory” demonstrating that the vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citation omitted). To satisfy this prong, petitioner’s “theory of causation must be supported by a ‘reputable medical or scientific explanation.’” Andreu, 569 F.3d at 1379 (quoting Althen, 418 F.3d at 1278). This theory need only be “legally probable, not medically or scientifically certain.” Id. at 1380 (emphasis omitted) (quoting Knudsen, 35 F.3d at 548).

Dr. Steinman proposed that the Prevnar 13 vaccination can cause GBS by molecular mimicry. Pet. Ex. 8 at 6; Pet. Ex. 33 at 7; Pet. Ex. 12. He identified two relevant mimics in the Prevnar 13 vaccine: 1) the phospholipid composition of the pneumococcal polysaccharide antigen mimics phospholipids found on myelin sheath in humans and 2) the CRM protein conjugate mimics contactin-1 present on the peripheral nerves of humans. Pet. Ex. 8 at 8, 19; Pet. Ex. 33 at 8, 24; Pet. Ex. 59 at 2. Dr. Steinman directed the Court’s attention to two cases that were decided in favor of petitioners in which he was the expert and offered the same theories and literature as in this case. Pet. Ex. 66 at 2. Notably, neither of those cases involved Drs. Fujinami nor Jamieson as respondent’s experts.

The experts in this case agreed that infectious illnesses often precede GBS. Pet. Ex. 8 at 18, 19; Pet. Ex. 33 at 23-24; Pet. Ex. 38 at 2-3; Pet. Ex. 54 at 1-2; Pet. Ex. 55 at 4-5; Pet. Ex. 66 at 2-3. Resp. Ex. A at 9; Resp. Ex. E at 2-3; Resp. Ex. H at 1-2; Resp. Ex. J at 1. Further, respondent’s experts did not dispute molecular mimicry as a theory or that molecular mimicry can cause disease and specifically GBS. 24 Instead, respondent’s experts disputed that Prevnar 13 vaccine can cause GBS via molecular mimicry or any other mechanism. Resp. Ex. C at 1; Resp. Ex. L at 2.

Dr. Fujinami countered Dr. Steinman’s argument that phospholipids are relevant to GBS because antiphospholipid antibodies are present in GBS patients, submitting that the literature petitioner relied on shows antiphospholipid antibodies are a result of myelin damage—not the cause of it. Resp. Ex. C at 3; Resp. Ex. L at 2-3; Pet. Ex. 14; Pet. Ex. 15; Pet. Ex. 16; Pet. Ex. 18. If antiphospholipid antibodies are pathogenic, one would expect to see both central and peripheral nervous system demyelination because phospholipids are present in both; but GBS is a disease of only the peripheral nervous system. Resp. Ex. C at 3, 5; Resp. Ex. F at 3; Resp. Ex. L at 1. Further, contactin-1 is not a known disease inducing site in GBS. Resp. Ex. L at 5.

As set forth above, many decisions have issued regarding whether a sound and reliable theory for Prong 1 has been provided for Prevnar 13 vaccine causing GBS. It is worth noting that many of the decisions in favor of petitioners involved more developed theories than what was submitted here. In this case, the basis of Dr. Steinman’s theory was that the presence of antiphospholipid antibodies suggests that phospholipids are targeted in GBS, while the literature he relied on did not directly support that conclusion. Pet. Ex. 14 at 3 (“autoantibodies [to phospholipids] are probably produced as a result of the myelin damage rather than cause the demyelination.”); see also Pet. Ex. 15 at 3 (“It is not established, however, whether apart from gangliosides other lipid antigens are also recognized as targets for antibodies in GBS.”); Pet. Ex. 16 at 2 (“Autoimmune responses directed against phospholipids and gangliosides contribute to the pathogenesis in systemic lupus erythematosus and Guillain-Barre syndrome, respectively.”) (emphasis added). He also asserted, seemingly without any basis, that contactin-1 is a “known target” in GBS. Pet. Ex. 8 at 19; Pet. Ex. 21 (discussing autoantibodies to contactin-1 in the context of chronic inflammatory demyelinating polyradiculoneuropathy—not GBS—but noting pathogenicity has not been proven); Pet. Ex. 22 at 6-7 (discussing anti contactin-1 IgG4 antibodies as “significantly associated with CIDP” and noting the presence of this biomarker may be useful in differentiating acute-onset CIDP from GBS); Moberly, 592 F.3d at 1324 (“[T]he special master is entitled to require some indicia of reliability to support the assertion of the expert witness.”). Without making an express finding as to Prong 1 in this case because of the findings under Prong 2, the undersigned notes that petitioner’s theory here was not very well developed and did not sufficiently address the rebuttals of respondent’s experts.

ii. Althen Prong 2 To satisfy the second prong of Althen, a petitioner must establish a “logical sequence of cause and effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. The sequence of cause and effect need only be “logical and legally probable, not medically or scientifically certain.” Knudsen, 35 F.3d at 548-49; accord Capizzano, 440 F.3d at 1326. In other words, even if the vaccination can cause the injury alleged, petitioner must show “that it did so in [this] particular case.” Hodges, 9 F.3d at 962 n.4 (citation omitted).

Under Prong 2, a petitioner need not eliminate other potential causes in order to be entitled to compensation. Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1149-52 (Fed. Cir. 2007). Nevertheless, “evidence of other possible sources of injury” in an off-Table claim can be relevant in determining “whether a prima facie showing has been made that the vaccine was a substantial factor in causing the injury in question.” Stone, 676 F.3d at 1379; Godfrey v. Sec’y of Health & Human Servs., 178 Fed. Cl. 220, 225 (2025). In other words, petitioner here does not need to disprove having suffered an infection prior to the onset of her GBS, nor must she prove that the Prevnar 13 vaccination was the only cause of her GBS; rather, to be entitled to compensation, petitioner must provide preponderant evidence that the Prevnar 13 vaccine was a substantial factor in her development of GBS, but the presence of other possible causal agents may be considered in reaching that determination. Winkler v. Sec’y of Health & Human Servs., 88 F.4th 958, 962 (Fed. Cir. 2023).

Dr. Steinman argued on one hand that the Prevnar 13 vaccine could cause and did cause petitioner’s GBS because there was no alternative explanation, such as an infection, for her symptoms. On the other hand, Dr. Steinman conceded that petitioner suffered an infection but submitted that he did not consider it causal because the specific pathogen was not identified. Pet. Ex. 8 at 18, 19; Pet. Ex. 31; Pet. Ex. 33 at 23-24; Pet. Ex. 38 at 2-3; Pet. Ex. 54 at 1-2; Pet. Ex. 55 at 4-5; Pet. Ex. 66 at 2-3. These arguments are contradictory, and neither argument—considered alone nor in combination—is persuasive.

As briefly discussed under Prong 1, the experts agreed that infections are associated with GBS. Pet. Ex. 8 at 18, 19; Resp. Ex. A at 9; Resp. Ex. E at 2-3; Resp. Ex. H at 1-2. The most common infections linked with the development of GBS are c. jejuni, EBV, and CMV. Pet. Ex. 8 at 18; Pet. Ex. 31; Resp. Ex. A at 9. Dr. Fujinami cited Hao, which studied fourteen infectious pathogens and found that 53% of GBS patients had a positive serologic test for recent infection with c. jejuni, EBV, CMV, influenza A & B, dengue virus, and mycoplasma pneumoniae. Resp. Ex. H at 2; Resp. Ex. H Tab 2.

Furthermore, the literature filed herein shows, and Dr. Steinman specifically notes, that mycoplasma pneumoniae has been identified as a precipitant of GBS. Pet. Ex. 8 at 18; Resp. Ex. A at 9; Pet. Ex. 31 at 1 (“Based on this evidence, infections with the gram negative enteropathogen Campylobacter jejuni, cytomegalovirus (CMV), Epstein-Barr virus, and Mycoplasma pneumoniae are precipitants of GBS…”); Resp. Ex. A Tab 6 at 1 (“Many infections have been associated with GBS, including . . . Mycoplasma pneumoniae…”); Resp. Ex. A Tab 7 at 1-2 (“Earlier studies have identified infections as a potential trigger in two-thirds of cases with . . . respiratory infections caused by Haemophilus influenzae, Mycoplasma pneumoniae, cytomegalovirus, influenza virus and enteroviruses being the most notable”); Resp. Ex. A Tab 8 at 2 (“Other pathogens that cause antecedent infections related to GBS are cytomegalovirus, Epstein–Barr virus, Mycoplasma pneumonia, Haemophilus influenzae, and influenza A virus.”).

Dr. Steinman conceded that “it can be argued that the respiratory infection with an unknown microbody could be a factor in the development of [petitioner’s] GBS,” given that most GBS cases are preceded by a respiratory or gastrointestinal infection. However, he placed less value on the infection here as a potential cause of petitioner’s GBS because the microbe involved was not identified. Pet. Ex. 54 at 1; Pet. Ex. 55 at 4.

Respondent argued that an infection need not be identified in order for it to have caused GBS. Resp. Ex. G at 1-2; Resp. Ex. H at 1; Resp. Ex. J at 1. Dr. Fujinami maintained that it is unnecessary to know a microbe’s identity to consider it a possible factor in the development of GBS. Resp. Ex. H at 1; Resp. Ex. J at 1. Respondent provided supportive literature that infections, even when unspecified, cause GBS. Donofrio found that “[a]pproximately 70% of [GBS] patients report a recent preceding upper or lower respiratory tract infection or gastrointestinal illness.” Resp. Ex. A Tab 6; see also Resp. Ex. A Tab 7 (Sipila & Soilu-Hanninen found in a study of 69 adult GBS patients that the “most common GBS triggers identified were respiratory tract infections . . . and gastroenteritis”). Lehmann noted that “[u]pper respiratory tract infection precedes GBS in many patients, but in most (around 60%) the infectious cause remains unidentified.” Resp. Ex. G Tab 1 at 3. Dr. Steinman acknowledged that two thirds of GBS patients report symptoms of upper respiratory tract or gastrointestinal tract infection 1-4 weeks prior to onset of GBS. Pet. Ex. 8 at 18; Pet. Ex. 33 at 23-24.

Despite Dr. Steinman’s contention, the caselaw supports that the presence of an infection is relevant to the determination of whether the subject vaccine was a substantial factor in petitioner’s development of GBS, even if the specific pathogen or microbe is not identified. De Bazan, 539 F.3d at 1353 (“The government, like any defendant, is permitted to offer evidence to demonstrate the inadequacy of the petitioner's evidence on a requisite element of the petitioner's case-in-chief.”); Pafford, 451 F.3d at 1358–59 (“[T]he presence of multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the vaccination...”); Stone, 676 F.3d at 1379–80 (“Indeed, in some cases a sensible assessment of causation cannot be made while ignoring the elephant in the room—the presence of compelling evidence of a different cause for the injury in question.”); K.A. v. Sec’y of Health & Human Servs., 164 Fed. Cl. 98, 118 (2022); (quoting the special master’s decision that “[t]he vaccine does not deserve greater weight simply because it is ‘known’ whereas the precise nature of the infection is not.”); Winkler, 88 F.4th at 963; see also Knudsen, 35 F.3d at 549 (holding “that a ‘viral infection’ can be an alternative [cause] even if not identified by specific type.”); White v. Sec’y of Health & Human Servs., 168 Fed. Cl. 660 (2023).

The literature filed by both parties shows that the majority of GBS cases are attributed to a preceding infection, though the specific infection is often unknown or unspecified. Pet. Ex. 31; Resp. Ex. A Tab 6; Resp. Ex. A Tab 7; Resp. Ex. G Tab 1; Resp. Ex. H Tab 2. The medical records in this case clearly show that petitioner suffered an infection prior to the onset of her GBS symptoms. Pet. Ex. 1 at 5, 21, 29-30 (hospital admission in July of 2015, prior to receiving the subject vaccine, for chronic respiratory failure from COPD, congestive heart failure, and community acquired pneumonia seen on chest x-ray and CT angiography); Pet. Ex. 3 at 10, 13 (neurology consultation from August 8, 2015 documenting recent hospitalization for community acquired pneumonia and respiratory failure). The presence of an infection, as well as her treating providers noting a possible association between her GBS and her recent pneumonia, preponderates in favor of the infection—even if unidentified—as the most likely cause of petitioner’s GBS.

Moreover, there is evidence in the record that suggests petitioner had mycoplasma pneumoniae, a known cause of GBS, prior to the onset of her symptoms. Though she was not tested for mycoplasma pneumoniae during her first hospitalization but rather diagnosed with community acquired pneumonia, laboratory testing during her second hospitalization revealed IgG antibodies for mycoplasma pneumonia. Lab work performed on August 9, 2015 revealed elevated mycoplasma pneumonia IgG levels at 0.316 [reference range <0.100]. Associated codes included that mycoplasma pneumonia IgG was “Equivocal. Borderline antibody result” 25 but that she was negative for mycoplasma pneumonia IgM antibodies. Pet. Ex. 3 at 54. According to Mosby’s Manual of Diagnostic and Laboratory Tests, mycoplasma pneumoniae serum antibodies (IgG and IgM) are “supportive of Mycoplasma infection.” MOSBY’S MANUAL OF DIAGNOSTIC AND LABORATORY TESTS 153 (6th ed. 2018). Positive IgM results are associated with acute infection, while positive IgG results indicate previous immunologic exposure. Id. at 328.

Based on the foregoing, preponderant evidence supports that petitioner suffered from an infection, likely mycoplasma pneumonia, prior to developing GBS. Dr. Steinman refused to consider petitioner’s infection at all, despite conceding that infections most often precede GBS. He submitted that “petitioner did not have an infection with Campylobacter, EBV or CMV;” Mycoplasma pneumoniae is conspicuously missing from his statement. Pet. Ex. 33 at 24. Dr. Steinman further attempted to undermine the evidence in the record that petitioner had pneumonia, relying on a single entry from a physician who examined petitioner upon admission on July 15, 2015 and wrote “[p]ossible pneumonia, but a normal white count with no left shift argues against that.” Pet. Ex. 54 at 1; Pet. Ex. 1 at 16. In singling out this record, Dr. Steinman disregarded the remainder of the records from her hospitalization describing her evolving pneumonia diagnosis, clinical impressions from petitioner’s treaters, objective testing, and imaging. Pet. Ex. 1 at 5, 21- 22, 29-31, 100. Dr. Steinman’s failure to discuss the potential role that petitioner’s pneumonia played in her development of GBS rendered his opinion less persuasive overall.

To be clear, petitioner is not required to eliminate other potential causes to be entitled to compensation. However, it is reasonable to consider “evidence of other possible sources of injury”—here infection generally and mycoplasma pneumoniae specifically—in determining whether petitioner sustained her burden in proving that the vaccine was a substantial factor in causing her injury. Stone, 676 3d. at 1358-59; see Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1149-52 (Fed. Cir. 2007) (finding petitioner does not bear the burden of eliminating alternative independent potential causes).

Because there is preponderant evidence of a known cause of GBS in this case (infection), along with petitioner’s relatively weak evidence of a causation theory related to the Prevnar 13 vaccine, petitioner has failed to satisfy Althen Prong 2. Ultimately, she cannot sustain her burden in proving the Prevnar 13 vaccine was a substantial factor in the development of her GBS. Godfrey, 178 Fed. Cl. at 224, 225 (sustaining the special master’s finding that the petitioner failed to satisfy his prima facie case in the presence of “multiple potential causative agents,” as well as the treating physician statements and the experts’ opinions regarding the medical literature).

iii. Althen Prong 3 The third Althen Prong requiring an appropriate temporal relationship contains two parts. First, a petitioner must establish the “timeframe for which it is medically acceptable to infer causation” and second, she must demonstrate that the onset of the disease occurred in this period. Shapiro v. Secʼy of Health & Human Servs., 101 Fed. Cl. 532, 542-43 (2011), recons. denied after remand on other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x 952 (Fed. Cir. 2013). The explanation for what is a medically acceptable timeframe must coincide with the theory of how the relevant vaccine can cause an injury utilized to satisfy the first prong. Id. at 542; Koehn v. Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

Dr. Steinman relied on Schonberger to show onset of GBS in the two weeks following the Prevnar 13 vaccine to be a medically acceptable timeframe to infer causation. Pet. Ex. 8 at 17, 19; Pet. Ex. 30; Pet. Ex. 33 at 23, 25. Dr. Jamieson disagreed that Schonberger was applicable since it addressed the swine flu vaccine—not the Prevnar 13 vaccine—and maintained that Prevnar 13 has not been shown to cause GBS. Resp. Ex. A at 8.

As previously noted, many cases involving the Prevnar 13 vaccination have been decided both in favor and against petitioners. Those in favor have found onset between 12 and 22 days post-vaccination reasonable. See, e.g., Simeneta v. Sec’y of Health & Human Servs., No. 18-859V, 2024 WL 4881411, at *34-35 (Fed. Cl. Spec. Mstr. Oct. 31, 2024) (finding a GBS onset of 18 days after Prevnar 13 vaccination to be appropriate); Bartoszek v. Sec’y of Health & Human Servs., No. 17-1254V, 2024 WL 4263604, at *24-25 (Fed. Cl. Spec. Mstr. Aug. 27, 2024) (finding a GBS onset of 22 days, or approximately three weeks, post-Prevnar 13 vaccination to be medically acceptable); Sprenger v. Sec’y of Health & Human Servs., No. 18-279V, 2023 WL 8543435, at *22 (Fed. Cl. Spec. Mstr. Nov. 14, 2023) (finding a GBS onset of approximately two weeks after Prevnar 13 vaccination to be appropriate); Gross, 2022 WL 9669651, at *38-39 (Fed. Cl. Spec. Mstr. Sept. 22, 2022) (finding a GBS onset of 13 days after Prevnar 13 vaccination to be appropriate); Koller, 2021 WL 5027947, at *23 (finding a GBS onset of 12 days after Prevnar 13 vaccination to be “within the medically accepted timeframe consistent with [P]etitioner’s theory of molecular mimicry [and] that has been accepted in other Vaccine Program cases”); see also Barone v. Sec’y of Health & Human Servs., No. 11-707V, 2014 WL 6834557, at *13 (Fed. Cl. Spec. Mstr. Nov. 12, 2014) (“[S]pecial masters have never gone beyond a two-month (meaning eight week) interval in holding that a vaccination caused a demyelinating illness.”).

However, a temporal association alone is insufficient to prove causation. Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992) (“[A] proximate temporal association alone does not suffice to show a causal link between the vaccination and the injury.”). Without a theory as to how the Prevnar 13 vaccine can cause GBS, it is impossible to determine a reasonable timeframe for that to occur. Thus, petitioner has not satisfied Prong 3 in this case.

VII. Conclusion I sympathize with petitioner for all that she has endured, but my decision must be based on the evidence in the record and application of the law. For the reasons discussed above, I find that petitioner has failed to provide preponderant evidence that the Prevnar 13 vaccination played any role in her subsequent condition. The Clerk of Court shall enter judgment accordingly. 26

IT IS SO ORDERED. s/ Mindy Michaels Roth Mindy Michaels Roth Special Master

Appendix: Medical Literature

Exhibit Citation Pet. Ex. 11 National Institute of Neurological Disorders and Stroke, Guillain-

Barre Syndrome Fact Sheet, National Institute of Health.

Pet. Ex. 12 Lawrence Steinman, Autoimmune Disease, 269 Scientific

American 106 (1993).

Pet. Ex. 14 B. Gilburd et al., Autoantibodies to Phospholipids and Brain

Extract in Patients with the Guillain-Barre Syndrome: Cross- Reactive or Pathogenic?, 16 Autoimmunity 23 (2009).

Pet. Ex. 15 G. Nakos et al., Anti-phospholipid Antibodies in Serum from

Patients with Guillain-Barre Syndrome, 31 Intensive Care

Medicine 1401 (2005).

Pet. Ex. 16 Jennifer L. Kanter el al., Lipid Microarrays Identify Key

Mediators of Autoimmune Brain Inflammation, 12 Nature

Medicine 138 (2006).

Pet. Ex. 17 Peggy P. Ho et al., Identification of Naturally Occurring Fatty

Acids of the Myelin Sheath that Resolve Neuroinflammation, 4

Science Translational Medicine 137ra73 (2012).

Pet. Ex. 18 Denong Wang et al., Uncovering Cryptic Glycan Markers in

Multiple Sclerosis (MS) and Experimental Autoimmune Encephalomyelitis (EAE), 75 Drug Development Research 172 (2014).

Pet. Ex. 19 Yi-Ping Chuang et al., Impact of the glpQ2 Gene on Virulence in a

Streptococcus pneumoniae Serotype 19A Sequence Type 320

Strain, 83 Infection and Immunity 682 (2015).

Pet. Ex. 25 Anand M. Gautam et al., A Polyalanine Peptide with only Five

Native Myelin Basic Protein Residues Induces Autoimmune Encephalomyelitis, 176 J. Experimental Medicine 605 (1992).

Pet. Ex. 26 Anand M. Gautam et al., Minimum Structural Requirements for

Peptide Presentation by Major Histocompatibility Complex Class II Molecules: Implications in Induction of Autoimmunity, 91 Proceedings of the National Academy of Sciences USA 767 (1994).

Pet. Ex. 27 Anand M. Gautam et al., A Viral Peptide with Limited Homology to a Self Peptide can Induce Clinical Signs of Experimental Autoimmune Encephalomyelitis, 161 J. Immunology 60 (1998).

Pet. Ex. 28 Hung Fu Tseng et al., Pneumococcal Conjugate Vaccine Safety in

Elderly Adults, Open Forum Infectious Diseases (2018).

Pet. Ex. 29 Roger Baxter et al., Lack of Association of Guillain-Barre

Syndrome with Vaccinations, 57 Clinical Infectious Diseases 197 (2013).

Pet. Ex. 30 Lawrence B. Schonberger et al., Guillain-Barre Syndrome Resp. Ex. A Tab 3 Following Vaccination in the National Influenza Immunization

Program, United States, 1976-1977, 110 Am. J. Epidemiology

105 (1979).

Pet. Ex. 31 Hans-Peter Hartung, Infections and the Guillain-Barre Syndrome,

66 Neurology Neurosurgery & Psychiatry 277 (1999).

Pet. Ex. 35 Janoi Chang et al., Relevance of 0-acetyl and Phosphoglycerol

Groups for the Antigenicity of Streptococcus Pneumoniae Serotype 18C Capsular Polysaccharide, 30 Vaccine 7090 (2012).

Pet. Ex. 36 Czeslaw Lugowski & Harold J. Jennings, Structural

Determination of the Capsular Polysaccharide of Streptococcus pneumoniae Type 18C (56), 131 Carbohydrate Research 119 (1984).

Pet. Ex. 39 Stefan Brocke et al., Treatment of Experimental Encephalomyelitis with a Peptide Analogue of Myelin Basic Protein, 379 Nature 343 (1996).

Pet. Ex. 41 Stefanie Kuerten & Paul V. Lehmann, The Immune Pathogenesis of Experimental Autoimmune Encephalomyelitis: Lessons Learned for Multiple Sclerosis?, 31 J. Interferon & Cytokine Research 907 (2011).

Pet. Ex. 42 Rosetta Pedotti et al., An Unexpected Version of Horror

Autotoxicus: Anaphylactic Shock to a Self-Peptide, 2 Nature Immunology 216 (2001).

Pet. Ex. 43 Rosetta Pedotti et al., Severe Anaphylactic Reactions to Glutamic

Acid Decarboxylase (GAD) Self Peptides in NOD Mice that Spontaneously Develop Autoimmune Type I Diabetes Mellitus, 4 BMC Immunology 3 (2003).

Pet. Ex. 44 Ludwig Kappos et al., Induction of a Non-encephalitogenic Type 2

T Helper-cell Autoimmune Response in Multiple Sclerosis After Administration of an Altered Peptide Ligand in a Placebo- controlled, Randomized Phase II Trial, 6 Nature Medicine 1176 (2000).

Pet. Ex. 45 Stephanie C. Eisenbarth et al., Crucial Role for the Nalp3

Inflammasome in the Immunostimulatory Properties of Aluminium Adjuvants, 453 Nature 1122 (2008).

Pet. Ex. 46 Anna Sokolovska et al., Activation of Dendritic Cells and

Induction of CD4+ T cell Differentiation by Aluminum-containing Adjuvants, 25 Vaccine 4585 (2007).

Pet. Ex. 47 J.W. Mannhalter et al., Modulation of the human immune response by the non-toxic and non-pyrogenic adjuvant aluminium hydroxide: effect on antigen uptake and antigen presentation, 61 Clinical & Experimental Immunology 143 (1985).

Pet. Ex. 48 Hanfen Li et al., Aluminum Hydroxide Adjuvants Activate

Caspase-1 and Induce IL-1 β and IL-18 Release, 178 J.

Immunology 5271 (2007).

Pet. Ex. 49 Kishan K. Nyati et al., Correlation of Matrix Metalloproteinases-2 and -9 with Proinflammatory Cytokines in Guillain-Barre Syndrome, 88 J. Neuroscience Research 3540 (2010).

Pet. Ex. 50 Sebastian Lander & Guido Stoll, Interleukin-18 is Induced in

Acute Inflammatory Demyelinating Polyneuropathy, 114 J.

Neuroimmunology 253 (2001).

Pet. Ex. 51 Shuo Yu et al., Neutralizing Antibodies to IL-18 Ameliorate

Experimental Autoimmune Neuritis by CounterRegulation of Autoreactive Th1 Responses to Peripheral Myelin Antigen, 61 J. Neuropathology & Experimental Neurology 614 (2002).

Pet. Ex. 56 Hassan El Khatib et al., Case Report: Guillain-Barre Syndrome with Pneumococcus - A New Association in Pediatrics, 11

IDCases 36 (2018).

Pet. Ex. 57 Nidhi Ravishankar, Guillain-Barre Syndrome Following PCV Resp. Ex. A Tab 13 Vaccine, 4 J. Neurology & Neurosurgery (2017).

Pet. Ex. 58 Nobuhiro Yuki & Koichi Hirata, Fisher's Syndrome and Group A

Streptococcal Infection, 160 J. Neurological Sciences 64 (1998). Pet. Ex. 60 Elisar Barbar et al., Binding of Phenylphosphocholine-Carrier

Conjugates to the Combining Site of Antibodies Maintains a Conformation of the Hapten, 35 Biochemistry 2958 (1996).

Pet. Ex. 62 Steve Bryson et al., Structures of Preferred Human IgV Genes-

Based Protective Antibodies Identify How Conserved Residues Contact Diverse Antigens and Assign Source of Specificity to CDR3 Loop Variation, 196 J. Immunology 4723 (2016).

Pet. Ex. 63 Robert Root-Bernstein, Rethinking Molecular Mimicry in

Rheumatic Heart Disease and Autoimmune Myocarditis: Laminin, Collagen IV, CAR, and B1AR as Initial Targets of Disease, 2 Frontiers in Pediatrics 1 (2014).

Pet. Ex. 64 Raghavanpillai Raju et al., Epitopes for Human CD4+ Cells on

Diphtheria Toxin: Structural Features of Sequence Segments Forming Epitopes Recognized by Most Subjects, 25 European J. Immunology 3207 (1995).

Pet. Ex. 65 Penina Haber et al., Post-licensure Surveillance of 13-valent Resp. Ex. A Tab 10 Pneumococcal Conjugate Vaccine (PCV13) in Adults Aged ≥ 19 Resp. Ex. C Tab 1 Years Old in the United States, Vaccine Adverse Event Reporting

System (VAERS), June 1, 2012-December 31, 2015, 34 Vaccine

6330 (2016).

Pet. Ex. 67 Tobias V. Lanz et al., Clonally Expanded B Cells in Multiple

Sclerosis Bind EBV and GlialCAM, Nature 1 (2021).

Resp. Ex. A Tab 1 Hung Fu Tseng et al., Pneumococcal Conjugate Vaccine Safety in

Elderly Adults, Open Forum Infectious Diseases 1 (2018).

Resp. Ex. A Tab 2 Roger Baxter et al., Lack of Association of Guillain-Barré

Syndrome With Vaccinations, 57 Clinical Infectious Diseases 197 (2013).

Resp. Ex. A Tab 4 Hugh J Willison et al., Guillain-Barré Syndrome, 388 Lancet 717

(2016).

Resp. Ex. A Tab 6 Peter D. Donofrio, Guillain-Barre Syndrome, 23 Continuum 1295

(2017).

Resp. Ex. A Tab 8 Bianca van den Berg et al., Guillain–Barré Syndrome:

Pathogenesis, Diagnosis, Treatment and Prognosis, 10 National Reviews Neurology 469 (2014).

Resp. Ex. A Tab 14 Nidhi Ravishankar, Guillain-Barre Syndrome Following PCV

Vaccine, 2 Clinical Surgery 1413 (2017).

Resp. Ex. C Tab 2 Maryline Sicotte et al., Immunization with Myelin or Recombinant

Nogo-66/MAG in Alum Promotes Axon Regeneration and Sprouting After Corticospinal Tract Lesions in the Spinal Cord, 23 Molecular and Cellular Neuroscience 251 (2003).

Resp. Ex. C Tab 3 Maja Wållberg et al., Vaccination with Myelin Oligodendrocyte

Glycoprotein Adsorbed to Alum Effectively Protects DBA/1 Mice from Experimental Autoimmune Encephalomyelitis, 33 European J. Immunology 1539 (2003).

Resp. Ex. E Tab 1 Yong Chen et al., Vaccines and the Risk of Guillain-Barre

Syndrome, 35 European J. Epidemiology 363 (2020).

Resp. Ex. E Tab 2 Gianpaolo Toscano et al., Guillain-Barre Syndrome Associated with SARS-CoV-2, 26 New Eng. J. Med. 382 (2020).

Resp. Ex. E Tab 3 Silas Webb et al., Guillain-Barre Syndrome Following COVID-

19: A Newly Emerging Post-infectious Complication, 13 BMJ

Case Report e236182 (2020).

Resp. Ex. E Tab 4 Clemence Grave et al., Seasonal Influenza Vaccine and Guillain-

Barre Syndrome, 94 Neurology 2168 (2020).

Resp. Ex. E Tab 5 Marek Petras et al., Is an Increased Risk of Developing Guillain-

Barre Syndrome Associated with Seasonal Influenza Vaccination? A Systematic Review and Meta-Analysis, 8 Vaccines 150 (2020).

Resp. Ex. G Tab 1 Helmar C. Lehmann et al., Guillain-Barre Syndrome After

Exposure to Influenza Virus, 10 Lancet Infectious Diseases 643 (2010).

Resp. Ex. H Tab 2 Yanlei Hao et al., Antecedent Infections in Guillain-Barre

Syndrome: A Single-center, Prospective Study, 6 Annals of Clinical & Translational Neurology 2510 (2019).