Diagnosis and management strategies for an elderly patient with Neisseria meningitidis sepsis complicated by multiple organ dysfunction: A case report

Abstract

An 88-year-old male presented with sepsis and multi-organ dysfunction due to Neisseria meningitidis serogroup B (MenB) infection, a severe and often atypical presentation in the elderly. His condition, characterized by subtle symptoms, rapidly improved with early broad-spectrum antibiotics, susceptibility-guided therapy, and multidisciplinary care. The patient fully recovered and was discharged on day 8, highlighting the importance of prompt diagnosis and aggressive support in this vulnerable population.

Introduction

Neisseria meningitidis (Nm) is a Gram-negative diplococcus acknowledged as the primary etiologic agent of invasive meningococcal disease (IMD). Its polysaccharide capsule antigens enable classification into 12 serogroups, of which serogroups A, B, C, W, and Y are the most commonly associated with invasive infections globally. ¹

Of these serogroups, MenB (serogroup B) poses a distinct and substantial challenge to vaccine development. The MenB capsular polysaccharide, primarily composed of α(2→8)-N-acetylneuraminic acid polymers, shares structural homology with glycans found in the human central nervous system. This molecular mimicry can induce immune tolerance, leading to suboptimal efficacy of traditional polysaccharide vaccines in eliciting a robust and protective immune response. Consequently, the MenB capsular polysaccharide is deemed an inappropriate vaccine antigen. ² Due to a lack of effective prevention and control measures, MenB has now become the predominant circulating strain in developed countries like Europe and the United States. ³

In China, MenB infections have historically been relatively rare and sporadic. However, recent surveillance data reveal an upward trend, indicating a potential shift in the epidemiological landscape. ⁴ . For instance, confirmed cases have been reported in Jiangsu and Gansu provinces, and surveillance data from multiple regions in China indicate a year-on-year rise in the proportion of MenB strains.^5,6

While most individuals infected with Neisseria meningitidis undergo an asymptomatic carriage phase, the correlation between carriage rates and age is statistically significant, characterized by an initial rise followed by a subsequent decline. Specifically, reported carriage rates are 4.5% in infancy, peaking at 23.7% among 19-year-olds, and decreasing to 7.8% in adults aged 50 years. ⁷ Despite the comparatively lower incidence in elderly individuals, infections in this demographic often progress rapidly and severely, culminating in systemic inflammatory response syndrome (SIRS), sepsis, and multi-organ dysfunction—posing significant challenges in the clinical management of older patients.

This case study reports a rare instance of successful treatment for an 88-year-old patient who developed sepsis and multi-organ dysfunction following MenB infection. This case exemplifies an atypical presentation of MenB infection among elderly individuals in China, suggesting potential evolution in the epidemiological characteristics of bacterial strains amid population aging. Our objective is to offer actionable insights for improving the diagnosis, treatment, and management of infectious diseases—especially meningococcal infections—in the aging population.

Case

Patient presentation

An 88-year-old male patient presented to the emergency department of our hospital on the initial day of consultation with fever (peak temperature 38.9°C), chills and fatigue. His past medical history was unremarkable, except for an appendectomy performed 50 years ago and cataract surgery 4 years ago, with no other chronic conditions. Upon arrival at the emergency room (ER), he was assessed using the ABCDE approach (Table 1). He was admitted to the hospital approximately 24 hours later (designated as hospital day 1).

Table 1.

ABCDE at admission.

Component	Definition	Findings
A	Patency of the upper airway	Patent; no stridor, snoring, or obstruction observed
B	Respiratory effort, rate, and oxygenation	Respiratory rate 18 breaths/min (normal range 12–20); SpO₂ 95% on room air; no use of accessory muscles; clear lung fields on auscultation
C	Perfusion status and hemodynamic stability	BP 173/63 mmHg (isolated systolic hypertension); HR 79 beats/min (regular); warm, dry skin with normal capillary refill (<2 seconds); no signs of shock
D	Neurological function (consciousness, pupillary response)	Conscious but lethargic; Glasgow Coma Scale (GCS) 14 (E4, V4, M6); pupils equal and reactive to light (3mm bilaterally)
E	Environmental exposure or skin abnormalities	No evidence of hypothermia, frostbite, or chemical exposure; no rashes, petechiae, or ecchymosis noted on full-body inspection

A: Airway; B: Breathing; C: Circulation; D: Disability; E: Exposure.

Upon admission, vital signs and initial assessment were performed (detailed findings are presented in Table 1). On general inspection, he was conscious but lethargic. A skin examination revealed no rash, petechiae, ecchymosis, or other abnormalities. His chest contour was normal, with bilateral lung breath sounds coarse but no added adventitious sounds. Cardiac examination demonstrated a regular heart rate with no murmurs. Abdominal palpation revealed a soft abdomen without tenderness or rebound tenderness, and both the liver and spleen were non-palpable. Mild 1+ pitting edema was noted in bilateral lower extremities. Muscle strength and tone in all four limbs were normal, and meningeal irritation signs were negative.

Diagnostic Workup and Results: Upon admission, laboratory tests showed white blood cell count (WBC) 15.4 × 10⁹/L (normal range:4–10× 10⁹/L), neutrophil percentage 84.1% (normal range: 40%–75%), C-reactive protein (CRP) 25.4 mg/L (normal range: <8 mg/L), serum amyloid A (SAA) 64.0 mg/L (normal range: <10 mg/L), procalcitonin (PCT) 16.01 ng/mL (normal range: <0.1 ng/mL), D-dimer 4297 μg/L FEU (normal range: <500 μg/L FEU), creatinine kinase (CK) 3205 U/L (normal range: 24–195 U/L), B-type natriuretic peptide (NT-pro BNP) 708 pg/ml (normal range: <125 pg/ml), creatinine 185 μmol/L (normal range: 44–133 μmol/L). Head CT scan revealed scattered lacunar infarcts and some encephalomalacia in the bilateral semi-oval centers and periventricular regions, consistent with senile cerebral changes and periventricular leukoaraiosis. Small amounts of bilateral frontal subdural effusion were suspected (Figure 1). Crucially, the scan showed no mass effect, hydrocephalus, or signs of acute meningeal enhancement. Abdominal CT scan showed bilateral renal calculi; a slightly low-density lesion in the right kidney; minimal perirenal exudation bilaterally. The gallbladder was full, and the common bile duct was mildly dilated with uneven density in the lower segment. Multiple enlarged lymph nodes were observed in the porta hepatis, retroperitoneum, mesenteric region, and along the bilateral iliac vessels. A small amount of mesenteric panniculitis was noted in the left mid-abdomen. Chest CT scan showed evidence of bronchitis. Further chest imaging showed scattered chronic inflammatory infiltrates and fibrotic lesions in both lungs with a tracheal mucous plug, cardiomegaly (enlarged cardiac silhouette), and multiple small mediastinal lymph nodes. Echocardiography showed structural abnormalities (enlarged left atrium, thickened interventricular septum, and dilated aorta), valvular changes (localized calcification of the aortic valve with mild regurgitation and mitral annulus calcification), and functional impairments (mild mitral and tricuspid regurgitation, impaired left ventricular diastolic function, and an ejection fraction of 0.62 [62%]), all consistent with senile degenerative cardiac changes. Collectively, the initial laboratory and imaging findings were consistent with Multiple Organ Dysfunction Syndrome (MODS) secondary to severe sepsis, primarily involving the cardiovascular system (sepsis-induced cardiomyopathy and diastolic dysfunction), musculoskeletal system (rhabdomyolysis, elevated CK), and coagulation system (disseminated intravascular coagulation, elevated D-dimer). Approximately two days following admission, blood cultures from two bottles suggested Gram-negative cocci infection, suspicious for Neisseria meningitidis. Two days later, blood culture and antimicrobial susceptibility testing results (as shown in Table 2) confirmed Neisseria meningitidis, sensitive to ceftriaxone but resistant to penicillin. Subsequently, the definitive serogrouping was performed: Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized, confirming the presence of the capsular biosynthesis gene siaD, which is specific to MenB.

Figure 1.

Head CT findings: Scattered lacunar infarcts and encephalomalacia in the bilateral centrum semiovale and periventricular regions (consistent with senile cerebral changes and periventricular leukoaraiosis), and suspicious small subdural effusions in the bilateral frontal regions.

Table 2.

Antimicrobial susceptibility results of Neisseria meningitidis.

Antimicrobial Agent	Susceptibility	Result Value	Breakpoint S	Breakpoint R	Unit	Method
Ceftriaxone	S	34	34	34	mm	K-B
Meropenem	S	34	30	30	mm	K-B
Azithromycin	S	24	20	20	mm	K-B
Minocycline	S	32	26	26	mm	K-B
Ciprofloxacin	R	29	35	32	mm	K-B
Sulfamethoxazole-Trimethoprim	R	6	30	25	mm	K-B
Penicillin	R	0.5	0.06	0.5	µg/mL	MIC
Ampicillin	I	1	0.12	2	µg/mL	MIC

S: Susceptible (meets CLSI criteria); I: Intermediate; R: Resistant.

Breakpoints: For K-B method, values are interpreted based on CLSI M100 (2023).

Treatment and Management: Upon admission (Day 1), the patient’s infection source was unclear, and the SOFA score was greater than 2. Considering the patient’s age, clinical manifestations, blood count, PCT, and other results, empirical broad-spectrum anti-infective treatment with Cefoperazone-Sulbactam was initiated, alongside supportive therapies including low molecular weight heparin anticoagulation, amlodipine besylate for blood pressure control, and other treatments.

After 2 days of empirical therapy, the patient’s C-reactive protein (CRP) increased significantly to 58.6 mg/L, suggesting inadequate infection control. Concurrently, on Day 3, the blood culture returned positive for Gram-negative diplococci. Respiratory isolation was immediately implemented upon receiving the preliminary bacteriology report, and the antibiotic regimen was switched to targeted therapy with Ceftriaxone Sodium (2 g IV Q12h).

Rationale for Antibiotic Adjustments:

• Day 1–2 (Cefoperazone-Sulbactam): This served as the empirical regimen for undiagnosed sepsis. While it covers typical community-acquired pathogens, its activity against Neisseria meningitidis is limited. Given the patient’s persistently rising inflammatory markers (PCT/CRP), this treatment was deemed insufficient.

• Day 3 (Switch to Ceftriaxone): The therapeutic shift was primarily driven by three critical factors: (a) Pathogen Confirmation: Blood culture confirmed N. meningitidis serogroup B. (b) Susceptibility Profile: Antimicrobial Susceptibility Testing (AST) showed sensitivity to ceftriaxone but, significantly, resistance to penicillin. (c) CNS Coverage: Ceftriaxone offers superior Cerebrospinal Fluid (CSF) penetration, which was prioritized due to the risk of CNS involvement despite the omission of Lumbar Puncture (LP).

Maintenance (Ceftriaxone): Continuation of ceftriaxone was justified by the patient’s sustained clinical improvement (fever resolution, decreasing PCT/CRP) and ongoing AST confirmation of N. meningitidis sensitivity.

The regimen changes underscore the transition from empirical broad-spectrum coverage to pathogen-specific, precision therapy. Follow-up blood cultures on Day 6 were negative; on Day 8, follow-up PCT was 0.14 ng/mL, and CRP was 34 mg/L (inflammatory marker trends shown in Figure 2). The antibiotic course was completed, and the patient was discharged with marked clinical improvement on Day 8 of hospitalization.

Figure 2.

Combination of line charts showing the changing trends of procalcitonin (PCT) and C-reactive protein (CRP) concentrations over time.

Epidemiological history: The patient’s native place is Zhejiang Province. He is a retiree and had been living at home for a long period before the onset of illness, with his main activities confined to his home and the downstairs community. He reported no history of recent travel to risk areas or recent medical visits. His history of meningococcal vaccination was unknown.

On Hospital Day 5, an epidemiological investigation and pharyngeal swab sampling were conducted for the patient’s family members and close contacts. Pathogen results for the patient’s immediate family were negative, while his caretakers tested positive for Neisseria meningitidis serogroup B by PCR amplification of the siaD gene. The caretakers were asymptomatic and subsequently tested negative after 3 days of oral azithromycin, a finding that supports a household transmission source rather than community-acquired high-virulence strains.

Rationale for Omission of Lumbar Puncture (LP): The patient presented with fever (peak 38.9°C), fatigue, and lethargy, diagnosed with MenB sepsis complicated by MODS. Lumbar puncture (LP) was not performed due to a multidimensional clinical trade-off, balancing diagnostic value against procedural risks in an unstable, high-risk patient. The omission of LP was based on three key considerations. First, the patient’s advanced age (88 years) and multi-organ involvement made him acutely unstable (SOFA score >2), posing significant procedural risks, including coagulopathy/bleeding (heightened by age-related hypercoagulability and a markedly elevated D-dimer of 4297 μg/L FEU) and the risk of cerebral herniation due to occult intracranial hypertension. Second, the patient lacked classic meningitis symptoms (e.g. severe headache, vomiting, or negative meningeal irritation signs), which significantly reduced the immediate urgency for LP and favored systemic sepsis management. Third, LP was deemed unnecessary because robust definitive diagnostic evidence was provided by the positive blood culture (identified MenB on Day 3) and significantly elevated serum biomarkers (PCT 16.01 ng/mL, CRP 25.4 mg/L). This evidence, combined with the favorable response (organ function stabilized and inflammatory markers rapidly declined within 8 days) following targeted ceftriaxone therapy, formed a rational diagnostic pathway. While LP remains the gold standard for suspected bacterial meningitis, ¹ the unique combination of advanced age, MODS, and atypical presentation in this case meant the acute-phase risks of LP substantially outweighed its immediate benefits.

To contextualize the unique features and management challenges of the present case, we compared its key clinical, diagnostic, and epidemiological characteristics with previously reported elderly Neisseria meningitidis serogroup B (MenB) cases. This comparative analysis is summarized in Table 3.

Table 3.

Comparison between the present case and previously reported elderly MenB cases.

Item	Present case (88-year-old male)	Previously reported elderly MenB cases (references 3, 5, 6)
Patient demographics	88-year-old male, retired, no underlying diseases	Mostly >65 years old, some with chronic diseases (e.g. Gansu case in Reference 5 reported hypertension/diabetes)
Clinical presentation	Fever (38.9°C), fatigue, no classic meningeal irritation signs (e.g. neck stiffness, Kernig’s sign)	Common: High fever (39–40°C), headache, rash; but elderly often present atypically (e.g. confusion without fever/rash)
Affected organs	Lungs (bronchitis), heart (EF 0.62), kidneys (calculi)	Predominantly: Kidney (dysfunction), shock, meningitis (e.g. Reference 6 noted 3/5 elderly cases with meningitis)
Laboratory findings	PCT 16.01 ng/mL, CRP 25.4 mg/L	Similar: Elevated PCT/CRP (values vary by study, but consistently high in severe cases)
Imaging findings	Head CT: Lacunar infarcts; Chest CT: Bronchitis	Some cases reported meningitis-related imaging changes (e.g. meningeal enhancement on MRI/CT, Reference 3)
Antimicrobial susceptibility	Sensitive to ceftriaxone/meropenem, resistant to penicillin	Majority sensitive to third-generation cephalosporins (consistent with this case)
Treatment regimen	Ceftriaxone (final) + supportive care	Third-generation cephalosporins as primary therapy, some combined with vancomycin
Vaccination status	Unknown	Mostly unvaccinated (traditional vaccines have poor efficacy against MenB, Reference 3)
Epidemiological notes	Zhejiang, China; Household transmission (positive caretakers)	Mostly sporadic; higher vaccine coverage in Europe/USA versus China (Reference 5)

Discussion

This case exemplifies a MenB infection in an elderly patient, manifesting as sepsis and multi-organ dysfunction. It underscores the insidious nature and atypical presentations of MenB infections in this demographic—a critical observation given the high morbidity and mortality associated with delayed diagnosis in older adults. MenB initiates infection by adhering to and penetrating the nasopharyngeal mucosal barrier, a process mediated by virulence structures such as pili (for attachment) and polysaccharide capsules (for immune evasion). Upon mucosal invasion, MenB replicates and releases lipooligosaccharide (LOS), a key pathogen-associated molecular pattern (PAMP). LOS activates the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/NF-κB signaling axis, triggering a cascade of pro-inflammatory cytokines (e.g. TNF-α, IL-6, IL-1). This unregulated cytokine storm culminates in systemic inflammatory response syndrome (SIRS) and progresses to sepsis. ⁸ Notably, when bacterial load in the bloodstream exceeds 10³ CFU/mL, LOS synergizes with matrix metalloproteinase 9 (MMP-9)—an enzyme upregulated during sepsis—to degrade the cerebrovascular basement membrane (composed primarily of type IV collagen). This disruption of the blood-brain barrier (BBB) integrity facilitates LOS and inflammatory cell infiltration into the CNS, potentially leading to epidemic cerebrospinal meningitis. ⁹ In this patient, despite the absence of classic meningeal irritation signs (e.g. neck stiffness, Kernig’s sign), strikingly elevated PCT levels (>20 ng/mL) and prolonged activated partial thromboplastin time (APTT) collectively indicated a robust systemic inflammatory storm. These findings align with the concept of "occult sepsis" in the elderly, where atypical clinical features mask underlying life-threatening pathology.

Typically, MenB infection presents with acute onset of high fever (39-40°C), severe headache, vomiting, petechiae/ecchymosis on the skin and mucous membranes, and meningeal irritation signs (e.g. neck stiffness, Kernig’s sign). ¹⁰ However, in elderly patients, age-related immunosenescence—characterized by impaired humoral immunity, reduced neutrophil chemotaxis and complement activation efficiency, and a compromised nasopharyngeal mucosal barrier—often leads to rapid disease progression despite a low nasal carriage rate (<7.8%). ¹¹ The interplay of two key factors underlies the absence of classic meningeal irritation signs in this population: reduced pro-inflammatory cytokine release (due to blunted innate immune responses) and an elevated meningeal pain threshold. Notably, while this patient maintained an acceptable cardiac ejection fraction, underlying diastolic dysfunction predisposed them to sepsis-induced myocardial depression and subsequent heart failure. Elderly individuals, owing to weakened immune responses, frequently manifest atypical infections—such as mild headache, apathy, and delirium—rather than classic meningeal signs, which contributes to diagnostic delays.

Heightened Risk of Sepsis-Associated Complications: Shock and Acute Kidney Injury (AKI). Beyond atypical presentations, elderly patients are highly susceptible to rapid deterioration into septic shock and Acute Kidney Injury (AKI), the two most common life-threatening complications of severe sepsis. Septic Shock: The reduced physiological reserve, coupled with pre-existing conditions like isolated systolic hypertension, makes the elderly heart less resilient to the massive cytokine release and vasodilation characteristic of meningococcal sepsis. This patient’s underlying diastolic dysfunction further increased the risk of cardiogenic component to the shock, making aggressive fluid resuscitation a high-risk strategy.

Acute Kidney Injury (AKI): AKI is frequently a key component of Multiple Organ Dysfunction Syndrome (MODS) in this population, often exacerbated by pre-existing conditions (e.g. bilateral renal calculi ), diminished baseline renal function due to age, and susceptibility to hypoperfusion during sepsis. Early and aggressive intervention is crucial, as the severity of AKI directly correlates with increased mortality in elderly sepsis patients.

Therefore, this case underscores the importance of early neuroimaging (e.g. CT/MRI) in elderly patients with sepsis lacking typical meningeal signs, to detect potential brain involvement and facilitate timely intervention.

Regarding etiology, blood culture confirmed Neisseria meningitidis as the causative pathogen. Antimicrobial susceptibility testing (AST) revealed that the isolate was resistant to penicillin and ciprofloxacin, exhibited low susceptibility to sulfamethoxazole-trimethoprim, and remained highly sensitive to ceftriaxone and meropenem (azithromycin also fell within the sensitive range; see Table 2). This susceptibility profile is critical for guiding targeted antimicrobial therapy, with particular concern raised by the emerging trend of multidrug resistance. The penicillin resistance observed in this strain warrants closer attention to its microbiological underpinnings. Recent global surveillance data, including that from the World Health Organization (WHO) Western Pacific Region, indicate a rising prevalence of penicillin-resistant N. meningitidis (resistant isolates accounting for 12%–18%), with strains harboring the blaROB-1 β-lactamase gene being particularly prevalent. ¹² Mechanistically, resistance arises from two key pathways: structural alterations in penicillin-binding proteins (PBPs) (e.g. mutations in the penA gene) and upregulated expression of β-lactamase. ¹³ Empirical broad-spectrum antibiotic therapy initiated at admission, followed by de-escalation to ceftriaxone based on AST results, led to significant clinical improvement and clearance of bacteremia. This outcome underscores the dual importance of early broad-spectrum coverage to prevent clinical deterioration and timely, susceptibility-guided therapy to optimize outcomes. Additionally, given the high prevalence of renal impairment in elderly patients, antibiotic dosing requires dynamic assessment (e.g. monitoring creatinine clearance) and individualized adjustment to avoid toxicity while maintaining therapeutic efficacy.

From an epidemiological perspective, the traditional dominance of serogroup A Neisseria meningitidis in China is shifting toward serogroup B (MenB). Recent data highlight a concerning upward trend: MenB incidence has surged in regions like Jiangsu and Zhejiang, with a marked increase in infections among individuals aged ⩾35 years. This shift mirrors global patterns—for example, a 2018 U.S. study reported that over half of meningococcal cases in 16–20-year-olds were attributed to MenB. In China, a Zhejiang provincial study spanning 2011–2021 revealed that 53.33% of meningococcal cases were caused by MenB, with no serogroup A isolates detected in Zhejiang since 2011. ¹⁴ Notably, this case—one of the few reported MenB infections in Chinese patients aged >65—suggests potential spread of MenB to the elderly population. A critical barrier to prevention lies in the structural similarity between MenB capsular polysaccharide and human central nervous system N-acetylneuraminic acid polymers, which induces immune tolerance and renders traditional polysaccharide vaccines ineffective. While protein-based vaccines (e.g. Bexsero, Trumenba) have been integrated into immunization programs in Europe and North America and can induce protective antibody responses in individuals aged ⩾55 years, ¹⁵ their widespread adoption for the elderly in China remains limited. This discrepancy creates a significant prevention gap for this vulnerable demographic, underscoring the urgency of optimizing MenB vaccination strategies for older adults.

This study was a single-center case report with a limited sample size, and the generalizability of the conclusions requires caution. The absence of lumbar puncture (LP) may have overlooked direct evidence of central nervous system (CNS) involvement, despite the absence of classic meningeal signs. Antibiotic regimen adjustments were based on clinical experience and antimicrobial susceptibility testing, but serum drug concentrations were not monitored—particularly given the potential impact of renal function fluctuations on pharmacokinetics. Furthermore, epidemiological investigations were restricted to the caretakers (confirmed as an asymptomatic Neisseria meningitidis serogroup B carrier), without screening other potential sources of exposure (e.g. community transmission or additional household contacts), which may limit the comprehensiveness of the transmission route analysis.

Conclusion

In summary, Neisseria meningitidis serogroup B infection in the elderly population is characterized by rapid progression, atypical symptoms, and poor prognosis. Its pathogenesis involves a dual interplay of high bacterial virulence and host immunosenescence. Clinicians should be highly vigilant for invasive infections in elderly individuals that present with mild initial symptoms but rapid progression, emphasizing the importance of rapid pathogen identification, precise antimicrobial treatment, dynamic assessment of organ function, and early intervention strategies. Simultaneously, promoting the accessibility of protein vaccines in high-risk elderly populations is expected to lay the foundation for effective prevention and control of such infections in an aging society. At discharge (day 8), the patient remained afebrile with marked improvement in inflammatory markers (PCT 0.14 ng/mL, CRP 34 mg/L). Given the history of severe sepsis and multi-organ dysfunction (including pulmonary, cardiac, and renal involvement), a structured follow-up plan was recommended: (1) Outpatient re-evaluation within 1 week, including complete blood count (CBC), PCT, and CRP to monitor for residual inflammation or infection relapse; (2) Repeat head CT at 2 weeks to assess the evolution of baseline lacunar infarcts (scattered in the bilateral centrum semiovale and periventricular regions); and (3) Family education to daily monitor the patient’s mental status, body temperature, and urine output for early detection of potential delayed complications (e.g. renal impairment or recurrent shock).